CHM-1

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

CHM-1 是一种细胞凋亡诱导剂，通过激活 Cdc2 激酶活性，在人肝细胞癌中显示出有效的抗肿瘤能力。 CHM-1 在体外和体内抑制微管蛋白聚合。

CHM-1 is an inducer of apoptosis, and displays potent antitumor ability in human hepatocellular carcinoma by activation of Cdc2 kinase activity. CHM-1 inhibits tubulin polymerization in vitro and in vivo.(In Vitro):CHM-1 (0-10 μM; 24 hours) significantly increased the binding of cyclin B1 to Cdc2 and induced change in expressed and phosphorylated status of G2-M regulators in HA22T cells. CHM-1 (0-100μM; 24 hours) induced significant concentration-dependent growth inhibition in HA22T, Hep3B, and HepG2 cells, with the most potent effects observed in HA22T cells with an IC50 of 0.75 μM).(In Vivo):In male severe combined immunodeficient mice, CHM-1 (10 mg/kg; i.p.) induced inhibition of HA22T tumor growth in a dose-dependent manner.

CHM-1 (0-100μM; 24 hours) induces significant concentration-dependent growth inhibition in HA22T, Hep3B, and HepG2 cells, with the most potent effects observed in HA22T cells (IC50 = 0.75 μM).CHM-1 (0-10 μM; 24 hours) significantly increases the binding of cyclin B1 to Cdc2 in HA22T cells. Cell Viability Assay Cell Line:HA22T, Hep3B, and HepG2 cells Concentration:0-100 μM Incubation Time:24 hours Result:Induced G2-M arrest of the cell cycle followed by apoptosis.Western Blot Analysis Cell Line:HA22T cells Concentration:0-10 μM Incubation Time:24 hours Result:Induced change in expressed and phosphorylated status of G2-M regulators in human hepatocellular carcinoma cells.

CHM-1 (10 mg/kg; I.p.) induces a dose-dependent inhibition of HA22T tumor growth. Animal Model:Male severe combined immunodeficient mice (HA22T)Dosage:10 mg/kg Administration:I.p.Result:Induced a dose-dependent inhibition of HA22T tumor growth.

NSC656158

Apoptosis

Apoptosis

Antibiotic|P-glycoprotein

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154554-41-3

283.258

C16H10FNO3

>98% (HPLC)

In Vitro:?DMSO : 5 mg/mL (17.65 mM)

Fc1ccccc1-c1cc(=O)c2cc3OCOc3cc2[nH]1

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(-20℃)

With Ice Pack

≥ 2 years