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for invention","granted":true,"earliest_filing_date":"2013-09-27","grant_date":"2018-06-26","anticipated_term_date":"2033-09-27","discontinuation_date":"2022-08-01","has_disclaimer":false,"patent_status":"INACTIVE","publication_count":2,"has_spc":false,"has_grant_event":true,"has_entry_into_national_phase":false},"abstract":{"en":[{"text":"Provided herein are compositions and methods for treating or preventing infection.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"}]},"abstract_lang":["en"],"has_abstract":true,"claim":{"en":[{"text":"1. A method of treating an enterococcal infection in a subject with an enterococcal infection, the method comprising administering to the subject an effective amount of a compound of Formula III or a pharmaceutically acceptable salt thereof, wherein R 1 and R 2 are independently selected from ethyl or methyl, n is 1 or 2, R 3 and R 4 are both phenyl or substituted phenyl, wherein the substituent can be halo, hydroxyl, a lower alkyl or a substituted lower alkyl wherein the substituent can be halo, hydroxy, or lower alkoxy, and R 5 is hydrogen, a halogen, a lower alkyl from about 1 to 4 carbon atoms or a substituted alkyl wherein the substituent can be halo, hydroxy, or lower alkoxy.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"2. The method of claim 1 , wherein the enterococcal infection is a respiratory infection.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"3. The method of claim 1 , wherein the enterococcal infection is a gastrointestinal infection.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"4. The method of claim 1 , wherein the enterococcal infection is a skin infection.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"5. The method of claim 1 , wherein the enterococcal infection is an Enterococcus faecium infection.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"6. The method of claim 1 , wherein the enterococcal infection is a small colony variant bacterial infection.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"},{"text":"7. The method of claim 1 , wherein the compound is selected from the group consisting of clomiphene or a pharmaceutically acceptable salt thereof; tamoxifen or a pharmaceutically acceptable salt thereof; and 4-hydroxy tamoxifen or a pharmaceutically acceptable salt thereof.","lang":"en","source":"USPTO_FULLTEXT","data_format":"ORIGINAL"}]},"claim_lang":["en"],"has_claim":true,"description":{"en":{"text":"CROSS REFERENCE TO RELATED APPLICATIONS This application is a divisional of U.S. application Ser. No. 14/431,031, filed on Mar. 25, 2015, which is a U.S. national stage application under 35 U.S.C § 371 of PCT/US2013/062309, filed on Sep. 27, 2013, which claims the benefit of U.S. Provisional Application No. 61/706,492, filed on Sep. 27, 2012, all of which are incorporated by reference herein in their entirety. STATEMENT REGARDING FEDERALLY FUNDED RESEARCH This invention was made with government support under Grant Nos. 1R01AI1075033-03 and 5P50GM069663 awarded by the National Institutes of Health. The government has certain rights in this invention. BACKGROUND Infectious diseases affect the health of people and animals around the world, causing serious illness and death. Thus, an urgent need exists for treatments for infections. SUMMARY Provided herein is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound of Formula I wherein R represents hydrogen or hydroxyl and R 1 represents hydrogen, or R and R 1 taken together form a second bond between the carbon atoms bearing R and R 1 ; R 2 represents hydrogen or phenyl; n is zero or a positive whole integer of from 1 to 4; X represents CH 2 , CHOH, NH, C═O, CHNR 3 R 4 , where R 3 and R 4 independently are hydrogen or lower alkyl; and Z represents thienyl, pyridinyl, substituted pyridinyl, phenyl or substituted phenyl wherein the substituents on the substituted pyridinyl or substituted phenyl are selected from phenyl, pyridinyl, nitro, a halogen atom, such as chlorine, fluorine, bromine, or iodine, a straight or branched lower alkyl chain of from 1 to 4 carbon atoms, a lower alkoxy group of from 1 to 4 carbon atoms, amino, a mono or di(lower)alkylamino group, a saturated monocyclic heterocyclic group such as pyrrolidino, piperidino, morpholino, or N-(lower)alkylpiperazino, or a group having the structure —COOR 5 , —CR 6 R 7 COOR 5 , —CF 3 , CHF 2 , CH 2 F, or where R 5 is hydrogen or lower alkyl, and R 6 and R 7 independently are hydrogen or methyl or a pharmaceutically acceptable salt thereof. Further provided is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound of Formula III or a pharmaceutically acceptable salt thereof, wherein R 1 and R 2 are independently selected from ethyl or methyl, n 1 or 2, R 3 and R 4 are both phenyl or substituted phenyl, wherein the substituent can be halo (for example, fluoro-, chloro-, iodo- or bromo-), hydroxyl, a lower alkyl or a substituted lower alkyl wherein the substituent can be halo, hydroxy, or lower alkoxy, and R 5 is hydrogen, a halogen, a lower alkyl from about 1 to 4 carbon atoms or a substituted alkyl wherein the substituent can be halo, hydroxy, or lower alkoxy. Also provided is a method of treating or preventing infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound selected from the group consisting of: a compound of Formula V wherein R 1 is a lower alkyl group having from 1 to 4 carbon atoms being substituted with one or several halogen atoms, Z is hydrogen or a lower alkyl group having from 1 to 4 carbon atoms, m is 2 or 3 and X 2 is the ethylene imino group or the group having the formula: wherein R is hydrogen or a lower alkyl group having from 1 to 4 carbon atoms which can be substituted with a chlorine atom or a hydroxy group, and Z and m have the above-given meaning, a compound of Formula X wherein R represents a lower alkyl or a lower alkenyl group, a phenyl group which can be substituted by halogen, methyl or lower alkoxy groups, or a benzyl group which can be nuclear substituted by halogen, methyl or lower alkoxy groups, X represents —O—, —S—, —SO—, or —SO 2 —, n represents an integer from 1-4, and Aryl represents a phenyl group which can be substituted by lower alkoxy or lower alkylmercapto groups; a compound of Formula XII wherein R and R 6 are the same or different and are hydroxy, lower alkoxy, lower alkenoxy, dilower alkylamino lower alkoxy (dimethylaminoethoxy), acylamino lower alkoxy (acetylaminoethoxy), acyloxy lower alkoxy (pivaloyloxymethoxy), aryloxy, such as phenoxy, arloweralkoxy, such as benzyloxy, substituted aryloxy or substituted arloweralkoxy wherein the substitutent is methyl, halo or methoxy, amino, loweralkylamino, diloweralkylamino, hydroxyamino, arloweralkylamino such as benzylamino; R 1 is hydrogen, alkyl of from 1 to 20 carbon atoms which include branched and cyclic and unsaturated (such as allyl) alkyl groups, substituted loweralkyl wherein the substituent can be halo, hydroxy, lower alkoxy, aryloxy such as phenoxy, amino, diloweralkylamino, acylamino, such as acetamido and benzamido, arylamino, guanidino, imidazolyl, indolyl, mercapto, loweralkylthio, arylthio such as phenylthio, carboxy or carboxamido, carboloweralkoxy, aryl such as phenyl or naphthyl, substituted aryl such as phenyl wherein the substituent is lower alkyl, lower alkoxy or halo, arloweralkyl, arloweralkenyl, heteroarlower alkyl or heteroarlower alkenyl such as benzyl, styryl or indolyl ethyl, substituted arloweralkyl, substituted arloweralkenyl, substituted heteroarlower alkyl, or substituted heteroarlower alkenyl, wherein the substituent(s) is halo, dihalo, lower alkyl, hydroxy, lower alkoxy, amino, aminomethyl, acylamino (acetyl amino or benzoylamino) diloweralkylamino, loweralkylamino, carboxyl, haloloweralkyl, cyano or sulfonamido; arloweralkyl or heteroarloweralkyl substituted on the alkyl portion by amino or acylamino (acetylamino or benzoylamino); R 2 and R 7 are the same or different and are hydrogen or lower alkyl; R 3 is hydrogen, lower alkyl, phenyl lower alkyl, aminomethyl phenyl lower alkyl, hydroxy phenyl lower alkyl, hydroxy lower alkyl, acylamino lower alkyl (such as benzoylamino lower alkyl, acetylamino lower alkyl), amino lower alkyl, dimethylamino lower alkyl, halo lower alkyl, guanidino lower alkyl, imidazolyl lower alkyl, indolyllower alkyl, mercapto lower alkyl, lower alkyl thio lower alkyl; R 4 is hydrogen or lower alkyl; R 5 is hydrogen, lower alkyl, phenyl, phenyl lower alkyl, hydroxy phenyl lower alkyl, hydroxy lower alkyl, amino lower alkyl, guanidino lower alkyl, imidazolyl lower alkyl, indolyl lower alkyl, mercapto lower alkyl or lower alkyl thio lower alkyl; R 4 and R 5 can be connected together to form an alkylene bridge of from 2 to 4 carbon atoms, an alkylene bridge of from 2 to 3 carbon atoms and one sulfur atom, an alkylene bridge of from 3 to 4 carbon atoms containing a double bond or an alkylene bridge as above substituted with hydroxy, loweralkoxy, loweralkylor diloweralky; a compound of Formula XIII wherein R 1 is H, alkyl, acyl or silyl(alkyl) 3 ; R 2 is H and R 3 is OH, O-acyl, O-alkyl or O-silyl (alkyl) 3 or R 3 is H and R 2 is OH. O-acyl, O-alkyl or O-silyl (alkyl) 3 ; or R 2 and R 3 together represent O; or R 2 and R 3 together represent acetal or cyclic acetal. R 1 might also represent a substituted alkyl such as e.g. methoxy ethoxy methyl; a compound of Formula XIV wherein PY is 4- or 3- or 2-pyridinyl or 4- or 3- or 2-pyridinyl having one or two lower-alkyl substituents, R is hydrogen, lower-alkyl or lower-hydroxyalkyl, and Q is nitro, carbamyl, halo, amino, lower-alkylamino, di(lower-alkyl)amino, or NHAc where Ac is lower-alkanoyl or lower-carbalkoxy; a compound of Formula XV a compound of Formula XVI a compound of Formula XVIII a compound of Formula XIX a compound of Formula (XX) or a pharmaceutically acceptable salt thereof. Further provided is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound selected from the group consisting of: Didanosine, Norcyclobenzaprine, Niridazole, Ifosfamide, Cefalonium, Tamoxifen citrate, Butoconazole, Suloctidil, Clomiphene, Sulconazole, Miconazole, Mefloquine, Sulfinpyrazone, Terfenadine, Lisinopril, Econzaole, Clofazimine, Equilin, Felodipine, Dacarbazine, Furazolidone, Perhexiline maleate, Oxethazaine, Pimozide, Trifluoperazine, Ellipticine, Fluspirilen, Hexestrol, Dienestrol, Zidovudine, Metoprolol, Napelline, Methimazole, Amrinone, Iopanoic acid, R-Propanolol, Rimexolone and Pyrvinium pamoate, wherein the infection is a bacterial infection. Also provided is a method of removing or preventing biofilm formation on a surface, the method comprising administering to a biofilm containing surface or a surface susceptible to biofilm formation an effective amount of a compound selected from the group consisting of: a compound of Formula I wherein R represents hydrogen or hydroxyl and R 1 represents hydrogen, or R and R 1 taken together form a second bond between the carbon atoms bearing R and R 1 ; R 2 represents hydrogen or phenyl; n is zero or a positive whole integer of from 1 to 4; X represents CH 2 , CHOH, NH, C═O, CHNR 3 R 4 , where R 3 and R 4 independently are hydrogen or lower alkyl; and Z represents thienyl, pyridinyl, substituted pyridinyl, phenyl or substituted phenyl wherein the substituents on the substituted pyridinyl or substituted phenyl are selected from phenyl, pyridinyl, nitro, a halogen atom, such as chlorine, fluorine, bromine, or iodine, a straight or branched lower alkyl chain of from 1 to 4 carbon atoms, a lower alkoxy group of from 1 to 4 carbon atoms, amino, a mono or di(lower)alkylamino group, a saturated monocyclic heterocyclic group such as pyrrolidino, piperidino, morpholino, or N-(lower)alkylpiperazino, or a group having the structure —COOR 5 , —CR 6 R 7 COOR 5 , —CF 3 , CHF 2 , CH 2 F, or where R 5 is hydrogen or lower alkyl, and R 6 and R 7 independently are hydrogen or methyl or a pharmaceutically acceptable salt thereof. DESCRIPTION OF DRAWINGS FIG. 1 depicts the adenylate kinase (AK) assay described in the Examples. Bactericidal agents compromise bacterial cell integrity, releasing cellular adenylate kinase. Extracellular AK is measured by the addition of a commercial ToxiLight AK cocktail containing ADP and luciferase, resulting in luminescence. FIG. 2 shows AK assay development. (A) AK assay measures of E. coli lysed cell supernatants. E. coli DH5α cells (1×10 9 ) were heat inactivated by boiling and diluted, and the AK assay was used to measure adenylate kinase release. Background signal is also shown (mock-treated cells (right-hand column in FIG. 2A ). “*” indicates a significant difference between results for boiled and mock treatment (Student's t test; P≤0.05). (B) AK assay results for colistin-treated A. baumannii strain 98-37-09. Cells were treated with the indicated concentration of colistin, and AK was measured; MIC (4 μg ml −1 is indicated. “*” indicates a significant increase in signal compared to that for mock treatment (0 μg ml −1 ; Student's t test, P≤0.05). FIG. 3 shows AK assay measures of S. aureus strain RN4220 treatment with bacteriostatic and bactericidal antibiotics. Standard MIC testing determined the MIC of each antibiotic class (in parentheses). Graphed are the fold changes in AK signal of cells treated with 0.5× or 1.0× the MIC value (left hand column and right hand column, respectively) for each antibiotic, in comparison to untreated control cells; “*” indicates a significant change in signal as determined by Student's t test; P≤0.05 (compared to results for untreated cells). FIG. 4 shows AK assay measures of antibiotic-treated biofilms and small-colony variants. (A) Graphed are AK signals generated by static biofilm-associated cells following mock or antibiotic treatment: colistin ( P. aeruginosa ) or ciprofloxacin ( S. aureus and A. baumannii ). (B) Fold change of AK measures of S. aureus SCV UAMS-1112 cells following treatment with 1× and 10× ciprofloxacin, meropenem, and vancomycin, compared to results for mock treated cells. “*” indicates a significant change in signal in comparison to results for mock-treated cells (Student's t test, P≤0.05). FIG. 5 shows AK-based HTS development and screening. (A) Z′ factor assay results for Klebsiella pneumoniae . Three-hundred-eighty-four-well microtiter plates were seeded with K. pneumoniae , and alternating rows were mock treated (DMSO) or treated with 50 μM colistin. Following 3 h of incubation, AK release was measured and plotted. DMSO-treated well measures are shown at the bottom of FIG. 5A ; colistin-treated wells are shown at the top of FIG. 5A . (B) Prestwick library Klebsiella pneumoniae screening results. In total, 26 compounds were determined to result in a 3-fold increase in AK signal, in comparison to results for DMSO-treated cells. Included among this list were polymyxin, cephalosporins, aminoglycosides, fluoroquinolones, and detergents; the complete Prestwick screening results for K. pneumoniae and all other organisms screened are provided in Table 4. FIG. 6 shows antimicrobial properties of terfenadine and tamoxifen. (A) Fold changes in AK signal of terfenadine-treated (10×MIC) S. aureus strain UAMS-1 static biofilms and the SCV strain UAMS-1112, compared to those for mock (DMSO)-treated populations, are plotted. “*” indicates a significant increase in signal over that with mock-treated cells (Student's t test,P≤0.05). (B) Plotted are the percent survival of G. mellonella larvae at 48 h post- E. faecium inoculation. Groups of larvae (n=45) were treated at 2 h and 24 h with either PBS (mock), DMSO, 80 mg kg −1 tamoxifen, 160 mg kg −1 tamoxifen, or 20 mg kg −1 vancomycin. DETAILED DESCRIPTION Provided herein is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound selected from the group consisting of: a compound of Formula I wherein R represents hydrogen or hydroxyl and R 1 represents hydrogen, or R and R 1 taken together form a second bond between the carbon atoms bearing R and R 1 ; R 2 represents hydrogen or phenyl; n is zero or a positive whole integer of from 1 to 4; X represents CH 2 , CHOH, NH, C═O, CHNR 3 R 4 , where R 3 and R 4 independently are hydrogen or lower alkyl; and Z represents thienyl, pyridinyl, substituted pyridinyl, phenyl or substituted phenyl wherein the substituents on the substituted pyridinyl or substituted phenyl are selected from phenyl, pyridinyl, nitro, a halogen atom, such as chlorine, fluorine, bromine, or iodine, a straight or branched lower alkyl chain of from 1 to 4 carbon atoms, a lower alkoxy group of from 1 to 4 carbon atoms, amino, a mono or di(lower)alkylamino group, a saturated monocyclic heterocyclic group such as pyrrolidino, piperidino, morpholino, or N-(lower)alkylpiperazino, or a group having the structure —COOR 5 , —CR 6 R 7 COOR 5 , —CF 3 , CHF 2 , CH 2 F, or where R 5 is hydrogen or lower alkyl, and R 6 and R 7 independently are hydrogen or methyl. The substituents on the substituted phenyl may be attached at the ortho, meta or para positions of the phenyl ring. Compounds of Formula I include compounds of Formula II, wherein R represents hydrogen or hydroxyl and R 1 represents hydrogen, or R and R 1 taken together form a second bond between the carbon atoms bearing R and R 1 ; n is zero or a positive whole integer of from 1 to 4; Z represents thienyl, pyridinyl, substituted pyridinyl, phenyl or substituted phenyl wherein the substituents on the substituted pyridinyl or substituted phenyl are selected from phenyl, pyridinyl, nitro, a halogen atom, such as chlorine, fluorine, bromine, or iodine, a straight or branched lower alkyl chain of from 1 to 4 carbon atoms, a lower alkoxy group of from 1 to 4 carbon atoms, amino, a mono or di(lower)alkylamino group, a saturated monocyclic heterocyclic group such as pyrrolidino, piperidino, morpholino, or N-(lower)alkylpiperazino, or a group having the structure —COOR 5 , —CR 6 R 7 COOR 5 , —CF 3 , CHF 2 , CH 2 F, or where R 5 is hydrogen or lower alkyl, and R 6 and R 7 independently are hydrogen or methyl or a pharmaceutically acceptable salt thereof. Compounds of Formula I also include terfenadine and derivatives thereof, including, but not limited to the following compounds. The compounds are identified by structure, name and registry number. The registry number for each compound is also set forth in Table 6 as an additional identifier for each compound. Also provided is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound selected from the group consisting of: a compound of Formula III or a pharmaceutically acceptable salt thereof, wherein R 1 and R 2 are independently selected from ethyl or methyl, n 1 or 2, R 3 and R 4 are both phenyl or substituted phenyl, wherein the substituent can be halo (for example, fluoro-, chloro-, iodo- or bromo-), hydroxyl, a lower alkyl or a substituted lower alkyl wherein the substituent can be halo, hydroxy, or lower alkoxy, and R 5 is hydrogen, a halogen, a lower alkyl from about 1 to 4 carbon atoms or a substituted alkyl wherein the substituent can be halo, hydroxy, or lower alkoxy. Examples of the compounds of Formula III include, tamoxifen and derivatives thereof, including but not limited to tamoxifen (Formula IV), 4-hydroxy tamoxifen and clomiphene. In the methods provided herein, wherein a one or more compounds of Formula III are used to treat or prevent infection, the infection can be an infection, wherein the infection is not a fungal infection or a parasitic infection. Further provided herein is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound selected from the group consisting of: a compound of Formula V wherein R 1 is a lower alkyl group having from 1 to 4 carbon atoms being substituted with one or several halogen atoms, Z is hydrogen or a lower alkyl group having from 1 to 4 carbon atoms, m is 2 or 3 and X 2 is the ethylene imino group or the group having the formula: wherein R is hydrogen or a lower alkyl group having from 1 to 4 carbon atoms which may be substituted with a chlorine atom or a hydroxy group, and Z and m have the above-given meaning, or a pharmaceutically acceptable salt thereof. As used throughout, the term “lower alkyl group containing from 1 to 4 carbon atoms” means methyl, ethyl, n-propyl, isopropyl, n-butyl, isobutyl, tertiary butyl, and I-methylpropyl. The term “halogen” means chlorine, bromine, fluorine, and iodine. Included herein are compounds of formula IV that correspond to formula VI: wherein R 1 , X 2 and m have the same meaning as in Formula IV. Additional compounds of formula IV, include the compounds of formula VII: wherein R 2 is a β-chloroethyl or a γ-chloropropyl group, and R 3 is hydrogen, a methyl group or an ethyl group, optionally substituted in the β-position with a chlorine atom or a hydroxy group. Among the compounds of formula VII, are the compounds of formula VIII and IX. The compound of formula VIII is 3-(2-chloroethyl)-2-[(2-chloroethyl)amino]tetrahydro-2H-1,3,2-oxazaphosphorine 2-oxide or ifosfamide. Ifosfamide is also known as IFEX. Further provided herein is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound selected from the group consisting of: a compound of Formula X wherein R represents a lower alkyl or a lower alkenyl group, a phenyl group which can be substituted by halogen, methyl or lower alkoxy groups, or a benzyl group which can be nuclear substituted by halogen, methyl or lower alkoxy groups, X represents —O—, —S—, —SO—, or —SO 2 —, n represents an integer from 1-4, and Aryl represents a phenyl group which can be substituted by lower alkoxy or lower alkylmercapto groups; or a pharmaceutically acceptable salt thereof. With respect to Formula X, R represents a lower alkyl or a lower alkenyl group, a phenyl group which can be substituted by halogen, methyl or lower alkoxy groups, or a benzyl group which can be nuclear substituted by halogen, methyl or lower alkoxy groups, X represents —O—, —S—, —SO—, or —SO 2 —, n represents an integer from 1-4, and aryl represents a phenyl group which can be substituted by lower alkoxy or lower alkylmercapto groups. For example, —R—X—C n H 2n — can represent the following groups: methoxy-, ethoxy-, propoxy-, isopropoxy-, butoxy-, isobutoxy-, allyloxy-, crotyloxy-, phenoxy-, o, -m- and p-methylphenoxy-, o,p-dimethylphenoxy-, m, p-dimethylphenoxy-, p-chlorophenoxy-, p-bromophenoxy-, -o, m and p-methoxyphenoxy-, p-ethoxyphenoxy-, benzyloxy-, o-, m-, and p-methylbenzyloxy-, p-chlorobenzyloxy-, p-bromobenzyloxy, o, m and p-methoxybenzyloxyand-, p-ethoxybenzyloxy-; methyl, -ethyl, -propyl, -isopropyl, and butyl radicals and analogous radicals with SO or SO 2 instead of O as divalent group X. Besides the phenyl group, aryl can be, for example, the o- or p-methylmercaptophenyl group, the o- or p-ethyl mercaptophenyl group, the o-; m-, or p-methoxyphenyl group or the o-, m- or p-ethoxyphenyl group. An example of the compound of formula X is set forth herein as formula XI. The compound of formula X is sulfinapyrazone. Sulfinapyrazone is also known as Anturane. Also provided herein is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound selected from the group consisting of: a compound of Formula XII wherein R and R 6 are the same or different and are hydroxy, lower alkoxy, lower alkenoxy, dilower alkylamino lower alkoxy (dimethylaminoethoxy), acylamino lower alkoxy (acetylaminoethoxy), acyloxy lower alkoxy (pivaloyloxymethoxy), aryloxy, such as phenoxy, arloweralkoxy, such as benzyloxy, substituted ayloxy or substituted arloweralkoxy wherein the substitutent is methyl, halo or methoxy, amino, loweralkylamino, diloweralkylamino, hydroxyamino, arloweralkylamino such as benzylamino; R 1 is hydrogen, alkyl of from 1 to 20 carbon atoms which include branched and cyclic and unsaturated (such as allyl) alkyl groups, substituted loweralkyl wherein the substituent can be halo, hydroxy, lower alkoxy, aryloxy such as phenoxy, amino, diloweralkylamino, acylamino, such as acetamido and benzamido, arylamino, guanidino, imidazolyl, indolyl, mercapto, loweralkylthio, arylthio such as phenylthio, carboxy or carboxamido, carboloweralkoxy, aryl such as phenyl or naphthyl, substituted aryl such as phenyl wherein the substituent is lower alkyl, lower alkoxy or halo, arloweralkyl, arloweralkenyl, heteroarlower alkyl or heteroarlower alkenyl such as benzyl, styryl or indolyl ethyl, substituted arloweralkyl, substituted arloweralkenyl, substituted heteroarlower alkyl, or substituted heteroarlower alkenyl, wherein the substituent(s) is halo, dihalo, lower alkyl, hydroxy, lower alkoxy, amino, aminomethyl, acylamino (acetyl amino or benzoylamino) diloweralkylamino, loweralkylamino, carboxyl, haloloweralkyl, cyano or sulfonamido; arloweralkyl or heteroarloweralkyl substituted on the alkyl portion by amino or acylamino (acetylamino or benzoylamino); R 2 and R 7 are the same or different and are hydrogen or lower alkyl; R 3 is hydrogen, lower alkyl, phenyl lower alkyl, aminomethyl phenyl lower alkyl, hydroxy phenyl lower alkyl, hydroxy lower alkyl, acylamino lower alkyl (such as benzoylamino lower alkyl, acetylamino lower alkyl), amino lower alkyl, dimethylamino lower alkyl, halo lower alkyl, guanidino lower alkyl, imidazolyl lower alkyl, indolyllower alkyl, mercapto lower alkyl, lower alkyl thio lower alkyl; R 4 is hydrogen or lower alkyl; R 5 is hydrogen, lower alkyl, phenyl, phenyl lower alkyl, hydroxy phenyl lower alkyl, hydroxy lower alkyl, amino lower alkyl, guanidino lower alkyl, imidazolyl lower alkyl, indolyl lower alkyl, mercapto lower alkyl or lower alkyl thio lower alkyl; R 4 and R 5 may be connected together to form an alkylene bridge of from 2 to 4 carbon atoms, an alkylene bridge of from 2 to 3 carbon atoms and one sulfur atom, an alkylene bridge of from 3 to 4 carbon atoms containing a double bond or an alkylene bridge as above substituted with hydroxy, loweralkoxy, loweralkylor diloweralky; or a pharmaceutically acceptable salt thereof. With respect to Formula XII, R and R 6 are the same or different and are hydroxy, lower alkoxy, lower alkenoxy, dilower alkylamino lower alkoxy (dimethylaminoethoxy), acylamino lower alkoxy (acetylaminoethoxy), acyloxy lower alkoxy (pivaloyloxymethoxy), aryloxy, such as phenoxy, arloweralkoxy, such as benzyloxy, substituted aryloxy or substituted arloweralkoxy wherein the substitutent is methyl, halo or methoxy, amino, loweralkylamino, diloweralkylamino, hydroxyamino, arloweralkylamino such as benzylamino; R 1 is hydrogen, alkyl of from 1 to 20 carbon atoms which include branched and cyclic and unsaturated (such as allyl) alkyl groups, substituted loweralkyl wherein the substituent can be halo, hydroxy, lower alkoxy, aryloxy such as phenoxy, amino, diloweralkylamino, acylamino, such as acetamido and benzamido, arylamino, guanidino, imidazolyl, indolyl, mercapto, loweralkylthio, arylthio such as phenylthio, carboxy or carboxamido, carboloweralkoxy, aryl such as phenyl or naphthyl, substituted aryl such as phenyl wherein the substituent is lower alkyl, lower alkoxy or halo, arloweralkyl, arloweralkenyl, heteroarlower alkyl or heteroarlower alkenyl such as benzyl, styryl or indolyl ethyl, substituted arloweralkyl, substituted arloweralkenyl, substituted heteroarlower alkyl, or substituted heteroarlower alkenyl, wherein the substituent(s) is halo, dihalo, lower alkyl, hydroxy, lower alkoxy, amino, aminomethyl, acylamino (acetyl amino or benzoylamino) diloweralkylamino, loweralkylamino, carboxyl, haloloweralkyl, cyano or sulfonamido; arloweralkyl or heteroarloweralkyl substituted on the alkyl portion by amino or acylamino (acetylamino or benzoylamino); R 2 and R 7 are the same or different and are hydrogen or lower alkyl; R 3 is hydrogen, lower alkyl, phenyl lower alkyl, aminomethyl phenyl lower alkyl, hydroxy phenyl lower alkyl, hydroxy lower alkyl, acylamino lower alkyl (such as benzoylamino lower alkyl, acetylamino lower alkyl), amino lower alkyl, dimethylamino lower alkyl, halo lower alkyl, guanidino lower alkyl, imidazolyl lower alkyl, indolyllower alkyl, mercapto lower alkyl, lower alkyl thio lower alkyl; R 4 is hydrogen or lower alkyl; R 5 is hydrogen, lower alkyl, phenyl, phenyl lower alkyl, hydroxy phenyl lower alkyl, hydroxy lower alkyl, amino lower alkyl, guanidino lower alkyl, imidazolyl lower alkyl, indolyl lower alkyl, mercapto lower alkyl or lower alkyl thio lower alkyl; R 4 and R 5 may be connected together to form an alkylene bridge of from 2 to 4 carbon atoms, an alkylene bridge of from 2 to 3 carbon atoms and one sulfur atom, an alkylene bridge of from 3 to 4 carbon atoms containing a double bond or an alkylene bridge as above substituted with hydroxy, loweralkoxy, loweralkylor diloweralky. The loweralkyl or lower alkenyl groups except where noted otherwise represented by any of the variables include straight and branched chain hydrocarbon radicals from one to six carbon atoms, for example, methyl, ethyl, propyl, isopropyl, butyl, isobutyl, t-butyl, pentyl, isopentyl, hexyl or vinyl, allyl, butenyl and the like. The aralkyl groups represented by any of the above variables have from one to four carbon atoms in the alkyl portion thereof and include for example, benzyl, p-methoxy benzyl and the like. Halo means chloro, bromo, iodo or fluoro. Aryl where it appears in any of the radicals except where noted represents phenyl or naphthyl. Heteroaryl groups where they appear include for example pyridyl, thienyl, furyl, indolyl, benzthienyl, imidazoyl and thiazolyl. The R 1 , R 3 and R 5 substituted lower alkyl moieties are exemplified by groups such as R 4 and R 5 when joined through the carbon and nitrogen atoms to which they are attached form a 4 to 6 membered ring which may contain one sulfur atom or a double bond. Preferred rings have the formulae: where Y is CH 2 , S, or CHOCH 3 . Compounds of Formula XI include compounds wherein: R and R 6 can each independently be hydroxy, lower alkoxy, lower alkenoxy, arloweralkyloxy, amino, dilower alkylamino lower alkoxy, acylamino lower alkoxy, acyloxy lower alkoxy wherein the substituent is methyl, halo or methoxy; R 2 and R 7 are hydrogen; R 3 is lower alkyl, amino lower alkyl, imidazoyllower alkyl, halo lower alkyl; R 4 and R 5 are joined to form the preferred rings as defined above where Y is CH 2 , S, or CH—OCH 3 ; R 1 is as defined previously. Other compounds include compounds of Formula XI wherein further R 1 is alkyl having from 1 to 8 carbon atoms, substituted lower alkyl wherein the alkyl group has 1-5 carbon atoms and the substituent is amino, arylthio, aryloxy or arylamino, aralkyl or heteroaralkyl wherein the alkyl portion has 1 to 3 carbon atoms such as phenethyl or indolylethyl or substituted arloweralkyl 65 (phenyl lower alkyl or naphthyl lower alkyl) and substituted heteroarloweralkyl wherein the alkyl groups have 1-3 carbons and wherein the substituent(s) is halo, dihalo, amino, aminoalkyl, hydroxy, lower alkoxy or lower alkyl. Other compounds of Formula XI include compounds wherein R and R 6 are hydroxy, lower alkoxy, aralkyloxy; R 2 and R 7 are hydrogen; R 3 is methyl or amino lower alkyl; R 4 and R 5 are joined through the carbon and nitrogen atom to form proline, 4-thiaproline or 4-methoxy proline; R 1 is alkyl having from 1 to 8 carbon atoms, substituted lower alkyl wherein the alkyl group has 1-5 carbon atoms and the substituent is amino, arylthio or aryloxy, aralkyl or heteroaralkyl wherein the alkyl portion has 1 to 3 carbon atoms such as phenethyl or indolylethyl or substituted aralkyl (phenyl lower alkyl or naphthyl lower alkyl) and substituted heteroaralkyl wherein the alkyl groups have 1-3 carbons and wherein the substituent(s) is halo, dihalo, amino, aminoalkyl, hydroxy, lower alkoxy or lower alkyl. Further examples of compounds of Formula XII include, but are not limited to: N-(1 (S)-carboxy-3-phenylpropyl)-L-alanyl-L-proline;N-(1(S)-ethoxycarbonyl-3-phenylpropyl)-L-alanyl-L-proline and its maleate salt;N-(1 (S)-ethoxycarbonyl-4-methylpentyl)-L-alanyl-L-proline;N-(1-carboxy-5-aminopentyl)-L-alanyl-L-proline;N-.alpha.-(1 (S)-carboxy-3-phenylpropyl)-L-lysyl-L-proline (lisinopril);N-.alpha.(1(S)-ethoxycarbonyl-3-phenylpropyl)-L-lysyl-L-proline;N-.alpha.[1 (S)-carboxy-3-(3-indolyl)propyl]-L-lysyl-L-proline;N-.alpha.-[1 (S)-carboxy-3-(4-chlorophenyl)-propyl]-L-lysyl-L-proline;N-.alpha.-[1(S)-carboxy-2-phenylthioethyl]-L-lysyl-L-proline;N-.alpha.-[1(S)-carboxy-3-(4-chlorophenyl)-propyl]-L-lysyl-L-4.alpha.-methoxyproline;N-.alpha.