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Also a method for determining the responsiveness of a mammalian tumor cell or cancer cell to treatment with a selective CDK9 inhibitor is described herein. In particular, the present invention provides for an in vitro method for the identification of a responder for or a patient sensitive to a selective CDK9 inhibitor, whereby the patient is suspected to suffer from NUT midline carcinoma (NMC). The present invention also relates to a method of monitoring or predicting the efficacy of a treatment of NUT midline carcinoma (NMC), wherein treatment with a selective CDK9 inhibitor is in particular envisaged. Also the use of a (transgenic) non-human animal or a (transgenic) cell having at least one rearrangement in the NUT gene for screening and/or validation of a medicament for the treatment NUT midline carcinoma (NMC) is described. Furthermore, a kit useful for carrying out the methods described herein as well as an olieo- or polynucleotide canable of detecting rearrangements in the NUT nene are provided.","lang":"en","source":"WIPO_FULLTEXT","data_format":"ORIGINAL"}],"fr":[{"text":"La présente invention concerne un procédé de sélection d'une ou des cellule(s), d'un ou des tissu(s) ou d'une ou des culture(s) cellulaire(s) présentant une susceptibilité à un inhibiteur sélectif de CDK9. L'invention concerne également un procédé pour la détermination de la sensibilité d'une cellule tumorale ou d'une cellule cancéreuse mammalienne à un traitement avec un inhibiteur sélectif de CDK9. En particulier, la présente invention concerne un procédé in vitro pour l'identification d'un répondeur pour un inhibiteur sélectif de CDK9 ou un patient sensible à celui-ci, le patient étant suspect d'être atteint de carcinome de la ligne médiane NUT (NMC). La présente invention concerne également un procédé pour le suivi ou la prédiction de l'efficacité d'un traitement de carcinome de la ligne médiane NUT (NMC), selon lequel un traitement avec un inhibiteur sélectif de CDK9 est envisagé. L'invention concerne en outre l'utilisation d'un animal non humain (transgénique) ou d'une cellule (transgénique) ayant au moins un remaniement dans le gène NUT pour le criblage et/ou la validation d'un médicament pour le traitement de carcinome de la ligne médiane NUT (NMC). L'invention concerne enfin une trousse utile pour la mise en œuvre des procédés selon la présente invention ainsi qu'un oligonucléotide ou un polynucléotide capable de détecter des remaniements dans le gène NUT.","lang":"fr","source":"WIPO_FULLTEXT","data_format":"ORIGINAL"}]},"abstract_lang":["en","fr"],"has_abstract":true,"claim":{"en":[{"text":"CLAIMS A method of selecting (a) cell(s), (a) tissue(s) or (a) cell culture(s) with susceptibility to a selective CD 9 inhibitor, comprising the steps: (a) determining the presence of a rearrangement in the NUT gene in said cell, tissue or cell culture; (b) selecting (a) cell(s), tissue(s) or cell culture(s) with at least one rearrangement in the NUT gene; (c) contacting said cell(s), tissue(s) or cell culture(s) with a selective CD 9 inhibitor; and (d) evaluating viability of said cell(s), tissue(s) or cell culture(s) contacted with said selective CD 9 inhibitor, wherein a decreased viability is indicative for susceptibility to said selective CD 9 inhibitor. A method for determining the responsiveness of a mammalian tumor cell or cancer cell to a selective CDK9 inhibitor, said method comprising determining the presence of at least one rearrangement in the NUT gene in said tumor or cancer cell, wherein said rearrangement in the NUT gene is indicative of whether the cell is likely to respond or is responsive to said selective CDK9 inhibitor. In vitro method for the identification of a responder for or a patient sensitive to a selective CD 9 inhibitor, said method comprising evaluating the presence of at least one rearrangement in the NUT gene in a sample obtained from a subject/patient suspected to suffer from or being prone to suffer from NUT midline carcinoma (NMC), whereby the presence of at least one rearrangement in the NUT gene is indicative for a responding patient or is indicative for a sensitivity of said patient to a selective CDK9 inhibitor. The method of claim 3, wherein said selective CDK9 inhibitor is a compound having the freneral formula Π\\ Fomiula (I) wherein L is a bond or -CR 5 R 6 -, -CR 5 R 6 -CR 7 R 8 - -CR 5 R 6 -CR 7 R 8 -CR 9 R 10 - -CRV-CRV-CR ^CR 1 'R 12 -; R 5 - R 12 represent independently of each other -H, -CH 3 , -C 2 H 5 , -C 3 H 7 , -F, -CI -Br, -I; R 3 is selected from -H, N( Ni l;-. -CN, -F, -CI, -Br, -I, -Ch\\. -C 2 H 5 , -Ph, - ;f i-. -CH(CH 3 ) 2 , -C 4 H 9 , -CH 2 -CH(CH 3 ) 2 , -CH(CH 3 )-C 2 H 5J -C(CH 3 ) 3 , -0-CH 3 , -0-C 2 H 5 , -0-C 3 H 7 , -0-CH(CH 3 ) 2 , -O-C4H9, -0-CH 2 -CH(CH 3 ) 2 , -0-CH(CH 3 )-C 2 H 5, -0-C(CH 3 ) 3 , -CR ,3 R 14 R 21 , -CR ,3 R 14 -CR ,5 R ,6 R 2I , -0-CR 13 R ,4 R 21 , ' -CR ,3 R ,4 -CR 15 R ,6 -CR ,7 R ,S R 21 , -CR 13 R 14 -CR ,5 R ,6 -CR 17 R 18 -CR ]9 R 20 R 21 , -0-CR 13 R ,4 -CR I5 R I6 R 21 , -0-CR 13 R 14 -CR I5 R 16 -CR 17 R 18 R 21 , -S0 2 R 22 , -CONR 23 R 24 , -NR 25 COR 22 , -O-CR 13 R 1 -CR 15 R 16 -CR 17 R 18 -CR 19 R 20 R 21 , -NR 25 S0 2 NR 23 R 24 , -NR 25 S0 2 R 22 , -NR 25 CONR 23 R 24 , -S0 2 NR 23 R 24 , -SO(NR 26 )R 27 , -NH-CO-NH-Ph; R 13 - R 21 , R 29 - R 32 and R 33 - R 48 represent independently of each other -H, -F, -CI, -Br, -I; ¾-¾26 ' IS ~~~Π,— , -CH(CH 3 )-C 2 H 5 , -C(CH 3 ) 3 , -C 5 H„, -CH(CH 3 )-C 3 H 7 , -CH 2 -CH(CH 3 )-C 2 H 5 , -CH(CH 3 )-CH(CH 3 ) 2 , -C(CH 3 ) 2 -C 2 H 5 , C ' !I; (CI1;);. -CH(C 2 H 5 ) 2 , -C 2 H 4 -CH(CH ) 2 , -C 6 H 13 , — C 3 H— CH(CH 3 ) 2 , — C2H4— CH(CH 3 )— C2H5, — CH(CH 3 )— C4H9, -CH 2 -CH(CH 3 )-C 3 H 7 , -CH(CH 3 )-CH 2 -CH(CH 3 ) 2 , -CH(CH 3 )-CH(CH 3 )-C 2 H 5 , -CH 2 -CH(CH 3 )-CH(CH 3 ) 2 , -CH 2 -C(CH 3 )2-C 2 H 5 , -C(CH 3 ) 2 -C 3 H 7 , -C(CH 3 ) 2 -CH(CH 3 ) 2 , -C 2 H 4 -C(CH 3 ) 3 , -CH(CH 3 )-C(CH 3 ) 3 , -CR 13 R 14 R 21 , -COR 28 , -CR 13 R 14 -CR , 5 R I 6 R 21 , -CR 13 R I4 -CR 15 R 16 -CR 17 R , 8 -CR 19 R 20 -CR 29 R 30 R 21 , -CR 13 R ,4 -CR 15 R I6 -CR I 7 R I8 R 21 , -CR 13 R , 4 ^CR 15 R , 6 ~CR 17 R 18 -CR I 9 R 20 R 21 , -CR 13 R 14 -CR 15 R 16 -CR 17 R 18 -CR 19 R 20 -CR 29 R 30 -CR 3 I R 32 R 2, , -COOR 28 , these C 3 -C6-cycloalkyl groups may further be substituted by one, two, three, four, five or more substituents selected from the group consisting of R 33 - R \"*0 ; R \" R 27 , and R 28 are independently selected from -CR 49 R 50 R 51 , -CR 49 R 50 -CR 52 R 53 R 51 , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -CR 56 R 57 -CR 58 R 59 R 51 , _ CR 49 R 50_ CR 52 R 5 3 _ CR 54 R 55 R 51 ; _ C R 49 R 50 -CR 5 R 53 -CR 54 R 55 -CR 56 R 57 R 51 , -CR 49 R 50 -CR 5 R 53 -CR 54 R 55 -CR 56 R 57 -CR 58 R 59 -CR 60 R 61 R 51 , -CH 2 Ph, -CH 2 Ph the phenyl group of which may further be substituted by one, two, three, four or five substituents selected from the group consisting of R 5 - R 12 ; C 3 -Ce-cycloalkyl groups listed for R 26 , which may further be substituted by one, two, three, four, five or more substituents selected from the group consisting of R 3j - R 48 ; R - R represent independently of each other -H, -CH 3 , -C2H5, (\\H-. -C 4 H 9 , F. -CI, -Br, -I, -OH, NC -NH 2 ; R 23 and R 24 are independently selected from -H, -CR 49 R 50 R 5! , -CR 49 R 50 -CR 5 R 5 R 51 , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -CR 56 R 57 ^CR 58 R 59 R 51 , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 R 51 , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -CR 56 R 57 R 51 , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -CR 56 R 57 -CR 58 R 59 -CR 60 R 61 R 51 , -CR 49 R 50 -CR 52 R 53 -O-R 51 ' , -CR 49 R 50 -CR 5 R 53 -CR 54 R 55 -O-R 51 ' , -CR 49 R 50 -CR 52 R 53 -NR 5 r R 51 \" , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -NR 5 r R 51 \" , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -CR 56 R 57 -NR 51 ' R 51 \" , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -CR 56 R 57 -CR 58 R 59 -NR 51 ' R 51 \" , phenyl, substituted phenyl, benzyl, substituted benzyl, or both residues R 23 and R 24 together form with the nitrogen atom to which they are attached a izetidine, pyrrolidine, piperidine, piperazine, azepane, or morpholine ring; R and R represent independently of each other -H, -CH 3 , -C2H5, -C 3 H 7 , -C4H9, -CH 2 Ph, -COOC(CH 3 ) 3 , -COOCH 3 , -COOCH 2 CH 3 , -COOCH 2 CH 2 CH 3 , -COOCH(CH 3 ) 2 , -COOCH 2 Ph, -COCH 3 ; and R 25 is -H, -CH 3 , -C 2 H 5 , -C 3 H 7 , -CH(CH 3 ) 2 , -C4H9, -CH 2 -CH(CH 3 ) 2 , -CH(CH 3 )-C 2 H 5 , -C(CH 3 ) 3 ; R 4 is selected from -H, -N0 2 , -NH 2 , -CN, -F, -CI, -Br, -I, -CR 62 R 63 R 64 , CON! i.;. -SO 2 CH 3 , -S0 2 C 2 H 5 , -S0 2 C 3 H 7 , -NH-S0 2 -CH 3 , -NH-S0 2 -C 2 H 5 , -NH-SO2-C 3 H 7 , -NHCO-CH 3 , -NHCO-C 2 H 5 , -NHCO-C 3 H 7 , -S0 2 NR 23 R 24 , -CH 2 -S0 2 NR 23 R 24 , -C 2 H 4 -S0 2 NR 23 R 24 , -C 3 H 6 -S0 2 NR 23 R 24 , -S0 2 NH 2 , -CH 2 -S0 2 NH 2 , -C : I L S():NI I;. -C 3 H 6 -S0 2 NH 2 , -0-CR 62 R 63 -CR 65 R 66 R 64 , — O— CR 62 R 63 — CR 65 R 66 — CR 67 R 68 R 64 — CR 62 R 63 — CR 65 R 66 — CR 67 R 68 — CR 69 R 70 R 64 -O-CR c ¾ 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 R 64 , -CR 62 R 63 -CR 65 R 66 -CR 67 R 68 R 64 , -O-CR 62 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 7, R 72 R 64 , -CR 62 R 63 -CR 65 R 66 R 64 , -O-CR 62 R 63 ^CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 71 R 72 -CR 73 R 74 R 64 , -0-CR 62 R 63 R 64 , -CR 6 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 71 R 72 R 64 , -CR 62 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 71 R 72 -CR 73 R 74 R 64 , -OCH 2 Ph, these C 3 -C6-cycloalkoxy groups and C 3 -C6-cycloalkyl groups may further be substituted by one, two, three, four, five or more substituents selected from the group consisting of R 3j - R 48 ; R 62 - R 74 represent independently of each other -H, -cyclo-C 3 Hs, cvdo-( ; ! !