Purvalanol A 是一種有效的，細胞滲透性 CDK 抑制劑，對cdc2-cyclin B，cdk2-cyclin A，cdk2-cyclin E，和 cdk4-cyclin D1的 IC50 分別為 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 是一種有效的，細胞滲透性 CDK 抑制劑，對cdc2-cyclin B，cdk2-cyclin A，cdk2-cyclin E，和 cdk4-cyclin D1的 IC50 分別為 4 nM，70 nM，35 nM，和 850 nM。Purvalanol A 可誘導(dǎo)內(nèi)質(zhì)網(wǎng)應(yīng)激介導(dǎo)的凋亡與自噬。

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

Purvalanol A劑量依賴性降低MCF-7和MDA-MB-231細胞系中細胞活性。Purvalanol A在MCF-7細胞中誘導(dǎo)50%的細胞活性損失，而MDA-MB-231細胞對Purvalanol A敏感性較低(細胞活性減少32 %)。Purvalanol A在MCF-7和MDA-MB-231細胞中誘導(dǎo)線粒體介導(dǎo)的細胞凋亡。 Purvalanol A通過抑制細胞周期進程和c-Src信號通路，有效防止c-Src介導(dǎo)轉(zhuǎn)化，并有效抑制一些c-Src上調(diào)的人類癌細胞貼壁不依賴性生長。 Purvalanol A對HT29和SW480人結(jié)腸癌細胞的貼壁依賴性生長具有強烈的抑制作用。