CCB02

CCB02 is a selective CPAP-tubulin interaction inhibitor, binding to tubulin and competing for the CPAP binding site of β-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 μM 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 μM, 72 hours) inhibits the proliferation of cancer cells with extra centrosomes, IC₅₀s are 0.86-2.9 μM^[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 (H1975^T790M cells) tumor xenografts^[1].
CCB02 also suppresses MDA-MB-231 cell migration and cuases multipolar mitosis in mouse xenografts^[1].