-. -cyclo- C 5 H 9 , -CR 75 R 76 R 77 , -CR 75 R 76 -CR 78 R 79 R 77 , -CR 75 R 76 -CR 78 R 79 -CR 80 R 81 R 77 , -CR 75 R 76 - CR 78 R 79 -CR 80 R 79 -CR 82 R 81 R 77 , -F, -CI, -Br, -I, -Ph; R - R represent independently of each other -H, -F, -CI, -Br, -I, -NH 2 ; R 4 together with R 22 , R 23 , R 24 , or R 2~ may form a group -CH 2 CH 2 - or -CH 2 CH 2 CH 2 - if R 4 is attached ortho to -L-R 3 ; R 2 is R is selected from -H, -OH, -N0 2 , -CN, -F, -CI, -Br, -I, -NR 2j R / ~!T τ V^IV IV Iv , — _-J\\. IX —IN IV CR 62 R 63 -CR 65 R 66 -NR 2 -CR 62 R 63 -CR 65 R 66 -CR 67 R 68 R 64 , -CR 6 R 63 -CR 65 R 66 -CR 67 R 68 -NR 23 R 2' -O-CR R R . 0-CR 62 R 63 -CR 05 R 00 R 04 , -CHO ηττ Αττ 23' -CR 23' 0, H.OR R 23 and R 24 represent independently of each other -H, CF . -C 2 H5, -C3H7, -CH(CH 3 ) 2 , -C4H9, -CH 2 -CH(CH 3 ) 2 , -CH(CH 3 )-C 2 H 5 , -C(CH 3 ) 3 ; -(cyclo-C 3 H 5 ); x is a value between 0 and 3; B is a bond, -CR 86 R 87 -, -CR 86 R 87 -CR 88 R 89 -, -CR 86 R 87 -CR 88 R 89 -CR 90 R 9i -, -CR 86 R 87 -CR 88 R 89 -CR 90 R 91 -CR 92 R 93 -, -CR 86 R 87 -CR 88 R 89 -CR 90 R 91 -CR 92 R 93 -CR 94 R 95 -, -CR 86 R 87 -CR 88 R 89 -CR 90 R 91 -CR 92 R 93 -CR 94 R 95 -CR 96 R 97 -; R 86 - R 97 represent independently of each other -H, -CH 3 , -C2H5, — C 3 H 7 , — C4H9, — F, —CI, —Br, —I; V is a bond. -0-, -S-, - SO--. -SO : - . SO : \\ l F . NHS ( ) . CO -COO-, -OOC-, -CONH-, -NHCO-, -NH- -N(CH 3 )-, -NH-CO-NH-, -0-CO-NH-, -NH-CO-0-; R 84 is selected from a bond, -CR 86 R 87 -, -CR 86 R 87 -CR 88 R 89 -CR 90 R 91 -, -CR 86 R 87 -CR 88 R 89 -CR 90 R 91 -CR 92 R 93 -, _ CR 86 R 87_ CR 88 R 89_ CR 90 R 91__ CR 92 R 93__ CR 94 R 95_ „ C R 86 R 87 -CR 88 R 89 -, _ CR 86 R 87_ CR 88 R 89_ CR 90 R 91__ CR 92 R 93_ CR 94 R 95_ CR 96 R 97_ R 85 is selected from (i) -H, -OH, -OCH,, -OC 2 H 5 , -OC 3 H 7 , -0-cyclo-C 3 H 5 , -OCH(CH 3 ) 2 , -OC(CH 3 ) 3 , -OC 4 H 9 , -Ph, -OPh, -OCH 2 -Ph, -OCPh 3 , -SH, -SCH 3 , -SC 2 H 5 , -SC 3 H 7 , -S-cyclo-C 3 H 5 , -SCH(CH 3 ) 2 , -SC(CH 3 ) 3 , -SC4H9, -N0 2 , -F, -CI, -Br, -I, -P(0)(OH) 2 , -P(0)(OCH 3 ) 2 , -P(0)(OC 2 H 5 ) 2 , -P(0)(OCH(CH 3 ) 2 ) 2 , -Si(CH 3 ) 2 (C(CH 3 )3), -Si(C 2 H 5 ) 3 , -Si(CH 3 ) 3 , -CN, -CHO, -COCH 3 , -COC 2 H 5 , -COC 3 H7, -CO-cyclo-C 3 H 5 , -COCH(CH 3 ) 2 , -COC(CH 3 ) 3 , -COC4H 9 , COOH, -COOCH3, -COOC 2 H 5 , -COOC3H7, -COOC 4 H 9 , -COO-cyclo-C 3 H 5 , -COOCHiCH^, -COOC(CH 3 ) 3 , -OOC-CH 3 , -OOC-C 2 H 5 , -OOC-C3H7, -OOC-C4H9, -OOC-cyclo-C 3 H 5 , -OOC-CH(CH 3 ) 2 , -OOC-C(CH 3 ) 3 , -CONR 23 R 24' , -NHCOCH 3 , -NHCOC2H5, -NHCOC3H7, -NHCO-cyclo-C 3 H 5 , -NHCO-CH(CH 3 ) 2 , -NHCOC 4 H 9 , -NHCO-C(CH 3 ) 3 , -NHCO-OCH 3 , -NHCO-OC 2 H 5 , -NHCO-OC3H7, -NHCO-0-cyclo-C 3 H 5 , -NHCO-OC 4 H 9 , -NHCO-OCH(CH 3 ) 2 , -NHCO-OC(CH 3 ) 3 , -NHCO-OCH 2 Ph, -NR 23 R 24 , -CF 3 , -SOCH 3 , -SOC 2 H 5 , -SOC 3 H7, -SO-cyclo-C 3 H 5 , -SOCH(CH 3 ) 2 , -SOC(CH 3 ) 3 , -S0 2 CH 3 , -S0 2 C 2 H 5 , -SO C 3 H 7 , -S0 2 -cyclo-C 3 H 5 , -S0 2 CH(CH 3 ) 2 , -S0 2 C 4 H 9 , -S0 2 C(CH 3 ) 3 , -SO 3 H, -S0 2 NR 2 R 24' , -OCF 3 , -OC 2 F 5 , -0-COOCH 3 , -0-COOC 2 H 5 , -O-COOC 3 H 7 , -0-COO-cyclo-C 3 H 5 , -O-COOC4H9, -0-COOCH(CH 3 ) 2 , -0-COOCH 2 Ph, -0-COOC(CH 3 ) 3 , NH -CO NH : . NH CO NHCH , -NH-CO-NHC 2 H 5 , -NH-CO- HC3H7, -NH-CO- HC4H9, -NH-CO-NH-CVCI0-C 3 H 5 , -OCH 2 -cyclo-C 3 H 5 , -NH-CO-NH[CH(CH 3 ) 2 ], -NH-CO-NH[C(CH 3 ) 3 ], -NH-CO-N(CH 3 ) 2 , -NH-CO-N(C 2 H 5 ) 2 , -NH-CO-N(C 3 H 7 ) 2 , -NH-CO-N(C 4 H 9 ) 2 , -NH-CO-N(cyclo-C 3 H 5 ) 2 , -NH-CO-N[CH(CH 3 ) 2 ] 2 , -NH-CO-N[C(CH 3 ) 3 ] 2 , -NH-C(=NH)-NH 2 , -NPi-C(=NFf)-NHCH 3 , -NH-C(=NH)-NHC 2 H 5 , -NH-C(=NH)- HC 3 H 7 , -NH-C(=NH)-NHC 4 H 9 , -NH-C(=NH)-NH-cyclo-C 3 H 5 , -NH-C(=NH)-NH[CH(CH 3 ) 2 ] , -NH-C(=NH)-NH[C(CH 3 ) 3 ] , -NH-C(=NH)-N(CH 3 ) 2 , -NH-C(=NH)-N(C 2 H 5 ) 2 , -NH-C(=NH)-N(C 3 H 7 ) 2 , -NH- C(=NH)-N(cyclo-C 3 H 5 ) 2 , -NH-C(=NH)-N(C 4 H 9 ) 2 , -NH-C(=NH)-N[CH(CH 3 ) 2 ] 2 , ~NH^C(=NH)-N[C(CH 3 ) 3 ] 2 , -0-CO-NH 2 , -O-CO-NHCH3, -O-CO-NHC 2 H 5 , -0-CO-NHC 3 H 7 , -O-CO-NHC4H 9 , -O-CO-NH- cyclo-C 3 H 5 , -0-CO-NH[CH(CH 3 ) 2 ], -0-CO-NH[C(CH 3 ) 3 ], -0-CO-N(CH 3 ) 2 , -0-CO-N(C 2 H 5 ) 2 , -0-CO-N(C 3 H 7 ) 2 , -0-CO-N(C 4 H 9 ) 2 , -0-CO-N(cyclo-C 3 H 5 ) 2 , -0-CO-N[CH(CH 3 ) 2 ] 2 , -0-CO-N[C(CH 3 ) 3 ] 2 , (ii) an aromatic or heteroaromatic mono- or bicyclic ring selected from 2- thienyl, 3-thienyl, 2-furanyl, 3-furanyl, 2-oxazolyl, 3-oxazolyl, 4-oxazolyl, 2-thiazolyl, 3-thiazolyl, 4-thiazolyl, 1-pyrazolyl, 3-pyrazolyl, 4- pyrazolyl, 5-pyrazolyl, 1 -imidazolyl. 2-imidazolyl, 4-irnidazolyl, 5- imidazolyl, phenyl, 1 -naphthyl, 2-naphthyl, 2-pyndyl, 3-pyndyl, 4-pyridyl, 2-pyrimidinyl, 4-pyrimidinyl, 5-pyrimidinyl, 2-pyrazinyl, 3- pyridazinyl, 4-pyridazinyl, l,3,5-triazin-2-yl, which optionally may be substituted by one or two substituents selected from -F, -CI, Br, ~I. -OCH 3 , -CH 3 , -NO,, -CN, -C : (iii) a saturated ring selected from cyclopentyl, azetidin-l -yl, R represents -H. -CH 3 , -CH 2 Ph, -COOC(CH 3 ) 3 , -COOCH 3 , -COOCH 2 CH 3 , -COOCH 2 CH 2 CH 3 , -COOCH(CH 3 ) 2 , -COOCH 2 Ph, the group -B-Y-R ' -R \" together with one substituent R ' may fonn a group -OCH 2 0- if R 83 is attached in position ortho to -B-Y-R 84 -R 85 ; with the pruviso that R \" is not -H, if the group -B-Y-R -R is hydrogen. R 98 is selected from -N0 2 , -CN, -F, -CI, -Br, -1, -NH 2 , -OH, -CR 62 R 63 R 64 , -CR 62 R 63 -CR 65 R 66 R 64 , -CR 62 R 63 -CR 65 R 66 -CR 67 R 68 R 64 , _ CR 62 R 63_ CR 65 R 66_ CR 67 R 68_ CR 69 R 70 R 64 5 _ 0 _ CR 62 R 63 R 64^ -0-CR 62 R 63 -CR 65 R 66 R 64 , -0-CR 2 R 63 -CR 65 R 66 -CR 67 R 68 R 64 , -U-CR K ^ - K'R\" -CR ' R ^ - -'R , -O-CR 62 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 71 R 72 R 64 , -O-CR 62 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 71 R 72 -CR 73 R 74 R 64 , -CR 62 R 63 -0-CR 65 R 66 R 64 , -CR 62 R 63 -0-CR 65 R 66 -CR 67 R 68 R 64 , _ CR 62 R 63_ o _ CR 65 R 66_ CR 67 R 68_ CR 69 R 70 R 64 5 -CR 62 R 63 -O-CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 7! R 72 R 64 , -CR 62 R 63 -O-CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 7, R 72 -CR 7 R 74 R 64 , ^CR 62 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 71 R 72 R 64 , -CR 62 R 63 -CR 65 R 66 -CR 67 R 68 ^CR 69 R 70 -CR 71 R 72 -CR 73 R 74 R 64 , -OCH 2 Ph, -OCH 2 -CH 2 -Ph, -CH 2 -0-CH 2 -Ph; with the proviso that R 98 is attached to a position ortho to the bond between the pyridine and the triazine ring if R 98 is not an amino group in para position to the bond between the pyridine and the triazine ring; R 100 is selected from -H, -N0 2 , -CN, -F, -CI, -Br, -I, -NH 2 , -OH, -CF 3 , -CH 3 , -CH2CH3, -CH2CH2CH3, -CH(CH 3 ) 2 , -OCH3, -OCH2CH3, -OCH2CH2CH3, -OCH(CH 3 ) 2 , -OCF 3 , -OCH 2 Ph; and with the proviso that if R 1 is a phenyl moiety and R 2 is also a phenyl moiety a chloro substituent is only allowed on the R 1 phenyl moiety or on the R 2 phenyl moiety but not on both simultaneously; and with the proviso that the compound 4-[4-(2-benzoylaminophenyl)-[l,3,5]triazin-2- ylaminojbenzamide is excluded; and enantiomers, stereoisomeric fon-ns, mixtures of enantiomers, diastereomers, mixtures of diastereomers, prodrugs, hydrates, solvates, acid salt forms, tautomers, and racemates of the above mentioned compounds and pharmaceutically acceptable salts thereof or salts of solvates thereof. The method of claim 4, wherein R 1 represents in which L is a bond, -CH 2 - -CH 2 CH 2 - or -CF 2 -; R 3 is -SO2NH2, -S0 2 NH(CH 3 ), -S0 2 N(CH 3 ) 2 , -S0 2 NH(CH 2 CH 2 OCH 3 ), -NHSO 2 CH 3 , -NHSO 2 CH 2 CH 3 , -NHSO 2 CH 2 CH 2 CH 3 , -NHS0 2 CF 3 , -S0 2 CH 3 , -NHS0 2 NH 2 , -SO(NH)CH 3 ; in which the group -B-Y-K -K is -UCH 3 , -L)CH 2 CH 3 , -OCH 2 C¾CH 3 , -OCH 2 CH 2 CH 2 C¾ -OCH(CH 3 ) 2 , -OPh, -OCH 2 Ph, -OCH 2 (4- pyridyl); R 83 is H. ~~F, or -CI; x is 0, 1, or 2; R 98 is -OCH 3 and R 100 is -H, with the proviso that R 98 is attached to a position ortho to the bond between the pyridine and the triazine ring. The method of claim 4 or 5, wherein R 1 represents in which the substituent -L-R 3 is SO : M I ; . -CH 2 S0 2 NH 2 , -CH 2 CH 2 S0 2 NH 2 , -CF 2 S0 2 NH 2 , M ISOAH:. --CH 2 NHS0 2 NH 2 , -S0 2 CH 3 , -SO(NH)CH 3 , -CH 2 SO(NH)CH 3 ; R is -H; R 2 represents 2-methoxyphenyl, 4-fluoro-2-methoxyphenyl, or 6-fluoro-2-methoxyphenyl. The method of claim 4, wherein L is a bond, -CH 2 - or -CH 2 CH 2 -; R 3 is -H, -S0 2 NR 23 R 24 , -CONR 23 R 24 , -N0 2 , -NH 2 , -NHS0 2 R 22 , -NHCOR 22 , -S0 2 R 22 , -NH-CO-NH- Ph. or -Ph, R 4 is -H, -C¾-S0 2 NR 23 R 24 , -SG 2 NR 23 R 24 , -CONH 2 , -C 2 H4-S0 2 NR. 23 R 24 , -NH-SO 2 -CH 3 , -NH-S0 2 -C,H 5 , -NH-S0 2 -C 3 H 7 , -NHCO-CH 3 , -NHCO-C 2 H 5 , -N0 2 , -NH 2 , -S0 2 CH 3 , or O R 23 and R 24 are independently selected from -H, -CH 3 , -C 2 H 5 , -C 3 H 7 , -(cyclo-C 3 H 5 ), CH 2 -CH 2 -CH 2 -CH 2 -NH 2 , or -CH 2 -CH 2 -CH 2 -CH 2 -NH-COOC(CH 3 ) 3 , R 2 represents B is a bond or -CH 2 -; Y is a bond, -0-, or -NH-; * is selected from -H, -CN, -F, -CI, -0-CR b R 6 , R , -CH 2 OR 23 ', -CR 23 '0, -CR 62 R 63 -NR 23 R 24' , -CR 62 R 63 R 64 ; R 23 ' and R 24 ' represent independently of each other -H. -CH 3 , -(cyclo-CiHs); R - R ' represent independently of each other -H, -CH 3 , -Ph, -F, -cyclo-C 3 H 5 ; R is selected from a bond, -CH 2 -, or t ' H - H- C ' ! 