Biological Activity |
CCB02 is a selective CPAP-tubulin interaction inhibitor, binding to tubulin and competing for the CPAP binding site of beta-tubulin, with an IC50 of 689 nM, and shows potent anti-tumor activity. CCB02 shows no inhibition on the cell cycle- and centrosome-related kinases, or the phosphorylation status of Aurora A, Plk1, Plk2, CDK2, and CHK1[1]. IC50 & Target: IC50: 689 nM (CPAP-tubulin)[1] In Vitro: CCB02 perturbs CPAP PN2-3-tubulin interaction with an IC50 of 0.441 uM in a PN2-3 CPAP-GST pull-down assay[1]. CCB02 shows no inhibition on the cell cycle- and centrosome-related kinases, or the phosphorylation status of Aurora A, Plk1, Plk2, CDK2, and CHK1[1]. CCB02 (0.1-15 uM, 72 hours) inhibits the proliferation of cancer cells with extra centrosomes, IC50s are 0.86-2.9 uM[1]. CCB02 activates spindle assembly checkpoint, induces PCM proteins recruitment to centrosomes, and enhances microtubule nucleation activities of centrosomes[1]. In Vivo: CCB02 (30 mg/kg, p.o. daily for 24 days) shows potent anti-tumor effect in nude mice bearing subcutaneous human lung (H1975T790M cells) tumor xenografts[1]. CCB02 also suppresses MDA-MB-231 cell migration and cuases multipolar mitosis in mouse xenografts[1]. |