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.

PI3K:7.11 μM (kd), PLK2:272 nM (kd), Aurora B:78 nM (kd), PLK3:456 nM (kd), Aurora A:23 nM (kd), ERK:5.32 μM (kd), Aurora C:289 nM (kd), CDK:8.02 μM , PLK1:55 nM (kd)

AAPK-25抑制HCT-116、Calu6、A549和MCF-7细胞增长(IC50s分别为0.4、5.3、11.6和2.3 μM)。在HCT-116细胞系中，AAPK-25按剂量依赖性诱导凋亡。AAPK-25显著增加组蛋白H3Ser10的磷酸化，表明明显的有丝分裂阻塞。AAPK-25对有丝分裂纺锤体检查点具有显著抑制作用。

AAPK-25在BALB/c裸鼠肿瘤异种移植模型中提高了存活率。