1- C I i - : R ■ is selected from -H, -CF 3 , -GCH 3 , -OCH(CH 3 ) 2 , -CN, -NHCOCH 3 , -OCH 2 -cyclo-C 3 H 5 , -M R , -Ph, -OPh, -NHCO-OC(CH 3 ) 3 , W represents -OCH 3 ; and salts, solvates or salts of solvates of the afore-mentioned compounds and especially the hydrochloride salt or the trifluoroacetate salt of these compounds. The method of claim 4, wherein R 1 represents in which the substituent -L -R is -S0 2 NH 2 or -CH 2 S0 2 NH 2 , R 4 is ~H; R represents 2-methoxyphenyl, 4-fluoro-2-methoxyphenyl or 2-benzyloxyphenyl, or their salts, solvates or salts of solvates and especially the hydrochloride salt or the trifluoroacetate salt. The method of claim 4, wherein the compound is selected from the group consisting of 3-[(4-(2-Methoxyphenyl)-l ,3,5-triazin-2-yl)amino]benzenemethanesulfonamide, 3-[(4-(4-Fluoro-2-methoxyphenyl)-l ,3,5-triazin-2-yl)amino]benzenemethane-sulfonamide, 3-[(4-(5-Fluoro-2-methoxyphenyl)-l ,3,5-triazin-2-yl)amino]benzenemethane-sulfonamide, 3-[(4-(6-Fluoro-2-methoxyphenyl)-l ,3,5-triazin-2-yl)amino]benzenemethane-sulfonamide, 3-[(4-(3,5-Difluoro-2-methoxyphenyl)-l ,3,5 riazin-2-yl)aminoJbenzenemethane- sulfonamide, 3-[(4-(4-Chloro-2-methoxyphenyl)-l ,3,5-triazin-2-yl)amino]benzenemethane-sulfonamide, 3-[(4-(5-Chloro-2-methoxyphenyl)- 1 ,3 ,5-triazin-2-yl)amino]benzenemethane-suifonamide, 3-[(4-(2-Methoxy-4-trifluoromethyl-phenyl)- 1 ,3 ,5-triazin-2-yl)amino]benzene- methanesulfonamide, 3-[(4-(2-Methoxy-5-trifluoromethyl-phenyl)-l ,3,5-triazin-2-yl)amino]benzene- methanesul fonamide, 3-[(4-(5-Hydroxymethyl-2-methoxyphenyl)-l ,3,5-triazin-2-yl)amino]benzene- methanesulfonamide, 3-[(4-(5-Formyl-2-methoxyphenyl)-l ,3,5-triazin-2-yl)amino]benzenemethane-sulfonamide, 3-[(4-(2-Ethoxyphenyl)-l ,3,5-triazin-2-yl)amino]benzenemethanesulfonamide, 3-[(4-(2-Benzyioxyphenyl)- 1 ,3 ,5-triazin-2-yl)amino] benzenemethanesulfonamide, l-(3-{[4-(2-phenoxyphenyl)-l ,3,5-triazin-2-yl]amino}phenyl)methanesulfonamide, 3-[(4-(l ,3-Benzodioxol-4-yl)-l ,3,5-triazin-2-yl)amino]benzenemethanesulfonamide, 3-[(4-(2-((4-Pyridinyl)methoxy)phenyl)-1 ,5 riazin-2-yl)amino]benzenemethane- sulfonamide, 3- (4-(2-(4-(tert-Butoxycarbonylamino)butoxy)phenyl)-l,3,5-triazin-2-yl)amino]- benzenemethanesulfonamide, 3-[(4-(4-Methoxypyridin-3-yl)-l,3,5-triazin-2-yl)amino]benzenemethane-sulfonamide, 3-[(4-(3-Methoxypyridin-4-yl)-l ,3^-triazin-2-yl)amino]benzenemethane-sulfonami 3-[(4-(2-((Mo holin-4-yl)methyl)phenyl)-l ,3,5-triazin-2-yl)amino]benzene- methanesulfonamide, 3-[(4-(2-((Piperidin-l-yl)methyl)phenyl)-l,3,5-triazin-2-yl)amino]benzene- methanesulfonamide, 3-[(4-(2-(Cyclopropylamino-methyl)phenyl)-l ,3,5-triazin-2-yl)amino]benzene- methanesulfonamide, 3-[(4-(6-Aminopyridin-3-yl)-l,3,5-triazin=2-yl)amino]benzenemethane-sulfonamide, 3-[(4-(2-(Me1iioxymethyl)phenyl)-l,3,5-triazin-2-yl)amino]benzene-methan 3-[(4-(2-Methoxyphenyl)- 1 ,3 ,5-triazin-2-yl)amino]benzenesulfonamide, 2-[3-((4-(2-Methoxyphenyl)-l ,3^-triazin-2-yl)amino)phenyl]ethanesulfonamide, 2- [3-((4-(4-Fluoro-2-methoxyphenyl)-l ,3,5-tri^ 3- [(4-(2-Methoxyphenyl)-l,3,5-triazin-2-yl)amino]benzamide, 6-[(4-(2-Methoxyphenyl)-l ,3,5-triazin-2-yl)amino]-2,3-dihydro-lH-in^ rac-S-[3-((4-(2-Methoxyphenyl)-l ,3,5-triazin-2-yl)amino)phenyl]-N-ethoxy-carbonyl-S- methyl-sulfoximide, 4- (2-Methoxyphenyl)-N-(3-nitrophenyl)-l,3,5-triazine-2-amine, 3-[(4-(2-(4-Aminobutoxy)phenyl)-l,3,5-triazin-2-yl)amino]benzenemethane-sulfonam N-(3-Aminophenyl)-4-(2-methoxyphenyl)-l,3,5-triazine-2-amine, N-[3-((4-(2-Methoxyphenyl)-l,3,5-triazin-2-yl)amino)phenyl]-methanesulfonamide N-[3-((4-(2-Methoxyphenyl)-l ,3,5-1xiazin-2-yl)amino)phenyl]-propanesulfonamide, N-[3-((4-(2-Methoxyphenyl)- 1 ,3,5-triazin-2-yl)amino)phenyl]acetamide, N-[3-((4-(2-Methoxyphenyl)-l ,3,5-triazin-2-yl)amino)phenyl]-N'-phenyl-urea, 3- [(4-(2-Methoxy-5-(methylamino-methyl)phenyl)- 1 ,3 ,5-triazin-2-yl)amino]- benzenemethanesulfonamide, 4- (2-Methoxyphenyl)-N-phenyl- 1 ,3,5-triazine-2-amine, tert-Butyl-[4-((3-((4-(4-Fluoro-2-methoxyphenyl)-l ,3,5- azin-2-yl)amino)phenyl)- methylsulfonamido) butyl ] carbamate , N-(4-Aminobutyl)-l-[3-((4-(4-fluoro-2-methoxyphenyl)-l ,3,5-triazin-2-yl)amino)- phenyl]methanesulfonamide, 4-(2-Methoxyphenyl)-N-(3-(methylsulfonyl)phenyl)-l,3,5-triazin-2-amine, 4-[(4-(2-Methoxyphenyl)- 1 ,3 ,5-triazin-2-yl)amino]benzenemethane-sulfonamide, 1 - [3 -( {4-[4-fluoro-2-(trifluoromethyl)phenyl] -1 ,3,5 -triazin-2-yl } amino)phenyl] - methanes lfonamide, l-[3-({4-[4-fluoro-2-(propan-2-yloxy)phenyl]-l ,3,5-triazin-2-yl}amino)phenyl]- methanesulfonamide, l-(3-{[4-(2-cyano-4-fluorophenyl)-l ,3,5-triazin-2-yl]amino}phenyl)methane-sulfonamide, N-[5-fluoro-2-(4- {[3-(sulfamoylmethyl)phenyl]amino}-l,3,5-triazin-2-yl)phenyl]-acetamide, 1 -[3-( {4-[2-(cyclopropylmethoxy)-4-fluoroplienyl]- 1 ,3 ,5-triazin-2-yl} amino)phenyl]- methanesulfonamide, l-(3-{[4-(3,4-difluoro-2-methoxyphenyl)-l ,3,5-triazin-2-yl]amino}phenyl)methane- sulfonamide, l-(3-{[4-(4,5-difluoro-2-methoxyphenyl)-l ,3,5-triazin-2-yl]amino}phenyl)methane- sulfonamide, 4-(4-fluoro-2-methoxyphenyl)-N-[6-(meth^ 3-[(4-(2-Methoxyphenyl)-l,3,5-triazin-2-yl)amino]benzenemethanesulfonam tnfluoroacetic acid salt, l-(3- {[4-(4-fluoro-2-methoxyphenyl)-l ,3,5- hydrochloride, 3-[(4-(4-Fluoro-2-methoxyphenyl)-l,3,5-triazin-2-yl)amino]benzene-methanesulfonamide tnfluoroacetic acid salt, 3-[(4-(2-Benzyloxyphenyl)-l ,3,5-triazin-2-yl)amino] benzenemethanesulfon-amide trifluoroacetic acid salt, 3 - [(4-(2 -Methoxyphenyl) - 1 ,3 ,5-triazin-2-yl)amino]benzenesulfonamide trifluoroacetic acid salt. The method of any of claims 1 to 3, wherein said inhibitor is selected from the group consisting of 3-[(4-(2-Methoxyphenyl)-l,3,5-triazin-2-yl)amino]benzenemethanesulfonamide (Cpd Bl); 3-[(4-(4-Fluoro-2-methoxyphenyl)-l ,3,5-triazin-2-yl)amino] benzenemethanesulfonamide (Cpd B2); 3-[(4-(5-Fluoro-2-methoxyphenyl)-l,3,5-triazin-2-yl)amino] benzenemethanesulfonamide (Cpd B3); 3-[(4-(6-Fluoro-2-methoxyphenyl)-l ,3,5-triazin-2-yl)amino] benzenemethanesulfonamide (Cpd B4); 3-[(4-(4-Chloro-2-methoxyphenyl)- 1 ,3 ,5-triazin-2-yl)amino] benzenemethanesulfonamide (Cpd B6); 3-[(4-(5-Chloro-2-methoxyphenyl)-l ,3,5-triazin-2-yl)amino] benzenemethanesulfonamide (Cpd B7); 3-[(4-(2-Ethoxyphenyl)-l ,3,5-triazin-2-yl)amino]benzenemethanesulfonamide (Cpd B12); 3-[(4-(2-Benzyloxyphenyl)-l ,3,5-triazin-2-yl)amino] benzenemethanesulfonamide (Cpd B13); 1 -(3- {[4-(2-phenoxyphenyl)-l ,3,5-triazin-2-yl]amino}phenyl)methanesulfonamide (Cpd B14); 3-[(4-(2-((4-Pyridinyl)methoxy)phenyl)-l ,3,5-triazin-2-yl)amino]benzenemethanesulfonamide (Cpd B 16); 3-[(4-(2-(4-(tert-Butoxycarbonylamino)butoxy)phenyl)-l ,3,5-triazin-2- yl)amino]benzenemethanesulfonamide (Cpd B17); 3-[(4-(3-Methoxypyridin-4-yl)-l ,3,5 riazin-2-yl)amino]benzenemethanesulfonamide (Cpd B18); 3-[(4-(6-Aminopyridin-3-yl)-l,3,5-triazm-2-yl)amino]benzenemethanesulfonamide (Cpd B23); 3- [(4-(2-Methoxyphenyl)-l ,3,5-triazin-2-yl)amino]benzenesulfonamide (Cpd B24); 2- [3-((4-(2-Methoxyphenyl)-l,3,5-triazin-2-yl)amino)phenyl]ethanesulfonamide (Cpd CI); N-[3-((4-(2-Metb±ox phenyl)-l,3,5 ria^ (Cpd Dl); N-[3-((4-(2-Methoxyphenyl)-l ,3,5-triazin-2-yl)amino)phenyl]-propanesulfonamide (Cpd LI ); tcrt-Butyl [4-((3-((4-(4-Fluoro-2-methoxyphenyl)- 1 ,3,5-triazin-2- yl)amino)phenyl)methylsulfonamido) butyl] carbamate (Cpd Ql ); N-(4-Aminobutyl)-l -[3-((4-(4-fluoro-2-methoxyphenyl)-l,3,5-triazin-2- yl (amino )phenyl]mcthanesulfonamidc (Cpd Rl); 4- (2-Methoxyphenyl) T -(3-(methylsulfonyl)phenyl)-l ,3,5-triazin-2-amine (Cpd SI); l-[3-({4-[4-Fluoro-2-(propan-2-yloxy)phenyl]-l ,3,5-triazin-2- yl}amino)phenyl]methanesulfonamide (Cpd U2); l-[3-({4-[2-(Cyclopropylmethoxy)-4-fluorophenyl]-l,3,5-triazin-2- yl}amino)phenyl]methanesulfonamide (Cpd U5); l-(3-{[4-(4,5-Difluoro-2-methoxyphenyl)-l,3,5-triazin-2- yl] amino }phenyl)methanesulfonamide (Cpd U7); 3- [(4-(2-Methoxyphenyl)pyridin-2-yl)amino]benzenesulfonamide (Cpd 24); 4- (2-Methoxyphenyl)-N-(3-(methylsulfonyl)phenyl)pyridin-2-amine (Cpd 25); [3-((4-(4-Fluoro-2-methoxyphenyl)pyridin-2-yl)amino)phenyl]methanesulfonamide (Cpd 26); [3-((4-(2-Methoxyphenyl)pyridin-2-yl)amino)phenyl]methanesulfonamide (Cpd 27); 1- [3-((4-(4-Fluoro-2-methoxyphenyl)pyridin-2-yl)amino)phenyl]-N,N- dimethylmethanesulfonamide (Cpd 28); 2- [3-((4-(2-Methoxyphenyl)pyridin-2-yl)amino)phenyl]ethanesulfonamide (Cpd 29); N-[3-((4-(4-Fluoro-2-methoxyphenyl)pyridin-2-yl)amino)phenyl]methanesulfonamide (Cpd 30); N-[3-((4-(4-Fluoro-2-methoxyphenyl)pyridin-2-yl)amino)phenyl]acetamide (Cpd 31); 1 - [3-((4-(4-Fluoro-2-methoxyphenyl)pyridin-2-yl)amino)phenyl]-N- propylmethanesulfonamide (Cpd 32); (R)-Methyl l-[4-((3-(Sulfamoylmethyl)phenyl)amino)-l ,3,5-triazin-2-yl]piperidine-2- carboxylate (Cpd 33); (R)_3-[(4-(2-(Methoxymethyl)pyrrolidin-l -yl)-l,3,5-triazm-2- yl)amino]benzenemethanesulfonamide (Cpd 34); (R)-Methyl l-[4-((3-(Sulfamoylmethyl)phenyl)amino)-l ,3,5-triazin-2-yl]pyrrolidine-2- carboxylate )Cpd 35); rac-3-[(4-(2-Phenylpyrrolidin-l-yl)-1 ,5-triazin-2-yl)amino]benzenemethanesulfonamide (Cpd 36); (R)-3-[(4-(2-Phenylpyrrolidin- 1 -yl)- 1 ,3 ,5-triazin-2-yl)amino]benzenemethanesulfonamide (Cpd 37); 3-[(4-(7,8-Dihydro-l,6-naphthyridin-6(5H)-yl)-l ,3,5-triazin-2- yl)amino]berizenemethanesulfonamide (Cpd 38); 3-[(4-(3,4-Dihydroquinolin- 1 (2H)-yl)- 1 ,3 ,5-triazin-2-yl)amino]benzenemethanesulfonamide (Cpd 39); 3-[(4-(6J-Dihydro-3H-imidazo[4,5-c]pyridin-5(4H)-yl)-l,3,5-triazin-2- yI )amino]benzenemethanesulfonamide (Cpd 40); 3-[(4-(lH-Pyrrolo[3,4-c]pyridin-2(3H)-yl)-l ,3,5-triazin-2- yl)amino]benzenemethanesulfonamide (Cpd 41); 3-[(4-( yrrolo[3,4-c]pyrazol-5(lH,4H,6H)-yl)-l,3.5-triazin-2- yl)amino]benzenemethanesulfonamide (Cpd 42); 3-[(4-(Indolin-l-yl)-l,3,5- azin-2-yl)amino]benzenemethanesulfonamide (Cpd 43); and (S)-3-[(4-(2-Methylpyrrolidin-l-yl)-l ,3,5-triaziii-2-yl)amino]benzenemethanesulfonamide (Cpd 44). The method of any one of claims 1 to 3, wherein said inhibitor is selected from the group consisting of Piperidine-4-carboxylic acid [5-(5-tert-butyl-oxazol-2-ylmethylsulfanyl)-thiazol-2-yl]-amide (SNS-032); 2- (2-Chloro-phenyl)-5,7-dihydroxy-8-(3-hydroxy-l-methyl-piperidin-4-yl)-chromen-4-one, (flavopiridol); N-(5-((6-(3-aminophenyl)pyrimidin-4-yl)amino)-2-methylphenyl)propane-l -sulfonamide (AX35427); [4-amino-2-(l methoxyphenyl)methanone (R-547); 3- [[6-(2-methoxyphenyl)-4-pyrimidinyl]amino]-Benzenemethanesulfonamide compound (1073485-20-7P); 3- ((6-(2-methoxyphenyl)pyrimidin-4-yl)amino)benzenesulfonamide (AX38679); l ,5,6,7-tetrahydro-2-(4-pyridinyl)-4H-pyrrolo[3,2-c]pyridin-4-one, (PHA767491); 5,6-dichloro-l-b-ribofuranosyl-benzimidazole (DRB); 6-Benzylamino-2[(R)-(r-ethyl-2'-hydroxyethylamino)]-9-isopropylpurine (Roscovitine); 4- [ [4- Amino-5 -(2,6-difluorobenzoyl)thiazol-2-yl] amino] -N-((R)-2-dimethyl amino- 1 - methylethyl)benzamide (AG-012986); 4H-l-Benzopyran-4-one, 2-(2-chlorophenyl)-5,7-dihydroxy-8-[(2R,3S)-2-(hydroxymethyl)-l- methyl-3-pyrrolidinyl]-, hydrochloride (1 : 1) (P276-00); 4- [3-Chloro-5-(4-methylpiperazin-l-yl)benzoylamino]-lH-pyrazole-3-carboxylic acid cyclohexylamide (ZK 304709); 4-(2,6-Dichlorobenzoylamino)-lH-pyrazole-3-carboxylic acid N-(piperidin-4-yl)amide (AT7519); N-[2-(dimethylarnino)ethyl]-2-fluoro-4-[[5-fluoro-4-[2-methyl-l-(l -methylethyl)-lH- imidazol-5-yl]-2-pyrimidinyl]amino] (Compound 7d); [4-[[5-fluoro-4-[2-methyl-l -(l-methylethyl)-lH-imidazol-5-yl]-2- pyTimidinyl]amino]phenyl][(3S)-3-(methylamino)-l-pyrrolidinyl](AZD5597); N-[l ,4-dihydro-3-[4-[[4-(2-methoxyethyl)-l-piperazinyl]methyl]phenyl]-4-oxoindeno[l ,2- ο]ρνταζο1-5-ν1]-Ν ^θφηο1ϊην1-, hydrochloride (1 :2) (RGB-286638); and 4-(2,6-dichlorobenzamido)-N-(l -(methylsulfonyl)piperidin-4-yl)-lH-pyrazole-3-carboxamide (LCQ195/AT931 1). 