-[1 (S)-carboxy-5-aminopentyl]-L-lysyl-L-proline;Ethyl N-(1 (S)-ethoxycarbonyl-3-phenylpropyl)-L-alanyl-L-prolinate hydrochloride; and the like. Also provided herein is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound selected from the group consisting of: a compound of Formula XIII wherein R 1 is H, alkyl, acyl or silyl(alkyl) 3 ; R 2 is H and R 3 is OH, O-acyl, O-alkyl or O-silyl (alkyl) 3 or R 3 is H and R 2 is OH. O-acyl, O-alkyl or O-silyl (alkyl) 3 ; or R 2 and R 3 together represent O; or R 2 and R 3 together represent acetal or cyclic acetal. R 1 might also represent a substituted alkyl such as e.g. methoxy ethoxy methyl; or a pharmaceutically acceptable salt thereof. Also provided herein is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound selected from the group consisting of: a compound of Formula XIV wherein PY is 4- or 3- or 2-pyridinyl or 4- or 3- or 2-pyridinyl having one or two lower-alkyl substituents, R is hydrogen, lower-alkyl or lower-hydroxyalkyl, and Q is nitro, carbamyl, halo, amino, lower-alkylamino, di(lower-alkyl)amino, or NHAc where Ac is lower-alkanoyl or lower-carbalkoxy; or a pharmaceutically acceptable salt thereof. With respect to Formula XIII, PY is 4- or 3- or 2-pyridinyl or 4- or 3- or 2-pyridinyl having one or two lower-alkyl substituents, R is hydrogen, lower-alkyl or lower-hydroxyalkyl, and Q is nitro, carbamyl, halo, amino, lower-alkylamino, di(lower-alkyl)amino, or NHAc where Ac is lower-alkanoyl or lower-carbalkoxy, or pharmaceutically-acceptable acid-addition salt thereof. Compounds of formula XIII where Q is amino, lower-alkylamino, di-(lower-alkyl) amino, or NHAc are provided herein. The compounds of formula XIII where Q is nitro or carbamyl are useful as intermediates for preparing the said compounds where Q is amino and those where Q is halo are useful as intermediates in the preparation of the compounds where Q is lower-alkylamino and di-(lower-alkyl)amino. Other compounds of Formula XIII include compounds where Q is amino, R is hydrogen and PY is 4-pyridinyl or 3-pyridinyl, for example, 3-amino-5-(4-pyridinyl)-2(1H)-pyridinone (amrinone). Further provided herein is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound selected from the group consisting of: a compound of Formula XV a compound of Formula XVI a compound of Formula XVII a compound of Formula XVIII a compound of Formula XIX a compound of Formula (XX) or pharmaceutically acceptable salt thereof. Formula XV is fluspirilen, Formula XVI is hexestrol, Formula XVII is dienestrol, Formula XVIII is napelline, Formula XIX is iopanoic acid and Formula XX is suloctodil. Further provided is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound selected from the group consisting of: Didanosine, Norcyclobenzaprine, Niridazole, Ifosfamide, Cefalonium, Tamoxifen citrate, Butoconazole, Suloctidil, Clomiphene, Sulconazole, Miconazole, Mefloquine, Sulfinpyrazone, Terfenadine, Lisinopril, Econzaole, Clofazimine, Equilin, Felodipine, Dacarbazine, Furazolidone, Perhexiline maleate, Oxethazaine, Pimozide, Trifluoperazine, Ellipticine, Fluspirilen, Hexestrol, Dienestrol, Zidovudine, Metoprolol, Napelline, Methimazole, Amrinone, Iopanoic acid, R-Propanolol, Rimexolone and Pyrvinium pamoate, or a pharmaceutically acceptable salt thereof. Further provided is a method of treating or preventing an infection in a subject with or at risk of developing an infection, the method comprising administering to the subject a compound selected from the group consisting of: Didanosine, Norcyclobenzaprine, Niridazole, Ifosfamide, Cefalonium, Tamoxifen citrate, Butoconazole, Suloctidil, Clomiphene, Sulconazole, Miconazole, Mefloquine, Sulfinpyrazone, Terfenadine, Lisinopril, Econzaole, Clofazimine, Equilin, Felodipine, Dacarbazine, Furazolidone, Perhexiline maleate, Oxethazaine, Pimozide, Trifluoperazine, Ellipticine, Fluspirilen, Hexestrol, Dienestrol, Zidovudine, Metoprolol, Napelline, Methimazole, Amrinone, Iopanoic acid, R-Propanolol, Rimexolone and Pyrvinium pamoate, or a pharmaceutically acceptable salt thereof, wherein the infection is a bacterial infection selected from the group consisting of Enterobacterium faecium, Staphylococcus aureus, Klebsiella pneumonia, Acinebacter baumannii, Pseudomonas aeruginosa and Enterobacter sp. Further provided is a method of treating or preventing a bacterial infection in a subject with or at risk of developing a bacterial infection in a subject comprising administering to the subject a compound that inhibits bacterial DNA gyrase or topoisomerase IV. The compound can be, for example, a compound of Formula I. As set forth above, a compound of Formula I can be terfenadine or a derivative thereof. In the methods set forth herein an inhibitor of bacterial DNA gyrase or topoisomerase IV can be used to treat or prevent Staphylococcus aureus infection. It is contemplated that one or more, for example, two, three, four, five, etc., of the compounds or derivatives of the compounds set forth herein can be administered to treat or prevent infection. Thus, combinations of the compounds set forth herein are also provided. Pharmaceutically acceptable salts of all of the compounds set forth herein are also provided. The term pharmaceutically acceptable salt as used herein refers to those salts of any of the compounds described herein or derivatives thereof that are, within the scope of sound medical judgment, suitable for use in contact with the tissues of subjects without undue toxicity, irritation, allergic response, and the like, commensurate with a reasonable benefit/risk ratio, and effective for their intended use, as well as the zwitterionic forms, where possible, of the compounds described herein. The term salts refers to the relatively non-toxic, inorganic and organic acid addition salts of the compounds described herein. These salts can be prepared in situ during the isolation and purification of the compounds or by separately reacting the purified compound in its free base form with a suitable organic or inorganic acid and isolating the salt thus formed. Representative salts include the hydrobromide, hydrochloride, sulfate, bisulfate, nitrate, acetate, oxalate, valerate, oleate, palmitate, stearate, laurate, borate, benzoate, lactate, phosphate, tosylate, citrate, maleate, fumarate, succinate, tartrate, naphthylate mesylate, glucoheptonate, lactobionate, methane sulphonate, and laurylsulphonate salts, and the like. These may include cations based on the alkali and alkaline earth metals, such as sodium, lithium, potassium, calcium, magnesium, and the like, as well as non-toxic ammonium, quaternary ammonium, and amine cations including, but not limited to ammonium, tetramethylammonium, tetraethylammonium, methylamine, dimethylamine, trimethylamine, triethylamine, ethylamine, and the like. The infection can be a viral infection, bacterial infection, fungal infection or a parasitic infection, to name a few. All strains and types of pathogenic infection are contemplated herein. The infection can also be a respiratory infection, a gastrointestinal infection or a skin infection, to name a few. In any of the methods of treating or preventing infection set forth herein, the infection can be any infection, wherein the infection is not a bacterial infection. In any of the methods of treating or preventing infection set forth herein, the infection can be any infection, wherein the infection is not a viral infection. In any of the methods of treating or preventing infection set forth herein, the infection can be any infection, wherein the infection is not a parasitic infection. In any of the methods of treating or preventing infection set forth herein, the infection can be any infection, wherein the infection is not a fungal infection. In any of the methods of treating or preventing infection set forth herein, the infection can be any infection, wherein the infection is not a protozoal infection. Examples of bacterial infections include, but are not limited to infections caused by the Gram negative or Gram positive bacteria. For example, the infection can be caused by Listeria (sp.), Franscicella tularensis, Enterobacter sp. Enterococcus faecium , other Enterococcus species, Klebsiella pneumonia, Acinetobacter baumannii, Mycobacterium tuberculosis, Rickettsia (all types), Ehrlichia or Chylamida . Further examples of bacteria include M. tuberculosis, Legionella pneumophila , other Legionella species, Salmonella typhi , other Salmonella species, Shigella species, Yersinia pestis, Pasteurella haemolytica, Pasteurella multocida , other Pasteurella species, Actinobacillus pleuropneumoniae, Listeria monocytogenes, Listeria ivanovii, Brucella abortus , other Brucella species, Chlamydia pneumoniae, Chlamydia trachomatis, Chlamydia psittaci, Coxiella burnetti , other Rickettsial species, Ehrlichia species, Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pyogenes, Streptococcus agalactiae, Bacillus anthracis, Escherichia coli, Vibrio cholerae, Kingella kingae, Campylobacter species, Neiserria meningitidis, Neiserria gonorrhea, Pseudomonas aeruginosa , other Pseudomonas species, Haemophilus influenzae, Haemophilus ducreyi , other Hemophilus species, Clostridium tetani , other Clostridium species, Yersinia enterolitica , and other Yersinia species. In the methods provided herein, one or more compounds set forth herein can treat or prevent one or more bacterial infections selected from the group consisting of Enterobacterium faecium, Staphylococcus aureus, Klebsiella pneumonia, Acinebacter baumannii, Pseudomonas aeruginosa and Enterobacter sp. In the methods set forth herein, the bacteria can be a small colony variant strain, for example a small colony strain of Staphylococcus aureus . In any of the methods set forth herein, the infection can be a bacterial infection, wherein the bacterial infection is not tuberculosis, for example, Mycobacterium tuberculosis . For example, and not to be limiting any of the compounds set forth herein, including compounds of Formula I and II can be used to treat or prevent infection in a subject with or at risk of developing an infection, wherein the infection is not tuberculosis. Examples of parasitic infections include, but are not limited to infections caused by the following parasites: Cryptosporidium, Plasmodium (all species), American trypanosomes ( T. cruzi ), African trypanosomes, Acanthamoeba, Entaoeba histolytica, Angiostrongylus, Anisakis, Ascaris, Babesia, Balantidium, Baylisascaris , lice, ticks, mites, fleas, Capillaria, Clonorchis, Chilomastix mesnili, Cyclspora, Diphyllobothrium, Dipylidium caninum, Fasciola, Giardia, Gnathostoma, Hetetophyes, Hymenolepsis, Isospora, Loa loa, Microsporidia, Naegleria, Toxocara, Onchocerca, Opisthorchis, Paragonimus, Baylisascaris, Strongyloides, Taenia, Trichomonas and Trichuris . In any of the methods set forth herein, the infection can be a parasitic infection, wherein the parasitic infection is not malaria, for example, malaria caused by any species of Plasmodium including Plasmodium falciparum . For example, and not to be limiting any of the compounds set forth herein, including compounds of Formula I and II can be used to treat or prevent infection in a subject with or at risk of developing an infection, wherein the infection is not malaria. Furthermore, examples of protozoan and fungal species contemplated within the present methods include, but are not limited to, Plasmodium falciparum , other Plasmodium species, Toxoplasma gondii, Pneumocystis carinii, Trypanosoma cruzi , other trypanosomal species, Leishmania donovani , other Leishmania species, Theileria annulata , other Theileria species, Eimeria tenella , other Eimeria species, Histoplasma capsulatum, Cryptococcus neoformans, Blastomyces dermatitidis, Coccidioides immitis, Paracoccidioides brasiliensis, Penicillium marneffei , and Candida species. In any of the methods set forth herein, the infection can be a protozoan infection, wherein the protozoan infection is not leishmaniasis, for example, leishmaniasis caused by a Leishmania species, for example, Leishmania major . For example, and not to be limiting any of the compounds set forth herein, including compounds of Formula I and III can be used to treat or prevent infection in a subject with or at risk of developing an infection, wherein the infection is not leishmaniasis. Examples of viral infections include but are not limited to, infections caused by RNA viruses (including negative stranded RNA viruses, positive stranded RNA viruses, double stranded RNA viruses and retroviruses) and DNA viruses. All strains, types, subtypes of DNA and RNA viruses are contemplated herein. Examples of RNA viruses include, but are not limited to picornaviruses, which include aphthoviruses (for example, foot and mouth disease virus O, A, C, Asia 1, SAT1, SAT2 and SAT3), cardioviruses (for example, encephalomycarditis virus and Theiller's murine encephalomyelitis virus), enteroviruses (for example polioviruses 1, 2 and 3, human enteroviruses A-D, bovine enteroviruses 1 and 2, human coxsackieviruses A1-A22 and A24, human coxsackieviruses B1-B5, human echoviruses 1-7, 9, 11-12, 24, 27, 29-33, human enteroviruses 68-71, porcine enteroviruses 8-10 and simian enteroviruses 1-18), erboviruses (for example, equine rhinitis virus), hepatovirus (for example human hepatitis A virus and simian hepatitis A virus), kobuviruses (for example, bovine kobuvirus and Aichi virus), parechoviruses (for example, human parechovirus 1 and human parechovirus 2), rhinovirus (for example, human rhinovirus 1-100 and bovine rhinoviruses 1-3) and teschoviruses (for example, porcine teschovirus). Additional examples of RNA viruses include caliciviruses, which include noroviruses (for example, Norwalk virus), sapoviruses (for example, Sapporo virus), lagoviruses (for example, rabbit hemorrhagic disease virus and European brown hare syndrome) and vesiviruses (for example vesicular exanthema of swine virus and feline calicivirus). Other RNA viruses include astroviruses, which include mamastorviruses and avastroviruses. Togaviruses are also RNA viruses. Togaviruses include alphaviruses (for example, Chikungunya virus, Sindbis virus, Semliki Forest virus, Western equine encephalitis, Getah virus, Everglades virus, Venezuelan equine encephalitis virus and Aura virus) and rubella viruses. Additional examples of RNA viruses include the the flaviviruses (for example, tick-borne encephalitis virus, Tyuleniy virus, Aroa virus, Dengue virus (types 1 to 4), Kedougou virus, Japanese encephalitis virus (JEV), West Nile virus (WNV), Kokobera virus, Ntaya virus, Spondweni virus, Yellow fever virus, Entebbe bat virus, Modoc virus, Rio Bravo virus, Cell fusing agent virus, pestivirus, GB virus A, GBV-A like viruses, GB virus C, Hepatitis G virus, hepacivirus (hepatitis C virus (HCV)) all six genotypes), bovine viral diarrhea virus (BVDV) types 1 and 2, and GB virus B). Other examples of RNA viruses are the coronaviruses, which include, human respiratory coronaviruses such as SARS—CoV, HCoV-229E, HCoV-NL63 and HCoV-OC43. Coronaviruses also include bat SARS-like CoV, turkey coronavirus, chicken coronavirus, feline coronavirus and canine coronavirus. Additional RNA viruses include arteriviruses (for example, equine arterivirus, porcine reproductive and respiratory syndrome virus, lactate dehyrogenase elevating virus of mice and simian hemorraghic fever virus). Other RNA viruses include the rhabdoviruses, which include lyssaviruses (for example, rabies, Lagos bat virus, Mokola virus, Duvenhage virus and European bat lyssavirus), vesiculoviruses (for example, VSV-Indiana, VSV-New Jersey, VSV-Alagoas, Piry virus, Cocal virus, Maraba virus, Isfahan virus and Chandipura virus), and ephemeroviruses (for example, bovine ephemeral fever virus, Adelaide River virus and Berrimah virus). Additional examples of RNA viruses include the filoviruses. These include the Marburg and Ebola viruses (for example, EBOV-Z, EBOV-S, EBOV-IC and EBOV-R. The paramyxoviruses are also RNA viruses. Examples of these viruses are the rubulaviruses (for example, mumps, parainfluenza virus 5, human parainfluenza virus type 2, Mapuera virus and porcine rubulavirus), avulaviruses (for example, Newcastle disease virus), respoviruses (for example, Sendai virus, human parainfluenza virus type 1 and type 3, bovine parainfluenza virus type 3), henipaviruses (for example, Hendra virus and Nipah virus), morbilloviruses (for example, measles, Cetacean morvilliirus, Canine distemper virus, Peste-des-petits-ruminants virus, Phocine distemper virus and Rinderpest virus), pneumoviruses (for example, human respiratory syncytial virus A2, B1 and S2, bovine respiratory syncytial virus and pneumonia virus of mice), metapneumoviruses (for example, human metapneumovirus and avian metapneumovirus). Additional paramyxoviruses include Fer-de-Lance virus, Tupaia paramyxovirus, Menangle virus, Tioman virus, Beilong virus, J virus, Mossman virus, Salem virus and Nariva virus. Additional RNA viruses include the orthomyxoviruses. These viruses include influenza viruses and strains (e.g., influenza A (H1N1 (including but not limited to A/WS/33 and A/California/04/2009 strains) H2N2, H3N2, H5N1, H7N7, H1N2, H9N2, H7N2, H7N3 and H10N7), B and C viruses, as well as avian influenza (for example, strains H5N1, H5N2, H7N1, H7N7 and H9N2) thogotoviruses and isaviruses. Orthobunyaviruses (for example, Akabane virus, California encephalitis, Cache Valley virus, Snowshoe hare virus,) nairoviruses (for example, Nairobi sheep virus, Crimean-Congo hemorrhagic fever virus Group and Hughes virus), phleboviruses (for example, Candiru, Punta Toro, Rift Valley Fever, Sandfly Fever, Naples, Toscana, Sicilian and Chagres), and hantaviruses (for example, Hantaan, Dobrava, Seoul, Puumala, Sin Nombre, Bayou, Black Creek Canal, Andes and Thottapalayam) are also RNA viruses. Arenaviruses such as lymphocytic choriomeningitis virus, Lujo virus, Lassa fever virus, Argentine hemorrhagic fever virus, Bolivian hemorrhagic fever virus, Venezuelan hemorrhagic fever virus, SABV and WWAV are also RNA viruses. Borna disease virus is also an RNA virus. Hepatitis D (Delta) virus and hepatitis E are also RNA viruses. Any of the compounds set forth herein, including, but not limited to the compounds of Formula I and II can be used to treat or prevent a viral infection, wherein the viral infection is not a Lassa fever virus infection. Additional RNA viruses include reoviruses, rotaviruses, birnaviruses, chrysoviruses, cystoviruses, hypoviruses partitiviruses and totoviruses. Orbiviruses such as African horse sickness virus, Blue tongue virus, Changuinola virus, Chenuda virus, Chobar Gorge Corriparta virus, epizootic hemorraghic disease virus, equine encephalosis virus, Eubenangee virus, Ieri virus, Great Island virus, Lebombo virus, Orungo virus, Palyam virus, Peruvian Horse Sickness virus, St. Croix River virus, Umatilla virus, Wad Medani virus, Wallal virus, Warrego virus and Wongorr virus are also RNA viruses. Retroviruses include alpharetroviruses (for example, Rous sarcoma virus and avian leukemia virus), betaretroviruses (for example, mouse mammary tumor virus, Mason-Pfizer monkey virus and Jaagsiekte sheep retrovirus), gammaretroviruses (for example, murine leukemia virus and feline leukemia virus, deltraretroviruses (for example, human T cell leukemia viruses (HTLV-1, HTLV-2), bovine leukemia virus, STLV-1 and STLV-2), epsilonretriviruses (for example, Walleye dermal sarcoma virus and Walleye epidermal hyperplasia virus 1), reticuloendotheliosis virus (for example, chicken syncytial virus, lentiviruses (for example, human immunodeficiency virus (HIV) type 1, human immunodeficiency virus (HIV) type 2, human immunodeficiency virus (HIV) type 3, simian immunodeficiency virus, equine infectious anemia virus, feline immunodeficiency virus, caprine arthritis encephalitis virus and Visna maedi virus) and spumaviruses (for example, human foamy virus and feline syncytia-forming virus). Examples of DNA viruses include polyomaviruses (for example, simian virus 40, simian agent 12, BK virus, JC virus, Merkel Cell polyoma virus, bovine polyoma virus and lymphotrophic papovavirus), papillomaviruses (for example, human papillomavirus, bovine papillomavirus, adenoviruses (for example, adenoviruses A-F, canine adenovirus type I, canined adeovirus type 2), circoviruses (for example, porcine circovirus and beak and feather disease virus (BFDV)), parvoviruses (for example, canine parvovirus), erythroviruses (for example, adeno-associated virus types 1-8), betaparvoviruses, amdoviruses, densoviruses, iteraviruses, brevidensoviruses, pefudensoviruses, herpes viruses 1, 2, 3, 4, 5, 6, 7 and 8 (for example, herpes simplex virus 1, herpes simplex virus 2, varicella-zoster virus, Epstein-Barr virus, cytomegalovirus, Kaposi's sarcoma associated herpes virus, human herpes virus-6 variant A, human herpes virus-6 variant B and cercophithecine herpes virus 1 (B virus)), poxviruses (for example, smallpox (variola), cowpox, monkeypox, vaccinia, Uasin Gishu, camelpox, psuedocowpox, pigeonpox, horsepox, fowlpox, turkeypox and swinepox), and hepadnaviruses (for example, hepatitis B and hepatitis B-like viruses). One or more of the compounds described herein can be contacted with a cell or populations of cells in vitro, ex vivo or in vivo. For example, the cell or population of cells can be in a subject, or in an in vitro culture. In another example, one or more compounds set forth herein can be used to inhibit bacterial growth, fungal growth, parasitic growth, protozoal growth or viral replication, in vitro, ex vivo or in vivo. Any of the compounds set forth herein can be used alone or in combination with other therapeutic agents such as antiviral compounds, antibacterial agents (for example, antibiotics), antifungal agents, antiparasitic agents, anti-inflammatory agents, anti-cancer agents, etc. In the methods described herein, the level of infection, for example, in a cell, or a population of cells, or a cell culture, can be assessed by measuring an antigen or other product associated with a particular infection. The level of infection can also be measured in a tissue sample or a culture of cells from a subject, either before or after administration of one or more compounds disclosed herein. For example, the level of viral infection can be measured by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) assay (See for example, Payungporn et al. “Single step multiplex real-time RT-PCR for H5N1 influenza A virus detection.” J Virol Methods . Sep. 22, 2005; Landolt et la. “Use of real-time reverse transcriptase polymerase chain reaction assay and cell culture methods for detection of swine influenza A viruses” Am J Vet Res. 2005 January; 66(1): 119-24). Methods of measuring bacterial growth and inhibition of bacterial growth are provided in the Examples. Further, one of skill in the art would know how to determine the concentration of a compound that inhibits bacterial infection (see, for example, Andrews, et al. “Determination of minimum inhibitory concentrations”. Journal of Antimicrobial Chemotherapy 48 (suppl 1): 5-16 (2001)). Other methods for determining antifungal and antibacterial activity are known in the art. See, for example, Hayhoe et al. “Screening for Antibacterial, Antifungal and Anti quorum Sensing Activity,” Methods Mol. Biol. 1055: 219-225 (2013)); Doddanna et al. “Antimicrobial activity of plant extracts on Candida albicans : An in vitro study Indian J. Dent. Res. 24(4): 401-405 (2013), both of which are incorporated by this reference in their entireties. As used throughout, by subject is meant an individual. Preferably, the subject is a mammal such as a primate, and, more preferably, a human. Non-human primates are subjects as well. The term subject includes domesticated animals, such as cats, dogs, etc., livestock (for example, cattle, horses, pigs, sheep, goats, etc.) and laboratory animals (for example, ferret, chinchilla, mouse, rabbit, rat, gerbil, guinea pig, etc.). Thus, veterinary uses and medical formulations are contemplated herein. As used herein, a biological sample is a sample derived from a subject such as a mammal or human and includes, but is not limited to, any biological fluid, including a bodily fluid. Examples of bodily fluids include, but are not limited to, whole blood, plasma, serum, urine, saliva, ocular fluid, ascites, a stool sample, spinal fluid, tissue infiltrate, pleural effusions, lung lavage fluid, and the like. The biological fluid includes a cell culture medium or supernatant of cultured cells from the subject. The methods and compounds as described herein are useful for therapeutic treatment. Use of one or more of the compounds set forth herein for the treatment or prevention of infection is also contemplated herein. One or more of the compounds set forth herein for use in a method of treating or preventing infection is also provided herein. Therapeutic treatment involves administering to a subject a therapeutically effective amount of one or more of the agents described herein, optionally, after diagnosis of an infection or risk of infection in the subject. Therefore, all of the methods disclosed herein, can optionally comprise the step of diagnosing a subject with an infection or diagnosing a subject in need of prophylaxis or prevention of infection. As used herein, the terms treatment, treat, or treating refers to a method of reducing the effects of a disease or condition or symptom of the disease or condition. Thus, in the disclosed methods, treatment can refer to a 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100% reduction in the severity of an established disease or condition or symptom of the disease or condition. For example, a method for treating a disease is considered to be a treatment if there is a 10% reduction in one or more symptoms of the disease in a subject as compared to a control. A control subject can be a subject that has not received a compound set forth herein. Thus, the reduction can be a 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, 100%, or any percent reduction in between 10% and 100% as compared to native or control levels. It is understood that treatment does not necessarily refer to a cure or complete ablation of the disease, condition, or symptoms of the disease or condition. As utilized herein, by preventing infection is meant a method of precluding, delaying, averting, obviating, forestalling, stopping, or hindering the onset, incidence, severity, or recurrence of infection. For example, the disclosed method is considered to be a prevention if there is about a 10% reduction in onset, incidence, severity, or recurrence of infection, or symptoms of infection (e.g., inflammation, fever, lesions, weight loss, etc.) in a subject exposed to an infection when compared to control subjects exposed to an infection that did not receive a composition for decreasing infection. Thus, the reduction in onset, incidence, severity, or recurrence of infection can be about a 10, 20, 30, 40, 50, 60, 70, 80, 90, 100%, or any amount of reduction in between as compared to a control subject. For example, and not to be limiting, if about 10% of the subjects in a population do not become infected as compared to subjects that did not receive preventive treatment, this is considered prevention. The compounds set forth herein can also be used to decrease infection in a cell. A decrease or inhibition of infection can occur in a cell, in vitro, ex vivo or in vivo. As utilized throughout, the term “infection” encompasses all phases of pathogenic life cycles including, but not limited to, attachment to cellular receptors, entry, internalization, disassembly, replication, genomic integration of pathogenic sequences, transcription of pathogen RNA, translation of pathogen RNA, transcription of host cell mRNA, translation of host cell mRNA, proteolytic cleavage of pathogenic proteins or cellular proteins, assembly of particles, endocytosis, cell lysis, budding, and egress of the pathogen from the cells. The compounds described herein can be provided in a pharmaceutical composition. Depending on the intended mode of administration, the pharmaceutical composition can be in the form of solid, semi-solid or liquid dosage forms, such as, for example, tablets, suppositories, pills, capsules, powders, liquids, or suspensions, preferably in unit dosage form suitable for single administration of a precise dosage. The compositions will include a therapeutically effective amount of the compound described herein or derivatives thereof in combination with a pharmaceutically acceptable carrier and, in addition, may include other medicinal agents, pharmaceutical agents, carriers, or diluents. By pharmaceutically acceptable is meant a material that is not biologically or otherwise undesirable, which can be administered to an individual along with the selected agent without causing unacceptable biological effects or interacting in a deleterious manner with the other components of the pharmaceutical composition in which it is contained. As used herein, the term carrier encompasses any excipient, diluent, filler, salt, buffer, stabilizer, solubilizer, lipid, stabilizer, or other material well known in the art for use in pharmaceutical formulations. The choice of a carrier for use in a composition will depend upon the intended route of administration for the composition. The preparation of pharmaceutically acceptable carriers and formulations containing these materials is described in, e.g., Remington's Pharmaceutical Sciences, 21st Edition, ed. University of the Sciences in Philadelphia, Lippincott, Williams & Wilkins, Philadelphia Pa., 2005. Examples of physiologically acceptable carriers include buffers such as phosphate buffers, citrate buffer, and buffers with other organic acids; antioxidants including ascorbic acid; low molecular weight (less than about 10 residues) polypeptides; proteins, such as serum albumin, gelatin, or immunoglobulins; hydrophilic polymers such as polyvinylpyrrolidone; amino acids such as glycine, glutamine, asparagine, arginine or lysine; monosaccharides, disaccharides, and other carbohydrates including glucose, mannose, or dextrins; chelating agents such as EDTA; sugar alcohols such as mannitol or sorbitol; salt-forming counterions such as sodium; and/or nonionic surfactants such as TWEEN® (ICI, Inc.; Bridgewater, N.J.), polyethylene glycol (PEG), and PLURONICS™ (BASF; Florham Park, N.J.). Compositions containing the compound(s) described herein suitable for parenteral injection may comprise physiologically acceptable sterile aqueous or nonaqueous solutions, dispersions, suspensions or emulsions, and sterile powders for reconstitution into sterile injectable solutions or dispersions. Examples of suitable aqueous and nonaqueous carriers, diluents, solvents or vehicles include water, ethanol, polyols (propyleneglycol, polyethyleneglycol, glycerol, and the like), suitable mixtures thereof, vegetable oils (such as olive oil) and injectable organic esters such as ethyl oleate. Proper fluidity can be maintained, for example, by the use of a coating such as lecithin, by the maintenance of the required particle size in the case of dispersions and by the use of surfactants. These compositions may also contain adjuvants such as preserving, wetting, emulsifying, and dispensing agents. Prevention of the action of microorganisms can be promoted by various antibacterial and antifungal agents, for example, parabens, chlorobutanol, phenol, sorbic acid, and the like. Isotonic agents, for example, sugars, sodium chloride, and the like may also be included. Prolonged absorption of the injectable pharmaceutical form can be brought about by the use of agents delaying absorption, for example, aluminum monostearate and gelatin. Solid dosage forms for oral administration of the compounds described herein or derivatives thereof include capsules, tablets, pills, powders, and granules. In such solid dosage forms, the compounds described herein or derivatives thereof is admixed with at least one inert customary excipient (or carrier) such as sodium citrate or dicalcium phosphate or (a) fillers or extenders, as for example, starches, lactose, sucrose, glucose, mannitol, and silicic acid, (b) binders, as for example, carboxymethylcellulose, alignates, gelatin, polyvinylpyrrolidone, sucrose, and acacia, (c) humectants, as for example, glycerol, (d) disintegrating agents, as for example, agar-agar, calcium carbonate, potato or tapioca starch, alginic acid, certain complex silicates, and sodium carbonate, (e) solution retarders, as for example, paraffin, (f) absorption accelerators, as for example, quaternary ammonium compounds, (g) wetting agents, as for example, cetyl alcohol, and glycerol monostearate, (h) adsorbents, as for example, kaolin and bentonite, and (i) lubricants, as for example, talc, calcium stearate, magnesium stearate, solid polyethylene glycols, sodium lauryl sulfate, or mixtures thereof. In the case of capsules, tablets, and pills, the dosage forms may also comprise buffering agents. Solid compositions of a similar type may also be employed as fillers in soft and hard-filled gelatin capsules using such excipients as lactose or milk sugar as well as high molecular weight polyethyleneglycol s, and the like. Solid dosage forms such as tablets, dragees, capsules, pills, and granules can be prepared with coatings and shells, such as enteric coatings and others known in the art. They may contain opacifying agents and can also be of such composition that they release the active compound or compounds in a certain part of the intestinal tract in a delayed manner. Examples of embedding compositions that can be used are polymeric substances and waxes. The active compounds can also be in micro-encapsulated form, if appropriate, with one or more of the above-mentioned excipients. Liquid dosage forms for oral administration of the compounds described herein or derivatives thereof include pharmaceutically acceptable emulsions, solutions, suspensions, syrups, and elixirs. In addition to the active compounds, the liquid dosage forms may contain inert diluents commonly used in the art, such as water or other solvents, solubilizing agents, and emulsifiers, as for example, ethyl alcohol, isopropyl alcohol, ethyl carbonate, ethyl acetate, benzyl alcohol, benzyl benzoate, propyleneglycol, 1,3-butyleneglycol, dimethylformamide, oils, in particular, cottonseed oil, groundnut oil, corn germ oil, olive oil, castor oil, sesame oil, glycerol, tetrahydrofurfuryl alcohol, polyethyleneglycols, and fatty acid esters of sorbitan, or mixtures of these substances, and the like. Besides such inert diluents, the composition can also include additional agents, such as wetting, emulsifying, suspending, sweetening, flavoring, or perfuming agents. Administration can be carried out using therapeutically effective amounts of the agents described herein for periods of time effective to treat or prevent infection in a subject. The effective amount may be determined by one of ordinary skill in the art and includes exemplary dosage amounts for a mammal of from about 0.5 to about 200 mg/kg of body weight of active compound per day, which may be administered in a single dose or in the form of individual divided doses, such as from 1 to 4 times per day. Alternatively, the dosage amount can be from about 0.5 to about 150 mg/kg of body weight of active compound per day, about 0.5 to 100 mg/kg of body weight of active compound per day, about 0.5 to about 75 mg/kg of body weight of active compound per day, about 0.5 to about 50 mg/kg of body weight of active compound per day, about 0.5 to about 25 mg/kg of body weight of active compound per day, about 1 to about 20 mg/kg of body weight of active compound per day, about 1 to about 10 mg/kg of body weight of active compound per day, about 20 mg/kg of body weight of active compound per day, about 10 mg/kg of body weight of active compound per day, or about 5 mg/kg of body weight of active compound per day. According to the methods taught herein, the subject is administered an effective amount of the compound. The terms effective amount and effective dosage are used interchangeably. The term effective amount is defined as any amount necessary to produce a desired physiologic response. Effective amounts and schedules for administering the agent may be determined empirically, and making such determinations is within the skill in the art. The dosage ranges for administration are those large enough to produce the desired effect in which one or more symptoms of the disease or disorder are affected (e.g., reduced or delayed). The dosage should not be so large as to cause substantial adverse side effects, such as unwanted cross-reactions, anaphylactic reactions, and the like. Generally, the dosage will vary with the activity of the specific compound employed, the metabolic stability and length of action of that compound, the species, age, body weight, general health, sex and diet of the subject, the mode and time of administration, rate of excretion, drug combination, and severity of the particular condition and can be determined by one of skill in the art. The dosage can be adjusted by the individual physician in the event of any contraindications. Dosages can vary, and can be administered in one or more dose administrations daily, for one or several days. Guidance can be found in the literature for appropriate dosages for given classes of pharmaceutical products. Any appropriate route of administration can be employed, depending on whether local or systemic treatment is desired, and on the area to be treated. The compositions are administered via any of several routes of administration, including topically, orally, parenterally, intravenously, intra-articularly, intraperitoneally, intramuscularly, subcutaneously, intracavity, transdermally, intrahepatically, intracranially, nebulization/inhalation, or by installation via bronchoscopy. Optionally, the composition is administered by oral inhalation, nasal inhalation, or intranasal mucosal administration. Administration of the compositions by inhalant can be through the nose or mouth via delivery by spraying or droplet mechanism, for example, in the form of an aerosol. Pharmaceutical compositions can be delivered locally to the area in need of treatment, for example by topical application or local injection. Multiple administrations and/or dosages can also be used. Effective doses can be extrapolated from dose-response curves derived from in vitro or animal model test systems. The disclosure also provides a pharmaceutical pack or kit comprising one or more containers filled with one or more of the ingredients of the pharmaceutical compositions. Optionally associated with such container(s) can be a notice in the form prescribed by a governmental agency regulating the manufacture, use or sale of pharmaceuticals or biological products, which notice reflects approval by the agency of manufacture, use or sale for human administration. Instructions for use of the composition can also be included. Also provided is a method of removing biofilm from a surface, comprising administering an effective amount of one or more of the compounds provided herein to a biofilm-containing surface, wherein the amount is effective to remove biofilm from the surface. Removal of the biofilm from this surface does not have to be complete as this can range from a reduction to complete removal of the biofilm. Thus, in the disclosed methods, removal can refer to a 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, or 100% reduction in the amount of biofilm on a surface. For example, a method for removing biofilm from a surface is considered to be removal if there is a 10% reduction in the amount of biofilm on the surface as compared to a control. A control surface can be a biofilm containing surface that has not received a compound set forth herein. Thus, the reduction can be a 10%, 20%, 30%, 40%, 50%, 60%, 70%, 80%, 90%, 100%, or any percent reduction in between 10% and 100% as compared to control. Further provided is a method of preventing biofilm formation on a surface comprising administering an effective amount of one or more of the compounds provided herein to the surface, wherein the amount is effective to prevent biofilm formation. The surface can be susceptible to biofilm formation. The biofilm can be produced by an organism selected from the group consisting of bacteria, algae, fungi and protozoa. The compound can be, but is not limited to, a compound of Formula I wherein R represents hydrogen or hydroxyl and R 1 represents hydrogen, or R and R 1 taken together form a second