(2R)-2-[[6-[(3-Chlorophenyl)amino]-9-(1-methylethyl)-9H-purin-2-yl]amino]-3-methyl-1-butanol (2R)-2-[[[6-[(3-氯苯基)-氨基]-9-异丙基-9H-嘌呤-2-基]氨基]-3-甲基-1-丁醇
CAS 212844-53-6 MFCD02179211
化学结构图
SMILES: CC(C)[C@H](CO)Nc1nc(Nc2cccc(Cl)c2)c2ncn(C(C)C)c2n1
化学属性
| Mol. Formula | C19H25ClN6O |
|---|---|
| Mol. Weight | 388.89 |
| Appearance | Grey to green solid powder |
| Solubility | Soluble in DMSO |
别名和识别编码
| Chemical Name | (2R)-2-[[6-[(3-Chlorophenyl)amino]-9-(1-methylethyl)-9H-purin-2-yl]amino]-3-methyl-1-butanol |
|---|---|
| Synonym | 2-(1R-Isopropyl-2-hydroxyethylamino)-6-(3-chloroanilino)-9-isopropylpurine NG-60 Purvalanol A Purvalanol A, Purv; NG60; NG-60; NG 60. |
| MDL Number | MFCD02179211 |
| PubChem Substance ID | 24898543 |
| Chemical Name Translation | (2R)-2-[[[6-[(3-氯苯基)-氨基]-9-异丙基-9H-嘌呤-2-基]氨基]-3-甲基-1-丁醇 |
| Formula | C19H25ClN6O |
| IUPAC Name | (R)-2-((6-((3-chlorophenyl)amino)-9-isopropyl-9H-purin-2-yl)amino)-3-methylbutan-1-ol |
| InChIKey | PMXCMJLOPOFPBT-HNNXBMFYSA-N |
| InChI | InChI=1S/C19H25ClN6O/c1-11(2)15(9-27)23-19-24-17(22-14-7-5-6-13(20)8-14)16-18(25-19)26(10-21-16)12(3)4/h5-8,10-12,15,27H,9H2,1-4H3,(H2,22,23,24,25)/t15-/m0/s1 |
| Canonical SMILES | CC(C)[C@@H](NC1=NC(NC2=CC=CC(Cl)=C2)=C3N=CN(C(C)C)C3=N1)CO |
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分类
- {SNA} Apoptosis and Cell Cycle, Bioactive Small Molecule Alphabetical Index, Cell Cycle Proteins, Antibodies and Reagents, Cell Cycle Regulators, Cyclin-Dependent Kinase (CDK), Enzymes, Substrates, Inhibitors &, Modulators for Stem Cell Biology, General Stem Cell Biology, Inhibitors, Kinase/Phosphatase Biology, PI-PZ, Serine/Threonine Kinase Biology, Serine/Threonine Kinase Inhibitors, Stem Cell Characterization, 干细胞生物学, 生物活性小分子, 细胞信号转导和神经科学, 细胞生物学
- {SNA} Apoptosis and Cell Cycle, Bioactive Small Molecules, Cell Biology, Cell Cycle Proteins and Antibodies, Cell Cycle Regulators, Cell Signaling and Neu
产品应用
- Purvalanol A is a potent CDK inhibitor, which effectively suppresses Src-mediated transformation by inhibiting both CDKs and c-Src. indicating that the activation of CDKs contributes to the c-Src transformation. Purvalanol A suppressed the c-Src activity as effectively as the Src-selective inhibitor PP2, and that it reverted the transformed morphology to a nearly normal shape with less cytotoxicity than PP2. Purvalanol A induced a strong G2-M arrest, whereas PP2 weakly acted on the G1-S transition. Furthermore, when compared with PP2, purvalanol A more effectively suppressed the growth of human colon cancer HT29 and SW480 cells, in which Src family kinases and CDKs are activated.
