AAPK-25

Research use only, not for human use.

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, 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.(In Vitro):AAPK-25 inhibited HCT-116, Calu6, A549, and MCF-7 cells growth (IC50s: 0.4, 5.3, 11.6, and 2.3 μM). AAPK-25 dose-dependently induced apoptosis in HCT-116 cell line.(In Vivo):In the BALB/c nude mice tumor xenograft model, AAPK-25 enhanced the survival rate.

AAPK-25 inhibits HCT-116, Calu6, A549 and MCF-7 cells growth with IC50s of 0.4, 5.3, 11.6, and 2.3 μM, respectively.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 in notably inhibition of the mitotic spindle checkpoint, which is mainly mediated by cell cycle signaling and mitotic pathways.

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

——

Apoptosis

Apoptosis

——

——

——

2247919-28-2

442.31

C21H13Cl2N3O2S

>98% (HPLC)

In Vitro:?DMSO : 50 mg/mL (113.04 mM)

Clc1ccc(cc1Cl)C(=O)Nc1ccc2cc(ccc2c1)C(=O)Nc1nccs1

——

(-20℃)

With Ice Pack

≥ 2 years