bond between the carbon atoms bearing R and R′; R 2 represents hydrogen or phenyl; n is zero or a positive whole integer of from 1 to 4; X represents CH 2 , CHOH, NH, C═O, CHNR 3 R 4 , where R 3 and R 4 independently are hydrogen or lower alkyl; and Z represents thienyl, pyridinyl, substituted pyridinyl, phenyl or substituted phenyl wherein the substituents on the substituted pyridinyl or substituted phenyl are selected from phenyl, pyridinyl, nitro, a halogen atom, such as chlorine, fluorine, bromine, or iodine, a straight or branched lower alkyl chain of from 1 to 4 carbon atoms, a lower alkoxy group of from 1 to 4 carbon atoms, amino, a mono or di(lower)alkylamino group, a saturated monocyclic heterocyclic group such as pyrrolidino, piperidino, morpholino, or N-(lower)alkylpiperazino, or a group having the structure —COOR 5 , —CR 6 R 7 COOR 5 , —CF 3 , CHF 2 , CH 2 F, or where R 5 is hydrogen or lower alkyl, and R 6 and R 7 independently are hydrogen or methyl or a pharmaceutically acceptable salt thereof. One or more of the compounds set forth herein can be combined with one or more biodegradable polymers to form a biodegradable antimicrobial composition. These compositions can be applied to a surface or used as a coating. The biodegradable polymers include but are not limited to polylactic acid, polyglycolic acid and copolymers and mixtures thereof such as poly(L-lactide) (PLLA), poly(D,L-lactide) (PLA), polyglycolic acid [polyglycolide (PGA)], poly(L-lactide-co-D,L-lactide) (PLLA/PLA), poly(L-lactide-co-glycolide) (PLLA/PGA), poly(D,L-lactide-co-glycolide) (PLA/PGA), poly(glycolide-co-trimethylene carbonate) (PGA/PTMC), poly(D,L-lactide-co-caprolactone) (PLA/PCL) and poly(glycolide-co-caprolactone) (PGA/PCL); polyethylene oxide (PEO), polydioxanone (PDS), polypropylene fumarate, poly(ethyl glutamate-co-glutamic acid), poly(tert-butyloxy-carbonylmethyl glutamate), polycaprolactone (PCL), polycaprolactone co-butylacrylate, polyhydroxybutyrate (PHBT) and copolymers of polyhydroxybutyrate, poly(phosphazene), polyphosphate ester), poly(amino acid), polydepsipeptides, maleic anhydride copolymers, polyiminocarbonates, poly [(97.5% dimethyl-trimethylene carbonate)-co-(2.5% trimethylene carbonate)], poly(orthoesters), tyrosine-derived polyarylates, tyrosine-derived polycarbonates, tyrosine-derived polyiminocarbonates, tyrosine-derived polyphosphonates, polyethylene oxide, polyethylene glycol, polyalkylene oxides, hydroxypropylmethylcellulose, polysaccharides such as hyaluronic acid, chitosan and regenerate cellulose, and proteins such as gelatin and collagen, and mixtures and copolymers thereof, among others as well as PEG derivatives or blends of any of the foregoing. In the methods of removing or preventing biofilm formation, the surface can be a hard (for example, glass, metal, wood, chrome, plastic, vinyl or formica) or a soft surface (for example, cloth or upholstery). The methods set forth herein can be used to remove or prevent biofilm formation in vitro, ex vivo or in vivo. The methods set forth herein can also be used to remove or prevent biofilm formation on a medical device or a part thereof. For example, the methods set forth herein can be used to remove or prevent biofilm formation on an implantable medical device such as a cardiac rhythm management device (for example, a pacemaker, a defibrillator, an implantable cardioverter defibrillator (ICD) and a cardiac resynchronization therapy defibrillator (CRT device), a neurostimulator, a pulse generator, a drug pump, an infusion device, a physiological monitoring device (for example, a glucose sensor), contact lenses, a stent, a catheter, tubing or a breast implant. Mesh, bandages, and implantable devices, for example, can be coated with a compositions comprising one or more of the compounds set forth herein. Further, organs can be treated with one or more of the compounds set forth herein prior to transplantation in a subject. One or more of the compounds set forth herein can be used to inhibit biofilm formation by one or more of Staphylococcus aureus, Pseudomonas aeuroginosa, Staphylococcus epidermidis, Escherichia coli or Acinetobacter baummanii. As utilized herein, by preventing biofilm formation is meant a method of precluding, delaying, averting, obviating, forestalling, stopping, or hindering the onset, incidence, severity, or recurrence of biofilm formation. For example, the disclosed method is considered to be prevention if there is about a 10% reduction in onset, incidence, severity, or recurrence of biofilm formation on a surface when compared to a control surface that did not receive a composition for preventing biofilm formation. Thus, the reduction in onset, incidence, severity, or recurrence of biofilm can be about a 10, 20, 30, 40, 50, 60, 70, 80, 90, 100%, or any amount of reduction in between as compared to a control surface. A biofilm can also exist or form in a biological subject, for example, on the teeth or gums of a subject. Therefore, one or more of the compounds set forth herein can be in a toothpaste, mouth rinse, gel, foam, varnish, polish, floss, dental strip, or copolymer membrane in order to remove or prevent biofilm formation on a dental surface. Further provided herein is a method of identifying an antimicrobial agent comprising contacting a bacterial culture with a test agent and measuring adenylate kinase release in the supernatant of the bacterial culture, wherein an increase in adenylate kinase release as compared to a control indicates that the test compound is an antimicrobial agent. The control can be a bacterial culture that was not contacted with the test compound. The bacterial culture can be a culture of any bacterial strain, for example, a culture of any of the bacteria disclosed herein. The bacterial culture can also be small colony variant bacterial culture or a biofilm associated bacterial culture. Examples of agents identified utilizing this method are provided in the Examples. Disclosed are materials, compositions, and components that can be used for, can be used in conjunction with, can be used in preparation for, or are products of the disclosed methods and compositions. These and other materials are disclosed herein, and it is understood that when combinations, subsets, interactions, groups, etc. of these materials are disclosed that while specific reference of each various individual and collective combinations and permutations of these compounds may not be explicitly disclosed, each is specifically contemplated and described herein. For example, if a method is disclosed and discussed and a number of modifications that can be made to a number of molecules including in the method are discussed, each and every combination and permutation of the method, and the modifications that are possible are specifically contemplated unless specifically indicated to the contrary. Likewise, any subset or combination of these is also specifically contemplated and disclosed. This concept applies to all aspects of this disclosure including, but not limited to, steps in methods using the disclosed compositions. Thus, if there are a variety of additional steps that can be performed, it is understood that each of these additional steps can be performed with any specific method steps or combination of method steps of the disclosed methods, and that each such combination or subset of combinations is specifically contemplated and should be considered disclosed. Publications cited herein and the material for which they are cited are hereby specifically incorporated by reference in their entireties. The following examples are put forth so as to provide those of ordinary skill in the art with a complete disclosure and description of how the compounds and/or methods claimed herein are made and evaluated, and are intended to be purely exemplary of the invention and are not intended to limit the scope of what the inventors regard as their invention except as and to the extent that they are included in the accompanying claims. Example I Identification of Antimicrobial Compounds Adenylate kinase (AK) is a ubiquitous intracellular enzyme that is released into the extracellular space upon cell lysis. As shown herein, AK release serves as a useful reporter of bactericidal agent activity and can be exploited for antimicrobial screening purposes. The AK assay exhibits improved sensitivity over that of growth-based assays and can detect agents that are active against bacteria in clinically relevant growth states that are difficult to screen using conventional approaches, such as small colony variants (SCV) and bacteria within established biofilms. The usefulness of the AK assay was validated by screening a library of off-patent drugs for agents that exhibit antimicrobial properties toward a variety of bacterial species, including Escherichia coli and all members of the “ESKAPE” pathogens ( Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa , and Enterobacter species). The assay detected antibiotics within the library that were expected to be active against the organism screened. Moreover, 38 drugs elicited AK release. Examples include, the antihistamine, terfenadine, which was active against S. aureus planktonic, SCV population, and biofilm-associated cells, to name a few. Tamoxifen, an estrogen receptor antagonist, was active toward E. faecium in vitro and also reduced E. faecium pathogenesis in a Galleria mellonella infection model. These data demonstrate that the AK assay provides an attractive screening approach for identifying new antimicrobial agents. Further, drugs identified using this screening approach, for example, terfenadine and tamoxifen, provide novel antimicrobial drug development scaffolds. The ESKAPE pathogens frequently cause health care-associated bacterial infections and can escape the effects of most currently available antibiotics. The most successful and widely applied method to identify agents with antibacterial activity has been whole-cell, bacterial growth assays. In this approach, libraries of small molecules or natural products are screened for agents that limit bacterial growth. However, growth-based assays have limitations. For example, the growth or no-growth readout has a limited dynamic range. This is likely to be problematic because growth assays lack the sensitivity required to detect antimicrobial molecules that are present in low concentrations within complex natural product extract libraries or compounds with limited antimicrobial activity. While the latter would obviously not represent a molecule that could be directly translated to clinical use, these low-activity hits could provide structurally novel scaffolds suitable for medicinal chemistry-based optimization. In addition, traditional growth-based assays are not readily amenable to screening for agents that target bacteria within certain clinically relevant bacterial growth states, such as established biofilms and small-colony variants. To address these limitations, provided herein is a high-throughput screen (HTS)-compatible whole-cell assay to detect agents that directly kill bacteria. The assay is based on the release of intracellular adenylate kinase (AK) into culture medium as a reporter of bacterial cell death. As shown herein, the AK assay exhibits improved sensitivity over that of conventional whole-cell growth assays and displays specificity for bactericidal agents. Further, the assay can be used to screen for agents that kill small-colony-variant bacteria and bacteria within established biofilms. To validate the AK assay as an HTS-compatible screening platform, the Prestwick library of off-patent drugs was screened against E. coli and each of the ESKAPE pathogens. This library contains representative examples of nearly all classes of antibiotics, and the bactericidal agents within the library that were expected to be active against the organism screened were identified. Additionally, agents with no previously reported antibiotic activity were identified. Traditional MIC testing confirmed the antimicrobial properties of many of these molecules, showing that they could be repurposed as antimicrobials or serve as lead molecules for antibiotic development. Consistent with that prediction, it was shown that one of these compounds, tamoxifen, is active against E. faecium in a Galleria mellonella model of infection. Further, it was shown that terfenadine is active against planktonic, small-colony variant, and biofilm-associated S. aureus . Taken together, these data demonstrate that the AK assay provides a general approach to screening for new antimicrobial agents active against a variety of pathogens during planktonic and other disease-associated growth states. Bacterial Growth Conditions— The bacterial species and strains used in these experiments are listed in Table 1. S. aureus strain UAMS-1112 (generous gift from M. Smeltzer, University of Arkansas Medical Center) is a stable small-colony variant of the common laboratory S. aureus strain 8325-4, which harbors a hemB deletion. Unless otherwise noted, bacteria were grown for 16 h in Mueller-Hinton (MB) (Becton. Dickinson. Franklin Lakes, N.J.) or brain heart infusion (BHI) (Becton, Dickinson) medium at 37° C. on a rotary shaker at 225 rotations per min (rpm) and then used to inoculate (1:100) fresh medium and processed, as described below. TABLE 1Bacterial StrainsSource orSpeciesStrainRelevant resistance areference bEnterococcus824-05Amp, Cf, Cp, Cl, Mp,ClinicalfaeciumTmp, Sul, Erm, KanisolateStaphylococcusUSA300-Amp, Cf, Cl, Sul, Kan6aureus0114UAMS-1ND7UAMS-1112ErmUniv. ofArkansasRN4220Cl8KlebsiellacKP1Amp, Cp, Sul, Erm, Van9pneumoniaeAcinetobacter98-37-09Amp, Lz10baumanniiPseudomonasPA01Amp, Kan, Lz, Sul, Van11aeruginosaEnterobacterPMD1001Amp, Erm, Lz, Sul, VanClinical isolatecloacaeEscherichia8295Erm, Lz, SulClinical isolatecolia Abbreviations: ampicillin, Amp; colistin, Cl; ceftriaxone, Cf; ciprofloxacin, Cp; erythromycin, Erm; kanamycin, Kan; linezolid, Lz; meropenem, Mp; minocycline, Min; Sulfamethoxazole, Sul; vancomycin, Van; not determined, ND; Univ., university.b Clinical isolates were obtained from the University of Rochester School of Medicine and Dentistry. Chemicals— The Prestwick Chemical Library of molecules with known biological activities was acquired from Prestwick Chemical (Illkirch, France). ToxiLight BioAssay kits were obtained to from Lonza (Basel, Switzerland). Terfenadine, suloctidil, clomiphene citrate, ceftriaxone, sulfamethoxazole, erythromycin, kanamycin, ciprofloxacin, rifampin, ampicillin, minocycline, tamoxifen, and trimethoprim were purchased from Sigma-Aldrich (St. Louis, Mo.). Meropenem, linezolid, and vancomycin were purchased from Thermo Fisher (Waltham, Mass.). Colistin was purchased from APP Pharmaceuticals (Schaumburg, Ill.). MIC Testing— MIC testing was performed to determine the antibiotic susceptibility profile of selected bacterial strains according to Clinical and Laboratory Standards (CLSI) protocols (Hindler et al. Antimicrobial susceptibility testing, section 5. Clinical microbiology procedures handbook, Vol. 1 America Society of Microbiology. Washington, D.C. (2010). Briefly, colonies of each bacterial species were collected from MH agar plates and suspended in individual tubes of MH medium to an optical density (600 nm) of 0.8. The resulting cultures were incubated at 37° C. in a rotary shaker at 225 rpm to exponential phase (˜1×10 8 CFU ml −1 ) and then diluted in fresh MH medium to a cell density of ˜3×10 7 CFU ml −1 . Ten microliters of the diluted cultures was added to 88 μl of MH medium in individual wells of a 96-well, round-bottom plate (Corning, Inc.), and 2 μl of a stock solution of the indicated reference antibiotic or test compound (0 to 256 μg ml −1 ) was added to each well. The carrier solvent was either water or dimethyl sulfoxide (DMSO); final DMSO concentrations were less than or equal to 2%. Plates were incubated at 37° C. for 24 h, and the MIC was defined as the lowest concentration of antibiotic in which there was no visible cell pellet in the wells. Heat-Killed Bacterial AK Release Assays— Overnight cultures of E. coli strain 8295 or S. aureus RN4220 were used to inoculate (1:100 dilution) 25 ml of fresh MH medium and grown at 37° C. on a rotary shaker at 225 rpm to exponential phase (˜1×10 8 CFU ml −1 ). Cells were pelleted by centrifugation (2,000×g) and resuspended in 2.5 ml of sterile water. One milliliter of the resulting suspension was boiled for 3 min and filter sterilized (0.45-μm filter) to remove cell debris. The filtrate was serially diluted in sterile water, and 100 μl of each dilution was added to individual wells of a white-walled, 96-well plate (Corning, Inc., Corning, N.Y.). To measure the AK activity in the supernatants at each dilution, 100 μl of ToxiLight AK reagent was added to each well, followed by incubation at room temperature for 30 min, and luminescence was measured using a SpectraMax M5 plate reader (Molecular Devices, Sunnyvale, Calif.). Cells were serially diluted and plated to enumerate CFU (CFU ml −1 ) before and after boiling to correlate cell lysis with viability. AK Assay 96-Well Format— Overnight cultures of each bacterial species were used to inoculate (1:100 dilution) 25 ml of fresh MH medium and grown at 37° C. on a rotary shaker at 225 rpm to exponential phase (˜1×10 8 CFU ml −1 ) Ninety-eight microliters of MH medium, 2 μl of the indicated antibiotic, and 5×10 6 bacteria were added to individual wells of a white-walled, 96-well microtiter plate. Well components were mixed by pipetting and incubated at 37° C. for 3 h. The plate was equilibrated to room temperature for 30 min. Next, 100 μl of ToxiLight AK reagent was added to each well and incubated at room temperature for 30 min, and luminescence was measured using a SpectraMax M5 plate reader. AK Assay 384-Well Format and High-Throughput Screening— Overnight cultures of each bacterial species were used to inoculate (1:100 dilution) 25 ml of fresh medium and grown at 37° C. on a rotary shaker at 225 rpm to exponential phase (˜1×10 8 CFU ml −1 ). In a white-walled, 384-well plate, 24 μl of MH medium, 0.3 μl (50 μM) of antibiotic or compound, and 5×10 6 bacteria were added to individual wells and incubated at 37° C. for 3 h. The plates were equilibrated at room temperature for 1 h. Twenty-five microliters of ToxiLight AK reagent was then added to each well, followed by incubation at room temperature for 30 min, and luminescence was measured using a SpectraMax M5 plate reader. AK Assay of Established Biofilms— Biofilms were grown as previously described (Beenken et al. Infect. Immun. 71: 4206-4211 (2003); Musken et al. Nat. Protoc. 5: 1460-1459 (2010); Tomaras et al. Microbiology 149: 3473-3483 (2003)). Briefly, P. aeruginosa and A. baumannii were cultured overnight in Luria-Bertani medium and then used to seed 96-well, flat-bottom plates. Plates were incubated at 37° C. in a humidified incubator for 48 h to allow the formation of static biofilms. Nonadherent cells were removed by aspiration and washing with sterile phosphate-buffered saline (PBS). Fresh LB medium supplemented with 0, 1, 10×, or 100×MIC of antibiotic was added to each well and incubated overnight at 37° C. Following treatment, 100 μl of each biofilm supernatant was transferred to 96-well, white-walled plates, 100 μl of ToxiLight AK reagent was added to each well, mixtures were incubated for 30 min at room temperature, and luminescence was measured using a SpectraMax M5 plate reader. Biofilm-associated bacteria were enumerated by resuspending each biofilm in fresh PBS and plating. For S. aureus UAMS-1 biofilms, 96-well, flat-bottom plates were first coated with 100 μl of 20% human plasma in carbonate buffer overnight at 4° C. Following coating, the plasma solution was removed and cells were inoculated in each well 1:200 in 100 μl of tryptic soy broth supplemented with 3% glucose and 0.5% NaCl. Biofilms were cultured for 48 h in a humidified incubator at 37° C. Established S. aureus biofilms were washed once with PBS and then treated with a 100 μl of ToxiLight lysis buffer for 3 h, after which the amount of AK released into supernatants was measured, as described above. Small-Colony Variant AK Assays— Thirty-six-hour cultures of S. aureus strain UAMS-1112 were used to inoculate (1:100 dilution) 100 ml of fresh MH medium and grown at 37° C. on a rotary shaker at 225 rpm to an optical density (600 nm) of 0.1 to 0.2, corresponding to ˜1×10 6 CFU ml −1 . Cells were pelleted by centrifugation and resuspended in 2 ml of fresh MH medium. Ninety-eight microliters of MH medium containing 5×10 6 bacteria and 2 μl of the indicated antibiotic were added to individual wells of a white-walled, 96-well microtiter plate. Well components were mixed by pipetting and incubated at 37° C. for 3 h. The plate was equilibrated to room temperature for 30 min. Next, 100 μl of ToxiLight AK reagent was added to each well, followed by incubation at room temperature for 30 min, and luminescence was measured using a SpectraMax M5 plate reader. Galleria mellonella Model of S. aureus Infection— A Galleria mellonella model of infection was used to measure the putative antimicrobial properties of tamoxifen against E. faecium and terfenadine against S. aureus . To do so, overnight cultures of E. faecium strain 824-05 or S. aureus strain USA300-0114 were used to inoculate (1:100 dilution) 25 ml of fresh MH medium and grown at 37° C. on a rotary shaker at 225 rpm to exponential phase (˜1×10 8 CFU ml −1 ). Cultures were pelleted by centrifugation (2,000×g), washed with sterile PBS, and resuspended at ˜1×10 9 CFU ml −1 in fresh PBS. Galleria mellonella larvae (Vanderhorst Wholesale, Inc., St. Marys, Ohio) weighing 200 to 300 mg were inoculated with 5 μl of E. faecium or S. aureus (5×10 6 CFU) into the last left proleg using a 10-μl Hamilton syringe. Worms were then mock treated with either DMSO (negative control), vancomycin (20 mg kg −1 positive control) at 2 h and 24 h postinoculation. For K. faecium studies, groups were also treated with the test compound tamoxifen at 80, 160, or 320 mg kg −1 , whereas groups were treated with the test compound terfenadine (80, 160, or 320 mg kg −1 ) for S. aureus studies. Treatments were administered in the same manner as infection, except that each injection was in the next left proleg moving toward the head of the worm. Larvae were housed in petri dishes in the dark at 37° C. and monitored for viability at the conclusion of the study (48 h postinoculation); worms were considered dead if they did not respond to physical stimuli. In addition to mock or compound treatment of infected larvae, studies included two additional noninfected negative-control groups: one group that did not receive injections and one group that was injected with PBS to control for the impact of physical trauma. All experimental groups contained 15 worms, and each experiment was repeated three times. Rationale for Adenylate Kinase as a Reporter of Bacterial Cell Lysis— Adenylate kinase (AK) is a ubiquitous intracellular enzyme that catalyzes the conversion of 2 ADP↔ATP+AMP and is released into the extracellular space upon cell lysis. The premise of the assay is that agents which disrupt cellular integrity, either directly through damage of the membrane/cell wall or indirectly following the death of the cell, will induce release of AK into the culture medium. Extracellular AK is subsequently detected by the addition of commercially available ToxiLight AK assay reporter cocktail (Lonza, Basel, Switzerland), which generates a luminescent signal by utilizing AK-generated ATP in the standard luciferase catalyzed reaction (see FIG. 1 ). As shown herein, an AK assay was developed as a high-throughput screening platform for antibacterial drug discovery. The AK Assay Provides a Sensitive Measure of Bacterial Lysis— As an initial test of AK release as a reporter of bacterial cell death for Gram-positive and Gram-negative organisms, the sensitivity with which the assay measures AK in the culture supernatants of heat-killed E. coli and S. aureus was determined. Each bacterial species was grown to exponential phase, harvested, and resuspended at 1×10 9 CFU per ml in Mueller-Hinton (MH) medium. Bacterial suspensions were heat killed, and a 10-fold dilution series of supernatants was prepared; an aliquot of each heat-killed sample was plated to ensure ≥99° % bacterial death. The AK activity of the dilution series was measured and compared to the AK activity of mock-treated (viable) bacteria by Student's t test. In comparison to untreated cells, a statistically significant increase in AK activity was detected at dilutions containing 1.7×10 3 or more heat-killed E. coli supernatants, compared to results for live bacteria (see FIG. 2A ). AK activity increased ˜433-fold and ˜1,574-fold in cultures with 1×10 7 and 1×10 8 heat-killed E. coli supernatants, respectively, compared to results for mock-treated bacteria. A comparison of AK released from heat-killed S. aureus to that of mock-treated cells revealed a statistically significant difference in AK activity was detected at dilutions containing 1.8×10 4 or more heat-killed S. aureus supernatants, with a maximum 122-fold increase in AK activity observed for 1×10 lysed cells. Taken together, these results indicate that the AK assay reproducibly detects AK release following bacterial cell lysis and that the assay is extremely sensitive, allowing the identification of agents that cause lysis in 0.0001% or 0.001% of the starting inoculum of E. coli or S. aureus cells, respectively. Furthermore, the AK assay exhibited a dynamic range of nearly 3 orders of magnitude and an excellent signal-to-noise ratio. The AK Assay Detects Bactericidal Molecules that are Active Against the ESKAPE Pathogens— Next, ability of the AK assay to detect the activities of bactericidal antibiotics toward E. coli and each of the ESKAPE pathogens was examined. To do so, the MICs of six classes of bactericidal antibiotics (penicillin, cephalosporin, quinolone, glycopeptide, carbapenem, and polymyxin) were determined for each organism (see Table 2). An AK assay was then performed at 0, 0.125×, 0.25×, 0.5×, 1×, and 2×MIC of each antibiotic. As discussed below, AK release was detected at antibiotic concentrations below the MIC for most antibiotics tested, showing that the AK assay is more sensitive than growth-based assays for detecting bactericidal agents. As a representative example, FIG. 2B presents the AK assay measured polymyxin (colistin)-mediated killing of A. baumannii strain 98-37-09. The MIC of colistin for this strain is 4 μg ml −1 , whereas AK release was robustly detected at 0.25×, 0.5×, and 1×MIC value. TABLE 2MIC and AK measures of bacterial species and antibiotic combinations aValue for agentTreatmentBactericidalBacteriostaticStrain and parameter(×MIC)AmpicillinCeftriaxoneCiprofloxacinVancomycinMeropenemColistinSulfamethoxazoleMinocyclineErythromycinKanamycinLinezolidEnterococcus faecium 824-05MIC>256>2562562>256>256>2561>256>25616Fold increase in AK signal0.5NDNDND1NDNDND3NDND21.0NDNDND2NDNDND4NDND2Staphylococcus aureusUSA300-0114MIC>256>256214>256>256164>2562Fold increase in AK signal0.5NDND31113NDND11ND11.0NDND5317NDND11ND1RN4220MIC22222>256282162Fold increase in AK signal0.54108311ND211111.031210611ND31111Klebsiella pneumoniae cKP1MIC>2562>256>25628>25664>2562>256Fold increase in AK0.5ND50NDND12834ND1ND1NDsignal1.0ND55NDND22033ND1ND1NDAcinetobacter baumannii 98-37-09MIC25680.0625642481162256Fold increase in AK0.5ND522791762333NDsignal1.0ND2124134495141214NDPseudomonas aeruginosa PA01MIC>25642>256242563232256>256Fold increase in AK0.5ND227ND455ND13NDNDsignal1.0ND14182ND3912ND61NDNDEnterobacter cloacae PMD1001MIC>2562<1>25622>25642562>256Fold increase in AK signal0.5ND206ND9910ND4ND1ND1.0ND177ND29632ND9ND1NDEscherichia coli 8295MIC12820.1251628>2561625632>256Fold increase in AK signal0.550511716015ND4ND55ND1.074763928522ND38ND70ND% increase expected0.510083.383.3401001005050504001.010010083.36010010010062.525400a Shading indicates significant increase in AK signal (greater than or equal to threefold over vehicle-treated cells). The MIC measures for each ESKAPE pathogen and each organism's corresponding fold increase in AK signal following treatment with 0.5× and 1.0×, the MIC are provided in Table 2 (bactericidal agents). For four of the six bactericidal antibiotics tested, the AK assay proved to be superior to growth-based assays with respect to detecting the killing properties of bactericidal agents at sub-MIC values. More specifically, 100% of the organisms that were determined to be susceptible to the cell wall-active antibiotics ampicillin, meropenem, and colistin exhibited a significant increase in AK signal (≥3-fold over that for vehicle-treated cells) at both 0.5× and 1.0× their MICs Eighty-three percent and 100% of ceftriaxone-susceptible species exhibited increased AK signal at 0.5× and 1× their MICs, respectively. Five of six (83%) ciprofloxacin-susceptible organisms exhibited AK signal at both 0.5× and 1.0×MIC. Interestingly, the cell wall-targeted glycopeptide, vancomycin, caused significant AK release at 0.5× and 1.0× their MICs in only 40% and 60% of susceptible species. To evaluate the specificity of the assay for detecting bactericidal agents, measured AK release by each of the ESKAPE pathogens following exposure to five classes of bacteriostatic agents (sulfonamide, tetracycline, macrolide, aminoglycoside, and oxazolidine) was also measured. To do this, the MIC value of each bacteriostatic antibiotic/organism pair was measured by a conventional growth-based approach. AK release by each bacterial species following treatment with 0.5× or 1.0×MIC of each bacteriostatic agent was subsequently measured. As shown in FIG. 3 , S. aureus strain RN4220 was susceptible to all agents tested but bacteriostatic agents generated very low AK release, whereas bactericidal antibiotics generated robust AK detection. In most instances, a similar trend was observed for the other ESKAPE pathogens, indicating that the assay enriches for the identification of bactericidal agents, which are arguably the most valuable antibiotics because they can be used to treat patients with immunological defects or rapidly lethal infections (Table 2, bacteriostatic agents). Two exceptions were noted. Surprisingly, A. baumannii generated significant AK signal in response to all the bacteriostatic agents evaluated, showing that AK release may be a feature of a more general stress response in this organism. Additionally, the bacteriostatic agent minocycline generated signal by five of the eight (63%) organisms tested. Taken together, these results show that the AK assay provides a viable screening approach for identifying bactericidal agents at sub-MICs that could otherwise be missed by growth-based assays. Further, because the AK assay relies on bacterial killing as opposed to growth changes to generate its readout, it was hypothesized that it would provide a format to develop screens that are not readily available by conventional, growth-based approaches. Use of the AK Assay to Identify Agents with Antimicrobial Activities Against Established Biofilms and Small Colony Variants— Established bacterial biofilms represent a particularly problematic disease state, in part because biofilm-associated bacteria are recalcitrant to conventional antibiotic therapy. Thus, they have been a focus of antibiotic development. As a result, a number of approaches to screening for molecules with activity toward bacterial biofilms have been developed recently (Benoit et al. Environ. Microb. 76: 4136-4142; Perez et al. Lett. App. Microb. 