| Name | CHM-1 |
| Description | 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)[3]. |
| 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[3]. |
| Storage | Shipping with blue ice/Shipping at ambient temperature. |
| Solubility Information | DMSO : 1.42 mg/mL (5.01 mM), Sonication is recommended. H2O : < 7.08 mg/mL, Sonication is recommended.
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| Keywords | Tubulin polymerization | NSC-656158 | NSC656158 | NSC 656158 | microtubule-destabilizing | MicrotubuleAssociated | Microtubule/Tubulin | Microtubule Associated | Inhibitor | inhibit | hepatocellular | CHM-1 | CHM1 | CHM 1 | Cdc2 | carcinoma | Apoptosis | antitumor | antimitotic |
| Inhibitors Related | Stavudine | Aceglutamide | Urea | Tamoxifen | Cysteamine hydrochloride | Metronidazole | Citric Acid Triammonium | Formamide | Dimethyl phthalate | Alginic acid | Sodium Molybdate | Sildenafil citrate |
| Related Compound Libraries | Apoptosis Compound Library | Bioactive Compound Library | Microtubule-Targeted Compound Library | Inhibitor Library | Bioactive Compounds Library Max | Fluorochemical Library | Cytoskeletal Signaling Pathway Compound Library | Anti-Cancer Compound Library | Anti-Cancer Active Compound Library | High-Efficiency Gene Editing Small Molecule Library |