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 H3^Ser10 phosphorylation and followed by a surge in apoptosis. AAPK-25 targets Aurora-A, -B, and -C with K_d values ranging from 23-289 nM, as well as PLK-1, -2, and -3 with K_d 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 H3^Ser10 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].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

AAPK-25 enhances survival rate in the BALB/c nude mice tumor xenograft model^[1].

Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.

442.32

C₂₁H₁₃Cl₂N₃O₂S

2247919-28-2

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• [1]. Qi B, et al. Discovery of inhibitors of Aurora/PLK targets as anti-cancer agents. J Med Chem. 2019 Aug 5.