Purvalanol A (NG-60) is an effective and cell-permeable CDK inhibitor with IC50 of 70/4/35/850 nM for cdk2-cyclin A/B/E, and cdk4-cyclin D1, respectively.

CDK2-CyclinA:70 nM, CDK4-CyclinD1:850 nM, ERK1:9000 nM, CDK2-CyclinE:35 nM, CDC2-cyclinB:4 nM, CDK5-p35:75 nM

In MCF-7 cells, Purvalanol A leads to a 50% reduction in cell viability, while MDA-MB-231 cells exhibit lower sensitivity to Purvalanol A, showing a 32% decrease in cell viability. Purvalanol A induces mitochondrial-mediated apoptosis in both MCF-7 and MDA-MB-231 cells. The compound's effect on reducing the viability of these cell lines is dose-dependent. By inhibiting cell cycle progression and the c-Src signaling pathway, Purvalanol A effectively prevents c-Src-mediated transformation and significantly inhibits anchorage-independent growth in certain human cancer cells with upregulated c-Src. Additionally, Purvalanol A markedly suppresses anchorage-dependent growth in HT29 and SW480 human colorectal cancer cells.

Cells are seeded at 10000 density in 96-well plates and treated with various concentrations of Purvalanol A (0-100 μM) for 24 h. Cells are exposed to 10 μL of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltet- razolium bromide dye (5 mg/mL) and are incubated at 37℃ for 4 h. In order to solubilize the formazan crystals 100 μL DMSO is added. Absorbance is determined at 570 nm spectrophotometrically.(Only for Reference)

DMSO: < 1 mg/mL (insoluble or slightly soluble), Sonication is recommended.

Ethanol: 19.5 mg/mL (50.14 mM), Sonication is recommended.