PURVALANOL A

Purvalanol A 是一种有效的，细胞渗透性 CDK 抑制剂，对cdc2-cyclin B，cdk2-cyclin A，cdk2-cyclin E，和 cdk4-cyclin D1的 IC50 分别为 4 nM，70 nM，35 nM，和 850 nM。Purvalanol A decreases cell viability in dose-dependent manner in MCF-7 and MDA-MB-231 cell lines. Purvalanol A induces cell viability loss by 50 % in MCF-7 cells but MDA-MB-231 cells sre less sensitive to Purvalanol A (32 % decreases in cell viability). Purvalanol A induces mitochondria-mediated apoptosis in MCF-7 and MDA-MB-231 cells. Purvalanol A effectively prevents c-Src-mediated transformation by inhibiting both cell cycle progression and c-Src signaling, and effectively suppresses the anchorage independent growth of some human cancer cells in which c-Src is up-regulated. Purvalanol A has a stronger inhibitory effect on the anchorage-independent growth of HT29 and SW480 human colon cancer cells.Purvalanol A 是一种有效的，细胞渗透性 CDK 抑制剂，对cdc2-cyclin B，cdk2-cyclin A，cdk2-cyclin E，和 cdk4-cyclin D1的 IC50 分别为 4 nM，70 nM，35 nM，和 850 nM。Purvalanol A 可诱导内质网应激介导的凋亡与自噬。

Target	Value
Cdc2/CyclinB ()	4 nM
CDK2/CyclinE	35 nM
CDK2/CyclinA	70 nM
CDK4/CyclinD1	850 nM

Purvalanol A剂量依赖性降低MCF-7和MDA-MB-231细胞系中细胞活性。Purvalanol A在MCF-7细胞中诱导50%的细胞活性损失，而MDA-MB-231细胞对Purvalanol A敏感性较低(细胞活性减少32 %)。Purvalanol A在MCF-7和MDA-MB-231细胞中诱导线粒体介导的细胞凋亡。 Purvalanol A通过抑制细胞周期进程和c-Src信号通路，有效防止c-Src介导转化，并有效抑制一些c-Src上调的人类癌细胞贴壁不依赖性生长。 Purvalanol A对HT29和SW480人结肠癌细胞的贴壁依赖性生长具有强烈的抑制作用。