VMY-1-103 is a potent CDK inhibitor, is also a novel dansylated analog of purvalanol B, was shown to inhibit cell cycle progression and proliferation in prostate and breast cancer cells more effectively than purvalanol B. VMY-1-103 , but not purvalanol B, significantly decreased the proportion of cells in S phase and increased the proportion of cells in G(2)/M. VMY-1-103 increased the sub G(1) fraction of apoptotic cells, induced PARP and caspase-3 cleavage and increased the levels of the Death Receptors DR4 and DR5, Bax and Bad while decreasing the number of viable cells, all supporting apoptosis as a mechanism of cell death. VMY-1-103 possesses unique antiproliferative capabilities and that this compound may form the basis of a new candidate drug to treat medulloblastoma.
CAS 1209002-43-6 MFCD309002436
化学结构图
SMILES: CC(C)[C@H](CO)Nc1nc(Nc2ccc(C(=O)NCCNS(=O)(=O)c3cccc4c(N(C)C)cccc34)c(Cl)c2)c2ncn(C(C)C)c2n1
化学属性
| Mol. Weight | 708.27 |
|---|---|
| Appearance | Solid powder |
| Solubility | Soluble in DMSO, not in water |
别名和识别编码
| Chemical Name | VMY-1-103 is a potent CDK inhibitor, is also a novel dansylated analog of purvalanol B, was shown to inhibit cell cycle progression and proliferation in prostate and breast cancer cells more effectively than purvalanol B. VMY-1-103 , but not purvalanol B, significantly decreased the proportion of cells in S phase and increased the proportion of cells in G(2)/M. VMY-1-103 increased the sub G(1) fraction of apoptotic cells, induced PARP and caspase-3 cleavage and increased the levels of the Death Receptors DR4 and DR5, Bax and Bad while decreasing the number of viable cells, all supporting apoptosis as a mechanism of cell death. VMY-1-103 possesses unique antiproliferative capabilities and that this compound may form the basis of a new candidate drug to treat medulloblastoma. |
|---|---|
| Formula | C34H42ClN9O4S |
| Synonym | VMY-1-103, VMY-1103, VMY 1103 |
| IUPAC Name | (R)-2-chloro-N-(2-(5-(dimethylamino)naphthalene-1-sulfonamido)ethyl)-4-((2-((1-hydroxy-3-methylbutan-2-yl)amino)-9-isopropyl-9H-purin-6-yl)amino)benzamide |
| InChIKey | NJNQGMFCZFMREY-MHZLTWQESA-N |
| InChI | InChI=1S/C34H42ClN9O4S/c1-20(2)27(18-45)40-34-41-31(30-32(42-34)44(19-37-30)21(3)4)39-22-13-14-25(26(35)17-22)33(46)36-15-16-38-49(47,48)29-12-8-9-23-24(29)10-7-11-28(23)43(5)6/h7-14,17,19-21,27,38,45H,15-16,18H2,1-6H3,(H,36,46)(H2,39,40,41,42)/t27-/m0/s1 |
| Canonical SMILES | O=C(NCCNS(=O)(C1=C2C=CC=C(N(C)C)C2=CC=C1)=O)C3=CC=C(NC4=C5N=CN(C(C)C)C5=NC(N[C@H](C(C)C)CO)=N4)C=C3Cl |
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- VMY-1-103 is a potent CDK inhibitor, is also a novel dansylated analog of purvalanol B, was shown to inhibit cell cycle progression and proliferation in prostate and breast cancer cells more effectively than purvalanol B. VMY-1-103 , but not purvalanol B, significantly decreased the proportion of cells in S phase and increased the proportion of cells in G(2)/M. VMY-1-103 increased the sub G(1) fraction of apoptotic cells, induced PARP and caspase-3 cleavage and increased the levels of the Death Receptors DR4 and DR5, Bax and Bad while decreasing the number of viable cells, all supporting apoptosis as a mechanism of cell death. VMY-1-103 possesses unique antiproliferative capabilities and that this compound may form the basis of a new candidate drug to treat medulloblastoma.
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