>>Signaling Pathways>> Cell Cycle/Checkpoint>> Microtubule/Tubulin>>CCB02

CCB02

Catalog No.GC33300

CCB02는 689nM의 IC50으로 tubulin에 결합하고 β-tubulin의 CPAP 결합 부위에 대해 경쟁하는 선택적 CPAP-tubulin 상호 작용 억제제이며 강력한 항종양 활성을 나타냅니다. CCB02는 세포주기 및 중심체 관련 키나제 또는 Aurora A, Plk1, Plk2, CDK2 및 CHK1의 인산화 상태에 대한 억제를 나타내지 않습니다.

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CCB02 Chemical Structure

Cas No.: 2100864-57-9

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Sample solution is provided at 25 µL, 10mM.

Description Chemical Properties Product Documents Related Products

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].

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. 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 inhibits the proliferation of cancer cells with extra centrosomes, IC50s are 0.86-2.9 μM. CCB02 activates spindle assembly checkpoint, induces PCM proteins recruitment to centrosomes, and enhances microtubule nucleation activities of centrosomes[1].

CCB02 (30 mg/kg, p.o. daily) shows potent anti-tumor effect in nude mice bearing subcutaneous human lung (H1975T790M cells) tumor xenografts. CCB02 also suppresses MDA-MB-231 cell migration and cuases multipolar mitosis in mouse xenografts[1].

[1]. Mariappan A, et al. Inhibition of CPAP-tubulin interaction prevents proliferation of centrosome-amplified cancer cells. EMBO J. 2019 Jan 15;38(2). pii: e99876.

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