BMI-1026 is a potent cdk inhibitor with potential anticancer activity. BMI-1026 induced a strong cell cycle alteration with potent inhibitory activities against cyclin-dependent kinases, collectively known as Cdks. BMI-1026 imposes a potent G(2)-M arrest and mild G(1)-S and S arrests. In vitro BMI-1026 induces a mitotic catastrophe and precocious mitotic exit even in the presence of nocodazole. These defects appeared to lead to apoptotic cell death in tumorigenic cell lines. Consistent with the induction of mitotic defects and apoptosis, BMI-1026 imposed a selective sensitivity to proliferating versus differentiating or growth-arrested mouse keratinocytes. These data suggest that BMI-1026 could be developed as a potential anti-Cdk1 chemotherapeutic agent. References: Seo HJ, Park HJ, Choi HS, Hwang SY, Park JS, Seong YS. BMI-1026 treatment can induce SAHF formation by activation of Erk1/2. BMB Rep. 2008 Jul 31;41(7):523-8. PubMed PMID: 18682036.

纯度：≥98%

CAS：477726-77-5