51:331-337 (2010)). Although each has its advantages, they also have a number of limitations, including reproducibility, reliance on specialized equipment, or low throughput. It was hypothesized that the AK assay would provide a solution to some of these problems because it is rapid, sensitive, and simple to perform and it detects bactericidal molecules, the type of antibiotics required to treat established biofilms. To determine whether the AK assay could detect agents with activity against established biofilms, S. aureus strain UAMS-1 , A. baumannii strain 98-37-09, and P. aeruginosa strain PAO1 static biofilms were formed in 96-well flat-bottom plates Forty-eight hours postinoculation, one well corresponding to each organism was stained with crystal violet to verify that biofilm formation had occurred, whereas the remaining wells were treated with 10× the MIC value with either colistin ( A. baumannii biofilms) or ciprofloxacin ( P. aeruginosa , and S. aureus biofilms). Following overnight antibiotic treatment, biofilm-associated bacteria were enumerated by plating, and the corresponding supernatants were analyzed by the AK assay. Plating verified that 10×MIC antibiotic treatment resulted in a significant reduction in biofilm-associated P. aeruginosa (a 3.1-log decrease), S. aureus (a 0.7-log decrease), and A. baumannii (a 1.8-log decrease) compared to findings for untreated biofilms. As shown in FIG. 4A , corresponding AK measures indicated that the assay robustly detects the mild effects of these antibiotics on each bacterial species tested, showing that it represents a promising approach to identify agents that exhibit bactericidal activity toward established bacterial biofilms. Another context in which the AK assay can be particularly valuable is in the identification of molecules that exhibit bactericidal activity toward bacterial small-colony variants (SCV). SCV are slow-growing populations of bacterial species that have been hypothesized to cause latent or recurrent infections and are tolerant of standard antibiotic treatment regimens. Based on the aberrant SCV growth characteristics, typical growth-based HTS assays would be difficult to employ. Accordingly, the ability of the AK assay to identify agents that kill S. aureus SCV strain UAMS-1112 was tested. To do so, 1×10 6 UAMS-1112 cells were treated with 1× or 10×MIC ciprofloxacin, meropenem, or vancomycin for 3 h. Following treatment, suspensions were plated to measure the antimicrobial properties of each antibiotic, and the AK assay was performed to measure adenylate kinase release. Plating revealed that ciprofloxacin and vancomycin had no effect on SCV viability at any concentration tested and exhibited no change in AK release in comparison to results for mock-treated cells ( FIG. 4B ), supporting the observation that S. aureus small-colony variants are recalcitrant to antibiotic treatment. Meropenem treatment resulted in a 0.5-log decrease in SCV viability, which corresponded to a 2.5-fold increase in AK signal compared to that for mock-treated cells ( FIG. 4B ). Taken together, these results show that the AK assay provides the sensitivity needed to detect the slight antimicrobial effects of antibiotics, such as meropenem, toward S. aureus SCV. Validation of AK as an HTS-Compatible Assay of Antibacterial Activity— To test the viability of the AK assay as a general tool in HTS-based antibacterial small-molecule discovery, optimized assay parameters, including inoculum, drug incubation time, and AK reaction time, for screening planktonic ESKAPE species as well as E. coli in a 384-well format were determined. Based on these experiments, a standardized assay, as described above, was developed. As part of this optimization process, control assays in a 384-well format were performed to measure the signal to noise and reproducibility of the assay in an HTS manner. For this, plates were seeded with E. coli or an ESKAPE pathogen. Alternating columns of the plate were then mixed with either 2% DMSO (negative control) or a bactericidal antibiotic (positive control), and AK signal was detected, a representative result for DMSO- and colistin-treated K. pneumoniae is shown in FIG. 5A . Comparisons of the variance in signal between positive- and negative-control measures indicated that the AK assay provides Z′-factor scores between 0.59 and 0.82 (depending on the specific organism), indicating that the assay is sufficiently robust for HTS. AK-Based Screening of Library of Off-Patent Drugs and Biologically Active Molecules— To further validate the AK assay protocol, E. coli and each of the ESKAPE pathogens was screened against the Prestwick library of FDA-approved drugs and biologically active molecules (1,120 compounds, total; 50 μM final drug concentration). The Prestwick library contains representatives of nearly all classes of antibiotics currently in clinical use, making it an ideal library for testing the ability of the AK assay to detect bactericidal agents in a high-throughput screening format. Accordingly, the library was screened for antimicrobial agents that were active against planktonic E. coli and each of the ESKAPE pathogens using the AK assay; the cutoff for positive-scoring molecules was set at a 3-fold increase in extracellular AK activity, corresponding to the detection limit of statistically significant increases in AK activity for planktonic bacteria. The hit rates for the different organisms ranged from 1.4% to 4.8%; a representative example of raw screening data for Klebsiella pneumoniae is shown in FIG. 5B . Screening results for all ESKAPE pathogens are summarized in Table 3, whereas results for all compounds within the Prestwick library are provided in Table 4. TABLE 3Preswick library screening resultsNo. of active agents for speciesCompoundE. coliE. faeciumS. aureus aK. pneumoniaeA. baumannii aP. aeruginosaE. cloacaeBactericidal4542519172116Bacteriostatic21140701Detergent2222210Other5910418112Total54165125442329a Tetracyclines were identified. TABLE 4AK-based Prestwick Library Screening Results.E. coliE. faeciumS. aureusK. pneumoniaeA. baumanniiP. aeruginosaE. cloacaeChemical nameMechanismTherapeutic group0.40.80.60.30.30.30.3Azaguanine-8Purine antimetaboliteAntineoplastic0.40.80.40.40.40.30.3MetronidazoleBacterial DNA damageAntibacterial0.40.71.40.40.40.30.3AllantoinPrecipitate proteinsVulnerary0.50.80.40.40.30.30.3Cotinine (−)Antidepressant0.40.90.40.40.40.30.3AcetazolamideCarbonic anhydrase inhibitorDiuretic0.40.80.40.50.40.40.3Edrophonium chlorideCholinergicMyasthenia Gravis test0.50.80.40.40.40.30.3Metformin hydrochloride—Antidiabetic0.50.80.40.40.40.30.3Moroxidine hydrochloride—Antiviral0.50.80.50.50.40.40.3Atracurium besylateNeuromuscular blocking agentCurarizing agent0.50.80.40.60.40.30.3Baclofen (R,S)GABAb agonistAntispasmodic0.50.90.40.50.40.40.4Isoflupredone acetateAnti-inflammatory0.50.90.50.50.40.40.3AcyclovirADN polymerase inhibitorAntiviral0.50.80.40.40.40.30.4Amiloride hydrochloride dihydrateAntialdosteronDiuretic0.50.90.50.40.40.40.4DiazoxideActivator of ATP-dependent K+ channelsAntihypertensor0.50.90.50.60.50.40.4Amprolium hydrochlorideThiamine transport inhibitorCoccidiostatic0.50.90.40.50.40.40.4AmidopyrineACTH secretorAntipyretic0.51.10.50.60.50.50.4HydrochlorothiazideNa+ Cl− transport inhibitorDiuretic0.42.80.10.40.50.40.5Ursolic acid—Diuretic0.51.00.50.60.50.50.4SulfaguanidineInhibitor of folic acid synthesisAntibacterial0.51.00.50.60.50.40.4PindololBeta adrenergic antagonistAntiarrhythmic0.61.00.70.60.60.60.6Isoniazid—Antibacterial0.60.90.70.60.50.70.7Mexiletine hydrochlorideNa+ channel blockerAntiarrhythmic0.61.00.70.50.60.70.6PentylenetetrazoleGABA antagonistCNS stimulant0.50.90.60.60.50.60.6Flavoxate hydrochloridePhosphodiesterase inhibitorAntispasmodic0.60.90.50.50.60.60.6Chlorzoxazone—Muscle relaxant0.50.90.40.50.50.50.6Bufexamac—Antiinflammatory0.60.90.50.50.60.60.6OrnidazoleBacterial DNA damageAntibacterial0.50.90.50.60.60.60.5Glutethimide, para-aminoAromatase inhibitorAntineoplasic0.60.90.50.60.50.50.6EthosuximideCa++ channel inhibitorAnticonvulsantvoltage dependant0.70.90.50.50.50.50.5Dropropizine (R,S)—Antitussive0.61.20.60.50.50.50.6Mafenide hydrochlorideInhibitor of folic acid biosynthesisAntibacterial0.50.90.50.50.50.50.6PinacidilK+ channel Ca++ dependant activatorVasodilatator0.20.30.20.20.20.20.5Riluzole hydrochlorideGlutamate antagonistNeuroprotective0.30.50.20.30.30.30.4Albendazole0.41.00.40.80.50.40.6NitrofurantoinBacterial DNA damageUrinary antiseptic0.50.90.50.50.60.50.6Clonidine hydrochlorideAlpha2 agonistAntihypertensor0.00.30.20.00.10.00.3Hydralazine hydrochlorideAdrenergic antagonistAntihypertensor0.51.00.50.50.50.50.5Bupropion hydrochloride—Antidepressant0.50.80.50.60.50.50.5Phenelzine sulfateMAO inhibitorAntidepressant0.60.90.60.50.70.50.4Alprenolol hydrochlorideBeta1 antagonistAntihypertensor0.60.90.80.50.80.60.7MeticraneNa+ channel blockerAntihypertensor0.60.90.70.60.70.70.7Khellin—Phototherapeutic agent0.70.80.70.60.70.60.7BenzonatateAntitussive0.70.90.80.50.70.60.8Zimelidine dihydrochloride5-HT uptake inhibitorAntidepressantmonohydrate0.70.90.50.50.70.50.7HydroflumethiazideNa+ Cl− transport inhibitorAntihypertensor0.60.90.70.60.60.60.9AzacyclonolH1 antagonistAnxiolytic0.60.90.70.52.20.50.7Sulfacetamide sodic hydrateAntipsoriasic0.60.80.70.50.70.60.8AzathioprineAntimetaboliteImmunosuppressant0.80.90.70.50.60.50.7Heptaminol hydrochloride—Antihypotensive0.70.90.50.61.40.60.7LynestrenolAntioestrogenProgestogen0.70.90.60.61.00.60.7SulfathiazoleInhibitor of folic acidAntibacterialsynthesis0.71.00.50.40.80.60.7Guanabenz acetateAlpha agonistAntihypertensor0.60.80.50.60.70.50.8LevodopaTyrosine aminotransferaseAntiparkinsonianinhibitor0.91.01.10.61.00.60.7DisulfiramDopamine beta-hydroxylaseAlcohol deterrentinhibitor0.71.00.70.60.70.60.8IdoxuridineNucleic acid synthesisAntiviralinhibitors0.61.00.70.60.70.60.8Acetylsalicylsalicylic acidCyclooxygenase inhibitorAntiinflammatory0.71.00.70.60.80.60.8CaptoprilAngiotensive convertingAntihypertensorenzyme inhibitor0.70.90.70.60.80.80.7Mianserine hydrochloride5-HT antagonistAntidepressant0.61.00.70.60.80.60.7MinoxidilK+ channel activatorAntihypertensor0.60.90.60.50.60.60.7NocodazoleMicrotubule poisonAntineoplastic0.81.10.70.70.80.90.9Tranexamic acidPlasminogen inhibitorHemostatic0.91.00.80.70.90.90.9ChlorothiazideNa+ Cl− transport inhibitorAntihypertensor0.81.00.80.60.80.70.9EtofyllinePhosphodiesterase inhibitorCardiac analeptic0.81.00.70.70.70.80.8Diphenidol hydrochloride—Antivertigo0.81.00.80.60.90.80.9Tranylcypromine hydrochlorideMAO inhibitorAntidepressant0.71.00.80.70.70.80.9Norethindrone—Progestogen0.90.90.70.70.90.80.9Alverine citrate saltAnticholinergicSpasmolytic0.90.91.00.70.90.80.9Nortriptyline hydrochlorideNorepinephrine uptakeAntidepressantinhibitor0.71.00.70.60.70.80.8AceclofenacCyclooxygenase inhibitorAntiinflammatory0.60.90.70.60.70.70.8Niflumic acidProstaglandine synthesisAnalgesicinhibitor0.81.01.00.70.70.70.8Iproniazide phosphateMonoamine oxydaseAntidepressantinhibitor (non selective)0.71.00.60.60.70.80.9Isotretinoin—Cystic acne0.71.00.70.61.30.70.7Sulfamethoxazole0.71.00.80.60.80.70.9Retinoic acid—Keratolytic0.71.00.80.70.80.60.8Mephenesin—Muscle relaxant0.71.00.80.60.80.70.8Antazoline hydrochlorideH1 antagonistAntihistaminic0.81.00.70.60.80.70.8Phenformin hydrochlorideNeoglucogenese inhibitorAntidiabetic0.71.31.40.60.80.70.8Ethacrynic acidNa+ Cl− uptake inhibitorDiuretic0.71.00.40.60.70.80.7FlutamideAndrogenic receptorAnticancerantagonist0.91.00.80.60.70.60.7PraziquantelModulates cell membraneAnthelminticpermeability0.80.80.80.71.40.80.8SulfaphenazoleInhibitor of folic acidAntibacterialsynthesis0.80.80.90.80.80.60.9R(−) Apomorphine hydrochlorideD1 agonistEmetichemihydrate0.90.80.60.70.80.71.0Panthenol (D)—Vitamin1.00.90.70.80.80.90.9AmoxapineDopamine-reuptakeAntidepressantinhibitor1.00.80.70.71.20.80.9SulfadiazineInhibitor of folic acidAntibacterialsynthesis0.90.90.60.60.90.90.9Cyproheptadine hydrochloride5-HT antagonistAntipruritic0.90.90.70.70.70.81.0Norethynodrel—Progestogen0.90.80.50.80.80.81.0FamotidineH2 histaminic antagonistAntiulcerative0.90.98.70.40.90.81.4ThiamphenicolRibosomal protein synthesisAntibacterialinhibitor0.70.90.60.60.90.80.9DanazolEstrogen antagonistAntigonadotropin0.90.90.80.70.80.81.0CimetidineH2 antagonistAntiulcer0.90.90.60.80.80.70.9NicorandilAntihypertensor0.80.90.70.60.80.81.0Doxylamine succinateH1 antagonistAntihistaminic0.91.00.80.71.00.81.1TomatineAntifungal0.90.90.60.70.80.71.1Ethambutol dihydrochlorideChelating agentAntibacterial0.90.90.70.80.80.81.0Nomifensine maleateDopamine uptake inhibitorAntidepressant0.91.00.70.71.00.81.0Antipyrine—Analgesic0.90.90.70.70.80.91.0Dizocilpine maleateProbe for NMDA receptors—0.91.00.70.70.80.81.0Antipyrine, 4-hydroxy—Antipyrine metabolite0.91.00.80.70.80.90.9AcenocoumarolVitamin K antagonistAnticoagulant0.91.00.80.70.91.01.0Ampyrone—Analgesic1.00.90.80.80.91.01.1Ethisterone—Progestogen1.01.00.90.71.11.01.0Levamisole hydrochlorideAlkaline phosphataseImmunomodulatorinhibitor1.01.00.60.70.91.01.0Triprolidine hydrochlorideH1 antagonistAntihistaminic1.00.90.80.80.91.00.9Pargyline hydrochlorideMonoamine oxidaseAntihypertensorinhibitor1.11.00.90.80.91.11.0Doxepin hydrochlorideAdrenaline uptake inhibitorAnticonvulsant0.90.90.80.60.90.91.0Methocarbamol—Muscle relaxant1.01.00.90.70.91.01.1Dyclonine hydrochlorideNa+ channel blockerLocal anesthesic15.91.00.62.65.49.118.4AztreonamBacterial transpeptidaseAntibacterialinhibitor1.01.00.80.70.81.01.2DimenhydrinateH1 antogonistAntihistaminic1.01.05.30.71.31.01.0Cloxacillin sodium saltBacterial transpeptidaseAntibacterialinhibitor0.90.92.70.60.90.91.0DisopyramideNa+ channel blockerAntiarrhythmic1.01.00.80.80.80.71.0Catharanthine1.01.32.01.03.31.01.0ClotrimazoleSpecific inhibitor of Ca2+Antibacterialactivated K+ channels0.80.90.70.71.01.01.1Pentolinium bitartrateGlanglionic blocking agentAntihypertensor0.91.00.80.80.91.01.0VinpocetinePhosphodiesterase inhibitorNootropic drug0.90.90.70.80.80.91.1Aminopurine, 6-benzylInhibitor of respiratorykinase in plants1.11.10.80.71.00.91.0Clomipramine hydrochlorideNoradrenaline reuptakeAntidepressantinhibitor0.81.00.70.80.90.91.0TolbutamideK+ channel ATP dependantHypoglycemicinhibitor1.01.10.80.81.51.10.9Fendiline hydrochlorideCa++ channel activatorAntianginal0.70.89.70.21.00.81.5ChloramphenicolRibosomalAntibacterialpeptidyltransferase inhibitor0.90.80.70.60.80.81.1Naloxone hydrochlorideOpiate antagonistOpioate antidote1.00.82.20.70.90.81.2EpirizoleAntiinflammatory0.80.80.70.60.80.71.0Metolazone—Diuretic1.00.90.70.60.80.71.1DiprophyllinePhosphodiesterase inhibitorCardiac analeptic33.61.21.50.82.229.74.7Ciprofloxacin hydrochlorideAnti-bacterial0.60.70.60.51.10.61.2TriamtereneNon competitiveDiureticaldosterone antagonist12.21.10.50.61.60.73.5Ampicillin trihydrateAntibacterial0.80.90.60.71.30.81.1DapsoneFolic acid antagonistAntiinflammatory0.90.90.80.61.00.91.1HaloperidolDopamine antagonistAntipsychotic0.91.06.50.60.80.71.1TroleandomycinRibosomal protein synthesisAntibacterialinhibitor0.91.00.70.60.90.81.3Naltrexone hydrochlorideOpioid antagonistAnalgesicdihydrate1.41.00.70.72.50.91.3PyrimethamineAntimalarial1.00.90.80.70.90.81.1Chlorpheniramine maleateH1 antagonistAntihistaminic0.90.90.70.70.90.81.2Hexamethonium dibromideGanglion blocking agentAntihypertensordihydrate0.90.90.70.70.90.81.2Nalbuphine hydrochlorideOpioid ligandAnalgesic0.70.90.60.60.70.61.2DiflunisalCyclooxygenase inhibitorAntiinflammatory0.90.90.70.80.90.81.2Picotamide monohydrateEicosenoid receptorAntithromboticantagonist0.10.10.40.10.20.10.5NiclosamideHelmintic DNA damageAnthelmintic1.01.00.80.70.90.71.2Triamcinolone—Antiinflamatory1.01.00.90.70.90.91.0Midodrine hydrochlorideAlpha adrenergicHypotensor0.90.90.70.70.91.01.2Vincamine—Cerebral antianoxic1.01.01.00.80.90.91.1Thalidomide—Immunosuppressant0.90.90.60.81.00.91.2IndomethacinCyclooxygenase inhibitorAntiinflammatory13.11.11.01.62.31.04.3Oxolinic acidTopoisomerase II inhibitorAntibacterial0.90.90.80.81.01.01.2CortisoneAntiinflammatory0.90.80.70.70.90.91.4NimesulideCyclooxygenase 2 inhibitorAntiinflammatory1.01.00.80.71.01.01.3Prednisolone—Glucocorticoid1.00.90.70.80.90.91.2Hydrastinine hydrochlorideDopamine receptor blockerCardiotonic0.80.80.80.60.70.81.2FenofibrateLipoprotein lipase activatorHypolipidemiant0.80.90.80.70.90.81.1PentoxifyllinePhosphodiesterase inhibitorVasodilatator0.90.90.70.70.80.81.3BumetanideVascular cyclooxygenaseDiureticactivator1.01.00.70.80.90.81.3Metaraminol bitartrateAdrenergic agonistVasoconstrictor0.90.90.80.70.90.91.3Labetalol hydrochloride0.91.00.80.70.90.81.4SalbutamolBeta adrenergic agonistBronchodilatator0.91.01.00.82.30.91.2CinnarizineH1 antagonistAntihistaminic0.90.90.80.70.90.91.3Prilocaine hydrochlorideNa+ channel blockerLocal anesthesic0.81.00.80.70.90.91.3Methylprednisolone, 6-alphaGlucocorticoid0.90.90.70.80.80.81.1Camptothecine (S,+)Topoisomerase I inhibitorAntitumor agent1.01.00.90.80.90.91.1Quinidine hydrochlorideHeme polymerase inhibitorAntiarrhythmicmonohydrate1.20.91.21.01.11.01.4Procaine hydrochlorideNa+ channel blockerLocal anesthesic1.30.90.61.11.41.11.4Bromocryptine mesylateProlactin inhibitorAntiparkinsonian1.20.91.11.01.11.11.6Moxisylyte hydrochorideAlpha antagonistVasodilatator1.31.01.21.01.11.11.3Metanephrine hydrochloride DLIsoprenaline uptake inhibitorextraneuronal1.31.01.20.91.21.01.4Betazole hydrochlorideHistamine analogGastric secretion stimulant1.31.01.00.81.01.01.4Dehydrocholic acid—Choleretic1.21.01.01.01.01.01.4IsoxicamCyclooxygenase inhibitorAntiinflammatory1.10.90.50.91.10.91.3HesperetinP450 inhibitor1.21.00.80.91.11.01.4NaproxenCyclooxygenase inhibitorAntiinflammatory1.51.20.91.31.61.11.4PerphenazineDopamine antagonistAntipsychotic1.31.11.00.81.11.01.5Naphazoline hydrochlorideAdrenergic ligandVasoconstrictor1.31.03.21.32.61.11.2Mefloquine hydrochlorideHeme polymerase inhibitorAntimalarial1.31.00.81.01.11.12.0Ticlopidine hydrochlorideADP antagonistPlatelet antiaggregant1.81.85.21.45.61.31.7IsoconazoleSterol 14-demethylaseAntibacterialinhibitor1.21.11.00.91.31.21.5Dicyclomine hydrochlorideAnticholinergicAntispasmodic1.41.01.21.01.11.01.3SpironolactoneAldosterone antagonistDiuretic1.41.11.10.81.10.91.2Amyleine hydrochlorideNa+ channel blockerLocal Anesthesic1.41.11.01.01.11.01.4Pirenzepine dihydrochlorideM1 antagonistAntiulcerative1.31.21.11.11.11.11.3Lidocaine hydrochlorideNa+ channel blockerLocal anesthesic1.41.21.21.11.11.01.2Dexamethasone acetateAntiinflammatory1.41.11.20.91.11.31.5Ranitidine hydrochlorideH2 antagonistAntiulcerative1.31.11.01.01.21.21.4Fludrocortisone acetate—Mineralocorticoid1.11.30.41.01.11.21.5Tiratricol, 3,3′,5-—Hypocholesterolemic drugtriiodothyroacetic acid1.31.11.00.91.31.11.4Fenoterol hydrobromideBeta adrenergic agonistBronchodilatator1.01.00.51.01.31.11.8Flufenamic acidCyclooxygenase inhibitorAnalgesic1.51.21.01.11.21.21.8HomochlorcyclizineH1 antagonistAntihistaminicdihydrochloride13.61.52.22.22.91.424.4FlumequineTopoisomerase II inhibitorAntibacterial1.31.21.10.91.11.11.7Diethylcarbamazine citrateLipoxygenase inhibitorAntihelmintic1.01.10.50.81.41.21.6Tolfenamic acidCyclooxygenase inhibitorAntiinflammatory1.21.01.70.81.01.21.5ChenodiolDetergentAnticholelithogenic1.11.20.61.01.21.21.4Meclofenamic acid sodium saltCyclooxygenase inhibitorAntiinflammatorymonohydrate1.81.20.81.63.41.41.5Perhexiline maleateCa2+ blocking agentVasodilatator1.11.11.01.01.21.01.4KawainCa++ channel blockerAntiaggregant1.41.11.20.91.11.01.6Oxybutynin chlorideAnticholinergicSpasmolytic1.21.11.00.83.11.17.2TrimethoprimFolic acid antagonistAntibacterial1.31.21.00.91.21.21.3SpiperoneD2 antagonistAntipsychotic1.31.20.90.91.21.11.6Metoclopramide5-HT3 antagonistAntiemeticmonohydrochloride1.41.21.41.01.11.11.4Pyrilamine maleateH1 antagonistAntihistaminic0.90.90.60.70.90.91.3FenbendazoleMicrotubule formationAntihelminticinhibitor1.31.13.51.01.21.01.2Sulfinpyrazone—Uricosuric1.20.81.11.10.91.01.5TrichlorfonCholinesterase inhibitorAntihelminthic1.20.91.20.81.01.01.3Glipizide1.00.81.00.90.91.01.5CarbamazepineCholinergic antagonistAnticonvulsivant1.00.91.11.01.00.91.3Loxapine succinateDopamine antagonistAnxiolytic1.10.91.11.01.51.01.6Triflupromazine hydrochlorideDopaminergic antagonist ?Antipsychotic1.00.90.90.81.01.01.6Hydroxyzine dihydrochlorideH1 antogonistAntihistaminic0.90.90.70.81.20.91.6Mefenamic acidCyclooxygenase inhibitorAntiinflammatory1.00.90.81.01.00.91.5Diltiazem hydrochlorideCa2+ channel inhibitor (L-AntianginalType)1.20.91.10.81.11.21.7AcetohexamideBlocking of ATP-sensitive K+Antidiabetic (type II,channelnoninsulin-dependent)1.10.80.90.81.01.01.3Methotrexate1.01.01.11.01.01.11.6SulpirideD2 antagonistAntipsychotic1.31.02.21.11.61.01.6AstemizoleH1 antagonistAntihistaminic1.30.91.01.01.10.91.4Benoxinate hydrochlorideNa+ channel blockerLocal anesthesic0.81.28.40.51.01.11.7Clindamycin hydrochlorideRibosomal protein synthesisAntibacterialinhibitor1.41.01.01.54.21.01.5OxethazaineNa+ channel blockerLocal anesthesic1.71.5###1.13.11.01.2TerfenadineH1 antagonistAntihistaminic1.41.01.01.01.01.01.7Pheniramine maleateH1 antagonistAntihistaminic21.91.02.95.52.210.022.0Cefotaxime sodium saltBacterial transpeptidaseAntibacterialinhibitor1.41.01.21.01.31.11.5Tolazoline hydrochlorideAlpha antagonistVasodilatator0.81.09.20.24.40.51.0Tetracycline hydrochlorideRibosomal protein synthesisAntibacterialinhibitor1.21.11.41.01.01.21.4PiroxicamCyclooxygenase inhibitorAntiinflammatory1.01.01.10.91.11.21.5Dantrolene sodium saltBlocker of Ca2+ releaseSkeletal muscle relaxant1.31.11.20.91.11.21.4Pyrantel tartrateNeuromuscular depolarizingAnthelminticagent0.91.00.91.01.01.21.3Trazodone hydrochloride5-HT uptake inhibitorAntidepressant1.31.01.11.01.21.11.6Fenspiride hydrochlorideBradykinin antagonistAntiinflammatory1.21.11.11.01.11.21.5Glafenine hydrochloride—Analgesic1.31.00.90.91.31.21.5Gemfibrozil—Antihyperlipoproteinemic1.41.10.91.21.11.11.4Pimethixene maleateAnticholinergicAntihistaminic1.21.00.90.91.01.11.3Mefexamide hydrochloride—Psychoanaleptic1.31.01.00.81.31.01.4Pergolide mesylateDopaminergic agonistAntiparkinsonian1.41.11.00.91.11.21.5Tiapride hydrochlorideDopamine antagonistAntidyskinetic1.21.01.10.91.11.11.3AcemetacinCyclooxygenase inhibitorAntiinflammatory0.80.90.90.80.70.81.2Mebendazole1.31.11.11.01.01.21.2Benzydamine hydrochloride5-HT receptor antagonistAnalgesic0.80.80.70.81.00.81.6FenbufenCyclooxygenase inhibitorAntiinflammatory1.31.10.91.11.01.01.3Fipexide hydrochlorideGlutamatergicNootropic1.10.91.01.11.01.01.5KetoprofenCyclooxygenase inhibitorAntiinflammatory1.31.10.70.91.11.01.4MifepristoneProgesterone receptorAbortifacientantagonist1.11.11.01.11.01.11.7IndapamideDiuretic1.41.11.20.91.11.11.4Diperodon hydrochloride—Local anesthesic1.40.81.20.91.11.21.3Morantel tartrateFumarate reductaseAnthelminticinhibitor1.30.91.20.91.51.21.2Verapamyl hydrochlorideAlpha1 antagonistAntyhypertensive1.40.81.10.91.31.11.4Homatropine hydrobromide (R,S)Muscarinic antagonistAntispasmodic1.30.90.80.91.21.11.4Dipyridamole1.40.90.50.91.51.01.4NifedipineL-type Ca2+ channels blockerAntihypertensor50.14.0###18.812.323.81.8ChlorhexidineDetergentBacteriostatic1.41.01.41.11.51.11.4Chlorpromazine hydrochlorideDopamine antagonistAntiemetic1.40.91.00.91.51.21.5Loperamide hydrochlorideCa2+ channel antagonistAntidiarrhoeic1.30.91.11.01.31.01.4Diphenhydramine hydrochlorideH1 receptor antagonistAntihistaminic0.80.96.80.23.90.71.0Chlortetracycline hydrochlorideRibosomal protein synthesisAntibacterialinhibitor1.30.81.00.91.31.11.3Minaprine dihydrochlorideDopamine agonistAntidepressant1.94.02.12.16.61.41.3Tamoxifen citrateOestrogen receptorantagonist1.42.52.21.44.71.21.6MiconazoleSterol 14-demethylaseAntifungalinhibitor1.31.01.41.01.41.21.2NicergolineAlpha agonistVasodilatator1.11.01.11.01.51.11.5Isoxsuprine hydrochloridebeta adrenergic agonistVasodilatator1.41.01.10.91.51.31.2Canrenoic acid potassium saltDetergentAntihypercholesterolemic1.31.11.10.91.31.11.2Acebutolol hydrochlorideBeta1 antagonistAntianginal1.51.01.01.11.71.11.3Thioproperazine dimesylateDopamine antagonistAntipsychotic1.11.01.30.91.51.01.2Tolnaftate—Antifungal1.31.01.00.91.51.21.3Dihydroergotamine tartrateSerotonine antagonistAntimigraine33.11.51.80.83.131.33.1NorfloxacinTopoisomerase II inhibitorAntibacterial1.21.04.31.01.31.21.5LisinoprilConverting enzyme inhibitorAntihypertensor1.31.11.01.01.41.11.3Antimycin AInhibitor of mitochondrialAntifungalelectron transport0.91.37.90.91.21.21.3Lincomycin hydrochlorideRibosomal protein synthesisAntibacterialinhibitor1.21.01.20.91.31.21.4Xylometazoline hydrochlorideVasoconstrictor1.51.11.31.01.61.21.4Telenzepine dihydrochlorideM1 muscarinic antagonistAntiulcerative1.11.01.11.11.41.21.3Oxymetazoline hydrochloridePartial alpha2A agonistVasoconstrictor1.31.53.71.36.71.31.3Econazole nitrateErgosterol synthesisAntifungalinhibition1.21.01.31.01.61.21.2NifenazoneCyclooxygenase inhibitorAnalgesic1.31.01.11.01.41.21.5Bupivacaine hydrochlorideNa+ channel blockerLocal anesthesic1.31.11.40.91.41.31.3GriseofulvinEnzymatic inductorAntifungal1.41.01.21.11.51.21.2Clemastine fumarateH1 antagonistAntihistaminic1.21.21.61.01.61.21.4Clemizole hydrochlorideH1 antagonistAntihistaminic1.00.93.40.25.30.51.1Oxytetracycline dihydrateRibosomal protein synthesisAntibacterialinhibitor1.21.01.11.11.51.21.4TropicamideMuscarinic antagonistMydriatic1.71.32.31.38.71.31.2PimozideDopamine antagonist ?Antipsychotic1.21.01.10.91.41.21.4Nefopam hydrochloride—Analgesic1.21.11.30.91.51.21.4Amodiaquin dihydrochlorideHeme polymerase inhibitorAntimalarialdihydrate1.41.01.11.11.41.21.2Phentolamine hydrochlorideAlpha adrenergic antagonistAntihypertensor1.31.01.11.01.41.11.3Mebeverine hydrochlorideAntispasmodic1.30.81.31.01.11.11.7Todralazine hydrochloride—Antihypertensor1.01.08.21.01.50.71.6ErythromycinRibosomal protein synthesisAntibacterialinhibitor1.20.91.21.01.31.11.7Imipramine hydrochloride5-HT transport inhibitorAntidepressant1.11.03.61.01.11.01.6Oleandomycin phosphateRibosomal protein synthesisAntibacterialinhibitor1.10.90.81.01.10.81.5SulindacCyclooxygenase inhibitorAntiinflammatory4.70.91.20.91.51.04.2DidanosineTransrcriptase inverseAntiviralinhibitor1.21.01.41.11.31.01.8Amitryptiline hydrochlorideAlpha 1 antogonistAntidiabetic1.31.08.41.01.10.91.4JosamycinRibosomal protein synthesisAntibacterialinhibitor1.21.01.31.01.30.91.5Adiphenine hydrochlorideAnticholinergicLocal anesthesic1.11.01.01.01.31.01.6PaclitaxelTubuline inhibitorAntineoplastic1.30.91.31.11.31.11.7DibucaineNa+ channel blockerLocal anesthesic1.31.22.11.01.51.01.6IvermectinGABA ligandAnthelmintic1.20.91.10.91.20.91.4Prednisone—Glucocorticoid1.31.01.11.11.21.01.5Gallamine triethiodideM2 antagonist allostericMuscle relaxant1.61.01.31.32.91.11.5Thioridazine hydrochlorideCa2+ channel antagonistNeuroleptic1.21.01.11.01.40.91.3Neomycin sulfateRibosomal protein synthesisAntibacterialinhibitor1.21.11.51.11.31.01.6Diphemanil methylsulfateAnticholinergicBronchodilatator1.21.01.20.71.20.91.3Dihydrostreptomycin sulfateRibosomal protein synthesisAntibacterialinhibitor1.21.11.21.11.21.01.3TrimethobenzamideD2 antagonistAntiemetichydrochloride1.31.01.11.01.50.91.4Gentamicine sulfateRibosomal protein synthesisAntibacterialinhibitor1.21.11.01.31.41.51.2EtodolacCyclooxygenase inhibitorAntiinflammatory1.21.01.11.31.41.21.3Ifenprodil tartrateAdrenergic antagonistVasodilatator1.21.11.41.21.41.31.5Scopolamin-N-oxideAnticholinergicAntiparkinsonianhydrobromide1.71.31.11.42.61.31.6Flunarizine dihydrochlorideNa+ channel blockerVasodilatator1.31.01.21.21.41.21.5Hyoscyamine (L)CholinergicAntispasmodic1.71.11.21.53.41.41.3Trifluoperazine dihydrochlorideDopamine antagonistPsycholeptic1.20.91.01.11.31.11.4Chlorphensin carbamate—Muscle relaxant1.21.11.31.21.31.21.3Enalapril maleateConverting enzyme inhibitorAntihypertensor16.81.61.31.01.11.34.3Metampicillin sodium saltBacterial transpeptidaseAntibacterialinhibitor2.31.16.90.63.90.70.9Minocycline hydrochlorideRibosomal protein synthesisAntibacterialinhibitor1.51.11.21.41.41.31.1Dilazep dihydrochlorideAdenosine uptake inhibitorVasodilatator1.21.00.91.11.31.21.4GlibenclamideATP-dependent K+ channelAntidiabeticinhibitor15.71.42.81.03.720.04.1OfloxacinTopoisomerase II inhibitorAntibacterial1.41.11.11.11.31.41.4Guanethidine sulfateCatecholamine depletorAntihypertensor26.81.53.41.03.830.23.5Lomefloxacin hydrochlorideTopoisomerase II inhibitorAntibacterial1.21.01.21.01.30.91.4Quinacrine dihydrochlorideMonoamine oxydaseAntimalarialdihydrateinhibitor1.31.01.01.21.31.11.2Orphenadrine hydrochlorideH1 antogonistAntihistaminic1.51.41.21.51.61.31.2Clofilium tosylateK+ channel blockerAntiarrhythmic1.31.01.11.21.31.11.5ProglumideGastrin inhibitorAntiulcerative1.31.11.01.51.61.11.6Fluphenazine dihydrochlorideDopamine antagonistAntipsychotic0.50.90.40.30.40.40.3Streptomycin sulfateRibosomal protein synthesisAntibacterialinhibitor0.50.90.30.40.50.40.3Testosterone propionate—Androgen0.50.90.30.40.40.40.4Alfuzosin hydrochlorideAlpha 1-adrenergicAntihypertensorantagonist0.40.90.40.40.40.40.3Arecoline hydrobromideCholinergicAnthelmintic0.40.90.40.40.30.30.3ChlorpropamideGlucagon secretogen,Antidiabeticsomatostatin secretogen0.51.00.20.40.40.40.3Thyroxine (L)Thyroid hormoneHypocholesterolemic drug0.50.80.30.50.40.40.4PhenylpropanolamineAlpha adrenergic agonistDecongestanthydrochloride0.60.90.40.40.40.40.4Tocopherol (R,S)—Anti-oxidant0.50.90.40.50.40.30.4Ascorbic acid—Vitamin0.50.80.40.50.40.40.4Pepstatin AAspartic proteasesAntiviralirreversible inhibitor0.60.90.40.60.50.40.5Methyldopa (L,−)L-aromatic aminoacidAntihypertensordecarboxylase inhibitor0.50.80.40.50.50.40.4SR-95639AM1 agonist receptor16.50.90.72.10.75.212.0Cefoperazone dihydrateBacterial transpeptidaseAntibacterialinhibitor0.50.90.40.50.50.40.4Adamantamine fumarateInhibition of viral uncoatingAntiviraland viral assembly,alteration of dopaminerelease and reuptake0.70.80.40.60.40.40.4ZoxazolamineUric acid uptake inhibitorMuscle relaxant0.73.30.60.72.00.50.5Butoconazole nitrateErgosterol inhibitorAntifungal0.50.90.50.40.50.50.4Tacrine hydrochloride hydrateCholinesterase inhibitorCognition enhancer0.71.70.70.62.20.50.5Amiodarone hydrochlorideNa+ channel blocker, K+Antiarrhythmicchannel blocker, non-competitive beta-adrenergicblocker0.50.90.60.50.50.50.6Bisoprolol fumarateBeta1 antagonistAntihypertensor0.50.90.50.70.50.40.5Amphotericin BErgosterol ligandAntibacterial0.80.90.60.60.60.60.6Serotonin hydrochloride5-HT agonistNeurotransmitter0.70.90.50.60.70.60.6Tubocurarine chlorideCurarisingMuscle relaxantpentahydrate (+)23.90.92.37.80.90.615.6Cefotiam hydrochlorideAntibacterial0.70.90.50.60.70.60.6Dihydroergocristine mesylate5-HT antagonist, partialVasodilatatoradrenergic agonist, partialdopaminergic agonist0.60.90.40.50.50.60.6Azathymine, 6AntimetaboliteAnticancer0.60.90.50.50.60.50.6NoscapineInhibitor of carbachol-Antitussivestimulated phosphoinositideturnover0.61.00.50.50.50.60.6BenperidolDopamine antagonist, 5-HTAntipsychoticantagonist0.60.90.30.50.60.50.6SyrosingopineCatecholamine depletor—10.70.90.52.51.50.50.7CefaclorBacterial transpeptidaseAntibacterialinhibitor0.60.80.50.50.50.50.5Atropine sulfate monohydrateMuscarinic antagonistAnticholinergic42.21.00.624.110.023.60.7Colistin sulfatePerforms membraneAntibacterialionophores0.70.90.40.50.50.60.7Eserine sulfate, physostigmineCholinesterase inhibitorOphtalmic agentsulfate0.92.32.10.50.60.50.6Daunorubicin hydrochlorideDNA intercalingAntineoplastic0.60.90.50.50.60.50.6AconitineOpen TTX-Na+ channelAnalgesic0.60.90.50.50.50.50.5Dosulepin hydrochloride—Antidepressant0.71.00.30.61.10.40.6RescinnaminCatecholamine depletorAntihypertensor11.50.90.43.20.57.812.9Ceftazidime pentahydrateAntibacterial0.60.80.40.50.50.40.6Dihydroergotoxine mesylateHigh affinity GABA AAnticonvulsantreceptor Cl− channel,prolactin inhibitor0.50.90.50.50.50.40.6Iobenguane sulfate—Antineoplastic if radiolabeled0.50.90.50.60.50.50.5Emetine dihydrochlorideProtein synthesis inhibitor,Antiamebic5-HT ligand0.71.00.50.60.70.60.7Tremorine dihydrochlorideCholinergicConvulsant0.61.00.50.50.70.60.7Androsterone—Antihypertensor0.70.90.60.50.70.60.8PractololBeta antagonistAntihypertensor0.71.00.70.50.70.70.7AnisomycinAcetylcholine esteraseAntiprotozoalinhibitor2.10.90.61.21.80.64.2Zidovudine, AZTTranscriptase reverseAntiviralinhibitor0.61.00.60.50.60.60.7CarbarsoneAntiamebic0.70.90.50.51.00.60.7SulfisoxazoleInhibitor of folic acidAntibacterialbiosynthesis, Eta endothelinreceptor antagonist0.20.30.00.20.20.20.5ApigeninMAP kinase inhibitorAntiproliferative0.71.00.60.50.60.70.8ZaprinastcGMP phosphodiesteraseErectogeninhibitor, phosphodiesterase5 inhibitor0.60.90.50.50.60.60.7Aspartic acid, N-acetyl (R,S)——0.71.00.70.60.70.60.7Chlormezanone—Skeletal muscle relaxant11.91.10.50.61.30.60.6Bacampicillin hydrochlorideBacterial transpeptidaseAntibacterialinhibitor0.61.00.60.60.70.60.9Procainamide hydrochlorideAlpha antagonist,Antiarrhythmicantinuclear antibodies,anticholinergic0.60.90.10.50.60.60.7Betulinic acidApoptosis inducer, PLA2Antimalarialinhibitor0.60.90.50.50.60.60.7N6-methyladenosineAntimetaboliteAnticancer0.60.91.40.60.80.70.8Biotin—Vitamin H0.81.10.60.50.70.70.9Guanfacine hydrochlorideAlpha 2A agonistAntihypertensor0.61.00.50.60.80.60.9BisacodylNa+ uptake inhibitorCathartic0.60.90.80.60.70.60.8DomperidoneDopamine AntagonistsAntiemetic0.80.90.50.70.70.70.7CalciferolStimulator of calcium andVitamin Dphosphate absorption0.91.00.70.81.00.80.8Metixene hydrochlorideAnticholinergicAntiparkinsonian0.90.90.60.60.80.80.9Tetracaine hydrochlorideLocal anesthesic0.71.00.50.21.00.80.8NitrofuralBacterial DNA damageAntibacterial0.91.00.40.70.90.60.9Mometasone furoate—Antiinflammatory0.70.80.20.60.80.60.8OmeprazoleNon competitive ATPase H+Antiulcerativepump inhibitor0.71.20.50.60.70.71.0TomatidineCholinesterase activityAntifungal0.71.00.70.60.80.71.1PropylthiouracilAntimetaboliteAntihyperthyroid2.01.10.73.81.60.90.8DacarbazineAlkylating agentAntineoplastic0.91.00.60.70.80.80.9TerconazoleSterol 14-demethylaseAntifungalinhibitor0.60.90.70.60.60.80.8Ipratropium bromideAntimuscarinic agentBronchodilatator0.60.80.50.50.70.60.8Tiaprofenic acidCyclooxygenase inhibitorAntiinflammatory0.81.00.80.60.80.70.8Acetopromazine maleate saltDopaminergic antagonist ?Tranquilizer1.21.5###0.81.10.90.9Vancomycin hydrochlorideBacterial mucopeptideAntibacterialbiosynthesis inhibitor0.71.00.70.60.80.60.8Rauwolscine hydrochlorideAlpha2 antagonistAntidepressant0.50.90.50.60.70.60.7ArtemisininOxidantAntimalarial0.71.00.70.60.60.70.8Corynanthine hydrochlorideAlpha1-adrenoreceptorAnti-leishmania drugantagonist1.01.00.70.60.70.70.8Propafenone hydrochlorideBeta adrenergic antagonistAntiarrhythmic0.71.00.80.50.70.70.9Palmatine chlorideAnticholinestrase activityUterine contractant0.61.00.60.60.90.60.9Ethamivan—Respiratory analeptic0.81.20.60.71.00.70.8Trimethylcolchicinic acidTubuline inhibitor ?Anticancer agent1.00.90.70.70.80.90.8FurosemideNa+ Cl− uptake inhibitor,Diureticcarbonic anhydrase inhibitor1.95.42.02.54.16.80.9Suloctidil—Vasodilatator0.91.00.50.60.90.90.8Methapyrilene hydrochlorideHistamine H1 antagonistAntihistaminic0.80.90.70.60.80.80.8Carcinine—Anti-oxidant0.90.80.70.70.70.90.8Desipramine hydrochlorideAdrenergic transportAntidepressantinhibitor, 5-HT transportinhibitor0.90.90.70.60.80.90.8Carisoprodol—Muscle relaxant0.70.70.50.50.60.70.8Clorgyline hydrochlorideMonoamine oxidase AAntidepressantinhibitor0.90.90.60.70.80.80.8Cephalosporanic acid, 7-aminoBacterial transpeptidaseAntibacterialinhibitor0.80.90.70.70.80.80.9Clenbuterol hydrochlorideBeta adrenergic agonistBronchodilatator0.50.50.00.30.40.40.9Chicago sky blue 6BCompetitive glutamate—uptake inhibitor0.80.81.10.60.80.90.9Maprotiline hydrochlorideNoradrenaline uptakeAntidepressantinhibitor, 5-HT uptakeinhibitor0.80.80.60.60.70.80.9Buflomedil hydrochloride—Vasodilatator0.80.90.50.70.90.80.9ThioguanosineAntimetaboliteAnticancer0.80.90.50.70.80.70.8Chlorogenic acidGlucose-6-phosphateAntiinflammatorytranslocase inhibitor1.01.00.60.81.20.91.0Chlorprothixene hydrochlorideD2 dopamine receptorNeurolepticantagonist, GABAA receptorsantagonist0.81.00.60.70.80.70.9Roxatidine Acetate HClAntiulcerative0.80.90.50.70.80.90.9Ritodrine hydrochlorideBeta2 agonistTocolytic1.00.90.70.70.80.91.0Cholecalciferol—Vitamin0.90.90.70.80.91.01.0Clozapine5-HT antagonist, dopamineAntipsychoticantagonist, GABA ligand0.90.90.60.71.10.90.9Cisapride5-HT antagonistPeristaltic stimulant1.00.90.70.81.10.90.8VigabatrinGABA transaminase inhibitorAnticonvulsant0.91.00.60.81.00.90.9Hydrastine hydrochlorideGABAa antagonistHypotensor1.00.90.60.80.80.80.9Biperiden hydrochlorideAnticholinergicAntiparkinsonian1.00.90.60.81.01.01.0Lobelanidine hydrochlorideNicotinic ligand—0.90.90.70.71.10.90.9Cetirizine dihydrochlorideH1 antagonistAntihistaminic0.91.00.60.80.81.00.9Papaverine hydrochloridePhosphodiesterase inhibitorVasodilator1.10.90.50.80.90.91.0EtifeninChelating agentDiagnostic agent0.80.90.60.80.80.91.0Yohimbine hydrochlorideAlpha antagonistMydriatic1.00.90.60.70.90.91.0Metaproterenol sulfate,Beta-adrenergic agonistBronchodilatatororciprenaline sulfate1.00.90.80.70.80.91.0Lobeline alpha (−) hydrochorideNicotinic receptor ligandRespiratory stimulant0.80.90.60.60.90.91.0Sisomicin sulfateRibosomal protein synthesisAntibacterialinhibitor1.01.00.70.70.90.91.1Berberine chlorideAnti-HIV reverseAntibacterialtranscriptase, cholinesteraseinhibitor0.70.80.10.60.40.60.9Quercetine dihydrateLipoxygenase inhibitorAntimalarial0.90.90.80.70.90.90.9CilostazolAntithrombotic0.00.00.00.00.00.00.1ResveratrolAntiinflammatory0.90.90.80.80.80.81.0Galanthamine hydrobromideCholinesterase inhibitor,Alzheimer treatmentnicotinic receptor agonist0.80.90.70.71.01.11.1BromperidolDopamine antagonistAntipsychotic0.80.90.60.80.80.90.9Bicuculline (+)GABAa receptor antagonistConvulsant0.91.00.90.81.00.90.9Cyclizine hydrochlorideH1 antagonistAntiemetic0.90.90.70.70.80.90.9Yohimbinic acid monohydrate——0.90.90.70.60.80.81.0ChlorthalidoneNa+ uptake inhibitor,Diureticcarbonic anhydrase inhibitor0.90.90.40.60.80.81.1Coralyne chloride hydrateTopoisomerase I inhibitorAnti-leukemic0.80.80.10.80.70.61.1Dobutamine hydrochlorideBeta1, Beta2 agonistBronchodilatator0.90.90.60.70.90.81.2Corticosterone—Glucocorticoid0.90.90.60.60.70.81.2MoclobemideMono amine oxidaseAntidepressantinhibitor (Type A)0.80.80.50.60.80.71.2Cyanocobalamin—Vitamin0.80.90.70.70.80.81.0ClopamideGonad stimuling agentAntihypertensor0.90.80.50.80.90.81.2CefadroxilBacterial transpeptidaseAntibacterialinhibitor0.91.20.80.70.80.81.1HycanthoneDNA intercaling agentAnthelmintic0.90.90.60.70.90.81.4Cyclosporin AIL 2 synthesis inhibitor,Immunosuppressantcalcineurine phosphataseinhibitor0.80.80.60.60.70.81.2Adenosine 5′-monophosphateCa++ channel block,Nutrientmonohydrateadenosine receptoractivation, activation ofoutward K+ current0.90.90.60.70.80.81.2DigitoxigeninNa+ K+ ATPase inhibitorCardiotonic10.61.40.40.71.70.71.0AmoxicillinBacterial transpeptidaseAntibacterialinhibitor0.80.90.80.70.90.81.2DigoxinNa+ K+ ATPase inhibitorCardiotonic0.80.90.70.70.90.81.4Cephalexin monohydrateBacterial transpeptidaseAntibacterialinhibitor1.01.70.90.71.00.61.2Doxorubicin hydrochlorideDNA intercalantAntibacterial0.80.90.70.70.80.81.1Dextromethorphan hydrobromideOpioid ligandAntitussivemonohydrate0.80.90.60.70.80.71.2CarbimazoleIodine oxidazing inhibitorAntityroidic hormone0.91.00.90.71.00.71.2DroperidolAlpha adrenergic antagonist,Antipsychotic5-HT antagonist, dopamineantagonist0.91.00.60.70.80.81.1Epiandrosterone—Anabolic steroid1.00.91.10.81.00.91.1Fluoxetine hydrochloride5-HT uptake inhibitorAntidepressant1.00.90.70.70.90.91.3Laudanosine (R,S)—Convulsant1.00.90.70.70.90.81.1Iohexol—Diagnostic aid0.90.90.50.70.90.91.2Ajmalicine hydrochlorideAlpha antagonistAntihypertensor6.30.80.60.91.11.01.3Norcyclobenzaprine—Antiulcerative0.90.90.80.70.90.81.2TrigonellineAntihyperglycaemic agent0.90.80.70.80.90.81.2Pyrazinamide—Antibacterial0.90.90.80.70.80.91.2Diclofenac sodiumCyclooxygenase inhibitorAntiinflammatory1.00.90.70.70.90.81.4TrimethadioneCa++ channel blockerAnticonvulsantvoltage dependant ?0.90.80.60.70.80.81.2CalycanthineCalcium channel blocker1.01.00.30.81.00.81.2LovastatinHMG CoA reductaseAntihypercholesterolemicinhibitor1.10.90.60.71.00.81.3Convolamine hydrochlorideCholinergic ligandVasodilatator1.00.80.70.80.90.81.4NystatinePerforms membraneAntifungalionophores0.90.90.70.70.90.81.3Isocorydine (+)GanglioblockerHypotensor0.90.90.60.70.90.91.4Budesonide—Antiinflammatory0.80.90.80.70.90.91.4XylazineAlpha-2 adrenergic agonistAntinociceptive12.10.92.51.71.21.02.4ImipenemBacterial transpeptidaseAntibacterialinhibitor0.90.90.80.70.80.81.2Seneciphylline—Antitumor activity0.80.90.80.71.10.81.1Sulfasalazine15-hydroxydehydrogenaseTreatment of ulcerative colitisinhibitor0.90.90.80.70.80.91.2BoldineSmooth muscle relaxantCholeretic1.31.11.20.91.01.21.2Bambuterol hydrochlorideBeta2 adrenergic receptorBronchodilatatoragonist1.10.90.80.80.81.01.3Estradiol-17 beta—Estrogen1.11.11.10.90.91.11.3Betamethasone—Glucocorticoid0.81.10.90.90.91.11.2Fusaric acidDopamine beta hydroxylaseAntibacterialinhibitor1.21.01.00.91.01.01.1ColchicineTubulin polymerisationAntiinflammatoryinhibitor1.01.11.10.81.11.01.3GabazineAntagonist GABA1.21.01.11.01.31.11.3Metergoline5-HT1 antagonist, D2Antiprolactinagonist, 5-HT2 antagonist1.31.01.11.01.01.11.2Ginkgolide ACholinergic antagonistAlzheimer treatment1.11.41.00.91.11.11.5BrinzolamideCarbonic anhydrase inhibitorAntiglaucoma drug1.31.01.00.91.21.11.2Cyclobenzaprine hydrochloride—Muscle relaxant1.01.01.01.01.21.21.5Ambroxol hydrochloride—Expectorant1.21.01.10.81.01.11.1Carteolol hydrochlorideAntihypertensor1.40.91.21.11.01.11.4Benfluorex hydrochlorideIncrease