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 In Vitro AAPK-25 inhibits HCT-116, Calu6, A549 and MCF-7 cells growth with IC 50 s 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 H3 Ser10 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. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo AAPK-25 enhances survival rate in the BALB/c nude mice tumor xenograft model . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Form:Solid IC50& Target: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)