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.
CAS 477726-77-5 MFCD77726775
化学结构图
SMILES: Nc1nccc(-c2ccc(O)c(-c3ccnc(N)n3)c2)n1
化学属性
Mol. Weight
280.28
Appearance
Solid powder
Solubility
Soluble in DMSO, not in water
别名和识别编码
Chemical Name
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.
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.
安全信息
Storage condition
Dry, dark and at 0 - 4 C for short term (days to weeks) or -20 C for long term (months to years).