• Purvalanol A is a cell-permeable, potent, and selective cyclin-dependent kinase (CDK) inhibitor. It inhibited CDK kinases with IC50 values of 4 nM for CDC2/cyclin B, 70 nM for CDK2/cyclin A, 35 nM for CDK2/cyclin E, 75 nM for CDK5/p35, and 850 nM for CDK4/cyclin D1. Gray N.S., et al. “Exploiting chemical libraries, structure and genomics in the search for kinase inhibitors.” Science 281: 533-538 (1998).
• Purvalanol A inhibited radiation-induced CDC2 kinase activity and induced apoptosis by increasing the levels of active fragments of caspase 3. Lizuka D., et al. “Purvalanol A enhances cell killing by inhibiting up-regulation of CDC2 kinase activity in tumor cells irradiated with high doses of X rays.” Radiat. Res. 167: 563-571 (2007).
• Purvalanol A prevented hippocampal proliferation in a time- and concentration -dependent manner. Mackowiak M., et al. “Purvalanol A, inhibitor of cyclin-dependent kinases attenuates proliferation of cells in the dentate gyrus of the adult rat hippocampus.” Pharmacol. Rep. 57: 845-849 (2005)
• Purvalanol A arrested cells at the G(2)-M phase and induced apoptosis in a concentration-dependent manner. It also concomitantly down-regulated the antiapoptotic protein survivin, a member of the inhibitors of apoptosis protein family. Pennati M., et al. “Potentiation of paclitaxel-induced apoptosis by the novel cyclin-dependent kinase inhibitor NU6140: a possible role for survivin down-regulation.” Mol. Cancer Ther. 4: 1328-1337 (2005).
• In synchronized cells, purvalanol A arrested cells in the G1 and G2 phases, but did not prevent DNA synthesis in S-phase cells. After mouse fibroblasts and human cancer cell lines were incubated with purvalanol A for 24 hr, inhibition of cell proliferation and cell death were observed. Villerbu N., et al. “Cellular effects of purvalanol A: a specific inhibitor of cyclin-dependent kinase activities.” Int. J. Cancer 97: 761-769 (2002).
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