CCB02 是一种选择性的 CPAP-tubulin 相互作用抑制剂，能够与 tubulin 结合，竞争 β-tubulin 的 CPAP 结合位点，IC₅₀ 值为 689 nM，具有高效抗肿瘤活性。CCB02 对其他的蛋白没有抑制作用，包括与细胞周期、中心体相关蛋白，同时对 Aurora A，Plk1，Plk2，CDK2 和 CHK1 的磷酸化状态无作用。

CCB02 is a selective CPAP-tubulin interaction inhibitor, binding to tubulin and competing for the CPAP binding site of β-tubulin, with an IC 50 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.

Solid

IC50: 689 nM (CPAP-tubulin)

CCB02 perturbs CPAP PN2-3-tubulin interaction with an IC50 of 0.441 μM in a PN2-3 CPAP-GST pull-down assay.
CCB02 shows no inhibition on the cell cycle- and centrosome-related kinases, or the phosphorylation status of Aurora A, Plk1, Plk2, CDK2, and CHK1.
CCB02 (0.1-15 μM, 72 hours) 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. has not independently confirmed the accuracy of these methods. They are for reference only.

CCB02 (30 mg/kg, p.o. daily for 24 days) shows potent anti-tumor effect in nude mice bearing subcutaneous human lung (H1975 cells) tumor xenografts.
CCB02 also suppresses MDA-MB-231 cell migration and cuases multipolar mitosis in mouse xenografts. has not independently confirmed the accuracy of these methods. They are for reference only.

Room temperature in continental US; may vary elsewhere.

-20°C, stored under nitrogen In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

[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.

In Vitro: DMSO : 25 mg/mL (106.27 mM; Need ultrasonic)配制储备液