12. The method of any one of claims 1 to 1 1 , wherein rearrangement in the NUT gene is a tl5;19 translocation as reflected in formation of a Brd4 NUT fusion gene. 13. The method of any one of claims 1 to 1 1 , wherein said rearrangement in the NUT gene is a formation of a NUT variant fusion gene. 14. The method of claim 13, wherein said NUT variant fusion gene is a Brd3 NUT fusion gene. 15. The method of any one of claims 12 to 14, wherein said rearrangement in the NUT gene is reflected in expression of the formed NUT fusion gene and whereby the expression level of the formed NUT fusion gene is detected. 16. The method of claim 15, wherein the expression level is detected by an immunohistochemical method, real-time PCR, and^or Northern Blot. 17. The method of any one of claims 1 to 14, wherein said rearrangement in the NUT gene is detected by an in situ hybridization method. The method of claim 17, wherein the in situ hybridization method is selected from the group consisting of fluorescent in situ hybridization (FISH), chromogenic in situ hybridization (CISH) and silver in situ hybridization (SISH). Use of an oligo- or polynucleotide capable of detecting at least one rearrangement in the NUT gene for diagnosing sensitivity to a selective CD 9 inhibitor as defined in any one of claims 1 to 1 1. The use of claim 19 wherein said oligonucleotide is about 15 to 100 nucleotides in length, A method of monitoring the efficacy of a treatment of NUT midline carcinoma (NMC) in a subject/patient suffering from said disorder or being prone to suffering from said disorder comprising the steps: a) determining in a cell or tissue sample obtained from said subject/patient the presence of at least one rearrangement in the NUT gene; and b) comparing the rearrangement status in the NUT gene as determined in a) with a reference or control rearrangement status in the NUT gene, wherein the extent of the difference between said rearrangement status determined in a) and said reference rearrangement status is indicative for said efficacy of a treatment of NUT midline carcinoma (NMC). The method of claim 21, wherein the treatment of NUT midline carcinoma (NMC) comprises treatment with a selective CD 9 inhibitor as defined in any one of claims 1 to 1 1. A method of predicting the efficacy of a treatment of NUT midline carcinoma (NMC) for a subject/patient suffering from said disorder or being prone to suffering from said disorder comprising the steps of a) determining in a cell or tissue sample obtained from said subject/patient the rearrangement status in the NUT gene; and b) comparing the rearrangement status in the NUT gene as determined in a) with a reference or control rearrangement status in the NUT gene determined in a cell or tissue sample obtained from a control subject/patient (responder and/or non-responder), wherein the extent of the difference between said rearrangement status determined in a) and said reference rearrangement status is indicative for the predicted efficacy of a treatment of NUT midline carcinoma (NMC). 24. The method of claim 23, wherein the treatment of NUT midline carcinoma (NMC) comprises treatment with a selective CD 9 inhibitor as defined in any one of claims 1 to 11.","lang":"en","source":"WIPO_FULLTEXT","data_format":"ORIGINAL"}]},"claim_lang":["en"],"has_claim":true,"description":{"en":{"text":"Susceptibility to selective CDK9 inhibitors The present invention relates to a method of selecting (a) cell(s), (a) tissue(s) or (a) cell culture(s) with susceptibility to a selective CDK9 inhibitor. Also a method for determining the responsiveness of a mammalian tumor cell or cancer cell to treatment with a selective CDK9 inhibitor is described herein. In particular, the present invention provides for an in vitro method for the identification of a responder for or a patient sensitive to a selective CDK9 inhibitor, whereby the patient is suspected to suffer from NUT midline carcinoma (NMC). The present invention also relates to a method of monitoring or predicting the efficacy of a treatment of NUT midline carcinoma (NMC), wherein treatment with a selective CD 9 inhibitor is in particular envisaged. Also the use of a (transgenic) non-human animal or a (transgenic) cell having at least one rearrangement in the NUT gene for screening and/or validation of a medicament for the treatment NUT midline carcinoma (NMC) is described. Furthermore, a kit useful for carrying out the methods described herein as well as an oligo- or polynucleotide capable of detecting rearrangements in the NUT gene are provided. NUT midline carcinomas (subsequently referred to as \"NMC\") is a highly lethal cancer that has previously been described to occur in young adults and children; see French (2004) J Clin Oncology 22(20), 4135-4139. However, recent publications indicate that NMC occurs in children and adults of all ages; see French (2010) J Clin Pathol 63: 492-496. NMC is a disease which is genetically defined by rearrangements in the nuclear protein in testis (NUT) gene on chromosome 15ql 4 most commonly in a balanced translocation with the BRD4 gene or the BRD3 gene. A corresponding rearrangement has first been disclosed in a cell line termed Ty-82 which had been derived from a 22-year old woman with undifferentiated thymic carcinoma; see Kuziime (1992) Int J Cancer 50, 259-264. Later, it has been found that this translocation involving rearrangement in the NUT gene is characteristic for a particularly aggressive form of a midline carcinoma and the term NUT midline carcinoma has been coined; see French (2001) Am J Pathol 159(6), 1987-1992. NMC as a genetically defined disease does not arise from a specific organ. Most cases occur in the mediastinum and upper aerodigestive tract, but in some cases tumors have arisen in bone, bladder, abdominal retroperitoneum, pancrease and salivary glands; see French (2010), Cancer Genetics and Cytogenetics 203, 16-20 and Ziai (2010) Head and Neck Pathol 4, 163-168. In about two thirds of NMC cases NUT is fused to BRD4 on chromosome 19; see French (2003) Cancer Res 63, 304-307 and French (2008) Oncogene 27, 2237-2242. French (2008) found that in certain cases NUT may also be fused to BRD3. Further, the authors of this document investigated the functional role of BRD-NUT fusion proteins using an siR A assay for silencing expression. It was found that the suppression of expression of such fusion genes results in squameous differentiation and cell cycle arrest and it was concluded that BRD-NUT fusion proteins contribute to carcinogenesis. It has been suggested in the art that NUT rearrangement is a very early, possible tumour-initiating event; see French (2010) J Clin Pathol (loc. cit). NUT rearrangements are restricted to NMC and, therefore, the diagnosis of NMC is not in question once NUT rearrangement has been detected by immunuohistochemical testing (e.g. FISH) or by molecular testing like detection of the expression of NUT fusion genes, in particular BRD4-NUT fusion genes, BRD3-NUT fusion genes or fusions of NUT with other uncharacterised genes (termed NUT -variant fusion genes). The expression of such fusion genes goes along with corresponding NUT rearrangements. Also NMC diagnosis via detection of NUT expression with a NUT specific monoclonal antibody has been disclosed in the art; see Haack (2009) Am J Surg Pathol 33(7), 984= 991. Thus, the challenge is not the diagnosis of NMC but rather the decision to perform the diagnosis on subject suspected of suffering from NMC. Generally, it is believed that NMC is a rare type of cancer; however, most cases of NMC currently go unrecognized due to its lack of characteristic histological features; see French (2010) J Clin Pathol loc. cit. NMCs are often mistaken for other cancer types such as thymic carcinoma, squamous cell carcinoma of the head and neck, lung carcinoma, Ewing sarcoma, and acute leukemia; see Schwartz (201 1) Cancer Res 71(7), 2686-2696. French (2010) J Clin Pathol loc. cit. has proposed to consider any poorly differentiated, monomorphic, midline neoplasm that does not stain for lineage-specific markers for NUT rearrangement testing. Many patients with presently undiagnosed NMC would profit enormously from diagnosis and subsequent effective treatment of NMC. Unfortunately, an effective therapy of NMC is presently not available resulting in a low survival rate (1 survival out of 22 reported cases) and a mean survival of less than 1 year (9.5 months) despite aggressive chemotherapy and radiation treatment, as summarized in Table 1 of French (2010) J Clin Pathol, loc. cit. and French (2010), Cancer Genetics and Cytogenetics 203, 16-20. Further, numerous NMC tumors might not be treated at all or treatment might commence late due to a late or absent NMC diagnosis. Though reliable diagnosis of NMC is, in principle, available, there is, thus, a need in the art for the early identification of patients eligible for efficient treatment of NMC. Clearly, in vitro methods for the identification of susceptible cells are also needed. Potential therapies of NMC have been proposed in the art. Schwartz (loc. cit.) has investigated the mechanism underlying an NMC subtype that is characterized by the expression of the BRD4-NUT fusion gene. Schwartz found that expression of BRD4-NUT is associated with globally decreased histone deacetylation and transcriptional repression. Therefore, the authors of this document suggest the use of histone deacetylase inhibitors (HDACi) such as vorinostat and romidepsin in order to revert this effect and to thereby treat NMC. Schwartz also suggests the use of small molecule bromodomain inhibitors (Brdi) to target BRD4-NUT; yet, the authors emphasize that the most