CCT 241533 dihydrochloride
Potent Chk2 inhibitor (IC50 = 3 nM). Shows >63-fold selectivity for Chk1 over Chk2 and a panel of 84 other kinases. Inhibits Chk2 activation in response to etoposide-induced DNA damage in HT29 cells. Blocks ionizing radiation-induced apoptosis of mouse thymocytes.
External Portal Information
Chemicalprobes.org is a portal that offers independent guidance on the selection and/or application of small molecules for research. The use of CCT 241533 is reviewed on the chemical probes website.
|Storage||Desiccate 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|
|water||5.15||10 with gentle warming|
Preparing Stock Solutions
The following data is based on the product molecular weight 515.41. 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||1.94 mL||9.7 mL||19.4 mL|
|5 mM||0.39 mL||1.94 mL||3.88 mL|
|10 mM||0.19 mL||0.97 mL||1.94 mL|
|50 mM||0.04 mL||0.19 mL||0.39 mL|
References are publications that support the biological activity of the product.
Caldwell et al (2011) Structure-based design of potent and selective 2-(quinazolin-2-yl)phenol inhibitors of checkpoint kinase 2. J.Med.Chem. 54 580 PMID: 21186793
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Keywords: CCT 241533 dihydrochloride, CCT 241533 dihydrochloride supplier, checkpoint, kinase, 2, CHK, inhibitors, inhibits, radioprotectant, potent, selective, Checkpoint, Kinases, Control, 4968, Tocris Bioscience
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Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.