of glucoseHypolipedimicpenetration and use by cells,decrease of triglycerideintestinal absorption1.11.01.30.91.31.11.4Hydrocortisone base—Glucocorticoid1.31.11.61.01.51.21.4Bepridil hydrochlorideCa++ channel blockerAntianginal1.31.03.01.01.01.01.3Hydroxytacrine maleate (R,S)Acetylcholine esteraseinhibitor1.00.92.00.80.90.91.2MeloxicamCyclooxygenase inhibitorAnti-inflammatory1.01.11.30.91.01.01.5Pilocarpine nitrateCholinergicAntiglaucoma drug1.11.20.40.91.41.51.4BenzbromaroneUric acid transport inhibitorCoronarodilatator1.21.07.10.91.51.41.2Dicloxacillin sodium saltBacterial transpeptidaseAntibacterialinhibitor1.11.11.21.01.11.11.4Glycocholic acidDetergentAnticholelithogenic1.21.01.01.01.31.11.6ScoulerineDopamine antagonist,Antiemeticalpha1 antagonist1.31.00.41.01.10.91.4ThiostreptonAntibacterial1.21.11.00.91.11.11.6AjmalineInhibitor of glucose uptakeAntihypertensorby heart tissue1.31.01.10.91.01.21.5Methionine sulfoximine (L)Glutamine synthetase—inhibitor1.31.11.01.01.21.21.3Monocrotaline—For inducing pulmonarydiseases in rats0.60.50.60.40.50.61.3TiabendazoleMicrotubule inhibitorAnthelmintic1.21.01.01.01.01.11.6Piperlongumine—Antifungal1.30.80.80.73.00.61.4RifampicinRNA polymerase inhibitorAntibacterial1.21.01.00.91.31.21.4Hydrocotarnine hydrobromide—Hemostatic1.11.01.31.01.21.11.4EthionamideAntibacterial1.31.00.90.81.11.11.6(−)-CinchonidineAntimalarial1.31.01.20.91.01.11.6TenoxicamCyclooxygenase inhibitorAntiinflammatory1.21.11.01.01.11.31.4Eburnamonine (−)—Cerebral vasodilatator1.21.01.40.91.01.21.3TriflusalCyclooxygenase inhibitorAntithrombotic1.21.11.61.01.11.11.5CinchonineHeme polymerase inhibitorAntimalarial1.11.11.31.01.01.21.3Mesoridazine besylateD antagonistAntipsychotic1.21.11.60.91.11.11.4Canavanine sulfate monohydrateNitric oxide inductibleAnticancer agent(L,+)synthetase inhibitor1.11.11.61.11.11.11.6Trolox—Vitamin E analog1.11.01.40.91.01.01.3Harmaline hydrochlorideMonoamine oxydaseAntihelminthicdihydrateinhibitor1.31.01.10.91.11.11.7Ketotifen fumarateH1 antagonistAntihistaminic1.01.01.00.91.11.11.4Alizapride HClAntiemetic1.21.00.90.80.91.01.7Debrisoquin sulfateCatecholamine depletorAntihypertensor1.01.00.80.91.11.01.2Lactobionic acid—Antithrombonic1.10.91.00.80.91.11.3Amethopterin (R,S)Dehydrofolate reductaseAntineoplasticinhibitor1.11.00.91.01.21.11.4Lumicolchicine gammaMicrotubule—depolymerizating agent1.00.90.81.00.90.91.6Methylergometrine maleate5-HT antagonist, alphaOxytocicadrenergic agonist1.10.90.90.81.01.11.6Lysergol5-HT antagonistAntipsychotic1.41.01.31.31.51.11.8Methiothepin maleate5-HT autoreceptor—antagonist, 5-HT1cantagonist, 5-HT releaseinhibitor electrical or K+induced1.11.00.90.80.91.11.5Mebhydroline 1,5-H1 antagonistAntihistaminicnaphtalenedisulfonate1.21.04.61.15.01.01.8Clofazimine—Antileprosy0.81.04.30.33.20.52.1Meclocycline sulfosalicylateRibosomal protein synthesisAntibacterialinhibitor1.01.00.91.01.01.11.4Nafronyl oxalatePhosphodiesterase inhibitorVasodilatator?, 5-HT antagonist,bradykinine antagonist1.21.22.10.91.91.21.4Meclozine dihydrochlorideHistamine antagonistAntiemetic0.90.81.10.70.81.01.5BezafibrateLipoprotein lipase activatorAntihyperlipoproteinemic0.91.01.30.81.21.11.4MelatoninMelatonin receptor ligandImmunostimulant1.01.01.40.90.91.11.5MimosineCell cycle blocker, apoptosisAnticancer agentinducer1.01.11.41.01.01.21.5Menadione—Vitamin K31.01.11.21.01.00.91.6Clebopride maleate—Spasmolytic1.01.01.41.01.21.01.1Dinoprost trometamolProtaglandin agonistSmooth muscle activator1.11.11.11.01.21.21.5Pirenperone5-HT2 antagonist1.21.00.80.81.11.21.6Harmalol hydrochloride dihydrate—Vasorelaxant1.30.91.01.01.01.21.5Isoquinoline, 6,7-dimethoxy-1-——methyl-1,2,3,4-tetrahydro,hydrochloride1.41.00.90.91.11.11.6Harmol hydrochlorideLiver conjugation probeAnxiolyticmonohydrate1.20.90.80.91.10.91.4PhenacetinCyclooxygenase inhibitorAnalgesic1.11.10.90.71.01.21.5Harmine hydrochlorideTopoisomerase II inhibitorAntibacterial1.11.01.20.81.21.01.4AtovaquoneAntipneumocystic1.31.30.81.04.11.21.8EllipticineIntercaling agentAnticancer1.11.00.91.01.01.21.4Methoxamine hydrochlorideAlpha adrenergic agonistAntihypotensive1.10.90.10.80.81.01.4Chrysene-1,4-quinone——1.21.01.20.91.11.11.7(S)-(−)-AtenololBlokage of the action ofAntihypertensoradrenergic mediators onbeta receptors1.41.00.81.01.11.32.0Demecarium bromideCholinergic (ophtalmic)1.10.91.01.00.91.11.4Piracetam—Nootropic drug1.11.01.00.81.01.21.3Quipazine dimaleate salt5-HT agonist, 5-HT3 ligand1.20.91.11.11.10.91.3PhenindioneAntivitamin KAnticoagulant1.31.01.11.01.01.01.7Sparteine (−)GanglioplegicAntiarrhythmic1.01.11.20.80.91.01.7ThiocolchicosideGABA agonist ?Muscle relaxant1.11.11.11.00.91.01.4Diflorasone DiacetateAnti-inflammatory (topical)1.01.41.51.01.01.11.7ClorsulonAnthelmintic1.11.01.30.61.00.91.4Harmane hydrochlorideImidazoline receptors ligandVasorelaxant1.41.01.41.12.91.31.4LidoflazineCa++ channel activatorCoronary vasodilatator1.11.00.90.81.31.11.3Tropisetron HCl5 HT3 antagonistAntiemetic1.20.90.91.01.41.11.6Betaxolol hydrochlorideBeta adrenergic antagonistAntihypertensor18.61.11.24.61.811.721.9CefiximeAntibacterial1.21.10.61.01.31.11.4Nicardipine hydrochlorideCa2+ channel antagonistAntihypertensor1.21.01.21.01.31.21.3Metrizamide—Contrasting product1.10.90.60.91.41.11.3Probucol—Antihyperlipoproteinemic1.11.01.01.01.51.11.4Muramic acid, N-acetylConstituent of bacterialpeptidoglycan1.50.80.71.01.50.91.2Mitoxantrone dihydrochlorideDNA topoisomerase IIAntineoplasticinhibitor0.90.80.50.90.80.91.2MyricetinNeutral endopeptidase—inhibitor1.41.31.51.02.21.21.5GBR 12909 dihydrochlorideDopamine reuptake inhibitorAntidepressant1.10.90.50.91.21.01.5NaringenineAntiestrogenic1.41.01.11.01.41.21.4Carbetapentane citrateSigma1 receptor ligandAntitussive1.31.01.20.91.21.31.2Naringin hydrate—Anti-oxidant3.01.11.21.63.22.31.8Dequalinium dichlorideBlocker of the apamin-Antibacterialsensitive small conductanceCa2+ activated K+ channel,detergent1.31.01.21.01.31.11.2Neostigmine bromideCholinesterase inhibitorSpinal analgesic1.30.91.21.21.51.11.5KetoconazoleCytochrome P450c17Antifungalinhibitor, sterol 14-demethylase inhibitor13.21.01.86.01.41.26.1NiridazoleHelminthic DNA damageAnthelmintic1.11.14.21.11.31.11.4Fusidic acid sodium saltProtein synthesis inhibitorAntibacterialGTPase coupled12.21.01.83.11.81.21.9CeforanideAntibacterial1.11.60.70.91.21.01.2Ciclopirox ethanolamineCell membrane proteinsAntifungalsynthesis inhibitor1.41.00.81.01.31.21.4Methoxy-6-harmalanBenzodiazepine receptorPsoriasis treatmentligand1.41.01.01.11.31.21.4ProbenecidUric acid uptake inhibitorUricosuric1.41.01.01.11.41.21.5Stachydrine hydrochloridePotent inhibitor oftyrosinase1.40.90.91.11.21.11.3Betahistine mesylateH1 agonist, H3 antagonistVasodilatator1.41.01.31.11.41.21.7Pyridoxine hydrochloride—Vitamin7.50.91.12.05.717.11.5TobramycinRibosomal protein synthesisAntibacterialinhibitor1.31.01.01.21.41.21.5Cytisine (−)Partial nicotinic receptorAntiinflammatoryantagonist1.31.01.11.11.41.21.4Tetramisole hydrochlorideAlkaline phosphataseAntihelminthicinhibitor1.40.91.01.21.21.11.5Pseudopelletierine hydrochloride——1.41.11.11.11.31.11.5PregnenoloneEstrogen1.21.01.91.11.31.21.5RacecadotrilEnkephalinase inhibitorAntidiarrhoeic1.40.90.91.01.21.11.5MolsidomineNO° production ?Vasodilatator1.31.11.01.01.31.11.3Folic acid—Vitamin Bc or M1.20.91.11.11.31.11.6Chloroquine diphosphateHeme polymerase inhibitorAntipaludic1.21.01.11.21.21.11.5Salsolinol hydrobromideDopamine analog—1.41.01.21.11.21.11.7Trimetazidine dihydrochloride—Antianoxic1.21.01.31.01.31.11.5GramineCholinesterase inhibitorAntibacterial1.51.01.31.11.31.21.4ParthenolideMAP kinase inhibitorAntiinflammatory1.31.01.31.21.51.21.5Dimethisoquin hydrochlorideLocal anesthesic1.21.01.11.31.11.11.4Terbutaline hemisulfateBeta-2 adrenergic agonistBronchodilatator1.21.01.10.91.21.11.7Strophantine octahydrateNa+ K+ ion dependantCardiotonicATPase inhibitor1.31.01.01.01.21.01.4Ketanserin tartrate hydrate5-HT1, 5-HT2, 5-HT2AAntihypertensorantagonist1.11.11.11.01.11.01.4Pantothenic acid calcium salt—Nutritional factormonohydrate1.10.91.01.01.20.92.0Hemicholinium bromideAcetylcholine stores—depleter, acetylcholineuptake inhibitor22.11.22.58.42.01.225.3CefotetanAntibacterial1.20.92.51.01.11.01.9Kanamycin A sulfateRibosomal protein synthesisAntibacterialinhibitor0.40.30.20.30.40.41.6PiperineEnzyme inhibitorAntidiarrhoeic22.11.01.36.27.614.24.9Amikacin hydrateRibosomal protein synthesisAntibacterialinhibitor1.41.01.11.11.21.12.0Brompheniramine maleateH1 Antagonist,Antihistaminicanticholinergic1.21.11.41.01.21.01.4EtoposideTopoisomerase II inhibitor,Antineoplastickinase inhibitor1.20.92.11.01.11.01.4Primaquine diphosphateHeme polymerase inhibitorAntimalarial1.84.42.01.65.41.41.9Clomiphene citrate (Z,E)Antioestrogen, gonad-Ovulation inductorstimulating agent1.01.11.11.11.11.01.7Progesterone—Progestogen1.11.01.31.01.11.01.8Oxantel pamoateFumarate reductaseAnthelminticinhibitor, neuromusculardepolarizing agent1.21.32.51.03.01.01.7FelodipineL-type Ca2+ channels blockerAntihypertensor1.21.11.11.21.61.22.0Prochlorperazine dimaleateDopamine antagonistAntiemetic1.11.11.00.91.01.01.5Methoxy-8-psoralenApoptosis inducer with UVPsoriasis treatment1.11.11.31.01.21.01.4Hesperidin—Anticancer1.11.11.11.11.61.01.4Puromycin dihydrochlorideAntimetaboliteAntiprotozoal1.51.11.21.43.01.11.6HexetidineDetergentAntifungal1.41.01.11.41.31.31.3Thiamine hydrochloride—Vitamin1.31.01.11.21.11.21.6Selegiline hydrochlorideMonoamine B oxydaseAntiparkinsonianinhibitor1.41.01.21.31.41.31.6Dipivefrin hydrochlorideAntiglaucoma drug1.41.41.91.21.21.21.4Pentamidine isethionate—Antiparasitic1.21.01.31.31.21.21.5ThiorphanNeutral endopeptidaseAntinociceptiveinhibitor1.51.01.01.41.21.41.6TolazamideATP-sensitive K+ ionAntidiabeticchannels blocker1.11.00.91.61.21.21.5Riboflavine—Vitamin1.21.00.71.81.11.21.5NifuroxazideBacterial DNA damageAntibacterial1.21.11.01.31.21.21.6Hydroquinine hydrobromide—Preventor of muscular cramphydrate1.21.11.11.51.21.21.3Mycophenolic acidInosine monophosphateAntineoplasticdehydrogenase inhibitor1.31.01.01.21.21.21.6EpivincamineAntiaggregant1.11.22.11.21.80.91.5DirithromycinRibosomal protein synthesisAntibacterialinhibitor1.31.01.21.21.21.21.5Retrorsine—Antineoplastic1.21.01.01.21.31.21.8GliclazideK+ channel voltageAntidiabeticdependant inhibitor1.51.11.21.21.41.21.6ConessineAntiamebic1.41.01.11.31.21.31.7DO 897/99D3 antagonist—1.11.01.21.21.21.11.3Protoveratrine AAcetylcholinesterase releaseAntihypertensorstimulant1.61.21.61.31.91.31.6Prenylamine lactateCa++ channel activatorVasodilatator1.21.01.21.21.31.21.7Solanine alphaButyrylcholinesteraseAntifungalinhibitor0.30.90.40.50.30.30.3SulmazolePhosphodiesterase IIICardiotonicinhibitor0.41.00.40.40.40.40.3AlthiazideNa+ Cl− transport inhibitorDiuretic0.40.90.30.40.30.30.3Epicatechin-(−)—Antidiarrhoeic0.40.80.40.40.30.40.3Isopyrin hydrochlorideCyclooxygenase inhibitorAntipyretic0.50.90.40.50.40.30.3Flunisolide—Glucocorticoid0.51.00.60.50.80.40.3Phenethicillin potassium saltBacterial transpeptidaseAntibacterialinhibitor0.50.80.40.40.40.30.7N-Acetyl-DL-homocysteineDisulfure bridge breakerExpectorantThiolactone0.50.90.40.50.70.30.3SulfamethoxypyridazineInhibitor of folic acidAntibacterialsynthesis0.50.80.40.50.50.40.3FlurandrenolideGlucocorticoid0.40.90.40.50.40.40.4Deferoxamine mesylateIron chelating agent0.50.90.40.50.40.40.4HelveticosideInhibitor of membrane ATPCardiotonic0.50.80.40.50.40.40.4Mephentermine hemisulfateAlpha-adrenergic receptorAntihypotensiveagonist0.50.90.40.50.50.40.4MyosmineCholinergic—0.40.70.20.50.50.40.4Ergocryptine-alphaVasoconstrictor0.40.90.40.60.40.40.4Betonicine——0.60.90.50.50.90.40.4SulfadimethoxineInhibitor of folic acidAntibacterialbiosynthesis0.50.80.40.50.50.40.4EtanidazoleDNA damageAntineoplastic adjunct(radiosensitizer)0.50.90.40.61.50.50.4SulfanilamideInhibitor of folic acidAntibacterialbiosynthesis0.50.80.50.50.50.50.4Butirosin disulfate saltRibosomal protein synthesisAntibacterialinhibitor0.50.90.40.70.50.50.4Balsalazide SodiumAnti-inflammatory0.70.80.60.60.70.60.7Carbinoxamine maleate saltHistamine antagonistAntihistaminic0.70.90.60.50.60.60.7NiacinAntihyperlipoproteine-mic0.51.50.60.50.50.60.7MethazolamideAnhydrase carbonic inhibitorDiuretic0.60.90.70.60.70.60.6BemegrideRespiratory stimulant0.70.80.60.60.50.60.7Pyrithyldione—Sedative0.70.80.60.60.60.50.7DigoxigeninMainly used as a non-Diagnosisisotopic label for DNA0.61.00.60.20.50.50.6Spectinomycin dihydrochlorideRibosomal protein synthesisAntibacterialinhibitor0.50.80.50.70.50.50.6MeglumineExpectorant0.60.90.70.60.50.50.6Piromidic acidTopoisomerase II inhibitorAntibacterial0.60.80.50.60.50.50.6CantharidinAphrodisiac0.60.90.50.60.60.60.6Trimipramine maleate saltnoradrednaline and 5-HTuptake inhibitor, alphaantagonist, anticholinergic,Dopamine and Histamineantagonist0.50.90.20.61.10.40.5ClioquinolAnti-infective0.70.90.50.60.60.50.6Chloropyramine hydrochlorideH1 antagonistAntihistaminic0.50.70.40.40.40.50.6OxybenzoneUltraviolet screen0.80.90.83.20.40.60.6FurazolidoneMonoamine oxidaseAntiinfectiveinhibitor and protozoal DNAdamage0.60.80.50.50.60.60.5Promethazine hydrochlorideAntihistaminic0.61.10.50.50.50.50.5DichlorphenamideCarbonic anhydrase inhibitor0.20.30.20.20.20.10.6Chrysin5-lipoxygenase inhibitorAntifungal0.83.50.70.92.60.50.6Sulconazole nitrateErgosterol synthesisAntifungalinhibition0.50.90.50.50.60.50.5ProxyphyllineVasodilator0.51.40.50.70.70.70.9GlimepirideAntidiabetic0.60.90.70.61.00.60.8Sulfaquinoxaline sodium saltInhibitor of folic acidAntibacterialsynthesis0.61.00.60.60.70.60.7PicrotoxininGABA channel blockerAnaleptic0.72.61.21.40.70.70.7StreptozotocinAntineoplastic0.61.00.60.60.70.60.7Mepenzolate bromideAnticholinergic andmuscarinic antagonist0.60.90.60.50.70.77.0Metoprolol-(+,−) (+)-tartrate saltBeta adrenergic antagonist0.70.90.50.60.70.60.8BenfotiamineVitamin0.60.90.60.60.70.70.8FlumethasoneAntiinflammatory0.60.90.60.50.70.70.8HalcinonideAntiinflammatory0.60.90.70.60.80.60.7Flecainide acetateAntiarrhythmic0.60.90.70.60.80.61.0Lanatoside CNa+ K+ ATPase inhibitorCardiotonic16.50.93.13.60.50.70.9Cefazolin sodium saltBacterial transpeptidaseAntibacterialinhibitor0.61.10.70.60.60.60.7Benzamil hydrochlorideNa+ channel blocker andblocker of Na+/Ca++exchanger0.70.90.70.60.80.60.8Atractyloside potassium saltNucleotide transportAnticancerinhibitor0.60.90.60.60.80.60.8Suxibuzone—Antiinflammatory0.71.00.70.60.70.60.7Folinic acid calcium salt—Antianemic0.70.90.60.50.70.70.96-Furfurylaminopurine—Plant growth accelerator0.71.00.60.80.80.70.7LevonordefrinAdrenergic receptor agonistVasoconstrictor0.81.21.70.60.80.60.9Avermectin B1Ligand GABA receptorsAntihelmetic0.60.90.50.60.70.60.7EbselenCyclooxygenase inhibitorAntiinflammatory0.70.90.90.80.90.81.1Bergenin monohydrate—Antiarrhythmic0.70.90.60.60.80.81.13-Acetylcoumarin0.70.90.70.70.90.81.0Cromolyn disodium salt—Antiasthmatic0.70.90.70.60.80.80.9Esculin HydrateSkin protectant0.70.90.70.60.80.80.9Bucladesine sodium saltAdenylate cyclase modulatorCardiotonic0.70.90.60.60.80.71.0FelbinacAnalgesic0.90.91.00.71.18.60.9Cefsulodin sodium saltBacterial transpeptidaseAntibacterialinhibitor0.50.50.70.40.60.61.0ButylparabenAntifungal0.70.90.70.60.80.70.8FosfosalCyclooxygenase inhibitorAnalgesic0.70.90.60.60.70.70.8Aminohippuric acidDiagnostic aid (renal function)0.70.90.60.70.80.70.9SuprofenCyclooxygenase inhibitorAnalgesic0.70.90.70.60.70.70.9N-Acetyl-L-leucineVertigo0.70.90.70.60.70.61.0Catechin-(+,−) hydrateAntidiarrhoeic14.71.10.71.70.90.91.0Pipemidic acidAntibacterial0.80.90.70.60.70.60.8NadololAdrenergic beta antagonistAntihypertensor0.80.80.50.70.60.71.0DioxybenzoneUltraviolet screen18.11.34.43.90.60.60.8Moxalactam disodium saltBacterial transpeptidaseAntibacterialinhibitor0.70.90.60.60.80.61.2AdrenosteroneAndrogenic activity0.60.90.60.60.70.80.8AminophyllineMastocytes degranulationVasodilatatorinhibitor andbenzodiazepines antagonist0.71.00.60.60.70.70.8Methylatropine nitrateMydriatic0.81.00.70.80.70.80.8VitexinAntiviral0.90.90.60.70.80.80.9NadideCoenzyme nicotinamide—adenine dinucleotide0.90.90.70.70.70.90.9GelsemineTumour inhibitor1.00.90.70.71.40.80.9SulfamethizoleInhibitor of folic acidAntibacterialsynthesis1.00.90.60.70.71.00.9SolasodineCytotoxic0.71.00.60.70.70.81.0Medrysone—Glucocorticoid0.80.90.70.70.90.91.2DelcorineNicotinic ligandAntiarrhythmic0.60.60.50.50.50.61.0Flunixin meglumineAnalgesic0.70.80.60.70.70.81.1EvoxineGlycine receptor antagonistSedative0.91.06.60.80.90.71.2SpiramycinRibosomal protein synthesisAntibacterialinhibitor0.90.90.40.71.40.81.0NisoldipineAntihypertensive0.90.90.70.80.80.91.1GlycopyrrolateAntispasmodic0.90.90.70.80.80.81.0Foliosidine—Anticonvulsant10.50.91.32.30.60.70.9Cefamandole sodium saltBacterial transpeptidaseAntibacterialinhibitor0.60.60.60.50.50.61.1Skimmianine5-HT ligandSedative0.91.10.70.60.70.91.1Monensin sodium saltPerforms membraneAntibacterialionophores1.00.90.60.80.80.91.0AnabasineInsecticide0.90.90.61.40.80.60.9Isoetharine mesylate saltBeta adrenergic agonistBronchodilator0.91.00.90.90.90.91.1TetrandrineAnalgesic1.01.00.90.80.90.80.9Mevalonic-D, L acid lactoneHMG CoA substrate—12.30.90.40.72.19.71.0Azlocillin sodium saltBacterial transpeptidaseAntibacterialinhibitor0.91.01.00.70.81.01.1HymecromoneAntispasmodic1.00.90.90.81.11.11.3Clidinium bromideAnticholinergicSpasmolytic1.00.90.80.80.80.91.0Caffeic acidAntineoplastic0.90.90.70.81.61.01.1SulfamonomethoxineInhibitor of folic acidAntisepticsynthesis1.00.80.70.70.91.01.2Diloxanide furoateAntiamebic0.91.40.80.80.90.91.1BenzthiazideNa+ Cl− transport inhibitorDiuretic0.90.80.80.71.01.01.2MetyraponeDiagnostic aid (pituitaryfunction)0.81.41.30.81.00.81.2TrichlormethiazideNa+ Cl− transport inhibitorDiuretic1.00.90.90.71.01.01.1Urapidil hydrochlorideAntihypertensor0.90.80.80.70.80.91.2Oxalamine citrate salt—Antiinflammatory1.31.31.41.16.60.81.0FluspirilenAntipsychotic0.90.80.80.81.00.91.3Propantheline bromideMuscarinic antagonistAntiulcerative0.90.90.80.70.80.91.3S-(+)-ibuprofenAnalgesic1.00.93.70.72.60.71.0Lasalocid sodium saltMembrane ionophoresAntibacterialproducer0.80.90.50.70.90.91.1Ethynodiol diacetateProgestogen0.90.90.70.80.80.81.0Dimethadione—Anticonvulsant0.50.40.40.50.40.61.0NabumetoneAnalgesic0.91.00.50.70.90.91.0Ethaverine hydrochlorideAntispasmodic0.91.00.70.70.80.90.9Nisoxetine hydrochlorideInhibitor of noradrenaline0.91.00.70.80.80.91.2DydrogesteroneProgestogen0.80.80.80.70.70.61.2Terazosin hydrochlorideAlpha adrenergic antagonistTreatment of benign prostatichyperplasia0.80.90.70.70.90.81.3(d,l)-Tetrahydroberberine—Sedative0.10.10.30.10.10.11.4Phenazopyridine hydrochloride—Analgesic0.90.90.80.70.80.81.1DeltalineNicotinic receptor ligandAntiarrhythmic0.50.97.10.23.40.41.3Demeclocycline hydrochlorideRibosomal protein synthesisAntibacterialinhibitor0.80.80.70.60.80.81.2Graveolinetopoisomerase II inhibitor?Antihypotensiveand CNS stimulant0.80.90.80.70.80.81.4Fenoprofen calcium salt dihydrateCyclooxygenase inhibitorAntiinflammatory0.90.90.70.60.80.91.4Hippeastrine hydrobromide—Hypotensor12.60.90.42.33.38.71.3Piperacillin sodium saltBacterial transpeptidaseAntibacterialinhibitor0.90.90.80.70.80.71.4Beta-EscinPeripheral vascular disorders0.91.10.60.71.80.81.4DiethylstilbestrolEstrogen0.61.30.20.30.40.51.5GossypolCa2+ uptake inhibitorLocal contraceptive0.91.00.80.80.80.81.4ChlorotrianiseneNuclear receptor ligandNon-steroidal estrogen0.80.90.90.80.80.71.3Ricinine0.90.90.80.70.80.81.2Ribostamycin sulfate saltRibosomal protein synthesisAntibacterialinhibitor0.90.90.80.70.90.81.3DelsolineNicotinic receptor antagonistand Ganglioblocker0.90.90.70.70.80.91.3Methacholine chlorideCholinergic agonist0.90.90.80.70.90.81.4Fluorocurarine chlorideMuscle relaxant0.90.90.80.70.70.80.9Pipenzolate bromideNicotinic receptor antagonistSpasmolytic0.90.90.80.80.91.01.4ButacaineNa+ channel blockerLocal anesthesic0.90.90.81.00.80.81.4(+)-Isoproterenol (+)-bitartrateSympathomimetic (VET)salt20.11.03.43.21.30.81.2Cefoxitin sodium saltBacterial transpeptidaseAntibacterialinhibitor0.70.60.60.50.50.71.4MonobenzoneDepigmentor9.00.80.80.70.80.91.4IfosfamideAntineoplastic1.10.90.80.70.90.91.42-AminobenzenesulfonamideLigand and potent inhibitorof carbonic anhydrase B3.21.54.50.71.11.01.6Novobiocin sodium saltDNA topoisomerase IVAntibacterialinhibitor0.80.80.70.70.80.81.4EstroneEstrogen0.90.90.80.81.10.91.3Tetrahydroxy-1,4-quinone—Keratolyticmonohydrate0.91.00.30.70.80.91.3Lorglumide sodium saltCCKa ligand0.20.10.20.10.20.21.5IndoprofenCyclooxygenase inhibitorAnalgesic0.80.90.40.80.90.91.4NitrendipineAntihypertensor0.80.91.60.71.10.91.4Carbenoxolone disodium saltMucus stimulating synthesisAntiulcerative0.80.90.60.70.90.81.6FlurbiprofenAnti-inflammatory0.90.90.80.80.80.91.4locetamic acidDiagnostic aid (radiopaquemedium)0.91.00.70.71.00.91.4NimodipineVasodilator0.90.90.90.70.80.91.4GanciclovirAntimetaboliteAntiviral1.01.30.40.81.10.81.2BacitracinAntibacterial0.90.90.70.81.01.01.3Ethopropazine hydrochlorideAnticholinergicAntiparkinsonian0.80.90.80.70.80.81.2L(−)-vesamicol hydrochloridePotent inhibitor of vesicularacetylcholine storage1.21.11.21.01.01.11.3Austricine hydrateAntiatherosclerotic0.80.81.10.60.70.91.7ButambenNa+ channel blockerAnesthetic1.21.01.30.91.01.21.3beta-BelladonnineMuscarinic receptor anddichloroethylatenicotinic receptor lignad1.21.01.40.92.21.11.6SulfapyridineAntibacterial1.11.01.11.01.11.11.5Pempidine tartrateNicotinic acetylcholineAntihypertensorreceptor antagonist1.21.01.21.01.01.11.4Meclofenoxate hydrochlorideAcetylcholine precursorCerebral stimulant1.21.01.41.01.01.01.7HeliotrineModel for hepatitis andcirrhosis in liver0.91.10.72.61.01.11.7Furaltadone hydrochlorideBacterial DNA damageAntibacterial1.21.01.31.11.01.11.4Nitrarine dihydrochloride—Hypotensor1.10.91.10.90.91.11.4Ethoxyquin—Antifungal1.01.01.40.81.01.11.5Lycorine hydrochlorideInhibitor of proteinAntitumoraltranslation1.20.91.20.81.01.11.5TinidazoleProtozoal and bacterial DNAAntiprotozoaldamage1.01.01.20.91.01.11.3KarakolineInhibitor of ACEHypotensor1.31.01.20.71.01.11.4Guanadrel sulfateAntihypertensor1.11.01.11.01.01.11.3EstropipateMenopause1.11.11.50.71.01.01.8VidarabineAdenosine antimetaboliteAntiviral1.31.01.21.01.11.11.4Ungerine nitrateEnhancer of analgesicsSedative1.31.01.21.02.31.11.2SulfameterInhibitor of folic acidAntibacterialsynthesis1.31.01.41.01.01.13.6NapellineAnticholinergic agentAntiarrhythmic1.31.11.21.11.01.21.5Isopropamide iodideAnticholinergic1.31.01.10.81.11.21.6Securinine—CNS stimulant1.31.01.20.91.01.21.7NizatidineH2 antagonistAntiulcerative1.21.01.10.91.11.21.5Trimeprazine tartrateHistamine antagonistAntipruritic1.21.01.11.01.01.31.6Thioperamide maleateH3 antagonistAntiemetic1.21.06.51.01.51.31.4Nafcillin sodium saltBacterial transpeptidaseAntibacterialmonohydrateinhibitor1.31.01.10.81.01.21.8Xamoterol hemifumaratebeta1-AdrenoceptorCardiotonicselective partial agonist1.41.11.20.91.11.21.8Procyclidine hydrochlorideMuscarinic antagonistAntiparkinsonian1.11.01.31.01.21.21.7RolipramNootropic drug1.31.11.30.91.21.11.5Amiprilose hydrochloride—Immunomodulator3.27.5###4.75.61.51.8Thonzonium bromideDetergent1.20.90.80.81.11.11.5Ethynylestradiol 3-methyl ether—Estrogen1.11.01.11.01.11.21.5Idazoxan hydrochlorideAlpha2 agonistAntiparkinsonian1.31.01.01.01.01.21.9(−)-Levobunolol hydrochlorideAdrenergic beta antagonistAntiglaucoma drug1.21.11.21.01.21.21.6Quinapril HClAngiotensin1.31.11.31.01.01.21.5IodixanolDiagnostic aid (radiopaquemedium)1.21.01.31.01.21.21.4NilutamideAntineoplastic1.11.01.11.01.21.11.7RolitetracyclineRibosomal protein synthesisAntibacterialinhibitor1.31.01.11.01.01.01.4Ketorolac tromethamineAnalgesic1.31.03.90.91.01.11.4Equilin—Estrogen1.21.02.81.11.11.21.4Protriptyline hydrochlorideAntidepressant1.21.01.00.80.91.21.8Fillalbin——1.11.01.11.10.91.01.2Alclometasone dipropionateCorticoideAnti-inflammatory1.01.01.00.90.91.21.5Citalopram Hydrobromide5HT uptake inhibitor0.80.70.60.60.80.81.5LeflunomideInhibitor of T and B cellImmunosuppressiveproliferation1.21.01.40.80.91.11.7Promazine hydrochlorideDopamine receptorAntipsychoticantagonist1.01.01.11.11.11.11.7Norgestrel-(−)-DProgestogenOral contraceptive1.11.00.91.02.11.01.9SulfamerazineInhibitor of folic acidAntibacterialsynthesis1.01.01.10.90.91.21.7FluocinonideAntiinflammatory0.70.50.70.60.30.61.6AcacetinInhibitor of glutathioneAntitumor agentreductase and oftopoisomerase I1.01.01.41.01.61.11.4Sulfamethazine sodium saltInhibitor of folic acidAntibacterialsynthesis1.21.01.21.01.10.91.6EthotoinAnticonvulsant1.11.01.20.81.01.11.6Guaifenesin—Expectorant1.21.01.00.90.91.11.93-alpha-Hydroxy-5-beta-androstan-17-one43.37.4###23.412.319.21.5Alexidine dihydrochlorideDetergentAntibacterial1.41.01.10.91.01.01.4Tetrahydrozoline hydrochlorideAdrenergicVasoconstrictor1.21.10.80.81.11.11.7Proadifen hydrochlorideCytochrome P450 mono-Local anesthesicoxygenases inhibitor, Na+channel blocker1.41.20.70.73.01.11.6HexestrolNuclear receptor ligandEstrogen antineoplastic1.11.10.91.01.10.91.6Zomepirac sodium saltCyclooxygenase inhibitor20.01.45.04.61.41.01.6Cefmetazole sodium saltBacterial transpeptidaseAntibacterialinhibitor10.31.11.32.11.31.21.4CinoxacinTopoisomerase II inhibitorAntibacterial1.40.91.41.21.31.31.6Paroxetine Hydrochloride5-HT uptake inhibitor1.31.01.21.11.01.01.7PropofolAnesthetic (intravenous)2.01.19.40.33.40.71.5Doxycycline hyclateRibosomal protein synthesisAntibacterialinhibitor0.91.01.61.11.01.31.8S(−)Eticlopride hydrochloride1.21.11.00.91.11.11.6LiothyronineThyroid hormoneThyroidic drug1.00.91.30.91.21.21.8PrimidoneAnticonvulsant0.91.42.81.11.00.91.5RoxithromycinRibosomal protein synthesisAntibacterialinhibitor1.10.91.10.81.21.11.8FlucytosineAntifungal1.11.00.50.91.01.01.5Beclomethasone dipropionate—Antiinflammatory1.21.01.11.01.11.31.9(−)-MK 801 hydrogen maleateNMDA antagonistAnticonvulsant0.90.80.90.60.81.02.0Tolmetin sodium salt dihydrateCyclooxygenase inhibitorAntiinflammatory1.21.01.21.00.91.02.0Bephenium hydroxynaphthoateAntihelmintic1.20.91.30.90.91.21.5(+)-Levobunolol hydrochlorideBeta adrenergic antagonistAntiglaucoma drug1.01.10.80.91.11.11.7Dehydroisoandosterone 3-acetateMenopausal syndrome1.41.11.20.91.31.11.5Doxazosin mesylateAlpha 1 adrenergicAntihypertensorantagonist1.30.91.41.21.01.11.8Benserazide hydrochlorideInhibitor of L-aromaticIn combination with levodopaamino acid decarboxylaseas antiparkinsonian1.31.01.00.90.91.01.7Fluvastatin sodium saltHMG CoA reductaseAnti-hyperlipoproteinemicinhibitor1.21.01.01.01.21.11.6IodipamideDiagnostic aid (radiopaquemedium-cholecystographic)1.41.11.31.01.01.12.0Methylhydantoin-5-(L)——1.41.01.11.21.10.91.4EsculetinAntifungal1.21.11.41.11.41.31.5Trihexyphenidyl-D,LAnticholinergicAntiparkinsonianHydrochloride1.21.00.91.01.31.11.3Clobetasol propionate—Glucocorticoid1.41.01.31.11.31.11.4SuccinylsulfathiazoleInhibitor of folic acidAntibacterialsynthesis1.20.91.01.21.21.11.3PodophyllotoxinAntiviral1.21.00.81.11.11.21.5FamprofazoneAntipyretic1.21.11.41.11.31.21.5Clofibric acidLipoproteine lipase activator ?Antihyperlipoproteinemic1.30.91.31.01.31.11.3BromoprideDopamine antagonistAntiemetic1.31.21.31.11.31.11.5BendroflumethiazideNa+ Cl− transport inhibitorDiuretic5.17.4###7.45.88.91.3Methyl benzethonium chlorideDetergentAntibacterial1.11.31.31.11.31.21.5DicumarolVitamin K antagonistAnticoagulant1.31.01.21.11.51.11.6Chlorcyclizine hydrochlorideHistamine antagonistAntihistaminic1.20.91.01.01.41.027.1MethimazoleIodine oxidazing inhibitorAntihyperthyroid1.31.11.21.01.31.11.4Diphenylpyraline hydrochlorideH1 antagonistAntihistaminic0.50.60.20.40.70.41.4Merbromin—Antibacterial2.96.2###5.75.45.81.3Benzethonium chlorideDetergentAntibacterial1.21.01.31.01.31.11.4Hexylcaine hydrochlorideLocal anesthesic1.20.90.91.01.21.01.3Trioxsalen—Pigmentation agent(photosensitizer)1.51.01.51.21.31.21.5Drofenine hydrochloride—Spasmolytic1.41.01.31.11.31.11.3StrophanthidinATPase inhibitorCardiotonic1.31.01.11.01.21.10.9Cycloheximide—Antibacterial1.41.01.51.11.41.31.6GabapentinGABA receptor ligandAnticonvulsant1.31.01.41.11.31.21.5Pentetic acidChelating agent (iron)1.50.91.21.11.51.21.3Raloxifene hydrochloride1.31.01.31.11.31.21.6Bretylium tosylateAntiadrenergic1.31.01.21.01.21.11.4Etidronic acid, disodium salt—Calcium regulator1.31.01.31.01.41.21.5Pralidoxime chloride1.21.01.21.11.31.21.5Methylhydantoin-5-(D)——1.40.91.11.21.31.11.4Phenoxybenzamine hydrochlorideNonselective alpha-Antihypertensoradrenergic blockade1.61.00.41.22.51.11.5SimvastatinHMG-CoA reductaseAntihyperlipidemicinhibitor1.41.01.91.11.51.21.5Salmeterolbeta 2 adrenergicBronchodilatoragonist2.21.01.20.91.41.21.5Azacytidine-5AntimetaboliteAntineoplastic1.31.01.11.01.31.21.4Altretamine1.40.91.31.01.51.01.4Paromomycin sulfateRibosomal protein synthesisAntiamebicinhibitor1.21.11.40.91.41.11.5Prazosin hydrochlorideAntihypertensor1.41.01.61.21.51.11.6AcetaminophenCyclooxygenase inhibitorAntipyretic1.31.01.31.11.51.11.4Timolol maleate saltAntiglaucoma drug1.41.01.41.01.41.01.2PhthalylsulfathiazoleInhibitor of folic acidAntibacterialsynthesis1.31.01.31.11.31.01.4(+,−)-Octopamine hydrochloridebeta-3 Adrenergic receptorAdrenergicagonist0.40.50.20.50.30.51.6Luteolin—Expectorant1.41.01.31.21.31.01.3(±)-Nipecotic acidActivates GABA-like ionchannels1.11.11.21.12.81.11.6SulfabenzamideInhibitor of folic acidAntibacterialsynthesis1.11.01.01.01.11.01.7(R)-Naproxen sodium saltCyclooxygenase inhibitorAntiinflammatory1.11.01.20.91.21.11.6BenzocaineNa+ channel blockerAnesthetic1.30.81.40.81.11.01.6Propidium iodideDetergentAntibacterial1.11.01.41.11.11.11.4DipyroneCyclooxygenase inhibitorAntipyretic1.21.11.31.21.41.22.0Cloperastine hydrochlorideHistamine antagonistAntitussive1.11.01.21.01.11.01.8Isosorbide dinitrateNitric oxide (NO) donorAntianginal1.21.11.30.91.11.11.6Eucatropine hydrochlorideAnticholinergic1.01.01.11.12.11.01.5SulfachloropyridazineInhibitor of folic acidAntibacterialsynthesis1.11.01.51.11.11.11.5IsocarboxazidAntidepressant1.11.01.31.11.11.21.5Pramoxine hydrochlorideLocal anesthesic0.81.21.10.81.01.01.7Lithocholic acidAnticholelithogenic,Cholagoguegastrointestinal agent1.11.11.00.91.21.11.8FinasterideAntialopecia agent1.31.01.21.01.11.11.8Methotrimeprazine maleat salt—Analgesic1.11.01.21.01.31.11.7Fluorometholone—Glucocorticoid1.11.30.40.93.21.121.9DienestrolNuclear receptor ligandNon-steroidal estrogen11.81.05.33.21.11.12.0Cephalothin sodium saltBacterial transpeptidaseAntibacterialinhibitor1.11.11.20.91.11.11.6Pridinol methanesulfonate saltAnticholinergicAntiparkinsonian12.11.03.42.41.41.61.6Cefuroxime sodium saltBacterial transpeptidaseAntibacterialinhibitor1.31.01.11.11.21.044.0AmrinoneTNF production inhibitor1.21.01.31.21.21.21.4IopamidolDiagnostic aid (radiopaquemedium)1.51.11.31.11.31.31.3CrotamitonScabicide1.21.01.31.11.11.21.4IopromideContrast molecule1.21.11.41.11.21.21.4Propranolol hydrochlorideBeta blocking agentAntiarrhythmic1.21.01.31.11.21.21.3Theophylline monohydrateMastocyte degranulationBronchodilatatorinhibitor in vitro1.31.01.21.21.31.21.3(R)-(+)-Atenolol1.21.11.31.21.11.21.4TheobromineAdenosine receptorCardiotonicantagonist1.41.01.41.51.31.21.2TyloxapolMucolytic1.31.11.31.21.51.41.5Reserpine1.21.0###0.31.21.41.4FlorfenicolAntibacterial0.70.60.90.70.80.81.2Arcaine sulfateLowers blood sugar1.11.20.91.01.21.21.6Megestrol acetateProgestogen1.21.01.21.11.21.11.5Scopolamine hydrochlorideNon-selective muscarinicAntiemeticantagonist1.21.21.61.21.31.31.3DeoxycorticosteroneCorticoideAntiinflammatory1.21.01.21.21.31.21.4IoversolDiagnostic aid (radiopaquemedium)1.21.01.21.01.31.21.4UrosiolAnticholelithogenic1.31.11.21.01.21.11.5CapsaicinVanilloid receptor ligandTopical analgesic1.31.01.21.11.41.11.2Proparacaine hydrochlorideLocal anesthesic (VET)1.21.11.41.21.31.21.2CarbacholCholinergic agonist,MyoticCholinesterase inhibitor ?1.21.11.21.21.31.11.6Aminocaproic acidAntiallergic0.50.90.40.40.30.40.4Denatonium benzoateBittering agent to preventpoisoning0.50.90.30.40.30.40.3EtomidateHypnotic0.40.90.30.40.40.40.3ScopoletinEicosanoid release inhibitorAntispasmodic0.40.80.40.40.40.40.3Tridihexethyl chlorideAntispasmodic0.51.10.40.50.40.40.4EnilconazoleAntifungal0.50.80.40.50.40.50.4Penbutolol sulfateAntiarrhythmic3.20.91.90.24.20.20.4Methacycline hydrochlorideAntibacterial0.40.90.40.50.40.40.3PrednicarbateGlucocorticoid (topical)0.50.80.40.50.40.40.4Gibberellic acidPlant growth regulator0.72.80.70.72.40.50.4Sertaconazole nitrateAntibacterial0.40.80.40.50.50.40.4Sotalol hydrochlorideBeta-blocker0.40.90.30.40.40.40.4RepaglinideAntidiabetic0.50.90.40.50.50.40.46-Hydroxytropinone0.50.80.40.50.40.40.4PiretanideAntihypertensor0.50.90.40.50.50.40.5Decamethonium bromideMuscle relaxant (skeletal)0.50.90.50.50.60.50.4PiperacetazineAntipsychotic0.50.80.40.40.40.40.43-AcetamidocoumarinAntiinflammatory0.50.90.40.50.50.50.5OxyphenbutazoneInhibition of cyclo-oxygenaseAnti-inflammatory0.40.80.60.40.50.50.5RoxarsoneControl of enteric infections.To improve growth and feedefficiency (VET)0.60.90.40.60.50.50.4QuinethazoneDiuretic0.70.90.60.60.70.70.8Remoxipride HydrochlorideDopaminergic antagonistAntipsychotic0.61.00.60.60.60.60.7Moricizine hydrochlorideAntiarrhythmic0.61.00.60.60.60.60.8THIP HydrochlorideGABAergic Agonist0.60.90.40.60.60.69.6Iopanoic acidContrast molecule0.70.90.60.60.70.70.7Pirlindole mesylateHighly selective reversibleAnti depressantinhibitor of monoamineSeizuresoxidase type A7.70.90.60.51.10.60.8Pivmecillinam hydrochlorideAntibacterial0.70.90.60.60.60.60.9Pronethalol hydrochlorideAntihypertensor0.61.00.60.60.70.70.7Levopropoxyphene napsylateAntitussive0.90.80.50.60.70.70.9Naftopidil dihydrochlorideAlpha1 agonistAntihypertensor0.71.00.60.60.60.70.7Piperidolate hydrochlorideAntispasmodic0.51.10.50.60.80.60.7Tracazolate hydrochlorideGABA receptor ligand0.90.90.71.11.10.60.7TrifluridineAntiviral (ophthalmic)0.61.00.60.70.70.70.9ZardaverinePhosphodiesterase III & IVinhibitor0.70.90.60.60.60.60.9Oxprenolol hydrochlorideBlocking beta-adrenergicAntiarrhythmicreceptors0.60.90.60.50.70.60.7Memantine HydrochlorideNMDA receptor antagonistAltzheimer disease0.71.10.60.60.70.70.8Ondansetron HydrochlorideAntagonist of 5-Antiemetichydroxytryptamine(serotonin) subtype 3 (5-HT3) receptors0.60.90.50.50.70.60.9Ozagrel hydrochlorideThromboxane synthaseAntianginalinhibitor0.61.00.70.60.80.70.8Propoxycaine hydrochlorideLocal anesthesic0.60.90.60.50.70.61.0Piribedil hydrochlorideDopaminergic agonistVasodilator (peripheral)0.61.10.50.60.70.70.9OxaprozinAnalgesic0.90.90.60.70.70.81.2Nitrocaramiphen hydrochlorideMuscarinic antagonist1.00.90.70.80.80.71.1PhensuximideAnticonvulsant0.91.00.70.70.80.91.0NandroloneAnabolic0.90.90.60.80.80.81.1loxaglic acidLow-osmolar, ionic contrastDiagnostic aid (radiopaquemediummedium)0.80.90.70.70.80.81.0Dimaprit dihydrochlorideHistamine H2 receptoragonist1.01.00.80.71.10.81.0Naftifine hydrochlorideAntifungal0.90.90.60.70.80.81.0Reserpinic acid hydrochloride0.90.90.60.70.80.90.8Meprylcaine hydrochlorideLocal anesthesic0.80.90.70.80.80.81.1Beta-sistosterolAnticholesteremic0.80.90.70.80.80.90.9MilrinoneCardiotonic0.90.80.60.70.80.90.9Proscillaridin AGlucoside cardiotonic0.90.90.70.80.80.91.1Methantheline bromideAntispasmodic0.60.30.10.20.70.30.9SanguinarinePotent cytotoxicAntimicrobial drug12.81.20.70.72.60.81.4Ticarcillin sodiumAntibacterial0.80.90.80.70.90.80.9HarpagosideAntiinflammatory1.11.00.81.02.10.81.0Thiethylperazine malateadrenergic antagonistAntiemetic0.80.90.80.70.80.81.0AsiaticosideAntibiotic0.90.90.70.70.90.91.0MesalamineAnti-inflammatory(gastrointestinal)0.80.90.30.70.80.71.3BetulinAntineoplastic0.81.00.90.70.80.90.9alpha-SantoninAnthelmintic0.80.90.50.70.70.81.1GliquidoneAntidiabetic0.90.90.70.70.80.81.2Imidurea1.01.00.70.70.80.81.3Pizotifen malateAntihistaminic0.60.60.20.50.60.71.0LansoprazoleAntiulcerative0.80.90.70.70.91.11.2RibavirinAntiviral1.00.90.70.70.80.70.9Bethanechol chlorideCholinergic0.80.90.70.80.80.81.2CyclopenthiazideDiuretic0.81.00.60.70.80.81.4Cyproterone acetateAntiandrogen0.90.80.70.70.90.81.1Fluvoxamine maleateAntidepressant0.80.90.80.70.90.817.3(R)-Propranolol hydrochlorideBeta-adrenergic receptorAntihypertensorblocking agent16.60.91.63.81.50.81.4CefaloniumProphylactic use in mastitisand dry udder therapy0.80.90.70.80.80.71.2CiprofibrateAntihyperlipoproteine-mic0.80.90.70.70.80.81.5Fluticasone propionateAnti-inflammatory0.90.90.70.80.80.81.2Tropine1.21.00.71.01.90.91.3Zuclopenthixol hydrochlorideBlocking of D1 and D2Schizophreniadopaminergic receptors11.31.70.80.62.90.71.2Benzylpenicillin sodiumAntibacterial0.90.80.90.70.90.81.1Proguanil hydrochlorideInhibition of dihydrofolatereductase0.90.90.80.70.90.81.2ChlorambucilAntineoplastic0.81.00.70.70.80.71.2LymecyclineAntibiotic0.40.51.30.40.50.51.3Methiazole1.21.11.00.91.01.01.4Alfadolone acetateIn combination with alfaxaloneas anesthesic (intravenous)1.21.11.01.01.01.11.6(S)-propranolol hydrochlorideBeta-adrenergic blockingAntihypertensoragent1.21.11.21.01.01.21.7AlfaxaloneIn