specific targeting of BRD4-NUT would be directed at NUT and that the potential difficulties in identifying deliverable NUT-directed inhibitors may be facilitated by the recent development of stapled peptides. In line with Schwartz (loc. cit.) the international patent application WO 2010/011700 describes the use of compounds, in particular histone deacetylase inhibitors, that promote increased acetylation of histones for the treatment of a cancer characterized by NUT or BRD chromosomal reaiTangments, Also Filippakopoulos (2010) propose the BRD4-NUT fusion as therapeutic target in NMC using a BRD4-directed inhibitor termed JQ1 (a thieno-triazolo-1,4- diazepine). Alsarraj (201 1) Cancer Res (author manuscript accepted for publication, doi: 10.1 158/0008- 5472.CAN-10-4417) explores the role of the bromodomain-containing chromatin modifying factor BRD4 in development of cancer. Alsarraj describes that ectopic Brd4 expression represses primary tumor growth and that Brd4 activation is predictive for good outcome in human breast cancer; the authors of this document speculate that the tumor- and the metastasis-suppressive properties of Brd4 may be associated with the presence of a proline-rich region in the C-tcrminal. part of one isoform while the extreme C-terminal domain containing a p_X£Fb binding region is found to act as a metastasis enhancer. However, Alsarraj does not suggest a potential treatment of cancer and is not ^OiiCciiicu i an wiui iimi ^ . Tone (2010) discloses a phase 1- study on the effect of the compound SNS-032 in the treatment of leukemia and multiple myeloma; Tong (2010) J Clinical Oncology 28, 3015-3022. Yan (201 1) investigates potential mechanisms underlying Nut Midline Carcinoma (NMC); see Yan (201 1) J Biol Chemistry 286, 27633-27675. Yan discloses that CDK9 can be one component of „P-TEFB\" („positive transcription elongation factor b\") in transcriptionally inactive BRD4-NUT Nuclear Foci. In these transcriptionally inactive BRD4-NUT Nuclear Foci the downstream target c- fos is repressed, thus contributing to oncogenic progression in nut midline carcinoma. Yan discloses that a knockdown of BRD4-NUT stimulates c-fos expression restoring the non-oncogenic, normal phenotype. Accordingly, Yan suggests the use of inhibitors of BRD4-NUT inhibitors as potential therapy of NMC. Thus, the technical problem underlying the present invention is the provision of means and methods allowing the therapeutic intervention in NMC. The technical problem is solved by provision of the embodiments characterized in the claims. Accordingly, the present invention relates to a method of selecting (a) cell(s), (a) tissue(s) or (a) cell culture(s) with susceptibility to a selective CD 9 inhibitor, comprising the steps: (a) determining the presence of a rearrangement in the NUT gene in said cell, tissue or cell culture; (b) selecting (a) cell(s), tissue(s) or cell culture(s) with at least one rearrangement in the NUT gene; (c) contacting said cell(s), tissue(s) or cell culture(s) with a selective CDK9 inhibitor; and (d) evaluating viability of said cell(s), tissue(s) or cell culture(s) contacted with said selective CD 9 inhibitor, wherein a decreased viability is indicative for susceptibility to said selective CDK9 inhibitor. As used herein, the term \"cell, tissue or cell culture\" is not only limited to isolated cells, tissues or cell cultures but also comprises the use of samples, i.e. biological, medical or pathological samples that consist of fluids that comprise such cells, tissues or cell cultures. Such a fluid may be a body fluid or also excrements and may also be a culture sample, like the culture medium from cultured cells or cultured tissues. The body fluids may comprise, but are not limited to blood, serum, plasma, urine, saliva, synovial fluid, spinal fluid, cerebrospinal fluid, tears, stool and the like. Accordingly, the gist of the present invention lies in the finding that the herein provided methods allow for the determination of the susceptibility of a given cell, tissue or cells in a tissue, (or a cell culture or individual cells in such a cell culture, or as will be explained below, (a) cell(s), tissue or cell culture in a biological/medical/pathological sample) for the anti-cancer or anti-proliferative treatment with a selective CD 9 inhibitor. As shown in the appended examples, it was surprisingly found that cells that comprise a rearrangement in the NUT gene are in particular susceptible to a selective CD 9 inhibitor. The examples provided herein also show that selective CDK9 inhibitor can successfully be employed in the treatment of NUT midline carcinoma (NMC) which is, by definition, characterized by rearrangements in the NUT gene. Nothing in the art suggested the use of selective CDK9 inhibitors m this context. Accordingly, and m a preferred embodiment, the cell(s), tissue(s) and/or cell culture(s) to be selected in accordance with the method as provided herein above is/are (a) cell(s), (a) tissue(s) or (a) cell culture(s) that is/are derived or obtained from a subject/patient suspected to suffer, being prone to suffer or who suffer from NUT midline carcinoma (NMC). Therefore, the present invention does not only provide for a method for selecting cells/tissues/cell cultures which are susceptible to (a) selective CD 9 inhibitor(s), but also for an in vitro method for assessing an individual, i.e. a human or animal patient, for its potential responsiveness to treatment of NMC with (a) selective CD 9 inhibitor(s). Thus, the present invention provides not only for the possibility to select cells, tissues and cell cultures that are susceptible for selective CD 9 inhibitor treatment (i.e. the selection of e.g. research tools whereon (a) novel selective CD 9 inhibitor(s) may be tested or which are useful in screening methods for compounds that are suspected to function as (a) selective CDK9 inhibitor(s)) but also for a method to evaluate whether a given patient, preferably a human patient, in need of treatment of NMC, is a responder for selective CDK9 inhibitor treatment. Preferably, the responsi veness of a given patient to Cpd B2 and Cpd B 1 is tested. These and further selective CD 9 inhibitor that may be tested are described herein below in more detail. Further it is expected that the use of CD 9 inhibitors, especially of the selective CD 9 inhibitors is associated with less side effects. The selection method of a responding cell/tissue/cell culture or a responding patient comprises a step wherein (a) cell(s), tissue(s) or cell culture(s) with at least one rearrangement in the NUT gene is selected. Said rearrangement is indicative for susceptibility to a selective CD 9 inhibitor. The term \"rearrangement in the NUT gene\" refers to any rearrangement in the NUT gene that is characteristic for NUT midline carcinoma (NMC) or a rearrangement resulting in the expression of a Brd/Nut fusion protein. Exemplary \"rearrangments in the NUT gene\" as well as methods for their detection are known in the art (see, for example, French (2010) J Clin Pathol, loc. cit.) and also described herein. In an alternative embodiment, the present invention relates m particular to a method for determining the responsiveness of a mammalian tumor cell or cancer cell to a selective CDK9 inhibitor, said method comprising determining the presence of at least one rearrangement in the NUT gene in said tumor cell, wherein said rearrangement in the NUT gene is indicative of whether the cell is likely to respond or is responsive to the selective CDK9 inhibitor. Such a determination may take place on an individual, isolated tumor cell. Such an evaluation may also be carried out on biological/medical/pathological samples, like body fluids, isolated body tissue samples and the like, wherein said samples preferably comprise cells or cell debris to be analyzed. Is/are (a) cell(s), (a) tissue(s) and/or (a) cell culture(s) selected and/or identified to be susceptible to a selective CDK9 inhibitor in accordance with this invention, said cell(s), tissue(s) and/or cell s ^ uiiure^bj C n uc uuii iuieu vVitu scieuu^c ^i r j' imuuiiui . 11 is iO Dc uiiQci suuuu Ulcu a contact may be in vivo as well as in vitro. Also, and as disclosed herein, the present invention also provides for means and methods how responders for patients sensitive to selective CD 9 inhibitors can be identified. The cell(s) and/or tissue(s) of these identified subject/patient can be contacted with a selective CDK9 inhibitor. As pointed out above, there is a need for stratification of patients who are to be subjected to an anti- NMC therapy with selective CDK9 inhibitors and distinguishing between selective CDK9 inhibitor \"responder\" and \"non-responder\" patients. Therefore, subject of the present invention is also a method for diagnosing an individual who is to be subjected to or is being subjected to an anti-NMC treatment to asses the responsiveness to selective CD 9 inhibitor prior, during and/or after selective CDK9 inhibitor treatment which comprises the steps of (a) detection of at least one rearrangement in the NUT gene in a biological/medical/pathological sample wherein the presence of said at least one rearrangement in the NUT gene is indicative for the responsiveness to a selective CDK9 inhibitor treatment prior, during and after treatment with such selective CD 9 inhibitor; and (b) sorting the individual into responder or non-responder based on detection of said at least one rearrangment in the NUT gene. The presence of at least one rearrangement in the NUT gene as defined herein correlates preferably significantly (p<0.05) with a responsiveness to a selective CDK9 inhibitor/susceptibility to a selective CDK9 inhibitor. The identification of rearrangments in the NUT gene as markers for susceptibility of (tumor) cell(s) to a selective CD 9 inhibitor provides an effective therapeutic approach for patients suffering from cancer characterized by the presence such rearrangments (i.e. NMC). Treatment of susceptible patients with a selective CD 9 inhibitor may lead to an increase in clinical response rate and/or an increase in survival. For