CAN-508 is an ATP-competitive inhibitor of cyclin-dependent kinase 9 (Cdk9; IC50 = 350 nM) and moderate inhibitor of similar enzymes including Cdk2-cyclin E. In the HT-29 cancer cell line, CAN-508 was observed to attenuate the frequency of the S-phase. Other CAN-508 effects were shown to involve inhibition of mRNA synthesis, induction of p53, inhibition of IL-6 signaling and reduced phosphorylation of both retinoblastoma protein and RNA polymerase II at the C-terminal domain. CAN-508 has been observed to be an effective antitumor and antimetastatic agent by disrupting TNFα signaling. CAN-508 is an inhibitor of Cdk4, cyclin D1 and p70 S6 Kinase. CAN508 inhibits endothelial cell migration and tube formation. In addition, it reduces phosphorylation of the C-terminus of RNA polymerase II and inhibits mRNA synthesis in endothelial cells, in accordance with previous observations that it has high selectivity towards the positive transcriptional regulator P-TEFb. Moreover, CAN-508 reduces expression of vascular endothelial growth factor by several human cancer cell lines. The findings suggest that P-TEFb may be an attractive target for anti-angiogenic therapy.