combination with alfadoloneacetate as anesthetic(intravenous)1.01.10.90.90.90.81.4(−)-Eseroline fumarate saltAnti-acetylcholinesterasePotent analgesicactivity & opiate agonistactivity1.11.00.80.90.91.01.5AzapropazoneCyclooxygenase inhibitorAnalgesic1.11.11.11.01.11.01.2Condelphine1.31.10.90.91.11.11.4Meptazinol hydrochlorideAnalgesic (narcotic)1.31.10.91.01.01.11.6Leucomisine1.21.00.90.81.01.11.4ApramycinAntibacterial1.41.02.40.91.11.01.3Dubinidine1.21.00.90.91.11.11.3EpitiostanolAntineoplastic1.41.21.41.11.01.21.2D-cycloserineCompetitive inhibition ofalanin racenase and D-alaninsynthase (bacterial cell wall)1.41.11.01.01.31.11.2Fursultiamine HydrochlorideAltzheimer's disease1.01.11.10.91.21.01.42-ChloropyrazineCardiotonic1.11.11.30.91.11.11.4Gabexate mesilateAnticoagulant1.31.11.01.01.11.11.3(+,−)-SynephrineHypertensive1.51.10.40.91.80.91.2PivampicillinAntibacterial1.31.11.11.01.11.11.6(S)-(−)-CycloserineTuberculosis15.21.41.20.80.81.11.6Talampicillin hydrochlorideAntibacterial1.31.11.21.11.81.11.5HomosalateTool for uv screen1.31.06.11.11.51.21.3Flucloxacillin sodiumAntibacterial1.41.11.00.90.91.11.6Spaglumic acidNMDA receptor ligands1.31.10.90.91.01.01.5TrapidilVasodilator (coronary)1.20.91.00.91.21.01.4RanolazineAntianginal1.51.11.10.91.31.01.6Deptropine citrateChronic bronchitis1.11.01.21.01.00.91.7(−)-Quinpirole hydrochlorideD2-dopaminereceptor agonist, someselectivity for D3 sites1.61.11.61.42.91.21.5Sertraline5-HT uptake inhibitor1.01.00.91.02.91.01.3SulfadoxineInhibition ofAntibacterialdihydropteroate synthase1.20.91.01.11.21.00.8EthamsylateRetinopathy1.21.01.11.01.01.11.3Cyclopentolate hydrochlorideMydriatic1.10.91.01.11.11.11.8MoxonidineImidazoline receptor ligandAntihypertensor1.11.11.20.81.21.01.4EstriolEstrogen1.01.01.10.81.41.11.5Etilefrine hydrochlorideAdrenergic agonistAntihypotensive1.20.90.91.20.91.12.3(−)-Isoproterenol hydrochlorideBeta Adrenergic AgonistCardiovascular drug (Sick SinusSyndrome)1.31.01.11.11.01.11.4AlprostadilVasodilator0.51.00.20.60.50.61.6KaempferolTopoisomerase I inhibitor,Anti-inflammatorytyrosin kinase, xanthinoxidase0.91.10.60.91.71.11.5TribenosideAntihaemorrhoidic drug1.21.11.20.91.01.21.4NialamideAntidepressant0.90.91.10.80.91.04.9RimexoloneCorticoidAnti-inflammatory (local)0.91.01.80.81.11.11.6Vitamin K2Dietary factor for controllingblood pressure1.11.10.71.11.21.11.4IsradipineAntianginal1.21.01.11.11.41.21.3PerindoprilAntihypertensive1.21.01.11.11.61.11.4Tiletamine hydrochlorideAnesthetic1.21.01.11.11.31.01.3Fexofenadine HClAntihistaminic1.21.01.21.11.51.11.2Isometheptene mutateAdrenergicSympathomimetic (VET)1.21.01.21.31.41.11.2Quinic acid1.11.00.81.21.51.11.3NifurtimoxAntiprotozoal (Trypanosoma)1.00.91.21.11.41.01.5Clonixin LysinateAnalgesic1.21.01.21.11.31.01.4LetrozoleAntineoplastic0.71.20.50.80.90.81.6VerteporfinTreatment of age-relatedmacular degeneration1.20.91.11.21.51.11.4ArbutinTyrosinase inhibitor andAntibacterialMelanin biosynthesisinhibitor13.41.03.93.61.514.81.2MeropenemAntibacterial1.21.01.11.11.61.11.4Tocainide hydrochlorideAntiarrhythmic1.11.01.21.01.31.21.1RamiprilConverting enzyme inhibitorAntihypertensor15.61.61.01.05.91.11.6Benzathine benzylpenicillinAntibacterial1.11.01.11.01.31.01.3MephenytoinAnticonvulsant1.11.01.31.11.51.11.3Risperidone5-HT2 antagonistAntipsychotic1.31.20.71.33.30.61.6RifabutinInhibition of RNA-Antibacterialpolymerase DNA-dependent1.11.01.51.31.61.11.4TorsemideDiuretic0.70.60.70.70.80.71.2ParbendazoleAnthelmintic (VET)1.01.01.21.11.31.11.3Halofantrine hydrochlorideAntimalarial1.41.11.41.01.21.11.6Mecamylamine hydrochlorideAntihypertensor1.11.21.11.11.21.01.6Articaine hydrochlorideLocal Anesthesic1.01.01.11.11.10.91.7Procarbazine hydrochlorideDNA depolymerization1.11.21.01.11.11.11.5Nomegestrol acetateProgestin1.01.01.30.91.10.91.6Viomycin sulfateAntibacterial1.11.01.11.01.10.91.6Pancuronium bromideCompetitive antagonist ofNeuromuscular blocking agentautonomic cholinergicreceptors1.31.20.91.11.51.01.8Saquinavir mesylateProtease inhibitor1.11.01.11.01.10.91.7Molindone hydrochlorideAntipsychotic1.11.11.31.71.61.01.6RonidazoleAntimicrobial1.41.01.21.01.41.02.2Alcuronium chlorideNeuromuscular blocking agent1.12.31.01.11.20.91.3Dorzolamide hydrochlorideAntiglaucoma drug1.31.11.11.11.21.01.8ZalcitabineReverse transcriptaseAntiviral (HIV)inhibitor1.11.01.21.01.21.01.9AzaperoneTranquilizer1.21.11.21.21.41.11.8Methyldopate hydrochlorideAntihypertensor19.31.03.14.93.415.61.9Cefepime hydrochlorideAntibacterial1.11.01.11.11.21.01.6Levocabastine hydrochlorideAntihistaminic1.01.11.11.01.21.01.6Clocortolone pivalateGlucocorticoid0.81.51.40.80.90.713.2Pyrvinium pamoateAnthelmintic (Nematodes,enterobiasis)13.42.84.35.22.917.71.7NadifloxacinAntibacterial Consistent with expectations, a detailed assessment of the hits revealed that AK screening enriches for the identification of bactericidal compounds (Table 3). More specifically, 100% of the antibiotics that were identified to be active against P. aeruginosa or K. pneumoniae represented bactericidal agents. Similarly, 96%, 94%, and 80% of the antibiotics that were active against E. coli, E. cloacae , and E. faecium , respectively, were bactericidal antibiotics. The assay identified 71% and 64% bactericidal antibiotics for A. baumannii and S. aureus. Among the bactericidal antibiotics detected, 3-lactam, cephalosporin, polymyxin, and fluoroquinolone antibiotics were active against Gram-negative pathogens ( E. coli and the ESKAPE pathogens A. baumannii, P. aeruginosa , and K. pneumoniae ), and penicillins, cephalosporins, quinolines, glycopeptides, and carbapenems were active toward S. aureus (see Table 4). It was also determined that clofazimine, which was initially developed as an antimycobacterial agent and was recently shown to exhibit bactericidal activity toward S. aureus , was indeed active against S. aureus . Bacteriostatic compounds, such as clindamycin, and macrolides, such as erythromycin, were not identified as being active toward any of the species tested. Interestingly, many tetracyclines were identified as killing S. aureus strain USA300-0114 and A. baumannii strain 98-37-09. In addition, the library contains membrane-active antiseptics, such as chlorhexidine, and with the exception of E. cloacae , these were also strong hits against all organisms tested. Screening results also revealed that the E. faecium strain tested proved to be resistant to most classes of antibiotics within the Prestwick library by MIC testing (Table 2), and this was also observed in the AK assay, indicating that the assay exhibits a low false-positive rate. Interestingly, the assay also detected 38 drugs with no known antimicrobial properties (denoted as “other” in Table 3) that were active against each organism; see Table 4 for a complete list of these compounds. Antimicrobial Activities of Nonantibiotic Drugs that Induce AK Release— Recently, the exploration of the so-called “off-target” activities of previously developed drugs has emerged as an approach to identify chemical scaffolds that could be exploited for new therapeutic indications. In that regard, Prestwick library screening results revealed that 4% to 56% (depending on the organism) of the members that generated significant AK signal were compounds with no previously reported antimicrobial activity (see Table 4). To determine whether the 38 nonantibiotics identified in the screen have potential for repurposing as anti-infectives, 4 nonantibiotic drugs that were commercially available were further evaluated by two secondary assays. First, dose-response assays were performed to validate that they induced AK activity, and all were reconfirmed. Second, the in vitro antimicrobial activity for each drug was measured by standard MIC testing. With the exception of one drug/organism pair, all drugs exhibited in vitro activity toward each organism. More specifically, tamoxifen, suloctidil, and clomiphene exhibited MICs of 8 μg ml −1 against E. faecium. S. aureus and A. baumannii were susceptible to terfenadine (16-μg ml −1 MIC and 64-Lag ml −1 MIC, respectively). Suloctidil was also detected to be active against P. aeruginosa by both primary and confirmatory AK screens, but the drug did not elicit an antimicrobial response by MIC measures. Some strains of P. aeruginosa secrete AK at high cell density, and it is possible that suloctidil may trigger a similar response. Terfenadine and tamoxifen, which exhibited antimicrobial properties toward planktonic S. aureus and E. faecium cells, respectively, were characterized further. Terfenadine was evaluated for activity against S. aureus biofilms and small-colony variants using the AK assays described above. Treatment of 48-h S. aureus strain UAMS-1 biofilms with 10×-MIC terfenadine elicited a modest 2.7-fold increase in AK release (see FIG. 6A ); plating-based viability assays determined that this correlated with a 1.1-log reduction in biofilm cell viability, which was comparable to the activity of ciprofloxacin under the same assay conditions (see FIG. 4A ). Similarly, treatment of S. aureus small-colony-variant UAMS-1112 cells with 10×MIC terfenadine elicited a 3.3-fold increase in AK signal in comparison to that for mock-treated cells (see FIG. 6A ). Conventional MIC testing subsequently verified that terfenadine is active against UAMS-1112 at 2 μg ml −1 . Next, the in vivo antimicrobial properties of terfenadine and tamoxifen were evaluated using a Galleria mellonella model of S. aureus and E. faecium infection, respectively. For terfenadine, groups of larvae (n=45) were infected with 1.0×10 6 S. aureus USA300-1114 cells. Worms were then treated at 2 h and 24 h with a range of terfenadine concentrations (20 to 160 mg kg −1 ), vehicle (DMSO; negative control), or 20 mg kg −1 vancomycin (positive control), and larval survival was assessed 48 h postinoculation. For tamoxifen studies, experiments were performed exactly as described above except that larvae were inoculated with 1.4×10 6 E. faecium strain 824-05 cells and larvae were treated with either 80 or 160 mg kg −1 tamoxifen. Terfenadine-treated larvae did not reproducibly exhibit increased survival relative to vehicle-treated larvae. However, tamoxifen treatment of E. faecium -infected larvae resulted in a dose-dependent increase in survival. As shown in FIG. 6B , treatment with 80 or 160 mg kg-1 resulted in a 4.2-fold- or 7-fold-higher survival, respectively, than was found with vehicle-treated controls. Taken together, these results indicate that terfenadine exhibits in vitro activity toward S. aureus planktonic, SCV, and biofilm populations and that tamoxifen is active toward planktonic E. faecium and against the organism in a simple animal model of infection. As discussed below, these data show that tamoxifen and terfenadine represent attractive new chemical scaffolds for antibacterial optimization. As set forth herein, Prestwick library screening revealed that each bacterial species studied was susceptible to members of the library with no previously reported antimicrobial activity. The antimicrobial properties of two of these drugs was studied in more detail: terfenadine and tamoxifen. Terfenadine is a nonsedating antihistamine based on a 4-substituted piperidine scaffold. Based on further studies, it was determined that terfenadine acts as a topoisomerase inhibitor and is structurally similar to certain topoisomerase inhibitors, including for example novel bacterial topoisomerase II inhibitor (NBTI). Based on the structural similarity between terfenadine and these molecules, it is likely that terfenadine is acting as a DNA gyrase and topoisomerase inhibitor. More specifically, terfenadine and derivatives thereof act as topoisomerase 4 inhibitors. Furthermore, it was found that terfenadine has activity against S. aureus small-colony variants and biofilms, properties not previously reported for this scaffold. A screen of E. faecium identified two structurally related nonsteroid estrogen receptor antagonists, tamoxifen and clomiphene. Tamoxifen is used to treat some forms of estrogen-receptor-positive breast cancer, while clomiphene is used in fertility treatment regimens. These two compounds are members of the triarylethylene class of estrogen receptors. Since the number of agents with activity toward enterococcus is quite limited, tamoxifen's in vivo activity was investigated using a Galleria model of enterococcus infection. Although it was not as active as vancomycin, tamoxifen did impart a survival benefit, indicating that it has in vivo antimicrobial activity. High-dose tamoxifen therapy has been used in experimental treatment of refractory human cancers, and dosing results in micromolar serum concentrations of tamoxifen corresponding to the levels of drug associated with antienterococcal activity observed in the studies provided herein. In addition to providing a powerful new HTS approach to identify antimicrobial agents active against planktonic bacteria, an AK assay that is easily amenable to screening bacteria in disease states that cannot be readily screened via conventional approaches is provided herein. In that regard, the AK assay is capable of measuring the killing properties of bactericidal agents administered to biofilms formed by both Gram-negative and Gram-positive representatives of the ESKAPE pathogens. Similarly, the AK assay can detect the bactericidal properties of antibiotics toward a phenotypically stable S. aureus small-colony variant. These features can be exploited to develop corresponding high-throughput screening assays for the identification of agents that kill established biofilms and small-colony variants or provide powerful secondary assays aimed at characterizing the potential antimicrobial properties of molecules of interest. Example II Antimicrobial Properties of Terfenadine and Terfenadine Derivatives Terfenadine derivatives were synthesized as described below. General Method A KSC-335-007 1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one To a vial was added the diphenyl(piperidin-4-yl)methanol (1.190 g, 4.45 mmol), 1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-one (1.012 g, 4.24 mmol), sodium bicarbonate (0.427 g, 5.09 mmol) with water:2-butanone (18 mL, 1:5). The reaction stirred at 85° C. for 16 h and was then cooled to rt and water (50 mL) was added. The reaction was extracted with EtOAc (3×50 mL). The EtOAc layer was dried with MgSO 4 , filtered, concentrated and purified by MPLC (20 min, 0-10% MeOH:DCM) to produce pure 1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl) piperidin-1-yl)butan-1-one (1.37 g, 2.92 mmol, 69% yield) as a colorless oil. 1 H NMR (500 MHz, CDCl 3 ): δ 7.90 (d, J=8.4 Hz, 2H), 7.49-7.45 (m, 6H), 7.31-7.25 (m, 4H), 7.20-7.14 (m, 2H), 2.97-2.92 (m, 4H), 2.45-2.36 (m, 3H), 2.09 (br s, 1H), 2.00-1.87 (m, 4H), 1.49-1.32 (m, 4H), 1.34 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 199.7, 156.5, 146.0, 134.5, 128.1, 128.0, 126.4, 125.7, 125.4, 79.4, 57.9, 43.9, 43.4, 44.1, 36.2, 35.0, 31.0, 26.2, 21.9. LCMS Retention time: 4.207 min. LCMS purity 99.5%. HRMS (ESI): m/z calcd for C 32 H 39 NO 2 [M+H] + 470.2981, found 470.3054. KSC-335-005 4-(4-(Hydroxydiphenylmethyl)piperidin-1-yl)-1-(4-isopropylphenyl)butan-1-one Method A: diphenyl(piperidin-4-yl)methanol (0.620 g, 2.317 mmol), 4-chloro-1-(4-isopropylphenyl)butan-1-one (0.496 g, 2.207 mmol), sodium bicarbonate (0.222 g, 2.65 mmol) with water (3 mL) and 2-butanone (15 mL, Ratio: 5). to produce pure 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-(4-isopropylphenyl)butan-1-one (0.481 g, 1.056 mmol, 48% yield) as a colorless oil. 1 H NMR (500 MHz, CDCl 3 ): δ 7.89 (d, J=8.4 Hz, 2H), 7.49-7.45 (m, 4H), 7.31-7.26 (m, 6H), 7.20-7.14 (m, 2H), 2.98-2.91 (m, 4H), 2.45-2.35 (m, 1H), 2.38 (t, J=6.8 Hz, 2H), 2.08 (br s, 1H), 1.99-1.89 (m, 4H), 1.61 (br s, 1H), 1.48-1.33 (m, 4H), 1.27 (d, J=6.8 Hz, 6H). KSC-335-006 1-(4-(tert-butyl)phenyl)-5-(4-(hydroxydiphenylmethyl)piperidin-1-yl)pentan-1-one Method A: diphenyl(piperidin-4-yl)methanol (0.544 g, 2.035 mmol), 1-(4-(tert-butyl)phenyl)-5-chloropentan-1-one (0.490 g, 1.938 mmol), sodium bicarbonate (0.195 g, 2.326 mmol) with water:2-butanone (18 mL, 1:5) to produce pure 1-(4-(tert-butyl)phenyl)-5-(4-(hydroxydiphenylmethyl)piperidin-1-yl)pentan-1-one (0.600 g, 1.240 mmol, 64.0% yield) as a colorless oil. 1 H NMR (500 MHz, CDCl 3 ): δ 7.89 (d, J=8.4 Hz, 2H), 7.49-7.45 (m, 6H), 7.32-7.26 (m, 4H), 7.20-7.14 (m, 2H), 2.98-2.92 (m, 4H), 2.48-2.32 (m, 3H), 2.14 (br s, 1H), 1.99-1.89 (m, 2H), 1.77-1.62 (m, 2H), 1.60-1.42 (m, 6H), 1.34 (s, 9H). 1-(4-(tert-butyl)phenyl)-3-(4-(hydroxydiphenylmethyl)piperidin-1-yl)propan-1-one Method A: diphenyl(piperidin-4-yl)methanol (0.543 g, 2.032 mmol), 1-(4-(tert-butyl)phenyl)-3-chloropropan-1-one (0.435 g, 1.936 mmol), sodium bicarbonate (0.195 g, 2.323 mmol) with water:2-butanone (18 mL, 1:5) to produce pure 1-(4-(tert-butyl)phenyl)-3-(4-(hydroxydiphenyl methyl)piperidin-1-yl)propan-1-one (0.838 g, 1.84 mmol, 95% yield) as a colorless oil. 1 H NMR (500 MHz, CDCl 3 ): δ 7.89 (d, J=8.4 Hz, 2H), 7.50-7.45 (m, 6H), 7.32-7.25 (m, 4H), 7.21-7.14 (m, 2H), 3.15 (t, J=7.1 Hz, 2H), 3.01-2.96 (m, 2H), 2.81 (t, J=7.1 Hz, 2H), 2.49-2.42 (m, 1H), 2.15-2.04 (m, 3H), 1.56-1.46 (m, 4H), 1.33 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 198.9, 171.1, 156.8, 145.8, 134.3, 128.2, 128.0, 126.5, 125.8, 125.5, 79.4, 60.4, 54.2, 53.4, 44.0, 36.3, 35.1, 31.1, 26.4, 21.1, 14.2. LCMS Retention time: 3.968 min. LCMS purity 98.1%. HRMS (ESI): m/z calcd for C 31 H 37 NO 2 [M+H] + 456.2824, found 456.2897. KSC-335-009 1-(4-chlorophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one Method A: diphenyl(piperidin-4-yl)methanol (0.626 g, 2.341 mmol), 4-chloro-1-(4-chlorophenyl) butan-1-one (0.484 g, 2.229 mmol), sodium bicarbonate (0.225 g, 2.68 mmol) with water:2-butanone (18 mL, 1:5) to produce pure 1-(4-chlorophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one (0.394 g, 0.879 mmol, 39.4% yield) as a colorless oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.90 (d, J=8.4 Hz, 2H), 7.48-7.44 (m, 4H), 7.42 (d, J=8.6 Hz, 2H), 7.31-7.26 (m, 4H), 7.20-7.15 (m, 2H), 3.96-2.89 (m, 4H), 2.45-2.34 (m, 3H), 2.08 (br s, 1H), 1.99-1.87 (m, 4H), 1.50-1.30 (m, 4H). General Method B KSC-335-014, Terfenadine 1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol. To a vial was added the 1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one (KSC-335-007 (0.198 g, 0.422 mmol) and MeOH (2 mL). The sodium borohydride (0.032 g, 0.844 mmol) was then added and the reaction stirred at rt for 3 h. The reaction was concentrated to dryness, water (5 mL) was added and a white precipitate formed. The precipitate was filtered out and then dissolved in DCM (10 mL), dried with MgSO 4 , filtered and concentrated to produce pure 1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol (0.151 g, 0.320 mmol, 76% yield) as on oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.52-7.46 (m, 4H), 7.33-7.25 (m, 8H), 7.21-7.15 (m, 2H), 4.61-4.56 (m, 1H), 3.16-3.11 (br m, 1H), 3.00-2.94 (m, 1H), 2.51-2.34 (m, 4H), 2.10-1.88 (m, 4H), 1.83-1.75 (m, 1H), 1.70-1.45 (m, 6H), 1.30 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 149.4, 146.1, 146.0, 142.7, 128.2, 128.1, 126.4, 126.3, 125.7, 125.6, 125.3, 125.0, 79.2, 73.4, 58.9, 54.7, 53.3, 44.2, 39.7, 34.4, 31.4, 26.0, 25.9, 24.1. LCMS Retention time: 4.137 min. LCMS purity 97.5%. HRMS (ESI): m/z calcd for C 32 H 41 NO 2 [M+H] + 472.3144, found 472.3219. KSC-335-012 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-(4-isopropylphenyl)butan-1-ol Method B: 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-(4-isopropylphenyl)butan-1-one (KSC-335-005) (0.154 g, 0.338 mmol) and MeOH (2 mL) sodium borohydride (0.026 g, 0.676 mmol) to produce pure 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-(4-isopropylphenyl)butan-1-ol (0.146 g, 0.319 mmol, 94% yield) as on oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.52-7.46 (m, 4H), 7.32-7.23 (m, 6H), 7.20-7.14 (m, 4H), 4.61-4.58 (m, 1H), 3.18-3.11 (br m, 1H), 3.00-2.94 (br m, 1H), 2.87 (septet, J=6.9 Hz, 1H), 2.50-2.33 (m, 3H), 2.29 (br s, 1H), 2.10-1.89 (m, 3H), 1.82-1.44 (m, 8H), 1.22 (d, J=6.9 Hz, 6H). 13 C NMR (125 MHz, CDCl 3 ): δ 147.2, 146.1, 146.0, 128.2, 128.1, 126.5, 126.4, 126.1, 125.7, 125.7, 79.2, 73.5, 58.9, 54.7, 53.3, 44.2, 39.9, 33.7, 26.0, 25.9, 24.2, 24.1, 24.0. LCMS Retention time: 4.056 min. LCMS purity 98.6%. HRMS (ESI): m/z calcd for C 31 H 39 NO 2 [M+H] + 458.2986, found 458.3062. KSC-335-013 1-(4-(tert-butyl)phenyl)-5-(4-(hydroxydiphenylmethyl)piperidin-1-yl)pentan-1-ol Method B: 1-(4-(tert-butyl)phenyl)-5-(4-(hydroxydiphenylmethyl)piperidin-1-yl)pentan-1-one (KSC-335-006) (0.204 g, 0.422 mmol) and MeOH (2 mL) and sodium borohydride (0.032 g, 0.844 mmol) to produce pure 1-(4-(tert-butyl)phenyl)-5-(4-(hydroxydiphenylmethyl)piperidin-1-yl)pentan-1-ol (0.156 g, 0.321 mmol, 76% yield) as on oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.50-7.45 (m, 4H), 7.36 (d, J=8.4 Hz, 2H), 7.31-7.24 (m, 6H), 7.19-7.14 (m, 2H), 4.65-4.60 (m, 1H), 2.98-2.90 (br m, 1H), 2.48-2.38 (m, 1H), 2.30 (t, J=7.2 Hz, 2H), 2.23 (br s, 1H), 1.97-1.87 (m, 2H), 1.84-1.60 (m, 4H), 1.55-1.35 (m, 8H), 1.31 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 150.3, 146.0, 142.0, 128.1, 126.4, 125.8, 125.5, 125.3, 79.4, 74.1, 58.4, 54.1, 54.0, 44.2, 38.5, 34.5, 31.4, 31.3, 26.5, 26.3, 26.2, 23.7. LCMS Retention time: 4.254 min. LCMS purity 96.4%. HRMS (ESI): m/z calcd for C 33 H 43 NO 2 [M+H] + 486.3294, found 486.3370. KSC-335-015 1-(4-chlorophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol Method B: 1-(4-chlorophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one (KSC-335-009) (0.156 g, 0.348 mmol) and MeOH (2 mL) sodium borohydride (0.026 g, 0.696 mmol) to produce pure 1-(4-chlorophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol (0.118 g, 0.262 mmol, 75% yield) as on oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.46 (m, 4H), 7.32-7.24 (m, 8H), 7.20-7.15 (m, 2H), 4.61-4.56 (m, 1H), 3.16-3.10 (br m, 1H), 2.97-2.91 (m, 1H), 2.51-2.33 (m, 4H), 2.12-1.88 (m, 3H), 1.83-1.75 (m, 1H), 1.78-1.46 (m, 8H). 13 C NMR (125 MHz, CDCl 3 ): δ 146.0, 145.9, 144.5, 139.1, 128.19, 128.18, 128.1, 127.1, 126.49, 126.45, 125.62, 125.57, 79.2, 72.9, 58.8, 54.7, 53.2, 44.2, 40.2, 26.0, 25.9, 24.1. LCMS Retention time: 3.845 min. LCMS purity 98.4%. HRMS (ESI): m/z calcd for C 28 H 32 ClNO 2 [M+H] + 450.2122, found 450.2194. KSC-335-016 1-(4-(tert-butyl)phenyl)-3-(4-(hydroxydiphenylmethyl)piperidin-1-yl)propan-1-ol Method B: 1-(4-(tert-butyl)phenyl)-3-(4-(hydroxydiphenylmethyl)piperidin-1-yl)propan-1-one (KSC-335-008) (0.116 g, 0.255 mmol) and MeOH (2 mL) and sodium borohydride (0.019 g, 0.509 mmol) to produce pure 1-(4-(tert-butyl)phenyl)-3-(4-(hydroxydiphenylmethyl)piperidin-1-yl)propan-1-ol (0.106 g, 0.232 mmol, 91% yield) as on oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.49-7.44 (m, 4H), 7.36-7.25 (m, 8H), 7.22-7.16 (m, 2H), 6.72 (br s, 1H), 4.90-4.85 (m, 1H), 3.21-3.15 (br m, 1H), 3.11-3.05 (br m, 1H), 2.70-2.62 (m, 1H), 2.57-2.40 (m, 2H), 2.14-2.06 (m, 2H), 1.91-1.79 (m, 3H), 1.57-1.45 (m, 4H), 1.31 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 149.6, 145.8, 145.7, 141.9, 128.2, 128.1, 126.6, 126.5, 125.8, 125.7, 125.2, 125.0, 79.4, 75.3, 57.3, 55.2, 53.2, 44.1, 34.4, 33.7, 31.4, 26.7, 26.4. LCMS Retention time: 4.006 min. LCMS purity 97.7%. HRMS (ESI): m/z calcd for C 31 H 39 NO 2 [M+H] + 458.2991, found 458.3066. KSC-335-018 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-phenylbutan-1-one Method A: diphenyl(piperidin-4-yl)methanol (0.524 g, 1.961 mmol), 4-chloro-1-phenylbutan-1-one (0.300 ml, 1.868 mmol), sodium bicarbonate (0.188 g, 2.241 mmol) with water:2-butanone (18 mL, 1:5) to produce pure 4-(4-(hydroxydiphenylmethyl)piperidin-1l-yl)-1-phenylbutan-1-one (0.177 g, 0.428 mmol, 23% yield) as a colorless oil. 1 H NMR (500 MHz, CDCl 3 ): δ 7.98-7.94 (m, 2H), 7.57-7.52 (m, 1H), 7.49-7.42 (m, 6H), 7.32-7.26 (m, 4H), 7.20-7.15 (m, 2H), 3.00-2.90 (m, 4H), 2.46-2.35 (m, 3H), 2.09 (br s, 1H), 2.00-1.87 (m, 4H), 1.50-1.33 (m, 4H). KSC-335-020 1-(tert-butyl)-4-(4-chlorobutyl)benzene To a vial was added the 1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-one (0.266 g, 1.114 mmol) and triethylsilane (0.518 g, 0.712 ml, 4.46 mmol) with TFA (4 mL). The reaction stirred at 75° C. for 18 h, was cooled to rt and concentrated in vacuo. The residue was then dissolved in DCM (5 mL) and washed with water (4 mL). The DCM layer was collected and washed with water (1×5 mL), dried with MgSO 4 , filtered and adsorbed to silica and purified by Teledyne ISCO Combiflash chromatography (20 min, 0-40% EtOAc:Hex) and fractions 4 and 5 were collected to produce pure 1-(tert-butyl)-4-(4-chlorobutyl)benzene (0.155 g, 0.690 mmol, 61.9% yield) as an oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.32 (d, J=7.6 Hz, 2H), 7.12 (d, J=7.6 Hz, 2H), 3.56 (t, J=6.5 Hz, 2H), 2.62 (t, J=7.5 Hz, 2H), 1.87-1.74 (m, 4H), 1.32 (s, 9H). KSC-335-021 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-phenylbutan-1-ol Method B: 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-phenylbutan-1-one (KSC-335-018) (0.065 g, 0.157 mmol) and MeOH (2 mL) and sodium borohydride (0.012 g, 0.314 mmol) to produce pure 4-(4-(hydroxydiphenylmethyl) piperidin-1-yl)-1-phenylbutan-1-ol (0.048 g, 0.116 mmol, 73% yield) as on oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.46 (m, 4H), 7.37-7.33 (m, 2H), 7.32-7.26 (m, 5H), 7.23-7.14 (m, 3H), 4.65-4.61 (m, 1H), 3.15 (d, J=11.7 Hz, 1H), 2.96 (d, J=11.7 Hz, 1H), 2.52-2.31 (m, 4H), 2.11-1.90 (m, 3H), 1.84-1.74 (m, 2H), 1.70-1.44 (m, 7H). 13 C NMR (125 MHz, CDCl 3 ): δ 146.0, 145.9, 145.8, 128.2, 128.1, 128.0, 126.6, 126.5, 126.4, 125.6, 125.6, 79.2, 73.6, 58.9, 54.7, 53.3, 44.2, 40.1, 26.0, 25.9, 24.1. LCMS Retention time: 3.711 min. LCMS purity 99.8%. HRMS (ESI): m/z calcd for C 28 H 33 NO 2 [M+H] + 416.2517, found 416.2592. KSC-335-022 Methyl 2-methyl-2-(4-(4-((methylsulfonyl)oxy)but-1-yn-1-yl)phenyl)propanoate To a vial was added the methyl 2-(4-(4-hydroxybut-1-yn-1-yl)phenyl)-2-methylpropanoate (0.051 g, 0.207 mmol) and dry DCM (2 mL). The methanesulfonyl chloride (0.047 g, 0.032 mL, 0.414 mmol) and pyridine (0.147 g, 0.151 mL, 1.864 mmol) were each added and the reaction and stirred at rt for 16 h. The reaction was then diluted with DCM (5 mL) and washed with 1% w/v sulfuric acid in water (3×7 mL), saturated NaHCO 3 (7 mL) and brine (7 mL). The organic layer was dried with MgSO 4 , filtered and concentrated to produce methyl 2-methyl-2-(4-(4-((methylsulfonyl) oxy)but-1-yn-1-yl)phenyl)propanoate (0.063 g, 0.194 mmol, 94% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.35 (d, J=8.6 Hz, 2H), 7.26 (d, J=8.6 Hz, 2H), 4.38 (t, J=6.8 Hz, 2H), 3.64 (s, 3H), 3.06 (s, 3H), 2.87 (t, J=6.8 Hz, 2H), 1.56 (s, 6H). KSC-335-023 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-(4-methoxyphenyl)butan-1-one Method A: diphenyl(piperidin-4-yl)methanol (0.490 g, 1.832 mmol), 4-chloro-1-(4-methoxyphenyl)butan-1-one (0.371 g, 1.744 mmol), sodium bicarbonate (0.176 g, 2.093 mmol) with water (3 mL) and 2-butanone (15 mL) to produce pure 4-(4-(hydroxydi phenylmethyl)piperidin-1-yl)-1-(4-methoxyphenyl)butan-1-one (0.282 g, 0.636 mmol, 36% yield) as a colorless oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.94 (d, J=9.0 Hz, 2H), 7.49-7.45 (m, 4H), 7.31-7.26 (m, 4H), 7.17 (tt, J 1 =7.3 Hz, J 2 =1.3 Hz, 2H), 6.92 (d, J=8.9 Hz, 2H), 3.87 (s, 3H), 2.97 (br s, 1H), 2.93 (t, J=7.3 Hz, 2H), 2.48-2.35 (m, 3H), 2.02-1.88 (m, 4H), 1.63-1.40 (m, 4H). KSC-335-024 1-(4-Fluorophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one Method A: diphenyl(piperidin-4-yl)methanol (0.385 g, 1.439 mmol), 4-chloro-1-(4-fluorophenyl)butan-1-one (0.275 g, 1.371 mmol), sodium bicarbonate (0.138 g, 1.645 mmol) with water (3 mL) and 2-butanone (15 mL) to produce pure 1-(4-fluorophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one (0.174 g, 0.403 mmol, 29% yield) as a colorless oil. 1 H NMR (400 MHz, CDCl 3 ): δ 8.00-7.96 (m, 2H), 7.48-7.44 (m, 4H), 7.31-7.26 (m, 4H), 7.20-7.15 (m, 2H), 7.14-7.08 (m, 2H), 2.97-2.94 (m, 4H), 2.46-2.36 (m, 3H), 2.15 (br s, 1H), 2.01-1.88 (m, 4H), 1.52-1.35 (m, 4H). KSC-335-025 1-(4-Bromophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one Method A: diphenyl(piperidin-4-yl)methanol (0.439 g, 1.642 mmol), 1-(4-bromophenyl)-4-chlorobutan-1-one (0.409 g, 1.564 mmol), sodium bicarbonate (0.158 g, 1.877 mmol) with water (3 mL) and 2-butanone (15 mL) to produce pure 1-(4-bromophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one (0.245 g, 0.498 mmol, 32% yield) as a colorless oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.83-7.79 (m, 2H), 7.60-7.56 (m, 2H), 7.48-7.45 (m, 4H), 7.31-7.26 (m, 4H), 7.20-7.15 (m, 2H), 2.95-2.90 (m, 4H), 2.45-2.35 (m, 3H), 2.17 (br s, 1H), 2.00-1.88 (m, 4H), 1.51-1.33 (m, 4H). KSC-335-030 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-(4-methoxyphenyl)butan-1-ol Method B: 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-(4-methoxyphenyl)butan-1-one (KSC-335-023) (0.113 g, 0.255 mmol) and MeOH (2 mL) and sodium borohydride (0.019 g, 0.509 mmol) to produce pure 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-(4-methoxyphenyl)butan-1-ol (0.062 g, 0.139 mmol, 55% yield) as on oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.46 (m, 4H), 7.32-7.24 (m, 6H), 7.20-7.15 (m, 2H), 6.84 (d, J=7.0 Hz, 2H), 4.60-4.56 (m, 1H), 3.78 (s, 3H), 3.14 (d, J=11.7 Hz, 1H), 2.95 (d, J=11.7 Hz, 1H), 2.50-2.35 (m, 4H), 2.10-2.02 (m, 1H), 1.99-1.86 (m, 2H), 1.80-1.73 (m, 1H), 1.69-1.45 (m, 7H). 13 C NMR (125 MHz, CDCl 3 ): δ 158.3, 146.1, 146.0, 138.1, 128.1, 128.1, 126.7, 126.4, 126.4, 125.7, 125.6, 113.5, 79.2, 73.2, 58.9, 55.2, 54.7, 53.2, 44.2, 40.0, 26.0, 25.9, 24.1. LCMS Retention time: 3.620 min. LCMS purity 98.3%. HRMS (ESI): m/z calcd for C 29 H 35 NO 3 [M+H] + 446.2652, found 446.2728. KSC-335-031 1-(4-fluorophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol Method B: 1-(4-fluorophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one (KSC-335-024) (0.064 g, 0.148 mmol) and MeOH (2 mL) and sodium borohydride (0.011 g, 0.297 mmol) to produce pure 1-(4-fluorophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol (0.059 g, 0.136 mmol, 92% yield) as on oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.46 (m, 4H), 7.33-7.25 (m, 6H), 7.20-7.14 (m, 2H), 6.96 (t, J=8.8 Hz, 2H), 4.61-4.57 (m, 1H), 3.14 (d, J=11.7 Hz, 1H), 2.94 (d, J=11.7 Hz, 1H), 2.51-2.35 (m, 4H), 2.13-2.02 (m, 1H), 2.02-1.86 (m, 2H), 1.78-1.45 (m, 7H). 13 C NMR (125 MHz, CDCl 3 ): δ 162.6, 160.7, 146.0, 145.9, 141.7, 141.6, 128.2, 128.1, 127.2, 127.1, 126.5, 126.4, 125.6, 125.5, 114.9, 114.7, 79.2, 73.0, 58.8, 54.8, 53.1, 44.2, 40.3, 30.9, 26.0, 25.9, 24.1. LCMS Retention time: 3.691 min. LCMS purity 98.5%. HRMS (ESI): m/z calcd for C 28 H 32 FNO 2 [M+H] + 434.2406, found 434.2482. KSC-335-032 1-(4-bromophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol Method B: 1-(4-bromophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one (KSC-335-025) (0.083 g, 0.169 mmol) and MeOH (2 mL) and sodium borohydride (0.013 g, 0.337 mmol) to produce pure 1-(4-bromophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol (0.053 g, 0.107 mmol, 63.6% yield) as on oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.46 (m, 4H), 7.41 (d, J=6.8 Hz, 2H), 7.32-7.26 (m, 4H), 7.22 (d, J=6.6 Hz, 2H), 7.20-7.15 (m, 2H), 4.60-4.56 (m, 1H), 3.14 (d, J=11.7 Hz, 1H), 2.93 (d, J=11.7 Hz, 1H), 2.50-2.42 (m, 1H), 2.41-2.34 (m, 2H), 2.11-2.05 (m, 1H), 2.01-1.95 (m, 1H), 1.94-1.86 (m, 1H), 1.78-1.45 (m, 8H). 13 C NMR (125 MHz, CDCl 3 ): δ 146.0, 145.9, 145.1, 131.1, 128.2, 128.1, 127.5, 126.5, 126.4, 125.6, 125.6, 120.2, 79.2, 72.9, 58.8, 54.7, 53.2, 44.1, 40.1, 26.0, 25.9, 24.1. LCMS Retention time: 3.902 min. LCMS purity 99.1%. HRMS (ESI): m/z calcd for C 28 H 32 BrNO 2 [M+H] + 494.1614, found 494.1673. KSC-335-041 (1-(4-(4-(tert-butyl)phenyl)butyl)piperidin-4-yl)diphenylmethanol To a vial was added the diphenyl(piperidin-4-yl)methanol (0.153 g, 0.571 mmol), 1-(tert-butyl)-4-(4-chlorobutyl)benzene (KSC-335-020) (0.154 g, 0.685 mmol) and potassium carbonate (0.473 g, 3.43 mmol) in acetonitrile. The reaction stirred overnight at 85° C. and for 18 h and was then cooled to rt and filtered. The filtrate was then diluted with brine and extracted with diethyl ether (3×15 mL). The ether layers were combined, dried with MgSO 4 , filtered and purified by reverse-phase MPLC (20 min, 10-100% MeCN:H 2 O) to produce pure (1-(4-(4-(tert-butyl)phenyl)butyl)piperidin-4-yl)diphenylmethanol (0.180 g, 0.395 mmol, 69% yield) as an oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.38-7.34 (m, 4H), 7.19-7.14 (m, 6H), 7.07-7.02 (m, 2H), 6.99-6.95 (m, 2H), 2.86-2.80 (m, 2H), 2.45 (t, J=7.3 Hz, 2H), 2.35-2.26 (m, 1H), 2.22-2.17 (m, 2H), 1.84-1.76 (m, 3H), 1.52-1.30 (m, 8H), 1.18 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 171.1, 148.4, 146.0, 139.4, 128.1, 128.0, 126.4, 125.8, 125.1, 79.5, 60.4, 58.8, 54.1, 44.2, 35.2, 34.3, 31.4, 29.5, 26.8, 26.4, 21.0, 14.2. LCMS Retention time: 3.928 min. LCMS purity 97.8%. HRMS (ESI): m/z calcd for C 32 H 41 NO [M+H] + 456.3188, found 456.3261. KSC-335-053 Methyl 4-(1,3-dithian-2-yl)benzoate. A flame dried vial was evaporated 3 times with argon and methyl 4-formylbenzoate (0.50 g, 3.05 mmol) was added with anhydrous DCM (8.70 mL) followed by 1,3-propanedithiol (0.339 mL, 3.35 mmol). The reaction began to stir at rt for 1.5 h. The reaction was then cooled to 0° C. and the BF3.OEt 2 (0.425 ml, 3.35 mmol) was added dropwise. The reaction was then warmed slowly to rt and stirred overnight. The reaction was then diluted with DCM (15 mL) and quenched with saturated NaHCO 3 (15 mL) and the DCM layer was dried with MgSO 4 , filtered and adsorbed to silica and purified by MPLC (20 min, 0-35% EtOAc:Hex) to produce methyl 4-(1,3-dithian-2-yl)benzoate (0.669 g, 2.63 mmol, 86% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 8.01 (d, J=8.4 Hz, 2H), 7.54 (d, J=8.3 Hz, 2H), 3.91 (s, 3H), 3.12-3.03 (m, 2H), 2.96-2.90 (m, 2H), 2.23-2.16 (m, 1H), 2.01-1.89 (m, 1H), 1.55 (s, 2H). KSC-335-054 Methyl 2-(4-(4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)but-1-yn-1-yl)phenyl)-2-methylpropanoate To a vial was added the diphenyl(piperidin-4-yl)methanol (0.528 g, 1.974 mmol), methyl 2-methyl-2-(4-(4-((methylsulfonyl)oxy)but-1-yn-1-yl)phenyl)propanoate (KSC-335-022) (0.582 g, 1.794 mmol) and potassium carbonate (0.744 g, 5.38 mmol) with acetonitrile (10 mL). The reaction stirred at 70° C. for 18 h and cooled to rt and filtered to remove the potassium carbonate. The filtrate was adsorbed to silica gel and purified by reverse-phase MPLC (20 min, 10-100% MeCN:H 2 O) to produce pure methyl 2-(4-(4-(4-(hydroxydiphenylmethyl) piperidin-1-yl)but-1-yn-1-yl)phenyl)-2-methylpropanoate (0.434 g, 0.876 mmol, 49% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.49-7.46 (m, 4H), 7.34-7.27 (m, 6H), 7.25-7.15 (m, 4H), 3.64 (s, 3H), 3.03-2.97 (m, 2H), 2.68-2.63 (m, 2H), 2.59-2.54 (m, 2H), 2.48-2.40 (m, 1H), 2.14-2.06 (m, 2H), 1.63 (br s, 1H), 1.55 (s, 6H), 1.55-1.45 (m, 4H). KSC-335-056 Methyl 4-(2-(3-chloropropyl)-1,3-dithian-2-yl)benzoate To a dry vial was added the methyl 4-(1,3-dithian-2-yl)benzoate (KSC-335-053) (0.256 g, 1.01 mmol) and this was evacuated with argon 3 times. The dry THF (7 mL) was added and the reaction was cooled to −78° C. at and the NaHMDS (1.258 mL, 1.258 mmol) was added. After 30 minutes the 1-chloro-3-iodopropane (0.531 mL, 5.03 mmol) was added. The reaction was then allowed to warm to rt overnight. The mixture was quenched with the addition of saturated NH 4 Cl (10 mL) at and diluted with EtOAc (15 mL) and shaken. The EtOAc layer was collected, dried with MgSO 4 , filtered and adsorbed to silica and purified by MPLC (20 min, −25% EtOAc:Hex) to produce pure methyl 4-(2-(3-chloropropyl)-1,3-dithian-2-yl)benzoate (0.102 g, 0.308 mmol, 31% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 8.07-8.03 (m, 2H), 8.01-7.98 (m, 2H), 3.93 (s, 3H), 3.41 (t, J=6.4 Hz, 2H), 2.74-2.62 (m, 4H), 2.19-2.13 (m, 2H), 1.99-1.92 (m, 2H), 1.78-1.70 (m, 2H). KSC-335-059 (S)-1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-ol To a flame-dried vial was added dry THF (2 mL) and then cooled to 0° C. The 1.0 M R-5,5-Diphenyl-2-methyl-3,4-propano-1,3,2-oxazaborlidine (0.105 mL, 0.105 mmol) in THF was added followed by the 2.0 M borane-methyl sulfide complex (0.654 mL, 1.309 mmol) in THF. The reaction began to stir at 0° C. for 30 minutes. To another flame-dried vial was added the 1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-one (0.250 g, 1.047 mmol) and this was evacuated with argon 3 times then dissolved in dry THF (5 mL) and the oxazaborlidine solution was added dropwise at 0° C. and the reaction was allowed to warm to rt stirred for 2 h. The reaction was quenched with MeOH (10 mL) extracted with EtOAc (20 mL) then was washed with 1.0 M HCl (3×25 mL). The EtOAc layer was dried with MgSO 4 , filtered and concentrated to produce pure (S)-1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-ol (0.248 g, 1.030 mmol, 98% yield). [alpha] 25 589=−24.0° (c=10 in CHCl 3 ). 