example, the clinical response rate may increase to at least 80 %. As mentioned above, rearrangements in the NUT gene have never been disclosed in context with susceptibility to selective CD 9 inhibitors. At most, HDAC inhibitors, BRD inhbitors or NUT inhbitors have been proposed in context of the development of potential NMC therapies; see Schwartz, loc. cit. Patients suffering from cancer with (a) rearrangement(s) in the NUT gene (like patients suffering from NMC) have a particularly low survival rate and a bad prognosis and known therapies are not effective. These patients will, therefore, profit enormously from the herein provided therapy with selective CD 9 and the identification of rearrangments in the NUT gene as markers for susceptibility to selective CD 9 inhibitors. Further, the herein described methods allow the identification of responders for/patients sensitive to an CDK9 inhibitor prior to initiation of clinical trials involving patients. The terms„susceptibility to a selective CDK9 inhibitor\" and \"responsiveness to treatment with a selective CD 9 inhibitor\" are used interchangeably in context of the present invention. Any explanations given herein in respect to \"susceptibility to a selective CDK9 inhibitor\" also apply to \"responsiveness to treatment with a selective CD 9 inhibitor\", mutatis mutandis, and vice versa. Technical means and methods for determining the susceptibility to drugs are known in the art. Such methods comprise, inter alia, cell or tissue culture experiments. It is also envisaged herein that two or more different selective CDK9 inhibitors (i.e. selective CDK9 inhibitors having different chemical formulae, optionally non- structurally related selective CD 9 inhibitors) may be tested simultaneously. However, it is preferred herein that only one selective CD 9 inhibitor is tested at one time. Preferred selective CD 9 inhibitors to be used and tested in the present invention are described herein below. The selection methods or method for determining the responsiveness to treatment with a selective CD 9 inhibitor provided herein may comprise a contacting step/exposing step which is explained in more detail herein below. These above-mentioned methods may also comprise an evaluation/determination step, which may, for example, include determining the viability of the cell(s), tissue(s) or cell culture(s) contacted with/exposed to a selective CD 9 inhibitor or (a) mammalian cell(s) treated with a selective CD 9 inhibitor. For example, (a) cell(s), (a) tissue(s) or (a) cell culture(s) described herein above may show decreased viability upon contacting/exposing/treating with a selective CDK9 inhibitor. Preferably, the cell(s), tissue(s) or cell culture(s) may show an at least 10 %, 20 %, 30 %, 40 %, 50 %, 60 %, 70 %, 80 %, and most preferably, at least 90 % reduction in viability compared to control cell(s), tissue(s) or cell culture(s) not contacted/ exposed/treated with a selective CDK.9 inhibitor. Preferably, the control cell(s), (a) tissue(s) or (a) cell culture(s) will be identical to the cell(s), (a) tissue(s) or (a) cell culture(s) to be tested as described herein with the only exception that the control (s), (a) tissue(s) or (a) cell culture(s) are not contacted with/exposed to the selective CDK9 inhibitor. Thus, (a) cell(s), (a) tissue(s) or (a) cell culture(s) contacted/exposed/treated with a selective CD 9 inhibitor and showing, for example, a decreased proliferation as described herein above, can be considered as being susceptible to a selective CD 9 inhibitor. Correspondingly, (a) mammalian cell(s) treated with a selective CD 9 inhibitor showing such a decreased proliferation can be considered as responsive to treatment with a selective CD 9 inhibitor. The step of determining the presence of a rearrangement in the NUT gene is described herein below. As already mentioned above, it has been surprisingly found in context of this invention that the presence of such a a rearrangement in the NUT gene is indicative of whether (a) cell(s), (a) tissue(s) or (a) cell culture(s) contacted/treated with or exposed to selective CD 9 inhibitor is susceptible to said inhibitor or responsive to treatment with a selective CD 9 inhibitor. A reduction in viability may, for example, be reflected in a decreased proliferation, such as 10 %, 20 %, 30 %, 40 %, 50 %, 60 %, 70 %, 80 %, and most preferably, 90 % reduction in proliferation compared to control cell(s), tissue(s) or cell culture(s) not contacted/exposed/treated with a selective CD 9 inhibitor The decreased proliferation may be quantitated, for example, by measuring the total cell volume, tissue volume or cell culture volume using standard techniques. The difference in proliferation between contacted/exposed/treated cell(s), tissue(s) or cell culture(s) and corresponding controls as defined herein may, for example, be evaluated/determined by measuring the volume of the cell(s), tissue(s) or cell culture(s) taking advantage of standard techniques. Said evaluation/determination may be performed in various points in time, for example, 15 minutes, 30 minutes, 60 minutes, 2 hours, 5 hours, 18 hours, 24 hours, 2 days, 3 days, 4 days, 5 days, six days and/or seven days after contacting/treating said cell(s), tissue(s) or cell culture(s) with a selective CD 9 inhibitor or exposing said cell(s), tissue(s) or cell culture(s) to a selective CDK9 inhibitor. It is envisaged herein that said evaluation/determination may be performed repeatedly, for example, at 15 minutes, 30 minutes and 60 minutes after said contacting/exposing/treating. It is of note that said cell(s), tissue(s) or cell culture(s) may be contacted /treated not only once with said selective CD 9 inhibitor or exposed to said selective CD 9 inhibitor but several times (e.g. 2 times, 3 times, 5 times, 10 times or 20 times) under various conditions (e.g. same concentration of inhibitor, different concentration of inhibitor, inhibitor comprised in a composition with different stabilizers, diluents, and/or carriers and the like). Accordingly, said optionally repeated evaluation/determination may be performed after the final contacting/treating with or exposing to said selective CDK9 inhibitor or in between said above-mentioned various contacting/exposing/treating steps. The explanations given herein above in respect of the exemplary determination/evaluation step, comprising determining the proliferation of the cell(s), tissue(s) or cell culture(s) contacted with/exposed to an selective CD 9 inhibitor apply to other expression of NUT fusion genes like BRD4-NUT fusion genes or B D3-NUT fusion genes and the like) and further determination/evaluation steps a person skilled in the art will be aware of, such as assays that quantitate the induction of apoptotic cell death, senescence or any other cell biology nhenotvoe that is associated with decreased viabilitv or proliferation of tumor cells. These selection methods or method for determining the responsiveness to treatment with a selective CDK9 inhibitor may also comprise determinining the level of NUT activity or activity of NUT fusion genes, wherein the activity of NUT activity or activity of NUT fusion genes is indicative whether the cell(s), tissue(s) or cell culture(s) is (are) susceptible to a selective CDK9 inhibitor or is (are) responsive to treatment with a selective CD 9 inhibitor. The term \"activity\" used herein expression level (e.g. mRNA or protein). Methods for determining the activity as defined herein are well known in the art and also described herein below. As used herein, a kinase \"inhibitor\" refers to any compound capable of downregulating, decreasing, suppressing or otherwise regulating the amount and/or activity of a kinase. Inhibition of these kinases can be achieved by any of a variety of mechanisms known in the art, including, but not limited to binding directly to the kinase polypeptide, denaturing or otherwise inactivating the kinase, or inhibiting the expression of the gene (e.g., transcription to mRNA, translation to a nascent polypeptide, and/or final polypeptide modifications to a mature protein), which encodes the kinase. Generally, kinase inhibitors may be proteins, polypeptides, nucleic acids, small molecules, or other chemical moieties. As used herein the term \"inhibiting\" or \"inhibition\" refers to the ability of a compound to downregulate, decrease, reduce, suppress, inactivate, or inhibit at least partially the activity of an enzyme, or the expression of an enzyme or protein and/or the virus replication. The term \"CD 9 inhibitor\" means accordingly in this context a compound capable of inhibiting the expression and/or activity of \"CD 9\" defined herein above. An CD 9 inhibitor may, for example, interfere with transcription of a CD 9 gene, processing (e.g. splicing, export from the nucleus and the like) of the gene product (e.g. unspliced or partially spliced mRNA) and/or translation of the gene product (e.g. mature mRNA). The CD 9 inhibitor may also interfere with further modification (like phosphorylation) of the polypeptide/protein encoded by the CD 9 gene and thus completely or partially inhibit the activity of the CDK9 protein as described herein above. Furthermore, the CD 9 inhibitor may interfere with interactions of the CD 9 protein with other proteins. In accordance with the above, the compounds according to the general formula (I) disclosed herein below as well as pharmaceutically acceptable salts thereof are used as an inhibitor for a protein iviuaafc, ui tiu ui v ao an iiuiiuiL i ιυι a t ii ui i uiuitm ivniaoC. In a preferred embodiment of this aspect said cellular protein kinase consists of Cyclin-dependent protein kinases (CDKs). The cyclin-dependent protein kinase can be selected from the group comprising: CD 1 , CD 2, CDK3, CDK4, CDK5, CD 6, CD 7, CDK8, CDK9, CDK10, CDKl l , CrkRS (Crk7, CDC2-related protein kinase 7), CD L1 (cyclin-dependent kinase-like 1); KIALRE, CD L2 (cyclin-dependent kinase-like 2), IAMRE, CDKL3 (cyclin-dependent kinase-like 3), NKIAMRE, CDKL4, similar to cyclin-dependent kinase-like 1 , CDC2L1 (cell division cycle 2-like 1 ), PITSLRE