AAPK-25 是选择性的AuRORa/PLK激酶双重抑制剂，显示出抗肿瘤活性。它可造成有丝分裂延迟并阻滞前中期细胞，通过生物标志物组蛋白 H3Ser10磷酸化反应，最终导致细胞凋亡激增。

AAPK-25, a potent and selective dual inhibitor of Aurora/PLK, causes mitotic delay and cell arrest in prometaphase, via phosphorylation of the biomarker histone H3Ser10, followed by a surge in apoptosis. AAPK-25 targets Aurora A, Aurora B, and Aurora C with Kd values ranging from 23-289 nM, and PLK1, PLK2, and PLK3 with Kd values ranging from 55-456 nM. AAPK-25 has antitumor activity.

AAPK-25 inhibits HCT-116, Calu6, A549, and MCF-7 cells growth (IC50s: 0.4, 5.3, 11.6, and 2.3 μM). AAPK-25 induces apoptosis as a dose-dependent manner in HCT-116 cell line. AAPK-25 has significantly increased histone H3Ser10 phosphorylation, indicating a markedly mitotic block. AAPK-25 is notably inhibition of the mitotic spindle checkpoint.

AAPK-25 enhances the survival rate in the BALB/c nude mice tumor xenograft model.

2247919-28-2

C21H13Cl2N3O2S

442.32

(< 1 mg/ml refers to the product slightly soluble or insoluble )
Powder: -20°C for 3 years
In solvent: -80°C for 2 years