MK-8745是一种高度选择性Aurora-A抑制剂，IC50 为0.6 nM,其对于Aurora-A的选择性高于Aurora B的选择性450倍。在非霍奇金淋巴瘤（NHL）的细胞系中， MK-8745导致细胞周期阻滞在G2/ M期伴随四倍体核的聚集，随后细胞死亡。MK-8745诱导p21（WAF1/CIP1）和CYCB1，表明细胞周期阻滞并增加了G2/M期细胞群。MK-8745处理导致Aurora-A底物（TACC3， Eg5和TPX2）迅速降解，随后磷酸化Aurora-A减少。

>98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

MK8745

固体粉末

Ethanol ：1 mg/mL (2.31 mM)

DMSO ：80 mg/mL (185.2 mM)

Aurora A

MK-8745 leads to cell cycle arrest at the G2/M phase with accumulation of tetraploid nuclei followed by cell death in non-Hodgkin lymphoma (NHL) cell lines. Treatment with MK-8745 induces p21(waf1/cip1) and CycB1, indicating cell cycle arrest and an increase in the G2/M phase cell population. Following MK-8745 treatment, Aurora-A substrates (TACC3, Eg5 and TPX2) are rapidly degraded following the reduction of phospho-Aurora-A. MK8745 induces apoptotic cell death in a p53-dependent manner when tested in vitro in cell lines of multiple lineages. Exposure of p53 wild-type cells to MK8745 results in the induction of p53 phosphorylation (ser15) and an increase in p53 protein expression. p53-dependent apoptosis by MK8745 is further confirmed in HCT 116 p53(-/-) cells transfected with wild-type p53.