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CAS No. 212844-53-6
Purvalanol A is a potent, and cell-permeable CDK inhibitor with IC50 of 4 nM, 70 nM, 35 nM, and 850 nM for cdc2-cyclin B, cdk2-cyclin A, cdk2-cyclin E, and cdk4-cyclin D1, respectively. Purvalanol A induces endoplasmic reticulum stress-mediated apoptosis and autophagy.
Selleck's Purvalanol A has been cited by 7 publications
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After 12 h PAB treatment, cells were treated with PAB in the absence and presence of RO-3306 or purvalanol A for 12 h and 36 h. (A) Expressions of p-histone h3 were detected by western blot.
Cancer Lett, 2016, 383(2):295-308. Purvalanol A purchased from Selleck.
（A）HeLa cells were treated with Nocodazole for 8 hours and then fixed. Before the cells were stained with phospho-specific antibody against S119 of Ajuba, they were pre-incubated with PBS (no peptide control), or non-phosphorylated (control) peptide, or the phosphorylated peptide used for immunizing rabbits. CDK1 inhibitors Purvalanol A (10 μM) together with MG132 (25 μM) were added 2 h before the cells were fixed (bottom two rows).（B）Experiments were done similarly as in (A) with phospho-specific antibody against Ser175 of Ajuba.
J Biol Chem, 2016, 291(28):14761-72.. Purvalanol A purchased from Selleck.
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|Description||Purvalanol A is a potent, and cell-permeable CDK inhibitor with IC50 of 4 nM, 70 nM, 35 nM, and 850 nM for cdc2-cyclin B, cdk2-cyclin A, cdk2-cyclin E, and cdk4-cyclin D1, respectively. Purvalanol A induces endoplasmic reticulum stress-mediated apoptosis and autophagy.|
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. 
|In vitro||DMSO||60 mg/mL warmed (154.28 mM)|
|Ethanol||'13 mg/mL warmed|
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