1 H NMR (400 MHz, CDCl 3 ): δ 7.38 (d, J=8.4 Hz, 2H), 7.28 (d, J=8.4, 2H), 4.71-4.67 (m, 1H), 3.61-3.53 (m, 2H), 1.98-1.79 (m, 4H), 1.32 (s, 9H). KSC-335-060 (R)-1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-ol Prepared the same as KSC-335-059 with 1.0 M (S)-5,5-diphenyl-2-methyl-3,4-propano-1,3,2-oxazaborlidine (0.105 ml, 0.105 mmol), 2.0 M Borane-methyl sulfide complex (0.654 ml, 1.309 mmol) and 1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-one (0.250 g, 1.047 mmol) to produce pure (R)-1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-ol (0.216 g, 0.897 mmol, 86% yield). [alpha] 25 589=+23.1° (c=10 in CHCl 3 ). 1 H NMR (400 MHz, CDCl 3 ): δ 7.38 (d, J=8.4 Hz, 2H), 7.28 (d, J=8.4, 2H), 4.71-4.67 (m, 1H), 3.61-3.53 (m, 2H), 1.98-1.79 (m, 4H), 1.32 (s, 9H). KSC-335-061 Methyl 4-(4-chlorobutanoyl)benzoate To a vial was added the methyl 4-(2-(3-chloropropyl)-1,3-dithian-2-yl)benzoate (KSC-335-056) (0.102 g, 0.308 mmol) and acetonitrile (1.5 mL) with water (0.2 mL). The (bis(trifluoroacetoxy)iodo)benzene (0.199 g, 0.462 mmol) was then added and the reaction stirred at rt for 1 h. The reaction was quenched with saturated NaHCO 3 (7 mL) then diluted with EtOAc (10 mL) and extracted. The EtOAc was collected and washed with water (2×8 mL) and then dried with MgSO 4 , filtered and adsorbed to silica and purified by MPLC (20 min, 0-25% EtOAc:hex to produce pure methyl 4-(4-chlorobutanoyl)benzoate (0.0512 g, 0.213 mmol, 69% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 8.11 (d, J=8.00 Hz, 2H), 8.00 (d, J=8.6 Hz, 2H), 3.93 (s, 3H), 3.67 (t, J=6.1 Hz, 2H), 3.19 (t, J=6.1 Hz, 2H), 2.22 (quintet, J=6.3 Hz, 2H). KSC-335-06 2 (S)-1-(4-(tert-butyl)phenyl)-4-chlorobutyl acetate To a vial was added the (S)-1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-ol (KSC-335-059) (0.248 g, 1.030 mmol) and diethyl ether (5.15 ml). The TEA (0.215 mL, 1.545 mmol) was added followed by the acetyl chloride (0.073 mL, 1.030 mmol) and the reaction began to stir at rt for 2 h. A white precipitate formed immediately. Water (5 mL) was added the reaction after 2 h and the ether layer was extracted. The aqueous was extracted again with more ether and the combined organics were dried with MgSO 4 , filtered and concentrated to produce pure (S)-1-(4-(tert-butyl)phenyl)-4-chlorobutyl acetate (0.250 g, 0.884 mmol, 86% yield). [alpha] 25 589=−42.11, (c=10, CH 2 Cl 2 ). 1 H NMR (400 MHz, CDCl 3 ): δ 7.36 (d, J=8.4 Hz, 2H), 7.25 (d, J=8.4 Hz, 2H), 5.78-5.73 (m, 1H), 3.53 (t, J=6.4 Hz, 2H), 2.06 (s, 3H), 2.02-1.68 (m, 4H), 1.31 (s, 9H). KSC-336-063 (R)-1-(4-(tert-butyl)phenyl)-4-chlorobutyl acetate Prepared the same as KSC-335-062 with (R)-1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-ol (KSC-335-060) (0.216 g, 0.897 mmol) and diethyl ether (4.5 mL), TEA (0.188 ml, 1.346 mmol) and acetyl chloride (0.064 ml, 0.897 mmol) to produce pure (R)-1-(4-(tert-butyl)phenyl)-4-chlorobutyl acetate (0.249 g, 0.880 mmol, 98% yield). [alpha] 25 589=+54.57, (c=10, CH 2 Cl 2 ). H NMR (400 MHz, CDCl 3 ): δ 7.36 (d, J=8.4 Hz, 2H), 7.25 (d, J=8.4 Hz, 2H), 5.78-5.73 (m, 1H), 3.53 (t, J=6.4 Hz, 2H), 2.06 (s, 3H), 2.02-1.68 (m, 4H), 1.31 (s, 9H). KSC-335-064 (S)-1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl acetate To a vial was added the diphenyl(piperidin-4-yl)methanol (0.154 g, 0.578 mmol), (S)-1-(4-(tert-butyl)phenyl)-4-chlorobutyl acetate (0.196 g, 0.693 mmol) (KSC-335-062) and potassium carbonate (0.319 g, 2.310 mmol) in acetonitrile (10 mL). The reaction stirred overnight at 70° C. for 18 h and was then cooled to rt and filtered. The filtrate was then diluted with DCM and washed with water (10 mL) and brine (10 mL). The DCM layers were combined, dried with MgSO 4 , filtered and purified by reverse-phase MPLC (20 min, 10-100% MeCN:water) to produce pure (S)-1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl acetate (0.135 g, 0.263 mmol, 46% yield) as a brown oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.48-7.45 (m, 4H), 7.35-7.14 (m, 10H), 5.73-5.68 (m, 1H), 2.93-2.87 (m, 2H), 2.46-2.37 (m, 1H), 2.87 (t, J=7.7 Hz, 2H), 2.11 (br s, 1H), 2.04 (s, 3H), 1.95-1.84 (m, 3H), 1.80-1.72 (m, 1H), 1.53-1.38 (m, 6H), 1.29 (s, 9H). KSC-335-065 (R)-1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl acetate Prepared the same way as KSC-335-064 with diphenyl(piperidin-4-yl)methanol (0.196 g, 0.734 mmol), (R)-1-(4-(tert-butyl)phenyl)-4-chlorobutyl acetate (KSC-335-063) (0.249 g, 0.880 mmol) and potassium carbonate (0.406 g, 2.93 mmol) in acetonitrile to produce pure (R)-1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl acetate (0.237 g, 0.461 mmol, 63% yield) as a brown oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.48-7.45 (m, 4H), 7.35-7.14 (m, 10H), 5.73-5.68 (m, 1H), 2.93-2.87 (m, 2H), 2.46-2.37 (m, 1H), 2.87 (t, J=7.7 Hz, 2H), 2.11 (br s, 1H), 2.04 (s, 3H), 1.95-1.84 (m, 3H), 1.80-1.72 (m, 1H), 1.53-1.38 (m, 6H), 1.29 (s, 9H). KSC-335-066 Methyl 2-(4-(4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butanoyl)phenyl)-2-methylpropanoate To a vial was added the methyl 2-(4-(4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)but-1-yn-1-yl)phenyl)-2-methylpropanoate (KSC-335-054) (0.074 g, 0.149 mmol). The mercuric oxide (1.493 ml, 0.045 mmol) was made into a 0.03 M solution in 4% w/v sulfuric acid and added to the starting material then heated to 55° C. and stirred for 3.5 h. The reaction turned a milky white color upon addition of the mercuric oxide solution. The reaction was removed from heat and diluted with saturated NaHCO 3 (10 mL) and extracted with DCM (3×10 mL). The DCM layers were combined and dried with MgSO 4 , filtered and concentrated then purified by reverse-phase MPLC (10-100% MeCN:water) to produce methyl 2-(4-(4-(4-(hydroxydiphenylmethyl) piperidin-1-yl)butanoyl)phenyl)-2-methylpropanoate (0.0217 g, 0.042 mmol, 28.3% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.93-7.91 (m, 2H), 7.48-7.45 (m, 4H), 7.42-7.39 (m, 2H), 7.30-7.26 (m, 4H), 7.19-7.14 (m, 2H), 3.63 (s, 3H), 2.96-2.88 (m, 4H), 2.44-2.34 (m, 3H), 2.08 (br s, 1H), 1.60 (s, 6H), 1.62-1.56 (m, 4H), 1.46-1.30 (m, 4H). KSC-335-069 (S)-1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol To a vial was added the (S)-1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl acetate (0.135 g, 0.263 mmol) and this vial was evacuated with nitrogen 3 times. The dry THF (9 mL) was then added. The 1.0 M lithium aluminum hydride (0.263 mL, 0.263 mmol) in THF was added dropwise at rt and the reaction stirred for 5 h. The reaction was quenched slowly with water (10 mL) and then extracted with diethyl ether (2×10 mL). The ether layer was dried with MgSO 4 , filtered, concentrated and purified by reverse-phase MPLC (20 min, 10-100%, MeCN:H 2 O) to produce pure (S)-1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol (0.100 g, 0.212 mmol, 81% yield). [alpha] 25 589=−38.8. 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.46 (m, 4H), 7.33-7.24 (m, 8H), 7.20-7.14 (m, 2H), 4.59 (dd, J=8.2 Hz, 2.8 Hz, 1H), 3.13 (br d, J=11.2 Hz, 1H), 2.97 (br d, J=11.2 Hz, 1H), 2.50-2.34 (m, 3H), 2.10-1.88 (m, 4H), 1.84-1.74 (m, 1H), 1.68-1.44 (m, 6H), 1.30 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 149.4, 146.1, 146.0, 142.7, 128.2, 128.1, 126.45, 126.43, 125.7, 125.6, 125.4, 125.0, 79.3, 73.4, 58.9, 54.7, 53.3, 44.2, 39.7, 34.4, 31.4, 26.1, 26.0, 24.1. LCMS Retention time: 4.159 min. LCMS purity 99.7%. HRMS (ESI): m/z calcd for C 32 H 41 NO 2 [M+H] + 472.3137, found 472.3210. KSC-335-070 (R)-1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol To a vial was added the (R)-1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl acetate (0.237 g, 0.461 mmol) and this vial was evacuated with nitrogen 3 times. The dry THF (Volume: 4.61 ml) was added and then the 1.0 M lithium aluminum hydride (0.461 mL, 0.461 mmol) in THE was added portionwise at rt for 5 h. The reaction was quenched slowly with water (10 mL) and then extracted with diethyl ether (2×10 mL). The ether layer was dried with MgSO 4 , filtered, concentrated and purified by reverse-phase MPLC (20 min, 10-100%, MeCN:H 2 O) to produce pure (R)-1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl) piperidin-1-yl)butan-1-ol (0.116 g, 0.246 mmol, 53% yield). [alpha] 25 589=+38.60. 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.46 (m, 4H), 7.33-7.24 (m, 8H), 7.20-7.14 (m, 2H), 4.59 (dd, J=8.2 Hz, 2.8 Hz, 1H), 3.13 (br d, J=11.2 Hz, 1H), 2.97 (br d, J=11.2 Hz, 1H), 2.50-2.34 (m, 3H), 2.10-1.88 (m, 4H), 1.84-1.74 (m, 1H), 1.68-1.44 (m, 6H), 1.30 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 149.4, 146.1, 146.0, 142.7, 128.2, 128.1, 126.45, 126.43, 125.7, 125.6, 125.4, 125.0, 79.3, 73.4, 58.9, 54.7, 53.3, 44.2, 39.7, 34.4, 31.4, 26.1, 26.0, 24.1. LCMS Retention time: 4.156 min. LCMS purity 97.8%. HRMS (ESI): m/z calcd for C 32 H 41 NO 2 [M+H] + 472.3137, found 472.3210. KSC-335-077 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-(p-tolyl)butan-1-ol Method B: 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-(p-tolyl)butan-1-one (0.073 g, 0.171 mmol) and MeOH (Volume: 2 mL) and SODIUM BOROHYDRIDE (0.013 g, 0.341 mmol) to produce pure 4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)-1-(p-tolyl)butan-1-ol (0.070 g, 0.163 mmol, 95% yield) as on oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.46 (m, 4H), 7.32-7.09 (m, 10H), 4.59 (dd, J=8.0, 2.8 Hz, 1H), 3.15-3.09 (m, 1H), 2.99-2.92 (m, 1H), 2.52-2.32 (m, 6H), 2.32 (s, 3H), 2.09-1.87 (m, 3H), 1.82-1.73 (m, 1H), 1.68-1.44 (m, 6H). 13 C NMR (125 MHz, CDCl 3 ): δ 146.1, 146.0, 142.9, 136.0, 128.7, 128.11, 128.10, 128.06, 126.39, 126.37, 125.7, 125.6, 125.5, 79.2, 73.3, 58.9, 54.6, 53.4, 53.3, 44.2, 39.9, 30.9, 26.0, 25.9, 26.0, 21.0. LCMS Retention time: 3.809 min. LCMS purity 94.1%. HRMS (ESI): m/z calcd for C 29 H 35 NO 2 [M+H] + 430.2668, found 430.2741. KSC-335-080 Methyl 2-(4-(1-hydroxy-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl)phenyl)-2-methylpropanoate Method B: methyl 2-(4-(4-(4-(hydroxydiphenylmethyl) piperidin-1-yl)butanoyl)phenyl)-2-methylpropanoate (KSC-335-066)(0.148 g, 0.288 mmol) and MeOH (1 mL) and sodium borohydride (0.016 g, 0.432 mmol) to produce pure methyl 2-(4-(1-hydroxy-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl)phenyl)-2-methylpropanoate (0.108 g, 0.209 mmol, 73% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.54-7.49 (m, 4H), 7.35-7.27 (m, 8H), 7.23-7.17 (m, 2H), 4.62 (dd, J=8.0, 2.8 Hz, 1H), 3.65 (s, 3H), 3.16 (d, J=11.7 Hz, 1H), 2.98 (d, J=11.7 Hz, 1H), 2.53-2.40 (m, 3H), 2.29 (br s, 1H), 2.14-2.06 (m, 1H), 2.01-1.93 (m, 2H), 1.84-1.50 (m, 14H). LCMS Retention time: 3.786 min. LCMS purity 98.2%. HRMS (ESI): m/z calcd for C 33 H 41 NO 4 [M+H] + 516.3036, found 516.3108. KSC-335-081 2-(4-(1-hydroxy-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl)phenyl)-2-methylpropanoic acid To a vial was added the methyl 2-(4-(1-hydroxy-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl)phenyl)-2-methylpropanoate (KSC-335-080) (0.094 g, 0.182 mmol) and THF (Volume: 3 mL,). The LiOH (0.022 g, 0.911 mmol) was dissolved in water (3.00 mL) and then added to the reaction stirred at 80° C. for 18 h. The reaction was removed from heat and cooled to rt and 1.0 M HCl in water was added to adjust to pH to 4 and a gummy off-white solid formed. DCM (5 mL) was added to the mixture and it was sonicated to break up the solid. The DCM layer was removed and the aqueous was extracted with DCM (2×5 mL). The DCM layer was concentrated and the residue was purified by reverse-phase MPLC (20 min, 10-100% MeCN:water) to produce the product with impurities. This was submitted to the purification core. The pure sample was recovered to produce 2-(4-(1-hydroxy-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl)phenyl)-2-methylpropanoic acid (0.0378 g, 0.075 mmol, 41% yield). 1 H NMR (400 MHz, DMSO-d 6 ): δ 8.22 (s, 1H), 7.52-7.49 (m, 4H), 7.29-7.26 (m, 8H), 7.15-7.10 (m, 2H), 4.47 (t, J=5.9 Hz, 1H), 2.94-2.86 (m, 3H), 2.35-2.30 (m, 2H), 2.05-1.95 (m, 2H), 1.60-1.35 (m, 12H), 1.28-1.22 (m, 2H). 13 C NMR (125 MHz, CDCl 3 ): δ 177.7, 163.7, 147.2, 144.4, 143.4, 127.8, 125.8, 125.7, 125.6, 125.1, 78.4, 71.8, 57.7, 53.4, 53.2, 45.5, 43.1, 37.3, 26.5, 25.6, 22.6. LCMS Retention time: 2.612 min. LCMS purity 100%. HRMS (ESI): m/z calcd for C 32 H 39 NO 4 [M+H] + 502.2879, found 502.2952. KSC-342-006 1-(4-(tert-butyl)phenyl)-2-(4-(hydroxydiphenylmethyl)piperidin-1-yl)ethanone Method A: diphenyl(piperidin-4-yl)methanol (0.4 g, 1.496 mmol), 1-(4-(tert-butyl)phenyl)-2-chloroethanone (0.300 g, 1.425 mmol), sodium bicarbonate (0.144 g, 1.710 mmol) with water (3 mL) and 2-butanone (Volume: 15 mL) to produce pure 1-(4-(tert-butyl)phenyl)-2-(4-(hydroxydiphenylmethyl)piperidin-1-yl)ethanone (0.452 g, 1.024 mmol, 71.8% yield) as a colorless oil. 1 H NMR (500 MHz, CDCl 3 ): δ 7.93 (d, J=8.6 Hz, 2H), 7.50-7.43 (m, 6H), 7.32-7.26 (m, 4H), 7.20-7.15 (m, 2H), 3.78 (s, 2H), 3.07-3.01 (m, 2H), 2.47 (tt, J=11.8 Hz, 3.5 Hz, 1H), 2.26-2.18 (m, 2H), 1.66-1.45 (m, 5H), 1.33 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 196.1, 157.0, 145.8, 133.5, 129.8, 128.2, 128.0, 126.5, 125.8, 125.5, 125.1, 79.5, 64.2, 54.2, 43.8, 35.1, 31.2, 31.0, 26.2. LCMS Retention time: 3.987 min. LCMS purity 98.8%. HRMS (ESI): m/z calcd for C 30 H 35 NO 2 [M+H] + 442.2668, found 442.2741. KSC-342-010 1-(4-(tert-butyl)phenyl)-2-(4-(hydroxydiphenylmethyl)piperidin-1-yl)ethanol Method B: 1-(4-(tert-butyl)phenyl)-2-(4-(hydroxydiphenylmethyl)piperidin-1-yl)ethanone (0.113 g, 0.256 mmol) and MeOH (1 mL) and SODIUM BOROHYDRIDE (0.019 g, 0.512 mmol) to produce pure 1-(4-(tert-butyl)phenyl)-2-(4-(hydroxydiphenylmethyl)piperidin-1-yl)ethanol (0.106 g, 0.239 mmol, 93% yield) as a solid. 1 H NMR (400 MHz, CDCl 3 ): δ 7.50-7.46 (m, 4H), 7.37-7.26 (m, 8H), 7.22-7.17 (M, 2H), 4.67 (m, 1H), 4.01 (br s, 1H), 3.20 (m, 1H), 2.86 (m, 1H), 2.50-2.45 (m, 3H), 2.37-2.30 (m, 1H), 2.10-2.02 (m, 1H), 1.60-1.45 (m, 5H), 1.31 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 150.3, 145.82, 145.78, 139.1, 128.20, 128.19, 126.59, 126.57, 125.7, 125.6, 125.2, 79.5, 68.6, 66.3, 55.8, 53.4, 52.2, 44.1, 34.5, 31.3, 26.8, 26.5. LCMS Retention time: 4.083 min. LCMS purity 94.2%. HRMS (ESI): m/z calcd for C 30 H 37 NO 2 [M+H] + 444.2824, found 444.2897. KSC-342-014 Methyl 4-(4-chloro-1-hydroxybutyl)benzoate Method B: methyl 4-(4-chlorobutanoyl)benzoate (KSC-335-061) (0.042 g, 0.175 mmol) and MeOH with sodium borohydride (0.013 g, 0.349 mmol). to produce methyl 4-(4-chloro-1-hydroxybutyl)benzoate (0.037 g, 0.152 mmol, 87% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 8.00 (d, J=8.4 Hz, 2H), 7.40 (d, J=8.2 Hz, 2H), 4.8-4.6 (m, 1H), 3.90 (s, 3H), 3.58-3.52 (m, 2H), 2.19 (br s, 1H), 1.96-1.78 (m, 4H) KSC-342-017 Methyl 4-(1-hydroxy-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl)benzoate To a vial was added the methyl 4-(4-chloro-1-hydroxybutyl)benzoate (KSC-342-014) (0.037 g, 0.152 mmol), diphenyl(piperidin-4-yl)methanol (0.122 g, 0.457 mmol), SODIUM BICARBONATE (0.026 g, 0.305 mmol), SODIUM IODIDE (1.143 mg, 7.62 μmol) and the vial was evacuated with argon 3 times. Dry acetonitrile (2 ml) was added and the reaction stirred overnight at reflux and was then cooled to rt after 18 h and the solvent was concentrated. The residue was dissolved in DCM (5 mL) and washed with 0.1 N HCl (5 mL), water (5 mL) and brine (5 mL). The product was purified by MPLC (0-10% MeOH:DCM) to produce pure methyl 4-(1-hydroxy-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl)benzoate (0.0268 g, 0.057 mmol, 37% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.97 (d, J=8.4 Hz, 2H), 7.52-7.47 (m, 4H), 7.42 (d, J=7.9 Hz, 2H), 7.32-7.29 (m, 4H), 7.20-7.14 (m, 2H), 4.66 (m, 1H), 3.90 (s, 3H), 3.14 (m, 1H), 2.94 (m, 1H), 2.78 (br s, 1H), 2.52-2.43 (m, 1H), 2.39 (t, J=4.8 Hz, 2H), 2.13-2.06 (m, 1H), 2.04-1.92 (m, 2H), 1.77-1.47 (m, 8H). 13 C NMR (125 MHz, CDCl 3 ): δ 167.2, 151.4, 146.0, 145.9, 129.5, 128.4, 128.2, 128.2, 126.51, 126.48, 125.64, 125.59, 79.2, 73.2, 58.8, 54.7, 51.9, 44.2, 40.0, 26.0, 25.9, 24.0. LCMS Retention time: 3.652 min. LCMS purity 100%. HRMS (ESI): m/z calcd for C 30 H 35 NO 4 [M+H] + 474.2566, found 474.2639. KSC-342-021 4-(1-hydroxy-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl)benzoic acid To a vial was added the methyl 4-(1-hydroxy-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl)benzoate (0.0195 g, 0.041 mmol) and THF (1 mL). The LiOH (6.90 mg, 0.288 mmol) was dissolved in water (1 mL) and added to the reaction. The reaction stirred at overnight and was then acidified with 1.0 M HCl to pH 2-3 then extracted with DCM (3×5 mL). The DCM layer was concentrated and purified by reverse-phase MPLC (10-100% MeCN:water) to produce pure 4-(1-hydroxy-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butyl)benzoic acid (0.009 g, 0.020 mmol, 47% yield). 1 H NMR (400 MHz, CD 3 OD): δ 7.85 (d, J=8.2 Hz, 2H), 7.53-7.49 (m, 4H), 7.34-7.26 (m, 6H), 7.19-7.14 (m, 2H), 4.70 (m, 1H), 3.46 (m, 1H), 3.35 (s, 2H), 3.01-2.96 (m, 2H), 2.92-2.77 (m, 3H), 1.84-1.64 (m, 8H). 13 C NMR (125 MHz, CD 3 OD): δ 174.7, 148.2, 147.2, 137.6, 130.4, 129.1, 127.6, 127.0, 126.4, 79.9, 74.0, 53.9, 49.8, 36.9, 25.5, 21.8. LCMS Retention time: 2.490 min. LCMS purity 100%. HRMS (ESI): m/z calcd for C 29 H 33 NO 4 [M+H] + 460.2410, found 460.2482. KSC-342-074 1-(Tert-butyl)-4-(2-chloroethyl)benzene To a vial was added the 1-(4-(tert-butyl)phenyl)-2-chloroethanone (0.171 g, 0.812 mmol) and triethylsilane (0.519 mL, 3.25 mmol) with TFA (4 mL). The reaction stirred at 75° C. for 17 h and was then concentrated in vacuo. The residue was dissolved in DCM (5 mL) and washed with water (4 mL). The DCM layer was collected and washed with water (1×5 mL), dried with MgSO 4 , filtered and adsorbed to silica and purified by MPLC (20 min, 0-40% EtOAc:hex) to produce pure 1-(tert-butyl)-4-(2-chloroethyl)benzene (0.114 g, 0.580 mmol, 71% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.34 (d, J=8.3 Hz, 2H), 7.16 (d, J=8.3 Hz, 2H), 3.71 (t, J=7.5 Hz, 2H), 3.05 (t, J=7.6 Hz, 2H), 1.32 (s, 9H). KSC-342-080 (1-(3-(4-(Tert-butyl)phenyl)propyl)piperidin-4-yl)diphenylmethanol To a vial was added the diphenyl(piperidin-4-yl)methanol (0.142 g, 0.530 mmol), 1-(tert-butyl)-4-(3-chloropropyl)benzene (0.134 g, 0.636 mmol) and POTASSIUM CARBONATE (0.439 g, 3.18 mmol) in acetonitrile. The reaction stirred overnight at 85° C. for 18 h and then filtered. The filtrate was then diluted with brine and extracted with diethyl ether (3×15 mL). The ether layers were combined, dried with MgSO 4 , filtered and purified by reverse-phase MPLC (20 min, 10-100% MeCN:water) to produce pure (1-(3-(4-(tert-butyl)phenyl)propyl)piperidin-4-yl)diphenylmethanol (0.152 g, 0.344 mmol, 65% yield) as an oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.49-7.45 (m, 4H), 7.31-7.24 (m, 6H), 7.19-7.14 (m, 2H), 7.11-7.08 (m, 2H), 2.96 (m, 2H), 2.57 (t, J=7.7 Hz, 2H), 2.48-2.32 (m, 3H), 2.22 (br s, 1H), 1.97-1.90 (m, 2H), 1.83-1.75 (m, 2H), 1.53-1.45 (m, 4H), 1.29 (s, 9H). LCMS Retention time: 2.965 min. LCMS purity 97.2%. HRMS (ESI): m/z calcd for C 31 H 39 NO [M+H] + 442.3032, found 442.3104. KSC-342-081 (1-(4-(Tert-butyl)phenethyl)piperidin-4-yl)diphenylmethanol To a vial was added the diphenyl(piperidin-4-yl)methanol (0.150 g, 0.561 mmol), 1-(tert-butyl)-4-(2-chloroethyl)benzene (KSC-342-074) (0.110 g, 0.561 mmol) and potassium carbonate (0.465 g, 3.37 mmol) in acetonitrile. The reaction stirred overnight at 85° C. for 18 h and then filtered. The filtrate was then diluted with brine and extracted with diethyl ether (3×15 mL). The ether layers were combined, dried with MgSO 4 , filtered and purified by reverse-phase MPLC (20 min, 10-100% MeCN:water) to produce pure (1-(4-(tert-butyl)phenethyl)piperidin-4-yl)diphenylmethanol (0.180 g, 0.421 mmol, 75% yield) as an oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.47 (m, 4H), 7.33-7.27 (m, 6H), 7.21-7.16 (m, 2H), 7.14-7.11 (m, 2H), 3.09-3.03 (m, 2H), 2.80-2.74 (m, 2H), 2.60-2.55 (m, 2H), 2.51-2.42 (m, 1H), 2.28 (br s, 1H), 2.08-2.00 (m, 2H), 1.57-1.50 (m, 4H), 1.30 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 148.8, 145.9, 137.3, 128.3, 128.1, 126.5, 125.8, 125.2, 79.5, 60.8, 54.0, 44.2, 40.9, 34.3, 33.1, 31.4, 26.4. LCMS Retention time: 4.384 min. LCMS purity 99.7%. HRMS (ESI): m/z calcd for C 30 H 37 NO [M+H] + 428.2875, found 428.2948. KSC-342-088 (1-(4-amino-4-(4-(tert-butyl)phenyl)butyl)piperidin-4-yl)diphenylmethanol To a vial was added the 1-(4-(tert-butyl)phenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one (0.200 g, 0.426 mmol), Ammonium acetate (0.328 g, 4.26 mmol) and Sodium cyanoborohydride (0.040 g, 0.639 mmol) with MeOH (Volume: 4 ml). The reaction stirred at rt at 2:56:22 PM. The reaction was stirred overnight and then concentrated and diluted with dilute aqueous ammonium hydroxide and extracted with DCM. The DCM layer was concentrated and the crude NMR showed product and starting material. The reaction then purified by reverse-phase Teledyne ISCO Combiflash chromatography (10-100% MeCN:basic water) and fractions 5 and 6 were collected. These were then subjected to normal phase purification (0-10% MeOH (5% NH 3 OH):DCM) to produce pure (1-(4-amino-4-(4-(tert-butyl)phenyl)butyl)piperidin-4-yl)diphenylmethanol (0.010 g, 0.021 mmol, 5% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.48-7.44 (m, 4H), 7.34-7.26 (m, 6H), 7.22-7.14 (m, 4H), 3.84 (t, J=6.7 Hz, 1H), 2.95-2.87 (m, 2H), 2.46-2.37 (m, 1H), 2.28 (t, J=7.6 Hz, 2H), 1.95-1.85 (m, 2H), 1.70-1.60 (m, 5H), 1.55-1.40 (m, 6H), 1.30 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 149.7, 146.0, 143.3, 128.1, 126.5, 125.9, 125.8, 125.3, 79.5, 58.7, 55.8, 54.2, 54.0, 44.2, 37.5, 34.4, 31.4, 26.4, 24.2. LCMS Retention time: 2.397 min. LCMS purity 100%. HRMS (ESI): m/z calcd for C 32 H 42 N 2 O [M+H] + 471.3297, found 471.3370. KSC-348-001 1-([1,1′-Biphenyl]-4-yl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one To a vial was added the 1-(4-bromophenyl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one (0.098 g, 0.199 mmol), 1,1′-bis(di-t-butylphosphino)ferrocene palladium dichloride, (2.71 mg, 3.98 μmol) and phenylboronic acid (0.029 g, 0.239 mmol) followed by acetonitrile (1.5 mL). The potassium carbonate (0.041 g, 0.299 mmol) was dissolved in water (1.5 mL) and added the reaction. The reaction stirred at 60° C. for 18 h. The reaction was stopped and the organic layer was diluted with EtOAc and extracted then washed with brine. The EtOAc layer was collected, dried with MgSO 4 , filtered and purified by reverse-phase MPLC (10-100% MeCN:water) to produce the desired 1-([1,1′-biphenyl]-4-yl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one (0.035 g, 0.071 mmol, 36% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 8.03 (d, J=8.6 Hz, 2H), 7.67 (d, J=8.4 Hz, 2H), 7.64-7.61 (m, 2H), 7.50-7.45 (m, 6H), 7.42-7.38 (m, 1H), 7.31-7.26 (m, 4H), 7.19-7.14 (m, 2H), 3.02-2.91 (m, 4H), 2.46-2.37 (m, 3H), 2.10 (br s, 1H), 1.97-1.92 (m, 4H), 1.50-1.35 (m, 4H). KSC-348-002 1-([1,1′-biphenyl]-4-yl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol Method B: 1-([1,1′-biphenyl]-4-yl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-one (KSC-348-001) (0.035 g, 0.071 mmol) and MeOH (2 mL) and sodium borohydride (5.41 mg, 0.143 mmol) to produce pure 1-([1,1′-biphenyl]-4-yl)-4-(4-(hydroxydiphenylmethyl)piperidin-1-yl)butan-1-ol (0.033 g, 0.067 mmol, 94% yield) as on oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.59-7.55 (m, 2H), 7.53-7.46 (m, 6H), 7.43-7.38 (m, 4H), 7.34-7.25 (m, 5H), 7.19-7.13 (m, 2H), 4.65 (dd, J=8.2 Hz, 2.7 Hz, 1H), 3.16-3.10 (m, 1H), 2.99-2.93 (m, 1H), 2.56 (br s, 1H), 2.50-2.34 (m, 3H), 2.10-1.92 (m, 3H), 1.86-1.76 (m, 1H), 1.70-1.45 (m, 6H).). 13 C NMR (125 MHz, CDCl 3 ): δ 146.1, 146.0, 145.0, 141.1, 139.4, 128.6, 128.2, 128.1, 127.01, 126.96, 126.8, 126.44, 126.41, 126.1, 125.7, 125.6, 79.2, 73.3, 58.9, 54.7, 53.3, 44.2, 40.0, 26.0, 25.9, 24.1. LCMS Retention time: 4.049 min. LCMS purity 97.6%. HRMS (ESI): m/z calcd for C 34 H 37 NO 2 [M+H] + 492.2824, found 492.2897. KSC-348-049 (4-(tert-butyl)phenyl)(4-(hydroxydiphenylmethyl)piperidin-1-yl)methanone To a vial was added the diphenyl(piperidin-4-yl)methanol (0.232 g, 0.868 mmol), acetonitrile (3 mL) and TEA (0.181 ml, 1.30 mmol). The 4-(tert-butyl)benzoyl chloride (0.173 mL, 0.954 mmol) was added and the reaction stirred at 70° C. for 6 h and was diluted with EtOAc (15 mL) and washed with saturated NaHCO 3 (15 mL). The EtOAc was collected, dried with MgSO 4 , filtered and adsorbed to silica and purified by MPLC (20 min, 0-30% EtOAc:Hex) to produce pure (4-(tert-butyl)phenyl)(4-(hydroxydiphenylmethyl)piperidin-1-yl)methanone (0.304 g, 0.711 mmol, 82% yield) as a white solid. 1 H NMR (400 MHz, CDCl 3 ): δ 7.50-7.44 (m, 4H), 7.38-7.14 (m, 10H), 4.77 (br s, 1H), 3.84 (br s, 1H), 3.05-2.63 (m, 3H), 2.25-2.17 (m, 1H), 1.75-1.35 (m, 4H), 1.29 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 170.4, 152.7, 145.4, 133.2, 128.3, 126.7, 125.7, 125.2, 79.5, 44.5, 34.7, 31.2. LCMS Retention time: 3.774 min. LCMS purity 100%. HRMS (ESI): m/z calcd for C 29 H 33 NO 2 [M+H] + 428.2511, found 428.2584. KSC-348-050 (1-(4-(tert-butyl)benzyl)piperidin-4-yl)diphenylmethanol To a vial was added the diphenyl(piperidin-4-yl)methanol (0.085 ml, 0.393 mmol), acetonitrile (2 mL) and TEA (0.082 ml, 0.589 mmol). The p-tert-butylbenzyl bromide (0.098 g, 0.432 mmol) was then added and the reaction stirred at 70° C. and stirred for 5 h then diluted with EtOAc (15 mL) and washed with saturated NaHCO 3 (15 mL). The EtOAc was collected, dried with MgSO 4 , filtered and adsorbed to silica and purified by reverse phase MPLC (20 min, 10-100% MeCN:water) to produce pure (1-(4-(tert-butyl)benzyl)piperidin-4-yl)diphenylmethanol (0.131 g, 0.317 mmol, 81% yield) as a brown oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.48-7.45 (m, 4H), 7.32-7.25 (m, 6H), 7.22-7.14 (m, 4H), 3.47 (s, 2H), 2.96-2.90 (m, 2H), 2.46-2.38 (m, 1H), 2.02-1.95 (m, 1H), 1.51-1.44 (m, 4H), 1.30 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 149.8, 146.0, 135.1, 128.9, 128.1, 126.4, 125.8, 125.0, 79.5, 62.8, 53.9, 44.2, 34.4, 31.4, 26.5, 21.0. LCMS Retention time: 4.186 min. LCMS purity 99.7%. HRMS (ESI): m/z calcd for C 29 H 35 NO [M+H] + 414.2719, found 414.2791. KSC-348-058 (1-(4-methoxyphenethyl)piperidin-4-yl)diphenylmethanol To a vial was added the diphenyl(piperidin-4-yl)methanol (0.381 g, 1.425 mmol), acetonitrile (5 mL) and TEA (0.298 ml, 2.138 mmol). The 1-(2-bromoethyl)-4-methoxybenzene (0.245 ml, 1.568 mmol) was then added and the reaction stirred at 75° C. and the stirred for 16 h then was quenched with saturated NaHCO 3 , extracted with EtOAc, dried with MgSO 4 , filtered and adsorbed to silica. The product was purified by MPLC (20 min, 0-10% MeOH:DCM) to produce pure (1-(4methoxyphenethyl) piperidin-4-yl)diphenylmethanol (0.289 g, 0.720 mmol, 50% yield) as a sticky solid. 1 H NMR (400 MHz, CDCl 3 ): δ 7.49-7.46 (m, 4H), 7.32-7.28 (m, 4H), 7.19 (tt, J=7.3 Hz, 1.9 Hz, 2H), 7.12 (d, J=8.6 Hz, 2H), 6.82 (d, J=8.5 Hz, 2H), 3.77 (s, 3H), 3.29-3.24 (m, 2H), 2.95-2.90 (m, 2H), 2.80-2.75 (m, 2H), 2.58-2.50 (m, 1H), 2.42-2.30 (m, 3H), 1.90-1.77 (m, 2H), 1.65-1.57 (m, 2H). 13 C NMR (125 MHz, CDCl 3 ): δ 158.3, 145.5, 129.6, 128.3, 126.7, 125.6, 114.0, 79.3, 55.3, 53.6, 53.4, 43.4, 31.5, 25.1. LCMS Retention time: 3.695 min. LCMS purity 100%. HRMS (ESI): m/z calcd for C 27 H 31 NO 2 [M+H] + 402.2355, found 402.2353. KSC-352-055 4-(4-Benzoylpiperidin-1-yl)-1-(4-(tert-butyl)phenyl)butan-1-one To a vial was added the 1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-one (0.060 g, 0.252 mmol) and potassium iodide (0.063 g, 0.377 mmol) with acetonitrile (2 mL). The reaction stirred at 85° C. for 1 h then the phenyl(piperidin-4-yl)methanone (0.050 g, 0.264 mmol) along with potassium carbonate (0.052 g, 0.377 mmol) was added. The reaction was then heated back to 85° C. for 48 h. The reaction was cooled to rt and diluted with water then extracted with EtOAc (3×15 mL). The EtOAc layer was dried with MgSO 4 , filtered and adsorbed to silica. The product was purified by reverse-phase MPLC (20 min, 10-100% MeCN:water) to produce 4-(4-benzoylpiperidin-1-yl)-1-(4-(tert-butyl)phenyl)butan-1-one (0.026 g, 0.066 mmol, 26% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.95-7.90 (m, 4H), 7.57-7.53 (m, 1H), 7.49-7.44 (m, 4H), 3.27-3.18 (m, 1H), 3.03-2.96 (m, 4H), 2.44 (t, J=7.04 Hz, 2H), 2.13-2.06 (m, 2H), 1.98-1.91 (m, 2H), 1.85-1.76 (m, 4H), 1.34 (s, 9H). KSC-352-060 (1-(4-nitrophenethyl)piperidin-4-yl)diphenylmethanol To a vial was added the diphenyl(piperidin-4-yl)methanol (0.513 g, 1.919 mmol), 1-(2-bromoethyl)-4-nitrobenzene (0.401 g, 1.744 mmol) and acetonitrile (10 mL). The TEA (0.365 ml, 2.62 mmol) was then added and the reaction stirred at 85° C. for 18 h then cooled to rt. The reaction was diluted with water and extracted with EtOAc (3×15 mL). The EtOAc layer was collected and dried with MgSO 4 , filtered and adsorbed to silica then purified by MPLC (15 min, 0-10% MeOH:DCM). to produce pure (1-(4-nitrophenethyl)piperidin-4-yl)diphenylmethanol (0.145 g, 0.348 mmol, 20% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 8.13 (d, J=8.7 Hz, 2H), 7.49-7.46 (m, 4H), 7.35 (d, J=8.7 Hz, 2H), 7.32-7.27 (m, 4H), 7.21-7.16 (m, 2H), 3.11-3.05 (m, 2H), 2.97-2.91 (m, 2H), 2.69-2.63 (m, 2H), 2.52-2.43 (m, 1H), 2.25 (br s, 1H), 2.20-2.10 (m, 2H), 1.63-1.53 (m, 4H). 13 C NMR (125 MHz, CDCl 3 ): δ 147.9, 146.5, 145.7, 129.5, 128.2, 126.6, 125.7, 123.7, 79.4, 59.4, 53.9, 43.9, 33.2, 26.1, 21.1. LCMS Retention time: 3.654 min. LCMS purity 98.8%. HRMS (ESI): m/z calcd for C 26 H 28 N 2 O 3 [M+H] + 417.2162, found 417.2173. KSC-352-061 (1-(4-bromophenethyl)piperidin-4-yl)diphenylmethanol To a vial was added the diphenyl(piperidin-4-yl)methanol (0.496 g, 1.855 mmol), 1-bromo-4-(2-bromoethyl)benzene (0.258 ml, 1.69 mmol) and acetonitrile (10 mL). The TEA (0.353 mL, 2.53 mmol) was then added and the reaction stirred at 85° C. for 18 h then cooled to rt. The reaction was diluted with water and extracted with EtOAc (3×15 mL). The EtOAc layer was collected and dried with MgSO 4 , filtered and adsorbed to silica then purified by MPLC (15 min, 0-10% MeOH:DCM). to produce pure (1-(4-bromophenethyl)piperidin-4-yl)diphenylmethanol (0.488 g, 1.083 mmol, 64% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.50-7.46 (m, 4H), 7.38 (d, J=8.3 Hz, 2H), 7.34-7.27 (m, 4H), 7.18 (tt, J=7.3 Hz, 1.8 Hz, 2H), 7.06 (d, J=8.4 Hz, 2H), 3.06-3.00 (m, 2H), 2.77-2.72 (m, 2H), 2.58-2.52 (m, 2H), 2.50-2.41 (m, 1H), 2.15-2.00 (m, 3H), 1.56-1.49 (m, 4H). 13 C NMR (125 MHz, CDCl 3 ): δ 145.8, 139.3, 131.4, 130.4, 128.2, 126.6, 125.8, 119.8, 79.5, 60.4, 54.0, 44.1, 33.1, 26.4, 21.1 LCMS Retention time: 3.969 min. LCMS purity 99.8%. HRMS (ESI): m/z calcd for C 26 H 28 BrNO [M+H] + 450.1354, found 450.1427. KSC-352-063 (1-(2-([1,1′-biphenyl]-4-yl)ethyl)piperidin-4-yl)diphenylmethanol To a vial was added the phenylboronic acid (0.019 g, 0.152 mmol), 1,1′-bis(di-tert-butylphosphino)ferrocene palladium dichloride (4.12 mg, 6.33 μmol), (1-(4-bromophenethyl)piperidin-4-yl)diphenylmethanol (KSC-352-061) (0.057 g, 0.127 mmol) and potassium carbonate (0.035 g, 0.253 mmol). The vial was then evacuated with argon 3 times and acetonitrile (1 mL) was added followed by water (1 mL). The reaction then stirred at 60° C. for 18 h then was diluted with EtOAc (5 mL) and saturated NaHCO 3 (5 mL). The EtOAc layer was collected and the aqueous layer was extracted with more EtOAc (2×5 mL). The EtOAc layers were combined and dried with MgSO 4 , filtered and concentrated. The reaction was purified by MPLC (10-100% MeCN:water) to produce pure (1-(2-([1,1′-biphenyl]-4-yl)ethyl)piperidin-4-yl)diphenylmethanol (0.045 g, 0.101 mmol, 79% yield) as a clear oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.59-7.45 (m, 2H), 7.53-7.48 (m, 6H), 7.45-7.40 (m, 2H), 7.35-7.25 (m, 7H), 7.22-7.16 (m, 2H), 3.11-3.05 (m, 2H), 2.87-2.81 (m, 2H), 2.65-2.59 (m, 2H), 2.53-2.44 (m, 1H), 2.22 (br s, 1H), 2.12-2.04 (m, 2H), 1.59-1.52 (m, 4H). 13 C NMR (125 MHz, CDCl 3 ): δ 145.9, 141.0, 139.5, 139.0, 129.1, 128.7, 128.2, 127.1, 127.03, 126.96, 126.5, 125.8, 79.5, 60.7, 54.0, 50.8, 44.2, 33.3, 26.4. LCMS Retention time: 4.086 min. LCMS purity 99%. HRMS (ESI): m/z calcd for C 32 H 33 NO [M+H] + 448.2562, found 448.2635. KSC-352-064 Diphenyl(1-(4-(pyridin-4-yl)phenethyl)piperidin-4-yl)methanol To a vial was added the (1-(4-bromophenethyl)piperidin-4-yl)diphenylmethanol (KSC-352-061) (0.050 g, 0.111 mmol), pyridin-4-ylboronic acid (0.018 g, 0.133 mmol), 1,1′-bis(di-tert-butylphosphino)ferrocene palladium dichloride (3.62 mg, 5.55 μmol) and potassium carbonate (0.031 g, 0.222 mmol). The vial was evacuated 3 times with argon and then acetonitrile (1 mL) followed by water (1 mL) was added. The reaction stirred at 60° C. for 18 h and was then cooled to rt and diluted with EtOAc (5 mL) and saturated NaHCO 3 (5 mL). The EtOAc layer was collected and the aqueous layer was extracted with more EtOAc (2×5 mL). The EtOAc layers were combined and dried with MgSO 4 , filtered and concentrated. The reaction was purified by reverse-phase MPLC (10-100% MeCN:water) to produce pure diphenyl(1-(4-(pyridin-4-yl)phenethyl)piperidin-4-yl)methanol (0.015 g, 0.033 mmol, 30% yield) as an oil. 1 H NMR (400 MHz, CDCl 3 ): δ 8.64-8.62 (m, 2H), 7.60 (d, J=8.2 Hz, 2H), 7.51-7.46 (m, 6H), 7.32-7.28 (m, 6H), 7.18 (tt, J=7.3 Hz, 1.8 Hz, 2H), 3.10-3.04 (m, 2H), 2.88-2.82 (m, 2H), 2.65-2.58 (m, 2H), 2.51-2.43 (m, 1H), 2.19 (br s, 1H), 2.12-2.03 (m, 2H), 1.58-1.51 (m, 4H). 13 C NMR (125 MHz, CDCl 3 ): δ 150.2, 148.1, 145.9, 141.7, 135.8, 129.5, 128.2, 127.0, 126.5, 125.8, 121.4, 79.5, 60.5, 54.1, 44.1, 41.0, 33.4, 26.4. LCMS Retention time: 3.585 min. LCMS purity 93.3%. HRMS (ESI): m/z calcd for C 31 H 32 N 2 O [M+H] + 449.2515, found 449.2587. KSC-352-065 Diphenyl(1-(4-(pyridin-3-yl)phenethyl)piperidin-4-yl)methanol To a vial was added the (1-(4-bromophenethyl)piperidin-4-yl)diphenylmethanol (0.057 g, 0.127 mmol), pyridin-3-ylboronic acid (0.019 g, 0.152 mmol), 1,1′-Bis(di-tert-butylphosphino)ferrocene palladium dichloride (4.12 mg, 6.33 μmol) and potassium carbonate (0.035 g, 0.253 mmol). The vial was evacuated with argon 3 times and then acetonitrile (1 mL) followed by water (1 mL) was added. The reaction stirred at 60° C. for 18 h and then cooled to rt and diluted with EtOAc (5 mL) and saturated NaHCO 3 (5 mL). The EtOAc layer was collected and the aqueous layer was extracted with more EtOAc (2×5 mL). The EtOAc layers were combined and dried with MgSO 4 , filtered and concentrated. The reaction was purified by RP MPLC (10-100% MeCN:water) to produce pure diphenyl(1-(4-(pyridin-3-yl)phenethyl)piperidin-4-yl)methanol (0.05 g, 0.111 mmol, 88% yield) as an oil. 1H NMR (400 MHz, CDCl 3 ): δ 8.79 (dd, J=2.4 Hz, 0.9 Hz, 1H), 8.53 (dd, J=4.8 Hz, 1.6 Hz, 1H), 7.86-7.83 (m, 1H), 7.51-7.47 (m, 6H), 7.36-7.27 (m, 7H), 7.20-7.15 (m, 2H), 3.10-3.03 (m, 2H), 2.87-2.81 (m, 2H), 2.71 (br s, 1H), 2.63-2.58 (m, 2H), 2.51-2.43 (m, 1H), 2.11-2.03 (m, 2H), 1.58-1.52 (m, 4H). 13 C NMR (125 MHz, CDCl 3 ): δ 148.04, 147.97, 146.0, 140.5, 136.5, 135.5, 134.3, 129.4, 128.1, 127.1, 126.4, 125.8, 123.5, 79.4, 60.5, 54.1, 44.1, 33.2, 26.2. LCMS Retention time: 3.582 min. LCMS purity 98.8%. HRMS (ESI): m/z calcd for C 31 H 32 N 2 O [M+H] + 449.2515, found 449.2587. KSC-352-066 1-(4-(tert-butyl)phenyl)-4-(4-(hydroxy(phenyl)methyl)piperidin-1-yl)butan-1-ol Method B: 4-(4-benzoylpiperidin-1-yl)-1-(4-(tert-butyl)phenyl)butan-1-one (KSC-352-055) (0.026 g, 0.066 mmol) and MeOH (2 mL) and sodium borohydride (10.05 mg, 0.266 mmol) to produce pure 1-(4-(tert-butyl)phenyl)-4-(4-(hydroxy(phenyl)methyl)piperidin-1-yl)butan-1-ol (0.019 g, 0.048 mmol, 72% yield) as a mixture of diastereomers. 