Inducer of apoptosis; displays potent antitumor ability in human hepatocellular carcinoma. Inhibits tubulin polymerization in vitro and in vivo. Causes cell cycle arrest at G2/M phase by activation of Cdc2 kinase activity. Induces translocation of apoptosis inducing factor (AIF) from the mitochondria to nucleus. Also exhibits vascular targeting activity through upregulation of p53 and induction of death receptor (DR5)-mediated apoptosis in HUVEC cells.
|Storage||Store at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 283.25. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||3.53 mL||17.65 mL||35.3 mL|
|5 mM||0.71 mL||3.53 mL||7.06 mL|
|10 mM||0.35 mL||1.77 mL||3.53 mL|
|50 mM||0.07 mL||0.35 mL||0.71 mL|
References are publications that support the biological activity of the product.
Wang et al (2008) CHM-1, a novel synthetic quinolone with potent and selective antimitotic antitumor activity against human hepatocellular carcinoma in vitro and in vivo. Mol.Cancer.Ther. 7 350 PMID: 18281518
Tsai et al (2010) CHM-1, a new vascular targeting agent, induces apoptosis of human umbilical vein endothelial cells via p53-mediated death receptor 5 up-regulation. J.Biol.Chem. 285 5497 PMID: 20007968
If you know of a relevant reference for CHM 1, please let us know.
Keywords: CHM 1, CHM 1 supplier, CHM1, apoptosis, inducer, inhibits, tubulin, polymerization, inhibitors, antitumor, antivascular, cell, cycle, arrest, Apoptosis, Inducers, 3868, Tocris Bioscience
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Literature in this Area
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Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.