Purvalanol A
CDK inhibitor / Cyclin-dependent kinase inhibitor. IC50s= 4, 70, 35, 75 and 850 nM for cdc2/cyclin B, cdk2/cyclin A, cdk2/cyclin E, cdk5/p35 and cdk4/cyclin D1 and respectively.1 Reversibly arrests synchronized cells in G1 and G2 phase.2 Induces ER stress-mediated apoptosis and autophagy in colon cancer cells.3 Suppresses Src-mediated transformation by inhibiting both CDKs and c-Src.4 In cells transformed with MYC, purvalanol A rapidly down-regulates survivin expression and induces MYC-dependent apoptosis.5 Cell permeable.
Biochemicals & reagents
212844-53-6
NG-60
1) Gray et al. (1998), Exploiting chemical libraries, structure, and genomics in the search for kinase inhibitors; Science, 281 533 2) Villerbu et al. (2002), Cellular effects of purvalanol A: a specific inhibitor of cyclin-dependent kinase activities; Int. J. Cancer, 97 761 3) Coker-Gurkan et al. (2015), Purvalanol induces endoplasmic reticulum stress-mediated apoptosis and autophagy in a time dependent manner in HCT116 colon cancer cells; Oncol. Rep., 33 2761 4) Hikita et al. (2010), Purcalanol A, a CDK inhibitor, effectively suppresses Src-mediated transformation by inhibiting both CDKs and c-Src; Genes Cells, 15 1051 5) Goga et al. (2007), Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC; Nat. Med., 13 820
-20°C
TARGET: Kinase -- PATHWAY: Apoptosis inducer; Cell cycle -- RESEARCH AREA: Cellular stress; Cell death; Stem cells