B, CDC2L1 (cell division cycle 2-like 1), PITSLRE A, CDC2L5 (cell division cycle 2-like 5), PCTKl (PCTAIRE protein kinase 1 ), PCTK2 (PCTAIRE protein kinase 2), PCTK3 (PCTAIRE protein kinase 3) or PFT 1 (PFTAIRE protein kinase 1). In a particularly preferred embodiment said cyclin-dependent protein kinase is CD 9. Thus, the ^ uiii wuiiu- wOi vaiii υιυ ^n l -i ijiiiiu-ia tx^ w ^n ΰ ii niii ^CutiC ii - ^^ ^ ii S ui l vji are, in a very preferred embodiment, used as an inhibitor for CD 9, in particular as a selective CDK9 inhibitor. Furthermore, in another particularly preferred embodiment the compounds according to the invention show a high potency (demonstrated by a low IC50 value) for inhibiting CD 9 activity. In context of the present invention, the IC 50 value with respect to CD 9 can be determined by the methods described in the method section of PCT patent application PCT/EP2011/001445 which is incorporated herein by reference in its entirety. Preferably, it is determined according to the method described in section 3.6 of said PCT patent application PCT/EP2011/001445. Surprisingly it turned out that the compounds according to the general formula (I) as well as pharmaceutically acceptable salts thereof selectively inhibit CD 9 in comparison to other protein kinases and in comparison to other cyclin-dependent protein kinases. Thus, the compounds according to the general formula (I) as well as pharmaceutically acceptable salts thereof are used as selective inhibitors for CDK9. Particularly preferred compounds of the present invention according to formula (I) show a stronger CD 9 than CDK2 inhibition. In context of the present invention, the IC 50 value with respect to CDK2 can be determined by the methods described in the method section of PCT patent application PCT/EP201 1/001445. Preferably, it is determined according to the method described in section 3.5 of PCT/EP2011/001445. Selectivity expresses the biologic fact that at a given compound concentration enzymes (or proteins) are affected to different degrees. In the case of enzymes selective inhibition can be defined as preferred inhibition by a compound at a given concentration. Or in other words, an enzyme is selectively inhibited over another enzyme when there is a concentration which results in inhibition of the first enzyme whereas the second enzyme is not affected. To compare compound effects on different enzymes it is crucial to employ similar assay formats, such as the LANCE assay as described in more detail below. The inhibitors to be used herein are t>referablv snecific for CD 9, i.e. the comnounds specifically inhibit CDK9. This is inter alia shown in Figure 3 where the inhibiting effect of exemplary compounds on CDK9 is demonstrated. A radiometric protein kinase assay (33PanQinase® Activity Assay) was used for measuring the kinase activity of protein kinases employing exemplary CDK9 inhibitors to be used in the present invention (see Figure 3). The low kinase activities of CDK9 show that exemplary compounds potently inhibit CD 9. Activities of other kinases are not inhibited. In the experimental part selectivity of the herein provided inhibitors for CDK9 is shown using, inter alia, the well known Lance Assay; see Figure 2. The Lance assay has been described for example in Moshinsky et al.; 2003 (A widely applicable, high-throughput TR-FRET assay for the measurement of kinase autophosphorylation: VEGFR-2 as a prototype. Moshinsky DJ, Ruslim L, Blake RA, Tang F. J Biomol Screen. 2003 Aug;8(4):447-52). The Lance Ultra KinaSelect Assay may be used to determine half maximal inhibitory concentration (IC 50 ) of inhibitor compounds and CDK/Cyclin complexes. The principle behind this enzymatic assay is based upon the phosphorylation of the Ulight-Peptide Substrat. It is detected by using a specific EU-labeled anti-phospho peptide antibody. The binding of the Eu labeled anti-phospho peptide antibody to the phosphorylated ULight labeled peptide gives rise to a FRET-signal. Binding of an inhibitor to the kinase prevents phosphorylation of the U% zt-MBP Substrat, resulting in a loss of FRET. Based on these results, the IC50 value can be determined. The Lance assay and the 33 PanQinase® assay may be performed as follows: Typically such experiments are started by generation of compounds which are serially diluted in multi titer plates in dimethylsulfoxide (DMSO). In the next step, working solutions for the enzymes, the substrates (protein and ATP separately) are generated in enzyme buffer. The preparation of the assay plate (definition of positive and negative control, reference inhibitors, test compounds and the pipetting of all solutions and compounds except the ATP working solution) is done within the next step. Finally the reaction is started by the addition of the ATP working solution. All pipetting steps can be done manually or by the help of robotics. Within the incubation of 1 h at room temperature the enzyme catalyzes the generation of phosphorylated substrate. This reaction is more ore less inhibited by the added compounds. Finally, to stop the reaction and to detect phosphorylated substrate detection buffer (see material and methods) is added followed by another incubation of 1 h. The data is evaluated by measuring the I RLI -Signal. Data is processed by subtraction of the backgroung signal (negative control) from all investigated activities. These activities are set into relation to the positive control. Altogether this is shown by the following equation: resulting activity (%) = 100 X [(signal of compound - signal of negative control) / (signal of positive control - signal of negative control)] Further analysis steps include the determination of IC50 values by using the activities of a dose response experiment and an algorithm (equation #205 in Excel fit) for calculation. A similar experimental procedure is performed when the resulting activity within j3 PanQinase® assay is done. In advance buffers are prepared but in this case the pipetting sequence is first ATP solution diluted with assay buffer, DMSO or compound solution. The reaction (Ih at 30°C) is started by addition of a substrate-kinase mix. During the incubation the kinase phosphorylates the substrate (different for each kinase). Due to the fact that the ATP solution contains 3j P-labelled ATP the substrate proteins are labeled with 3j P. The reaction is stopped by addition of excess H 3 PO 4 . If the reaction is performed in plates binding substrate proteins, said plates are washed to reduce unspecific signals (mainly not used ATP). The incorporation of j3 P into substarte proteins is a direct measure of activity of the respective kinase. Therefore, the incorporated radioactivity is detected by scintillation counting. Data is evaluated, processed and analyzed as described for the LANCE assays. From Figure 2 it can be deduced that a known CDK7-inhibitor (BS-181) has an IC50 value of 1.944 in the CDK9 Lance Assay. As shown in the experimental part, the IC50 value determined for exemplary selective CDK9 inhibitors, for example according to the Lance Assay, is low, preferably below 0.2 μΜ, more preferably, below 0.15 μΜ, 0.14 μΜ, 0.13 μΜ, 0.12 μΜ or even lower. More preferably, the IC50 value is below 0.1 μΜ, 0.095 μΜ, 0.090 μΜ, 0.085 μΜ, 0.080 μΜ, 0.075 μΜ, 0.070 μΜ, 0.065 μΜ, 0.060 μΜ, 0.055 μΜ, 0.050 μΜ, 0.045 μΜ, 0.040 μΜ , 0.035 μΜ, 0.030 μΜ , or even below 0.025 μΜ, wherein the lower values are preferred over the higher values. Even more preferably, the IC50 value is below 0.024 μΜ, 0.023 μΜ, 0.022 μΜ, 0.021 μΜ, 0.020 μΜ, 0.019 μΜ, 0.018 μΜ, 0.017 μΜ, 0.016 μΜ, 0.015 μΜ, 0.014 μΜ, 0.013 μ.Μ, 0.012 μΜ, or 0.01 1 μΜ. The IC50 value may even be lower, for example, below 0.010 μΜ, 0.009 μΜ, 0.008 μΜ, 0.007 μΜ, 0.006 μΜ, or 0.005 μ\\1. Generally, the lower values are preferred herein over the higher values. It is preferred herein that the ratio of IC50 values of selective CDK9-inhibitors determined according to the CDK9 Lance assay and IC50 values of selective CD 9-inhibitors determined according to the CDK1 Lance assay, CD 2 Lance assay, CD 4 Lance assay, and/or the CDK6 Lance assay is about 1 : 10 or lower. A ratio of 1 : 10 or lower also indicates selectivity of the inhibitor for CD 9. More preferred is a ratio of 1 : 10, 1 :20, 1 :30, 1 :40, 1 :50, 1 :60, 1 :70, 1 :80, 1 :90 or 1 : 100 or even lower. The following selective CDK9 inhibitors are preferably used in accordance with the present invention; these and further selective CD 9 inhibitors for use in the present invention are described in PCT/EP201 1/001445, EP 10075 1 3 1.2 (filing date 22.03.2010) EP11075037.9 (filing date 02.03.201 1) and EP11075038.7 (filing date 02.03.201 1) which are incorporated herein by reference in their entirety. The disubstituted triazine compounds to be used according to the present invention are defined by the general formula (I) Formula (I) wherein L is a bond or -CR 5 R 6 -, -CR 5 R 6 -CR 7 R 8 -, -CR 5 R 6 -CR 7 R 8 -CR 9 R 10 - -CRV-CR -CR^^-CR 1 2 -; R 5 - R 12 represent independently of each other -H, -CH 3 , -C 2 H 5 , -C 3 H 7 , -F, -CI, -Br, -I; R 3 is selected from -H, -N0 2 , Nil;. -CN, -F, -CI, -Br, -I, -CH 3 , -C 2 H 5 , -Ph, -C3H7, -CH(CH 3 ) 2 , -C4H9, -CH 2 -CH(CH 3 ) 2 , -CH(CH 3 )-C 2 H 5; -C(CH 3 ) 3 , -0-CH 3 , -0-C 2 H 5 , -0-C 3 H 7 , -0-CH(CH 3 ) 2 , -O-C4H 9 , -0-CH 2 -CH(CH 3 ) 2 , -0-CH(CH 3 )-C 2 H 5, -0-C(CH 3 ) 3 , -CR 13 R 14 R 21 , -CR 13 R ,4 -CR 15 R !6 R 21 , -0-CR !3 R 14 R 2! , -CR !3 R 14 -CR I5 R !6 -CR 17 R !8 R 21 , -CR 13 R 14 -CR 15 R 16 -CR 17 R ,8 -CR 19 R 20 R 21 , O CR¾ ,4 -CR¾ S \"R 21 , -0-CR L3 R 14 -CR L5 R L6 -CR L7 R L8 R 21 , -S0 2 R 22 , -CONR 23 R 24 , -NR 25 COR 22 , -O-CR ,3 R ,4 -CR I5 R I6 -CR 17 R ,8 -CR 19 R 20 R 21 , -NR 25 S0 2 NR 23 R 24 , -NR 25 S0 2 R 22 , -NR 25 CONR 23 R 24 , -S0 2 NR 23 R 24 , -SO(NR 26 )R 27 , -NH-CO-NH-Ph; R 13 - R 21 , R 29 - R 32 and R 33 - R 48 represent independently of each other -h, -t, — tsr, -1; R 26 is -H, -CH 3 , -C 2 H 5 , -C 3 H 7 , -CH(CH 3 ) 2 , -C 4 H 9 , -CH 2 -CH(CH 3 ) 2 , -CH(CH 3 )-C 2 H 5 , -C(CH 3 ) 3 , -C 5 H„, -CH(CH 3 )-C 3 H 7 , -CH 2 -CH(CH 3 )-C 2 H 5 , -CH(CH 3 )-CH(CH 3 ) 2 , -C(CH 3 ) 2 -C 2 H 5 , -CH 2 -C(CH 3 ) 3 , -CH(C 2 H 5 ) 2 , -C 2 H 4 -CH(CH 3 ) 2 , -C 6 H 13 , — C 3 Hg— CH(CH 3 ) 2 , — C 2 H 4 — CH(CH 3 )— C 2 H 5 , — CH(CH 3 )— C 4 H9, -CH 2 -CH(CH 3 )-C 3 H 7 , -CH(CH 3 )-CH 2 -CH(CH 3 ) 2 , -CH(CH 3 )-CH(CH 3 )-C 2 H 5 , -CH 2 -CH(CH 3 )-CH(CH 3 ) 2 , -CH 2 -C(CH 3 ) 2 -C 2 H 5 , -C(CH 3 ) 2 -C 3 H 7 , -C(CH 3 ) 2 -CH(CH 3 ) 2 , -C 2 H 4 -C(CH 3 ) 3 , -CH(CH 3 )-C(CH 3 ) 3 , -CR !3 R 14 R 21 , -COR 28 , -CR 13 R ,4 -CR 15 R I6 -CR 17 R ,8 R 21 , -CR 13 R ,4 -CR I5 R 16 -CR 17 R I8 -CR 19 R 20 R 21 , -CR 13 R 14 -CR 15 R ,6 -CR 17 R ,8 -CR 19 R 20 -CR 29 R 0 -CR 3I R 32 R 21 , -COOR 28 , these Ca-Ce-cycloalkyl groups may further be substituted by one, two, three, four, five or more substituents selected from the group consisting of R' R 22 , R 27 , and R 28 are independently selected from -CR 49 R 5(! R 51 , -CR 49 R 50 -CR 52 R 53 R 5! , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -CR 56 R 57 -CR 58 R 59 R 51 , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 R 51 , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -CR 56 R 57 R 51 , κ κ κ — -K _ -t^K. f , -^n 2 rn; -CH;Ph the phenyl group of which may further be substituted by one, two, three, four or five substituents selected from the group consisting of R - R C3-C 6 -cycloalkyl groups listed for R , which may further be substituted by one, two, three, four, five or more substituents selected from the group consisting of R j3 - R 48 ; K *' ' - R° ' represent independently of each other -H, -CH 3 , -C 2 H 5 , -C3H7, CM,. -F, -CI, Br. -I, -OH, ( -NH 2 ; R 23 and R 24 are independently selected from -H, -CR 49 R 50 R 51 , -CR 49 R 50 -CR 52 R 53 R 51 , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -CR 56 R 57 -CR 58 R 59 R 5 -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 R 51 , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -CR 56 R 57 R 5 -CR 49 R 50 ^CR 52 R 53 -CR 54 R 55 -CR 56 R 57 -CR 58 R 59 -CR 60 R 6, R 51 , -CR 49 R 50 -CR 52 R 53 -O-R 51 ' , ^CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -O-R 51 ' , -CR 49 R 50 -CR 52 R 53 -NR 51 R 51'' , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -NR 5r R 51\" , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -CR 56 R 57 -NR 5 r R 51 \" , -CR 49 R 50 -CR 52 R 53 -CR 54 R 55 -CR 56 R 57 -CR 58 R 59 -NR 51 ' R 51 \" , 23 24 5 phenyl, substituted phenyl, benzyl, substituted benzyl, or both residues R and R together form with the nitrogen atom to which they are attached a azetidine, pyrrolidine, piperidine, piperazine, azepane, or morpholine ring; R 51 and R 51 represent independently of each other - H, -CH 3 , -C2H5, 10 -C3H 7 , -C 4 H9, -CH 2 Ph, -COOC(CH 3 ) 3 , -COOCH 3 , -COOCH 2 CH 3 , -COOCH 2 CH 2 CH3, -COOCH(CH 3 ) 2 , -COOCH 2 Ph, -COCH 3 ; and R s is selected from -H, -CH 3 , -C 2 H 5 , -C3H 7 , -CH(CH 3 ) 2 , -C 4 H 9 -CH 2 -CH(CH 3 ) 2 , -CH(CH 3 )-C 2 H 5 or -C(CH 3 ) 3 ; R is selected from— H,— N0 2 ,— NH 2 ,— CN,— F,—CI,—Br,—I, — CONH 2 ,— SO 2 CH 3 , -SO 2 C 2 H 5 , -S0 2 C 3 H 7 , -NH-S0 2 -CH 3 , -NH-S0 2 -C 2 H 5 , -NH-S0 2 -C 3 H 7 , -NHCO-CH 3 , -NHCO-C 2 H 5 , -NHCO-C 3 H 7 , -S0 2 NR 2 R 24 , -CH 2 -S0 2 NR 23 R 24 , -C 2 H4-S0 2 NR 23 R 24 , -C 3 H 6 -S0 2 NR 23 R 24 , SO N! ! , ( S i SO NH . C H_ SO N! i . C ,! !,. SOXI K -CR 62 R 63 R 64 , -CR 62 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 R 64 , -0-CR 62 R 63 -CR 65 R 66 R 64 , o r r ^r> 62-r> 63 65 ώ 66 r^n 67-p 68r> 64 ,-,- 0 62- 0 63 65 π 66 67-p 68-p 64 -O-CR 62 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 R 64 , -CR 62 R 63 -CR 65 R 66 R 64 , -O-CR 62 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 71 R 72 R 64 , -0-CR 62 R 63 R 64 , -O-CR 6 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 71 R 72 -CR 73 R 74 R 64 , -CR 62 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 71 R 72 R 64 , 30 -CR 6 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 -CR 71 R 72 -CR 73 R 74 R 64 , -OCH 2 Ph, R - R represent independently of each other -H, -cyclo-C 3 H 5 , -cyclo-C 4 H 7 , ^yclo-C 5 H 9 , -CR 75 R 76 R 77 , -CR 75 R 76 -CR 78 R 79 R 77 , -CR 75 R 76 -CR 78 R 79 -CR 80 R 81 R 77 , _ CR 75 R 76_ CR 78 R 79_ CR 80 R 79_ CR 82 R 81 R 77 ? ^ _ ¾ _^ __ ph; R - R represent independently of each other -H, -F, -CI, -Br, -I, -NH 2 ; R 4 together with R 22 , R 23 , R 24 , or R 25 may form a group -CH 2 CH 2 - or -CH 2 CH 2 CH 2 - ifR 4 is attached ortho to -L-R 3 ; R 2 is R 83 is selected from -H, -OH, -N0 2 , -CN, -F, -CI, -Br, -I, -NR 23' R 24' , -CF 3 , -CR 62 R 63 R 64 , -CR 62 R 63 -NR 23' R 24' , -CR 62 R 63 -CR 65 R 66 R 64 , -CR 62 R 63 -CR 65 R 66 -NR 23 R 24' , -CR 62 R 63 -CR 65 R 66 -CR 67 R 68 R 64 , -CR 62 R 63 -CR 65 R 66 -CR 67 R 68 -NR 23 R 24' , -0-CR 62 R 63 R 64 , -0-CR 62 R 63 -CR 65 R 66 R 64 , _o-rR 62 R 63 -r 65 R 66 -rR 67 TJ 68 64 -ΓΗΠ -PR ^ OH _PT? 23 'O -rw.ni? 23 '- R 23' and R 24' represent independently of each other -H, -CH 3 , -C 2 H 5 , -C 3 H 7 , -CH(CH 3 ) 2 , -C 4 H 9 , -CH 2 -CH(CH 3 ) 2 , -CH(CH 3 )-C 2 H 5 , -C(CH 3 ) 3 ; -(cyclo-C 3 H 5 ); x is a value between 0 and 3; B is a bond, -CR 86 R 87 -, -CR 86 R 87 -CR 88 R 89 - -CR 86 R 87 -CR 88 R 89 -CR 90 R 91 -, -CR 8 V 7 -CR 88 R 89 -CR 9 1 -CR 92 R 93 -, -CR 86 R 87 -CR 88 R 89 -CR 90 R 91 -CR 92 R 93 ^CR 94 R 95 -, - CR 86 R 87 -CR 88 R 89 -CR 90 R 91 -CR 92 R 93 -CR 94 R 95 -CR 96 R 97 -; R 86 - R 97 represent independently of each other -H, -CH 3 , -C 2 H 5 , ;l 1-. -C 4 H 9 , -F, -CI, -Br, -I; Y is a bond, -0-, -S-, -SO-, -S0 2 - -S0 2 NH- -NHS0 2 - -CO-, -COO-, -OOC-, -CONH-, -NHCO-, -NH- -N(CH 3 )-, -NH-CO-NH- -O-CO- H- - H-CO-0-; R 84 is selected from a bond, -CR 86 R 87 - -CR 86 R 87 -CR 88 R 89 -CR 90 R 91 -, -CR 86 R 87 -CR 88 R 89 -CR 90 R 91 -CR 92 R 93 -, -CR 86 R 87 -CR 88 R 89 -CR 90 R 91 -CR 92 R 93 -CR 94 R 95 -, -CR 86 R 87 -CR 88 R 89 -, -CR 86 R 87 -CR 88 R 89 -CR 90 R 91 -CR 92 R 93 -CR 94 R 95 -CR 96 R 97 -; R 85 is selected from (i) -H, -OH, -OCH 3 , -OC2H5, -OC3H7, -0-cyclo-C 3 H 5 , -OCH(CH 3 ) 2 , -OC(CH 3 ) 3 , -OC 4 H 9 , -Ph, -OPh, -OCH 2 -Ph, -OCPI13, -SH, -SCH 3 , -SC 2 H 5 , SC M l-. -S-cyclo-C 3 H 5 , SCI KCI -SC(CH 3 ) 3 , -SC4H9, NO;. -F, -CI, -Br, -I, -P(0)(OH) 2 , -P(0)(OCH 3 ) 2 , -P(0)(OC 2 H 5 ) 2 , -P(0)(OCH(CH 3 ) 2 ) 2 „ -Si(CH 3 ) 2 (C(CH 3 ) 3 ), -Si(C 2 H 5 ) 3 , -Si(CH 3 ) 3 , -CN, -CHO, -COCH 3 , -COC2H5, -COC3H7, -CO-cyclo-C 3 H 5 , -COCH(CH 3 ) 2 , -COC(CH 3 ) 3 , -COC 4 H 9 , -COOH, -COOCH 3 , -COOC 2 H 5 , -COOC 3 H 7 , -COOC 4 H 9 , -COO-cyclo-C 3 H 5? -COOCH(CH 3 ) 2 , -COOC(CH 3 ) 3 , -OOC-CH3, -OOC-C 2 H 5 , -OOC-C 3 H 7 , ^ OOC-C 4 H 9 , -OOC-cyclo-C 3 H 5 , -OOC-CH(CH 3 ) 2 , -OOC-C(CH 3 ) 3 , -CONR 23 R 24' , -NHCOCH 3 , -NHCOC 2 H 5 , -NHCOC 3 H 7 , -NHCO-cyclo-C 3 H 5 , -NHCO-CH(CH 3 ) 2 , -NHCOC 4 H 9 , -NHCO-C(CH 3 ) 3 , - HCO OCH ;. -NHCO-OC 2 H 5 , -NHCO-OC 3 H 7 , -NHCO-O-CVCI0-C3H5, -NHCO-OC 4 H 9 , -NHCO-OCH(CH 3 ) 2 , -NHCO-OC(CH 3 ) 3 , -NHCO-OCH 2 Ph, -NR 23 R 24 , -CF 3 , -SOCH3, -SOC 2 H 5 , -SOC 3 H 7 , -SO-cyclo-QHs, -SOCH(CH 3 ) 2 , -SOC(CH 3 ) 3 , -S0 2 CH 3 , -SO9C 2 H 5 , -S0 2 C 3 H 7 , -S0 2 -cyclo-C 3 H 5 , -S0 2 CH(CH 3 ) 2 , -S0 2 C 4 H 9 , -S0 2 C(CH 3 ) 3 , -SO 3 H, -S0 2 NR 23' R 24' , -OCT;. -OC 2 F 5 , O -COOCH 3 . -0-COOC 2 H 5 , -0-COOC 3 H 7 , -0-COO-cyclo-C 3 H 5 , -0-COOC 4 H 9 , -0-COOCH(CH 3 ) 2 , -O-COOCH 2 PI1, -0-COOC(CH 3 ) 3 , -NH-CO-NH 2 , -NH-CO-NHCH 3 , -NH-CO-NHC 2 H 5 , N H C O NHC J k NH CO ΝΊ !( ' .,! !.,. -NH-CO-NH-cyclo-C 3 H 5 , -NH-CO-NH[CH(CH 3 ) 2 ], -NH-CO-NH[C(CH 3 ) 3 ], -NH-CO-N(CH 3 ) 2 , -NH-CO-N(C 2 H 5 ) 2 , -NH-CO-N(C 3 H 7 ) 2 , -NH-CO-N(C 4 H 9 ) 2 , -NH-CO-N(cyclo-C 3 H 5 ) 2 , -NH-CO-N[CH(CH 3 ) 2 ] 2 , -NH-CO-N[C(CH 3 ) 3 ] 2 , -NH-C(=NH)-NH 2 , N H C( N i l ) M ICH ;. -NH-C(=NH)-NHC 2 H 5 , -NH-C(=NH)-NHC 3 H 7 , -NH-C(=NH)-NHC 4 H 9 , -NH-C(=NH)-NH-cyclo-C 3 H 5 , -OCH 2 -cyclo-C 3 H 5 , -NH-C(=NH)-NH[CH(CH 3 ) 2 ], -NH-C(= H)-NH[C(CH 3 ) 3 ] , -NH-C(=NH)-N(CH 3 ) 2 , -NH-C(=NH)-N(C 2 H 5 ) 2 , -NH-C(=NH)-N(C 3 H 7 ) 2 , -NH-C(=NH)~-N(cyclo-C 3 H 5 ) 2 , -NH-C(=NH)-N(C 4 H 9 ) 2 , -NH-C(=NH)-N[CH(CH 3 ) 2 ] 2 , -NH-C(=NH)-N[C(CH 3 ) 3 ] 2 , -0-CO-NH 2 , -0-CO-NHCH 3 , -O^CO-NHC 2 H 5 , -0-CO-NHC 3 H 7 , -0-CO-NHC 4 H 9 , -0-CO-NH-cyclo-C 3 H 5 , -0-CO-NH[CH(CH 3 ) 2 ], -O-C0-NH[C(CH 3 ) 3 ], -0-CO-N(CH 3 ) 2 , -0-CO-N(C 2 H 5 ) 2 , -0-CO-N(C 3 H 7 ) 2 , -0-CO~N(C 4 H 9 ) 2 , -0-CO-N(cyclo-C 3 H 5 ) 2 , -0-CO-N[CH(CH 3 ) 2 ] 2 , -0-CO-N[C(CH 3 ) 3 ] 2 , (ii) an aromatic or heteroaromatic mono- or bicyclic ring selected from 2-thienyl, 3-thienyl, 2-furanyl, 3-furanyl, 2-oxazolyl, 3-oxazolyl, 4-oxazolyl, 2-thiazolyl, 3-thiazolyl, 4-thiazolyl, 1-pyrazolyl, 3-pyrazolyl, 4-pyrazolyl, 5-pyrazolyl, 1-imidazolyl, 2-imidazolyl, 4-imidazolyl, 5-imidazolyl, phenyl, 1-naphthyl, 2-naphthyl, 2-pyridyl, 3-pyridyl, 4-pyridyl, 2-pyrimidinyl, 4-pyrimidinyl. 5-pyrimidinyl, 2-pyrazinyl, 3-pyridazinyl, 4-pyridazinyl, l,3,5-triazin-2-yl, R y represents -H, -CH 3 , -CH 2 Ph, -COOC(CH 3 ) 3 , -COOCH 3 , COOCH ; CH , -COOCH 2 CH 2 CH 3 , -COOCH(CH 3 ) 2 , COOCH : Ph. -COCH 3 ; 84 85 83 the group -B-Y-R -R together with one substituent R \" may form a group -OCH 2 O-, if R 83 is attached in position ortho to -B-Y-R 84 -R 85 ; with the proviso that R 8 is not -H. if the group -B-Y-R 84 -R 85 is hydrogen. R 98 is selected from -NO,, -CN, -F, -CI, -Br, -I, -NH 2 , -OH, -CR 62 R 63 -CR 65 R 66 -CR 57 R 68 --CR 69 R 70 R 64 , -0-CR 62 R 63 R 64 , -0-CR 62 R 63 -CR 65 R 66 R 6 -O- CR 0/ R 0j -CR o;> R 00 -CR' -O-CR 62 R 63 -CR 65 R 66 -CR 67 R 68 -CR 69 R 70 R 64 , ^ ^^ fi?.„ 3 ^^ fi „6 ^^ ,67 ^ 8 ^ 6 ^ 70 ^ , ^ 71 ^ 79 ^ 6 ^^ 2 ^ 63 ^ ,,-.6^66 ^^ fi7 ^ fiS- ^ fi4 -U -i. K K --«. K K K K I K K -U K K , -UK ~ K \" -UK ~ K \"\" -UK K , O-CR 62 R 63 -CR 65 R 66 --CR 67 R 68 -CR 69 R 70 -CR 71 R 72 -CR 73 R 74 R 64 ,-CR 62 R 63 -CR 65 R 66 R 64 , CR 62 R 63 -O-CR 5 R 66 -CR 67 R 68 -CR 69 R 70 R 64 , -CR 62 R 63 -O^CR 65 R 66 -CR 67 R 68 R 64 , Γ UΏK 62 Ώ Κ 63 O ) - Γ κ Ώ 65 Ώ κ 66 — Γ υ\"Ρ 67 Ρ κ 68 — Γ υ1? 69 Ρ κ 70 — Γ υΏκ ΊΙ Ώ κ 71 κΏ 64 , — Γ UΏK 62 Ώ Κ 63 — Γ>»— Γυ\"Ρκ 65 Τ κ? 66 Ρ 64 , CR 62 R 63 ^o^CR 65 R 66_ CR 67 R 68 ^CR 69 R 70_ CR 71 R 72_ CR 73 R 74 R 64^ CR 62 R 63 R 64 5 r-