purvalanol a

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.

Purvalanol B (NG 95) is a CDK inhibitor that targets Cdk2/cyclin A, Cdk2/cyclin E, Cdk5/p35, and Cdk2/cyclin B, with IC50 values of 6, 9, 6, and 6 nM, respectively.

(S)-Purvalanol B, the S enantiomer of Purvalanol B, is an inhibitor of cyclin-dependent kinase (CDK).

Aminopurvalanol A is a competitive, selective and cell-permeable inhibitor of cyclin-dependent kinase (CDK) that potently inhibits Cyclin A/cdk2, Cyclin B/cdk1, Cyclin E/cdk2, and P35/cdk5 with IC50 of 33 nM, 33 nM, 28 nM and 20 nM, respectively.

VMY-1-103 is a potent CDK inhibitor, is also a novel dansylated analog of purvalanol B, was shown to inhibit cell cycle progression and proliferation in prostate and breast cancer cells more effectively than purvalanol B. VMY-1-103 , but not purvalanol B, significantly decreased the proportion of cells in S phase and increased the proportion of cells in G(2)/M. VMY-1-103 increased the sub G(1) fraction of apoptotic cells, induced PARP and caspase-3 cleavage and increased the levels of the Death Receptors DR4 and DR5, Bax and Bad while decreasing the number of viable cells, all supporting apoptosis as a mechanism of cell death. VMY-1-103 possesses unique antiproliferative capabilities and that this compound may form the basis of a new candidate drug to treat medulloblastoma.

VMY-1-101 is a synthesized fluorescent CDK inhibitor. VMY-1-101 demonstrates potent CDK inhibitory activity, enhanced induction of G2/M arrest and modest apoptosis as compared to purvalanol B.