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Purvalanol B is a selective inhibitor of CDK1, CDK2 and CDK4.

CDKs (cyclin-dependent kinases) family has the ability to regulate cell cycle.

Purvalanol B is reported as one of the most potent and selective CDK inhibitors. When tested with Chinese hamster lung fibroblast CCL39 cell line, treatment with Purvalanol B inhibited cells proliferate via targeting CKD1 which induced a G2/M block with a GI50 of 2.5 μM. In asynchronous cells, exposed to Purvalanol B led to an accumulation of cells in G2/M phase [1].

In a mouse model with NCI-H2228 subcutaneous xenograft, oral administration of ASP3026 caused significant reduction of phosphorylated ALK and tumor growth. 30 mg/kg/d ASP3026 for 2 weeks induced tumor regression by 78%. In mice injected with Karpas 299 cells, ASP3026 treatment caused remarkable lymphoma regression [2, 3].

Purvalanol B also interacts with p42/p44 MAPK proteins when tested with several mammalian cell lines including MCF-7 cell line [1].

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