1 H NMR (400 MHz, CDCl 3 ): δ 7.36-7.24 (m, 9H), 4.63-4.57 (m, 1H), 4.33 (d, J=7.6 Hz, 1H), 3.23-2.83 (m, 2H), 2.42-2.35 (m, 2H), 2.13-1.89 (m, 3H), 1.86-1.52 (m, 6H), 1.46-1.16 (m, 4H), 1.31 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 149.4, 143.4, 142.8, 128.3, 127.63, 127.61, 126.6, 125.4, 125.0, 78.74, 78.67, 73.4, 58.9, 54.30, 54.26, 52.8, 52.7, 43.21, 43.2, 39.9, 34.4, 31.4, 28.4, 28.3, 28.2, 24.2, 24.1. LCMS Retention time: 3.707 min. LCMS purity 97.1%. HRMS (ESI): m/z calcd for C 26 H 37 NO 2 [M+H] + 396.2824, found 396.2897. KSC-352-069 (1-(4-aminophenethyl)piperidin-4-yl)diphenylmethanol To a vial was added the (1-(4-nitrophenethyl) piperidin-4-yl)diphenylmethanol (KSC-352-060) (0.135 g, 0.324 mmol) with MeOH (1 mL) and DCM (1 mL). The reaction was cooled to 0° C. and the Raney Nickel (1.902 mg, 0.032 mmol) was added. The sodium borohydride (0.031 g, 0.810 mmol) was then added portionwise and the reaction stirred at rt for 28 h and the Raney Nickel filtered through celite. The reaction was diluted with DCM and washed with water and the DCM layer was dried with MgSO 4 , filtered and adsorbed to silica then purified by MPLC (0-15% MeOH:DCM) to produce pure (1-(4-aminophenethyl)piperidin-4-yl)diphenylmethanol (0.077 g, 0.199 mmol, 61% yield). H NMR (400 MHz, CDCl 3 ): δ 7.51-7.47 (m, 4H), 7.32-7.27 (m, 4H), 7.18 (tt, J=7.3 Hz, 1.8 Hz, 2H), 6.97 (d, J=8.3 Hz, 2H), 6.61 (d, J=8.3 Hz, 2H), 3.52 (br s, 2H), 3.07-3.01 (m, 2H), 2.70-2.65 (m, 2H), 2.54-2.41 (m, 3H), 2.22 (br s, 1H), 2.07-1.98 (m, 2H), 1.56-1.49 (m, 4H). 13 C NMR (125 MHz, CDCl 3 ): δ 145.9, 144.4, 130.4, 129.4, 128.1, 126.5, 125.8, 115.2, 79.5, 61.2, 54.1, 44.2, 32.8, 26.4, 21.0. LCMS Retention time: 3.328 min. LCMS purity 93.1%. HRMS (ESI): m/z calcd for C 26 H 30 N 2 O [M+H] + 387.2358, found 387.2431. KSC-352-075 (1-(4-(Dimethylamino)phenethyl)piperidin-4-yl)diphenylmethanol To a vial was added the (1-(4-aminophenethyl)piperidin-4-yl)diphenylmethanol (KSC-352-069) (0.030 g, 0.078 mmol) and acetic acid (1 mL). The paraformaldehyde (0.058 mL, 0.776 mmol) solution in water followed by sodium cyanoborohydride (0.015 g, 0.233 mmol) was then added and the reaction stirred at rt for 20 h. The reaction was concentrated and diluted with saturated NaHCO 3 and extracted with EtOAc (3×5 mL). The EtOAc layer was dried with MgSO 4 , filtered and concentrated. The product was purified by reverse-phase MPLC (10-100% MeCN:water) to produce (1-(4-(dimethylamino)phenethyl)piperidin-4-yl)diphenylmethanol (0.027 g, 0.065 mmol, 84% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.50-7.46 (m, 4H), 7.31-7.26 (m, 4H), 7.17 (tt, J=7.3 Hz, 1.8 Hz, 2H), 7.06 (d, J=8.3 Hz, 2H), 6.68 (d, J=8.3 Hz, 2H), 3.08-3.02 (m, 2H), 2.90 (s, 6H), 2.72-2.67 (m, 2H), 2.56-2.50 (m, 2H), 2.48-2.42 (m, 1H), 2.30 (br s, 1H), 2.07-2.00 (m, 2H), 1.56-1.51 (m, 4H). 13 C NMR (125 MHz, CDCl 3 ): δ 149.1, 146.0, 129.2, 128.4, 128.1, 126.4, 125.8, 112.9, 79.4, 61.1, 54.0, 44.2, 41.0, 40.8, 32.6, 26.4. LCMS Retention time: 2.50 min. LCMS purity 96.1%. HRMS (ESI): m/z calcd for C 28 H 34 N 2 O [M+H] + 415.2671, found 415.2744. KSC-352-082 Diphenyl(1-(4-(trifluoromethyl)phenethyl)piperidin-4-yl)methanol To a vial was added the diphenyl(piperidin-4-yl)methanol (0.100 g, 0.374 mmol), 1-(2-bromoethyl)-4-(trifluoromethyl)benzene (0.057 ml, 0.340 mmol) and acetonitrile (10 mL). The TEA (0.071 mL, 0.510 mmol) was then added and the reaction stirred at 85° C. for 18 h. The reaction was diluted with water and extracted with EtOAc (3×15 mL). The EtOAc layer was collected and dried with MgSO 4 , filtered and adsorbed to silica then purified by MPLC (15 min, 0-10% MeOH:DCM) to produce pure diphenyl(1-(4-(trifluoromethyl)phenethyl)piperidin-4-yl)methanol (0.074 g, 0.168 mmol, 49% yield) as an oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.54-7.47 (m, 4H), 7.33-7.27 (m, 6H), 7.19 (tt, J=7.3 Hz, 1.8 Hz, 2H), 3.06-3.00 (m, 2H), 2.86-2.80 (m, 2H), 2.60-2.55 (m, 2H), 2.51-2.42 (m, 1H), 2.14 (br s, 1H), 2.10-2.03 (m, 2H), 1.57-1.47 (m, 4H). 13 C NMR (125 MHz, CDCl 3 ): δ 145.9, 144.6, 129.0, 128.3 (q, J=32 Hz), 128.2, 126.5, 125.8, 125.2 (q, 3.8 Hz), 124.2 (q, J=271.8 Hz), 79.5, 60.2, 54.1, 44.1, 33.6, 26.4, 21.0. LCMS Retention time: 3.877 min. LCMS purity 99.1%. HRMS (ESI): m/z calcd for C 27 H 28 F 3 NO [M+H] + 440.2123, found 440.2196. KSC-352-088 (1-(4-Fluorophenethyl)piperidin-4-yl)diphenylmethanol To a vial was added the diphenyl(piperidin-4-yl)methanol (0.099 g, 0.370 mmol), 1-(2-bromoethyl)-4-fluorobenzene (0.047 mL, 0.337 mmol) and acetonitrile (10 mL). The TEA (0.070 mL, 0.505 mmol) was then added and the reaction stirred at 85° C. at for 19 h and was cooled to rt. The reaction was diluted with water and extracted with EtOAc (3×15 mL). The EtOAc layer was collected and dried with MgSO 4 , filtered and adsorbed to silica then purified by MPLC (15 min, 0-10% MeOH:DCM) to produce pure (1-(4-fluorophenethyl)piperidin-4-yl)diphenylmethanol (0.123 g, 0.316 mmol, 94% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.47 (m, 4H), 7.32-7.27 (m, 4H), 7.21-7.11 (m, 4H), 6.98-6.92 (m, 2H), 3.06-3.00 (m, 2H), 2.78-2.72 (m, 2H), 2.56-2.51 (m, 2H), 2.50-2.42 (m, 1H), 2.21 (br s, 1H), 2.08-1.99 (m, 2H), 1.57-1.48 (m, 4H). 13 C NMR (125 MHz, CDCl 3 ): δ 161.2 (d, J=243.6 Hz), 145.9, 136.5 (d, J=3.2 Hz), 129.9 (d, J=7.9 Hz), 128.1, 126.5, 125.8, 115.0 (d, J=21.2 Hz), 79.5, 60.8, 54.1, 44.2, 33.0, 26.4, 21.0. LCMS Retention time: 3.733 min. LCMS purity 96.8%. HRMS (ESI): m/z calcd for C 26 H 28 FNO [M+H] + 390.2155, found 390.2228. KSC-352-090 2-(3-(Tert-butyl)phenyl)ethanol To a vial was added the 1-bromo-3-(tert-butyl)benzene (0.107 g, 0.502 mmol) and dry THF. The reaction was then cooled to −78° C. and the BuLi (0.221 mL, 0.552 mmol) (2.5 M in hexanes) was added dropwise and the reaction stirred for 30 min at −78° C. and then ethylene oxide (0.502 mL, 1.255 mmol) (2.5-3.3M solution in THF) was added dropwise and the reaction stirred for 10 minutes at −78° C. then warmed to rt and stirred for 1 h. The reaction was then quenched with 1.0 M HCl (2 mL) and extracted with EtOAc (3×5 mL). The EtOAc layer was combined, concentrated and purified by reverse-phase MPLC (10-100% MeCN:water) to produce pure 2-(3-(tert-butyl)phenyl)ethanol (0.035 g, 0.196 mmol, 39% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.31-7.27 (m, 3H), 7.10-7.07 (m, 1H), 3.90 (t, J=6.6 Hz, 2H), 2.91 (t, J=6.5 Hz, 2H), 1.52 (br s, 1H), 1.36 (s, 9H). KSC-352-093 3-(Tert-butyl)phenethyl 4-methylbenzenesulfonate To a vial was added the 2-(3-(tert-butyl)phenyl)ethanol (KSC-352-090) (0.035 g, 0.196 mmol), TEA (0.082 mL, 0.589 mmol) and DCM (2 mL) followed by p-toluenesulfonyl chloride (0.056 g, 0.294 mmol). The reaction began to stir at rt for 20 h and was then diluted with saturated NaHCO 3 and extracted with EtOAc. The EtOAc was then dried with MgSO 4 , filtered and concentrated then purified by reverse-phase MPLC (10-100% MeCN:water) to provide pure 3-(tert-butyl)phenethyl 4-methylbenzenesulfonate (0.060 g, 0.180 mmol, 92% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.70 (d, J=8.4 Hz, 2H), 7.30-7.24 (m, 3H), 7.19 (t, J=7.52 Hz, 1H), 7.14-7.12 (m, 1H), 4.22 (t, J=7.2 Hz, 2H), 2.96 (t, J=7.2 Hz, 2H), 2.43 (s, 3H), 1.29 (s, 9H). KSC-352-097 (1-(3-(Tert-butyl)phenethyl)piperidin-4-yl)diphenylmethanol To a vial was added the 3-(tert-butyl)phenethyl 4-methylbenzenesulfonate (KSC-352-093) (0.060 g, 0.180 mmol), diphenyl(piperidin-4-yl)methanol (0.048 g, 0.180 mmol) and acetonitrile (1 mL). The TEA (0.038 mL, 0.271 mmol) was added and the reaction stirred at 85° C. for 18 h and was cooled to rt then diluted with water and extracted with EtOAc. The EtOAc layer was concentrated and the crude product was purified by reverse-phase MPLC (10-100% MeCN:water) to produce the pure (1-(3-(tert-butyl)phenethyl)piperidin-4-yl)diphenylmethanol (0.065 g, 0.152 mmol, 84% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.47 (m, 4H), 7.32-7.27 (m, 4H), 7.23-7.16 (m, 5H), 7.01-6.98 (m, 1H), 3.09-3.04 (m, 2H), 2.81-2.76 (m, 2H), 2.61-2.55 (m, 2H), 2.51-2.43 (m, 1H), 2.28 (br s, 1H), 2.10-2.02 (m, 2H), 1.30 (s, 9H), 1.32-1.26 (m, 4H). 13 C NMR (125 MHz, CDCl 3 ): δ 151.2, 145.9, 140.0, 128.1, 128.0, 126.5, 125.8, 125.71, 125.68, 123.0, 79.5, 54.1, 44.2, 34.6, 34.0, 31.6, 31.4, 26.4, 22.6. LCMS Retention time: 4.214 min. LCMS purity 96.4%. HRMS (ESI): m/z calcd for C 30 H 37 NO [M+H] + 428.2875, found 428.2948. KSC-352-099 3-((Phenylsulfonyl)methylene)oxetane To an oven-dried vial was added (methylsulfonyl)benzene (0.570 g, 3.65 mmol) and the vial was evacuated with argon 3 times. The dry THF (17 mL) was added and the reaction was cooled to 0° C. The 2.5 M BuLi in hexanes (3.21 mL, 8.03 mmol) was added dropwise and the reaction began to stir at 0° C. and stirred for 45 minutes. The diethyl chlorophosphate (0.528 mL, 3.65 mmol) was then added at 0° C. and the reaction stirred for 30 minutes. The reaction was then cooled to −78° C. and the oxetan-3-one (0.330 mL, 5.15 mmol) was then added dropwise and the reaction stirred for 2 h. The reaction was then warmed to rt and filtered through a silica plug. The reaction was then concentrated onto silica and purified by MPLC (20 min, 0-40% EtOAc:hex) to provide pure 3-((phenylsulfonyl)methylene)oxetane (0.579 g, 2.75 mmol, 75% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.91-7.87 (m, 2H), 7.69-7.64 (m, 1H), 7.60-7.55 (m, 2H), 6.12 (quintet, J=2.3 Hz, 1H), 5.66-5.63 (m, 2H), 5.30-5.27 (m, 2H). KSC-367-003 2-(4-(3-((Phenylsulfonyl)methyl)oxetan-3-yl)phenyl)ethanol To a vial was added the chloro(1,5-cyclooctadiene)rhodium(I), dimer (0.012 g, 0.025 mmol) and 1,4-dioxane (10 mL). The 1.5 M aqueous KOH (0.496 mL, 0.745 mmol) was then added and the reaction stirred for 1 minute at rt. Then the (4-(2-hydroxyethyl)phenyl)boronic acid (0.103 g, 0.621 mmol) and 3-((phenylsulfonyl)methylene)oxetane (KSC-352-099) (0.052 g, 0.248 mmol) in 1 mL dioxane was added and the reaction stirred for 30 minutes at 100° C. in waves. The reaction was then cooled to rt and diluted with EtOAc and washed with 1.0 M HCl. The water layer was extracted with EtOAc (3×15 mL). The EtOAc layer was collected and the water was extracted with EtOAc again. The EtOAc layers were combined and dried with MgSO 4 , filtered and concentrated then purified by reverse-phase MPLC (30 min, 10-100% MeCN:water) to produce pure 2-(4-(3-((phenylsulfonyl)methyl) oxetan-3-yl)phenyl)ethanol (0.063 g, 0.190 mmol, 76% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.55-7.52 (m, 2H), 7.50-7.46 (m, 1H), 7.36-7.31 (m, 2H), 7.09 (d, J=8.4 Hz, 2H), 7.01 (d, J=8.3 Hz, 2H), 5.03 (d, J=6.4 Hz, 2H), 4.93 (d, J=6.4 Hz, 2H), 4.03 (s, 2H), 3.82 (t, J=7.3 Hz, 2H), 2.80 (t, J=7.3 Hz, 2H). KSC-367-027 4-(diphenylmethylene)piperidine To a vial was added the diphenyl(piperidin-4-yl)methanol (0.514 g, 1.922 mmol) and TFA (4 mL). The reaction stirred at 75° C. at for 24 h and was concentrated in vacuo. The residue was then dissolved in DCM (5 mL) and washed with water (4 mL). The DCM layer was collected and washed with water (1×5 mL), dried with MgSO 4 , filtered concentrated then purified by reverse-phase MPLC (10-100% MeCN:Hex) to produce pure 4-(diphenylmethylene)piperidine (0.296 g, 1.187 mmol, 62% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.34-7.28 (m, 4H), 7.25-7.20 (m, 2H), 7.18-7.14 (m, 4H), 2.96-2.92 (m, 4H), 2.37-2.33 (m, 4H), 1.75 (br s, 1H). KSC-367-032 4-(4-Benzylpiperidin-1-yl)-1-(4-(tert-butyl)phenyl)butan-1-one To a vial was added the 4-benzylpiperidine (0.25 ml, 1.422 mmol), 1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-one (0.407 g, 1.707 mmol), acetonitrile and TEA (0.297 mL, 2.133 mmol). The reaction stirred at 85° C. for 17 h. The reaction was cooled to rt and diluted with saturated NaHCO 3 then extracted with EtOAc. The EtOAc was dried with MgSO 4 , filtered and concentrated. The crude material was purified by reverse-phase MPLC (10-100% MeCN:water) to produce 4-(4-benzylpiperidin-1-yl)-1-(4-(tert-butyl)phenyl)butan-1-one (0.291 g, 0.771 mmol, 54% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.91 (d, J=8.6 Hz, 2H), 7.47 (d, J=8.5 Hz, 2H), 7.29-7.24 (m, 2H), 7.20-7.16 (m, 1H), 7.14-7.11 (m, 2H), 2.96 (t, J=7.2 Hz, 2H), 2.90-2.84 (m, 2H), 2.50 (d, J=7.0 Hz, 2H), 2.36 (t, J=7.3 Hz, 2H), 1.96-1.82 (m, 4H), 1.63-1.56 (m, 2H), 1.53-1.46 (m, 1H), 1.34 (s, 9H), 1.28-1.18 (m, 2H). KSC-367-033 3-(4-(Hydroxydiphenylmethyl)piperidin-1-yl)propan-1-ol To a vial was added the diphenyl(piperidin-4-yl)methanol (0.502 g, 1.878 mmol), 3-bromopropan-1-ol (0.204 mL, 2.253 mmol), acetonitrile and TEA (0.393 mL, 2.82 mmol). The reaction stirred at 85° C. for 3 h. The reaction was cooled to rt and diluted with saturated NaHCO 3 and extracted with EtOAc. The EtOAc layer was concentrated and purified by reverse-phase MPLC (10-100% MeCN:water) to provide 3-(4-(hydroxydiphenylmethyl)piperidin-1-yl)propan-1-ol (0.395 g, 1.214 mmol, 65% yield) as a white solid. 1 H NMR (400 MHz, CDCl 3 ): δ 7.48-7.44 (m, 4H), 7.31-7.27 (m, 4H), 7.20-7.15 (m, 2H), 5.45 (br s, 1H), 3.75 (t, J=5.2 Hz, 2H), 3.12-3.06 (m, 2H), 2.57 (t, J=5.7 Hz, 2H), 2.47-2.36 (m, 1H), 1.98-1.91 (m, 2H), 1.70-1.65 (m, 3H), 1.54-1.42 (m, 4H). KSC-367-036 3-(4-(Hydroxydiphenylmethyl)piperidin-1-yl)propyl 4-methylbenzenesulfonate Prepared with same method at KSC-352-093 using 3-(4-(hydroxydiphenylmethyl)piperidin-1-yl)propan-1-ol (KSC-367-033) (0.395 g, 1.214 mmol), 4-methylbenzene-1-sulfonyl chloride (0.347 g, 1.821 mmol), DCM (5 mL) and TEA (0.508 mL, 3.64 mmol) to produce pure 3-(4-(hydroxydiphenylmethyl)piperidin-1-yl)propyl 4-methylbenzenesulfonate (0.193 g, 0.402 mmol, 33% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.69-7.66 (m, 2H), 7.46-7.41 (m, 4H), 7.24-7.19 (m, 4H), 7.15-7.05 (m, 4H), 4.26-4.12 (m, 4H), 3.73-3.65 (m, 2H), 3.27-3.18 (m, 2H), 2.68-2.60 (m, 1H), 2.47-2.37 (m, 2H), 2.30 (s, 3H), 1.88-1.76 (m, 2H), 1.52-1.43 (m, 2H). KSC-367-039 4-(4-Benzylpiperidin-1-yl)-1-(4-(tert-butyl)phenyl)butan-1-ol Method B: 4-(4-benzylpiperidin-1-yl)-1-(4-(tert-butyl)phenyl)butan-1-one (KSC-367-032) (0.291 g, 0.771 mmol) and MeOH (5 mL) and sodium borohydride (0.117 g, 3.08 mmol) to produce pure 4-(4-benzylpiperidin-1-yl)-1-(4-(tert-butyl)phenyl)butan-1-ol (0.232 g, 0.611 mmol, 79% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.35-7.25 (m, 6H), 7.21-7.12 (m, 3H), 4.64-4.60 (m, 1H), 3.13-3.07 (m, 1H), 2.94-2.88 (m, 1H), 2.54 (d, J=7.0 Hz, 2H), 2.44-2.34 (m, 2H), 2.03-1.93 (m, 2H), 1.90-1.38 (m, 10H), 1.31 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 149.4, 142.9, 140.7, 129.1, 128.2, 125.8, 125.4, 125.0, 73.5, 59.0, 54.6, 52.9, 42.9, 40.1, 38.0, 34.4, 31.8, 31.6, 31.4, 24.3. LCMS Retention time: 4.330 min. LCMS purity 99.1%. HRMS (ESI): m/z calcd for C 26 H 37 NO [M+H] + 380.2875, found 380.2948. KSC-367-043 (1-(3-((4-(Tert-butyl)phenyl)amino)propyl)piperidin-4-yl)diphenylmethanol To a vial was added the 3-(4-(hydroxydiphenylmethyl)piperidin-1-yl)propyl 4-methylbenzenesulfonate (KSC-367-036) (0.088 g, 0.183 mmol), 4-(tert-butyl)aniline (0.035 mL, 0.220 mmol) and TEA (0.038 mL, 0.275 mmol) with acetonitrile (3 mL). The reaction began to stir at 85° C. for 18 h and was then cooled to rt and diluted with saturated NaHCO 3 then extracted with EtOAc. The EtOAc was concentrated and purified by reverse-phase MPLC (10-100% MeCN:water) to produce pure (1-(3-((4-(tert-butyl)phenyl)amino) propyl)piperidin-4-yl)diphenylmethanol (0.038 g, 0.083 mmol, 45% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.50-7.46 (m, 4H), 7.33-7.28 (m, 4H), 7.21-7.16 (m, 4H), 6.51 (d, J=8.7 Hz, 2H), 3.13 (t, J=6.4 Hz, 2H), 3.02-2.96 (m, 2H), 2.49-2.41 (m, 3H), 2.15 (br s, 1H), 2.00-1.93 (m, 2H), 1.80-1.73 (m, 2H), 1.57-1.43 (m, 5H), 1.27 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 146.4, 145.9, 139.7, 128.2, 126.5, 125.9, 125.8, 112.4, 79.6, 57.4, 54.2, 44.2, 43.7, 33.8, 31.5, 26.6, 26.2. LCMS Retention time: 4.208 min. LCMS purity 100%. HRMS (ESI): m/z calcd for C 30 H 38 N 2 O [M+H] + 457.6620, found 457.3194. KSC-367-044 (1-(3-(4-(Tert-butyl)phenoxy)propyl)piperidin-4-yl)diphenylmethanol To a vial was added the 3-(4-(hydroxydiphenylmethyl)piperidin-1-yl)propyl 4-methylbenzenesulfonate (KSC-367-036) (0.105 g, 0.219 mmol), 4-(tert-butyl)phenol (0.039 g, 0.263 mmol) and TEA (0.046 mL, 0.328 mmol) with acetonitrile (3 mL). The reaction stirred at 85° C. for 18 h then diluted with saturated NaHCO 3 and extracted with EtOAc. The EtOAc layer was concentrated and purified by RP MPLC (10-100% MeCN:water) to produce pure (1-(3-(4-(tert-butyl)phenoxy)propyl)piperidin-4-yl)diphenylmethanol (0.015 g, 0.033 mmol, 15% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.49-7.46 (m, 4H), 7.31-7.26 (m, 6H), 7.19-7.14 (m, 2H), 6.81 (d, J=8.8 Hz, 2H), 3.96 (t, J=6.4 Hz, 2H), 3.01-2.94 (m, 2H), 2.51-2.40 (m, 3H), 1.99-1.89 (m, 5H), 1.52-1.45 (m, 4H), 1.28 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 156.7, 145.9, 143.2, 128.1, 126.5, 126.1, 125.7, 116.3, 113.9, 79.5, 66.3, 60.4, 55.4, 54.1, 44.1, 34.0, 31.5, 29.7, 27.0, 26.4. LCMS Retention time: 4.293 min. LCMS purity 95.2%. HRMS (ESI): m/z calcd for C 30 H37NO 2 [M+H] + 458.6470, found 458.3068. KSC-367-047 2-(6-(tert-butyl)pyridin-3-yl)ethanol Prepared by same method as KSC-352-090 with 5-bromo-2-(tert-butyl)pyridine (0.303 g, 1.415 mmol), dry THF (10 mL), 2.5 M BuLi in hexanes (0.623 mL, 1.557 mmol) and ethylene oxide (1.415 ml, 3.54 mmol) (2.5-3.3M solution in THF) to produce pure 2-(6-(tert-butyl)pyridin-3-yl)ethanol (0.211 g, 1.177 mmol, 83% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 8.40 (br d, J=2.4 Hz, 1H), 7.48 (dd, J=8.2 Hz, 2.4 Hz, 1H), 7.26 (dd, J=8.2 Hz, 0.8 Hz, 1H), 3.85 (br t, J=6.0 Hz, 2H), 2.82 (t, J=6.5 Hz, 2H), 2.29 (br s, 1H), 1.33 (s, 9H). KSC-367-049 2-(6-(tert-butyl)pyridin-3-yl)ethyl 4-methylbenzenesulfonate Prepared by same method at KSC-352-093 with 2-(6-(tert-butyl)pyridin-3-yl)ethanol (KSC-367-047) (0.211 g, 1.177 mmol), TEA (0.492 mL, 3.53 mmol) and DCM (2 mL) followed by p-toluenesulfonyl chloride (0.337 g, 1.766 mmol) to provide pure 2-(6-(tert-butyl)pyridin-3-yl)ethyl 4-methylbenzenesulfonate (0.260 g, 0.780 mmol, 66% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 8.29 (br d, J=2.4 Hz, 1H), 7.69 (d, J=8.3 Hz, 2H), 7.40 (dd, J=8.2 Hz, 2.4 Hz, 1H), 7.30-7.27 (m, 2H), 7.23 (dd, J=8.2 Hz, 0.8 Hz, 1H), 4.19 (t, J=6.9 Hz, 2H), 2.92 (t, J=6.8 Hz, 2H), 2.43 (s, 3H), 1.34 (s, 9H). KSC-367-052 (1-(2-(6-(Tert-butyl)pyridin-3-yl)ethyl)piperidin-4-yl)diphenylmethanol To a vial was added the diphenyl(piperidin-4-yl)methanol (0.250 g, 0.936 mmol), 2-(6-(tert-butyl)pyridin-3-yl)ethyl 4-methylbenzenesulfonate (KSC-367-049) (0.260 g, 0.780 mmol) and acetonitrile (5 mL). The TEA (0.163 mL, 1.170 mmol) was then added and the reaction stirred at 50° C. for 20 h and was then cooled to rt and diluted with saturated NaHCO 3 then extracted with DCM. The DCM layer was concentrated and purified by reverse-phase MPLC (10-100% MeCN:water) to produce pure (1-(2-(6-(tert-butyl)pyridin-3-yl)ethyl)piperidin-4-yl)diphenylmethanol (0.308 g, 0.719 mmol, 92% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 8.39-8.38 (m, 1H), 7.51-7.48 (m, 4H), 7.42 (dd, J=8.1 Hz, 2.4 Hz, 1H), 7.32-7.27 (m, 4H), 7.25-7.22 (m, 1H), 7.20-7.15 (m, 2H), 3.07-3.01 (m, 2H), 2.76-2.71 (m, 2H), 2.57-2.52 (m, 2H), 2.50-2.42 (m, 1H), 2.31 (br s, 1H), 2.09-2.01 (m, 2H), 1.57-1.48 (m, 4H), 1.35 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 166.9, 148.7, 145.9, 136.3, 132.3, 128.1, 126.5, 125.8, 118.6, 79.4, 60.2, 54.0, 44.1, 37.0, 30.3, 30.2, 26.4. LCMS Retention time: 3.802 min. LCMS purity 99.5%. HRMS (ESI): m/i calcd for C 29 H 36 N 2 O [M+H] + 429.2828, found 429.2900. KSC-367-053 1-(4-(Tert-butyl)phenyl)-4-(4-(diphenylmethylene)piperidin-1-yl)butan-1-one To a vial was added the 4-(diphenylmethylene)piperidin-1-ium 2,2,2-trifluoroacetate (KSC-367-027) (0.0475 g, 0.131 mmol), 1-(4-(tert-butyl)phenyl)-4-chlorobutan-1-one (0.037 g, 0.157 mmol) and TEA (0.046 mL, 0.327 mmol) in acetonitrile. The reaction stirred at 75° C. for 20 h. The reaction was removed from heat and diluted with saturated NaHCO 3 , extracted with EtOAc. The EtOAc layer was concentrated and purified by reverse-phase MPLC (10-100% MeCN:water) to produce pure 1-(4-(tert-butyl)phenyl)-4-(4-(diphenylmethylene)piperidin-1-yl)butan-1-one (0.019 g, 0.042 mmol, 32% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.91 (d, J=8.2 Hz, 2H), 7.46 (d, J=8.3 Hz, 2H), 7.30-7.25 (m, 4H), 7.21-7.17 (m, 2H), 7.13-7.10 (m, 4H), 2.99 (t, J=7.2 Hz, 2H), 2.51-2.32 (m, 10H), 1.98-1.91 (m, 2H), 1.34 (s, 9H). KSC-367-055 (1-(4-Chlorophenethyl)piperidin-4-yl)diphenylmethanol To a vial was added the diphenyl(piperidin-4-yl)methanol (0.221 g, 0.827 mmol), 1-(2-bromoethyl)-4-chlorobenzene (0.165 g, 0.752 mmol), acetonitrile (4 mL) and TEA (0.157 mL, 1.128 mmol). The reaction stirred at 75° C. for 18 h then was cooled to rt and diluted with saturated NaHCO 3 and extracted with EtOAc. The EtOAc layer was concentrated and purified by reverse-phase MPLC (10-100% MeCN:water) to produce pure (1-(4-chlorophenethyl)piperidin-4-yl)diphenylmethanol (0.224 g, 0.552 mmol, 73% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.39-7.36 (m, 4H), 7.20-7.15 (m, 4H), 7.12-7.09 (m, 2H), 7.08-7.03 (m, 2H), 6.99-6.96 (m, 2H), 2.92-2.87 (m, 2H), 2.64-2.58 (m, 2H), 2.43-2.38 (m, 2H), 2.37-2.30 (m, 1H), 2.22 (br s, 1H), 1.95-1.88 (m, 2H), 1.44-1.35 (m, 4H). 13 C NMR (125 MHz, CDCl 3 ): δ 145.9, 145.8, 138.9, 131.6, 129.9, 128.3, 128.0, 126.4, 125.7, 79.4, 79.3, 60.4, 57.0, 44.1, 33.0, 26.4. LCMS Retention time: 3.903 min. LCMS purity 99.6%. HRMS (ESI): m/z calcd for C 26 H 28 ClNO [M+H] + 406.1859, found 406.1932. KSC-367-058 1-(4-(Tert-butyl)phenyl)-4-(4-(diphenylmethylene)piperidin-1-yl)butan-1-ol Method B: 1-(4-(tert-butyl)phenyl)-4-(4-(diphenylmethylene)piperidin-1-yl)butan-1-one (KSC-367-053) (0.019 g, 0.042 mmol) and sodium borohydride (6.37 mg, 0.168 mmol) to produce pure 1-(4-(tert-butyl)phenyl)-4-(4-(diphenylmethylene)piperidin-1-yl)butan-1-ol (0.010 g, 0.022 mmol, 52% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.35-7.26 (m, 8H), 7.23-7.18 (m, 2H), 7.13-7.10 (m, 4H), 4.68-4.65 (m, 1H), 2.66-2.60 (m, 2H), 2.55-2.42 (m, 8H), 2.00-1.94 (m, 1H), 1.90-1.81 (m, 1H), 1.73-1.63 (m, 3H), 1.30 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 149.5, 142.7, 142.3, 136.4, 134.6, 129.7, 128.0, 126.4, 125.3, 125.0, 73.3, 58.7, 55.0, 39.6, 34.4, 31.6, 31.4, 31.1, 24.0, 22.6. LCMS Retention time: 4.454 min. LCMS purity 97.1%. HRMS (ESI): m/z calcd for C 32 H 39 NO [M+H] + 454.3032, found 454.3104. KSC-367-066 4-(3-((phenylsulfonyl)methyl)oxetan-3-yl)phenethyl 4-methylbenzenesulfonate Prepared by the same method as KSC-352-093 with 2-(4-(3-((phenylsulfonyl)methyl)oxetan-3-yl)phenyl)ethanol (KSC-367-003) (0.104 g, 0.313 mmol), TEA (0.131 mL, 0.939 mmol) and DCM (2 mL) followed by p-toluenesulfonyl chloride (0.089 g, 0.469 mmol) to produce 4-(3-((phenylsulfonyl)methyl)oxetan-3-yl)phenethyl 4-methylbenzenesulfonate (0.041 g, 0.084 mmol, 27% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.75 (d, J=8.3 Hz, 2H), 7.57-7.46 (m, 4H), 7.36-7.32 (m, 4H), 7.02-6.96 (m, 3H), 5.00 (d, J=6.4 Hz, 2H), 4.93 (d, J=6.4 Hz, 2H), 4.17 (t, J=7.0 Hz, 2H), 4.01 (s, 2H), 2.90 (t, J=7.0 Hz, 2H), 2.45 (s, 3H). KSC-367-069 Diphenyl(1-(4-(3-((phenylsulfonyl)methyl)oxetan-3-yl)phenethyl)piperidin-4-yl)methanol To a vial was added the 4-(3-((phenylsulfonyl)methyl)oxetan-3-yl)phenethyl 4-methylbenzenesulfonate (KSC-367-066) (0.041 g, 0.084 mmol) and diphenyl(piperidin-4-yl)methanol (0.025 g, 0.093 mmol) in acetonitrile. The TEA (0.018 ml, 0.126 mmol) was then added and the reaction stirred at 50° C. for 18 h. The reaction was removed from heat and cooled to rt then diluted with saturated NaHCO 3 . The reaction was then extracted with EtOAc (3×5 mL) and the EtOAc layer was dried with MgSO 4 , filtered and concentrated. The crude residue was purified by reverse-phase MPLC (15 min, 10-100% MeCN:water) to produce diphenyl(1-(4-(3 ((phenylsulfonyl) methyl)oxetan-3-yl)phenethyl)piperidin-4-yl)methanol (0.024 g, 0.041 mmol, 49% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.53-7.43 (m, 6H), 7.33-7.27 (m, 7H), 7.21-7.16 (m, 2H), 7.04 (d, J=8.2 Hz, 2H), 6.96 (d, J=8.2 Hz, 2H), 5.02 (d, J=6.4 Hz, 2H), 4.92 (d, J=6.4 Hz, 2H), 4.01 (s, 2H), 3.08-3.02 (m, 2H), 2.74-2.69 (m, 2H), 2.56-2.44 (m, 3H), 2.10-2.02 (m, 2H), 1.60-1.50 (m, 5H). KSC-367-072 (1-(4-(3-Methyloxetan-3-yl)phenethyl)piperidin-4-yl)diphenylmethanol To a vial was added the diphenyl(1-(4-(3-((phenylsulfonyl)methyl)oxetan-3-yl)phenethyl)piperidin-4-yl)methanol (KSC-367-069) (0.024 g, 0.041 mmol) and MeOH (10 mL) and the reaction as heated to 50° C. The magnesium was added in 3 additions (0.016 g, 0.066 mmol, 16 equiv) 1.5 h apart. The reaction was removed from heat 1.5 h after the final magnesium addition, cooled to rt and poured into 1.0 M HCl with ice. The aqueous layer was then extracted with DCM (3×10 mL) and the organic layers were combined and dried with MgSO 4 , filtered and concentrated then purified by reverse-phase MPLC (15 min, 10-100% MeCN:water). To produce (1-(4-(3-methyloxetan-3-yl)phenethyl)piperidin-4-yl)diphenylmethanol (0.0045 g, 10.19 μmol, 24.70% yield) as a light brown solid. 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.47 (m, 4H), 7.32-7.27 (m, 4H), 7.21-7.16 (m, 4H), 7.13-7.10 (m, 2H), 4.95 (d, J=5.5 Hz, 2H), 4.61 (d, J=5.5 Hz, 2H), 3.09-3.02 (m, 2H), 2.81-2.75 (m, 2H), 2.59-2.54 (m, 2H), 2.50-2.42 (m, 1H), 2.16 (br s, 1H), 2.09-2.00 (m, 2H), 1.71 (s, 3H), 1.56-1.48 (m, 4H). 13 C NMR (125 MHz, CDCl 3 ): δ 145.9, 144.1, 138.4, 128.8, 128.2, 126.5, 125.8, 125.1, 83.8, 79.5, 60.7, 54.1, 44.1, 43.1, 33.3, 27.8, 26.4. LCMS Retention time: 3.652 min. LCMS purity 97.9%. HRMS (ESI): m/z calcd for C 30 H 35 NO 2 [M+H] + 442.2668, found 442.2741. KSC-367-088 2-(Tert-butyl)phenyl trifluoromethanesulfonate To a vial was added the 2-(tert-butyl)phenol (1.0 ml, 6.51 mmol) and DCM (4 mL) followed by pyridine (1.053 mL, 13.02 mmol). The reaction was then cooled to 0° C. and the triflic anhydride (1.320 mL, 7.81 mmol) was added dropwise and the reaction stirred for 2 h. The reaction was then allowed to warm to rt and was diluted with DCM and quenched with 1.0 M HCl. The DCM layer was collected and washed with saturated NaHCO 3 and brine. The organic layer was then dried (MgSO 4 ), filtered and adsorbed to silica and purified by MPLC (0-25% EtOAc:hex) to produce pure 2-(tert-butyl)phenyl trifluoromethanesulfonate (1.66 g, 5.88 mmol, 90% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.49-7.46 (m, 1H), 7.37-7.34 (m, 1H), 7.31-7.27 (m, 2H), 1.43 (s, 9H). KSC-381-009 2-(2-(Tert-butyl)phenyl)-4,4,5,5-tetramethyl-1,3,2-dioxaborolane To a flame-dried vial was added molecular sieves and 2-(tert-butyl)phenyl trifluoromethanesulfonate (KSC-367-088) (0.475 g, 1.683 mmol) and 1,1′-Bis(diphenylphosphino)ferrocenedichloropalladium(II) (0.042 g, 0.050 mmol). The vial was evacuated with argon 3 times and then dioxane (1 mL), TEA (0.704 mL, 5.05 mmol) and 4,4,5,5-tetramethyl-1,3,2-dioxaborolane (0.732 mL, 5.05 mmol) were added via syringe. The reaction stirred at reflux (100° C.) for 2 h. The reaction was then removed from heat and diluted with water then extracted with DCM (3×5 mL). The DCM layer was then washed again with water (3×10 mL). The DCM layer was dried with MgSO 4 , filtered and concentrated. The residue was diluted with hexanes and filtered through MgSO 4 to remove the residual Pd complex. The hexanes layer was then concentrated to produce pure 2-(2-(tert-butyl)phenyl)-4,4,5,5-tetramethyl-1,3,2-dioxaborolane (0.093 g, 0.357 mmol, 86% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.45 (dd, J=7.2 Hz, 1.2 Hz, 1H), 7.41-7.39 (m, 1H), 7.29 (td, J=7.6 Hz, 2.0 Hz, 1H), 7.14 (td, J=7.6 Hz, 2.0 Hz, 1H), 1.41 (s, 9H), 1.38 (s, 12H). KSC-381-011 1-Bromo-2-(tert-butyl)benzene To a vial was added the 2-(2-(tert-butyl)phenyl)-4,4,5,5-tetramethyl-1,3,2-dioxaborolane (KSC-381-009) (0.180 g, 0.692 mmol) and MeOH (1.5 mL). The copper (H) bromide (0.464 g, 2.075 mmol) was then dissolved in water and added to the reaction then stirred at 80° C. for 24 h. The reaction was then removed from heat and diluted with water and extracted with EtOAc. The EtOAc was dried with MgSO 4 , filtered and concentrated to produce 1-bromo-2-(tert-butyl)benzene (0.103 g, 0.483 mmol, 70% yield) as a brown liquid. 1 H NMR (400 MHz, CDCl 3 ): δ 7.59 (dd, J=8.0 Hz, 1.6 Hz, 1H), 7.44 (dd, J=8.0 Hz, 1.6 Hz, 1H), 7.24 (td, J=7.6 Hz, 2.0 Hz, 1H), 7.02 (td, J=7.6 Hz, 2.0 Hz, 1H), 1.51 (s, 9H). KSC-381-015 2-(2-(Tert-butyl)phenyl)ethanol Prepared by same method as KSC-352-090 with 1-bromo-2-(tert-butyl)benzene (KSC-381-011) (0.147 g, 0.690 mmol), dry THF, 2.5 M BuLi in hexanes (0.303 ml, 0.759 mmol) and then ethylene oxide (0.690 ml, 1.724 mmol) (2.5-3.3M solution in THF) to produce pure 2-(2-(tert-butyl)phenyl)ethanol (0.018 g, 0.101 mmol, 14.64% yield) as a clear oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.43-7.37 (m, 1H), 7.23-7.19 (m, 1H), 7.18-7.14 (m, 2H), 3.90 (t, J=7.6 Hz, 2H), 3.19 (t, J=7.6 Hz, 2H), 1.44 (s, 9H). KSC-381-018 2-(Tert-butyl)phenethyl 4-methylbenzenesulfonate Prepared according to same procedure as KSC-352-093 with 2-(2-(tert-butyl)phenyl)ethanol (KSC-381-015) (0.018 g, 0.101 mmol), TEA (0.042 mL, 0.303 mmol) and DCM (2 mL) followed by p-toluenesulfonyl chloride (0.029 g, 0.151 mmol) to provide pure 2-(tert-butyl)phenethyl 4-methylbenzenesulfonate (0.022 g, 0.066 mmol, 66% yield) and a clear oil. 1 H NMR (400 MHz, CDCl 3 ): δ 7.76 (d, J=8.0 Hz, 2H), 7.37-7.31 (m, 3H), 7.17-7.04 (m, 3H), 4.19 (t, J=7.6 Hz, 2H), 3.25 (t, J=7.6 Hz, 2H), 2.44 (s, 3H), 1.33 (s, 9H). KSC-381-020 (1-(2-(Tert-butyl)phenethyl)piperidin-4-yl)diphenylmethanol To a vial was added the 2-(tert-butyl)phenethyl 4-methylbenzenesulfonate (KSC-381-018) (0.022 g, 0.066 mmol), diphenyl(piperidin-4-yl)methanol (0.018 g, 0.066 mmol) and acetonitrile. The TEA (0.014 mL, 0.099 mmol) was added and the reaction stirred at 85° C. for 20 h. The reaction was cooled to rt and diluted with water then extracted with EtOAc. The EtOAc layer was concentrated and the crude product was purified by reverse-phase MPLC (10-100% MeCN:water) to produce the pure (1-(2-(tert-butyl)phenethyl) piperidin-4-yl)diphenylmethanol (0.013 g, 0.030 mmol, 46% yield). 1 H NMR (400 MHz, CDCl 3 ): δ 7.51-7.48 (m, 4H), 7.37-7.28 (m, 5H), 7.21-7.09 (m, 5H), 3.15-3.04 (m, 4H), 2.65-2.60 (m, 2H), 2.52-2.42 (m, 1H), 2.17-2.08 (m, 3H), 1.60-1.53 (m, 4H), 1.41 (s, 9H). 13 C NMR (125 MHz, CDCl 3 ): δ 147.7, 145.9, 138.5, 132.1, 128.2, 126.5, 126.1, 125.9, 125.84, 125.79, 79.5, 61.7, 54.2, 44.2, 35.7, 31.7, 29.7, 26.4. LCMS Retention time: 4.200 min. LCMS purity 99.3%. HRMS (ESI): m/z calcd for C 30 H 37 NO [M+H] + 428.2875, found 428.2948. Bacterial Strains and Conditions All strains used to evaluate the antimicrobial activity of terfenadine and corresponding structural derivatives are shown below in Table 5. S. aureus strain UAMS-1 is an osteomyelitis clinical isolate (Gillaspy et al. “Role of the accessory gene regulator (agr) in pathogenesis of staphylococcal osteomyelitis. Infect. Immun. 63:3373-3380 (1995)), whereas ciprofloxacin-resistant strains CRC118 and CRC61 are spontaneous ciprofloxacin-resistant derivatives of UAMS-1 that were selected by growth on Mueller-Hinton agar (MHA) (Becton, Dickinson & Company, Franklin Lakes, N.J.) at 1.5×MIC ciprofloxacin (0.75 μg/ml). TABLE 5Bacterial Strains Used in Terfenadine StudySpeciesStrainSourceS. aureusUAMS-11CRC61Dunman Lab, URMCCRC118Dunman Lab, URMC Minimum Inhibitory Concentration (MIC) Testing Minimum Inhibitory Concentration (MIC) testing was performed to determine the minimum concentration of test compound that is necessary to inhibit visible growth of bacteria according to Clinical and Laboratory Standards (CLSI) guidelines (Clinical and Laboratory Standards Institute (CLSI). Methods for Dilution Antimicrobial Susceptibility Tests for Bacteria That Grow Aerobically; Approved Standard—Ninth Edition. CLSI document M07-A9. 2012. Clinical and Laboratory Standards Institute, 940 West Valley Road, Suite 1400, Wayne, Pa. 19087-1898 USA.) To do so, 10 5 colony forming units of an overnight bacterial culture were seeded into individual wells of 96-well round-bottom microtiter plates containing 88 μl of MHB medium. To the first column, 2 μl of the test compound's corresponding solvent was also added to each well (negative control). To the next ten columns, 2 μl of the test compound (dissolved in DMSO for terfenadine and its derivatives or sterile water for ciprofloxacin) was added in increasing 2-fold increments of 0.5 μg/ml to 256 μg/ml to each successive well. Each test compound was evaluated in duplicate. Plates were incubated at 37° C. incubator for 16 h at which point the minimum inhibitory concentration was determined to be the lowest concentration of test compound that inhibited bacterial growth, as judged by the unaided eye. S. aureus DNA Gyrase Supercoiling Assay (TopoGEN) The gyrase supercoiling assays were performed to determine if test compounds interfered with S. aureus DNA gyrase activity, following the manufacturer's recommendations (TopoGEN). Reactions (20 μl) contained kit provided assay buffer, ATP, potassium glutamate, relaxed plasmid DNA (0.4 μg/ml), 2 Units of S. aureus DNA gyrase, and various amounts of test compound. Reactions were incubated at 37° C. for 30 min and then stopped by the addition of 10% SDS, filtered through 0.025 μm Millipore membrane filters in a 10 mM Tris-HCl buffer (pH 8), and electrophoresed in a 1% agarose TAE gel. Gels were stained with 0.5 μg/ml ethidium bromide and images were analyzed using densitometry (Image J, NIH). The IC 50 values for each test compound was determined to be the compound concentration that inhibited S. aureus DNA gyrase activity by 50%. S. aureus Topoisomerase IV Decatenation Assay (Inspiralis) A Topoisomerase IV assay was performed on test compounds to determine if they interfered with the ability of S. aureus topoisomerase IV to decatenate kDNA, according to the recommendations of the manufacturer (Inspiralis). To do so, 0.25 U S. aureus topoisomerase IV enzyme was mixed with 200 ng kDNA in kit provided reaction buffer, in the absence or presence of various concentrations of test compounds at 37° C. for 30 min. The reaction was stopped by the addition of STEB stop buffer and 30 μl of 24:1 chlorform:isoamyl alcohol (total volume 90 μl). Reaction products then electrophoresed in a 1% agarose TAE gel, stained with 0.5 μg/ml ethidium bromide and images were analyzed using densitometry (Image J, NIH). The IC 50 value for each test compound was determined as the compound concentration that inhibited S. aureus topoisomerase IV activity by 50%. The results are set forth in Table 6. 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or a pharmaceutically acceptable salt thereof, wherein R1 and R2 are independently selected from ethyl or methyl, n is 1 or 2, R3 and R4 are both phenyl or substituted phenyl, wherein the substituent can be halo, hydroxyl, a lower alkyl or a substituted lower alkyl wherein the substituent can be halo, hydroxy, or lower alkoxy, and R5 is hydrogen, a halogen, a lower alkyl from about 1 to 4 carbon atoms or a substituted alkyl wherein the substituent can be halo, hydroxy, or lower alkoxy."],"number":1,"annotation":false,"claim":true,"title":false},{"lines":["The method of claim 1, wherein the enterococcal infection is a respiratory infection."],"number":2,"annotation":false,"claim":true,"title":false},{"lines":["The method of claim 1, wherein the enterococcal infection is a gastrointestinal infection."],"number":3,"annotation":false,"claim":true,"title":false},{"lines":["The method of claim 1, wherein the enterococcal infection is a skin infection."],"number":4,"annotation":false,"claim":true,"title":false},{"lines":["The method of claim 1, wherein the enterococcal infection is an Enterococcus faecium infection."],"number":5,"annotation":false,"claim":true,"title":false},{"lines":["The method of claim 1, wherein the enterococcal infection is a small colony variant bacterial infection."],"number":6,"annotation":false,"claim":true,"title":false},{"lines":["The method of claim 1, wherein the compound is selected from the group consisting of clomiphene or a pharmaceutically acceptable salt thereof; tamoxifen or a pharmaceutically acceptable salt thereof; and 4-hydroxy tamoxifen or a pharmaceutically acceptable salt thereof."],"number":7,"annotation":false,"claim":true,"title":false}]}},"filters":{"npl":[],"notNpl":[],"applicant":[],"notApplicant":[],"inventor":[],"notInventor":[],"owner":[],"notOwner":[],"tags":[],"dates":[],"types":[],"notTypes":[],"j":[],"notJ":[],"fj":[],"notFj":[],"classIpcr":[],"notClassIpcr":[],"classNat":[],"notClassNat":[],"classCpc":[],"notClassCpc":[],"so":[],"notSo":[],"sat":[]},"sequenceFilters":{"s":"SEQIDNO","d":"ASCENDING","p":0,"n":10,"sp":[],"si":[],"len":[],"t":[],"loc":[]}}