AAPK-25 |
| カタログ番号GC35216 |
AAPK-25 は、抗腫瘍活性を備えた強力かつ選択的な Aurora/PLK 二重阻害剤であり、有糸分裂の遅延を引き起こし、前中期で細胞を停止させ、バイオマーカーのヒストン H3Ser10 リン酸化を反映し、その後にアポトーシスが急増します。 AAPK-25 は、23 ～ 289 nM の範囲の Kd 値を持つ Aurora-A、-B、および -C と、55 ～ 456 nM の範囲の Kd 値を持つ PLK-1、-2、および -3 をターゲットにしています。
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 2247919-28-2
Sample solution is provided at 25 µL, 10mM.
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AAPK-25 is a potent and selective Aurora/PLK dual inhibitor with anti-tumor activity, which can cause mitotic delay and arrest cells in a prometaphase, reflecting by the biomarker histone H3Ser10 phosphorylation and followed by a surge in apoptosis. AAPK-25 targets Aurora-A, -B, and -C with Kd values ranging from 23-289 nM, as well as PLK-1, -2, and -3 with Kd values ranging from 55-456 nM[1]. Kd: 23 nM (Aurora-A), 78 nM (Aurora-B), 289 nM (Aurora-C), 55 nM (PLK-1), 272 nM (PLK-2), 456 nM (PLK-3), 5.32 μM (ERK), 7.11 μM (PI3K), 8.02 μM (CDK)[1]
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[1].AAPK-25 induces apoptosis as a dose-dependent manner in HCT-116 cell line[1].AAPK-25 has significantly increased histone H3Ser10 phosphorylation, indicating a markedly mitotic block[1].AAPK-25 is in notably inhibition of the mitotic spindle checkpoint, which is mainly mediated by cell cycle signaling and mitotic pathways[1].
AAPK-25 enhances survival rate in the BALB/c nude mice tumor xenograft model[1].
[1]. Qi B, et al. Discovery of inhibitors of Aurora/PLK targets as anti-cancer agents. J Med Chem. 2019 Aug 5.
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