VMY-1-103 is a potent CDK inhibitor, is also a novel dansylated analogue 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. References: Ringer L, Sirajuddin P, Tricoli L, Waye S, Choudhry MU, Parasido E, Sivakumar A, Heckler M, Naeem A, Abdelgawad I, Liu X, Feldman AS, Lee RJ, Wu CL, Yenugonda V, Kallakury B, Dritschilo A, Lynch J, Schlegel R, Rodriguez O, Pestell RG, Avantaggiati ML, Albanese C. The induction of the p53 tumor suppressor protein bridges the apoptotic and autophagic signaling pathways to regulate cell death in prostate cancer cells. Oncotarget. 2014 Nov 15;5(21):10678-91. PubMed PMID: 25296977; PubMed Central PMCID: PMC4279402.

纯度：≥98%

CAS：1209002-43-6