AZD 7762 hydrochloride
Potent and selective ATP-competitive inhibitor of Chk1 and Chk2 (IC50 vales are 5 nM for both kinases); displays at least >10 fold selectivity over a panel of 164 kinases. Potentiates cytotoxicity of DNA-damaging agents. Active in vivo. Also improves efficiency of CRISPR-Cpf1-mediated genome editing in hPSC lines (2.7-fold at 1 μM).
Sold for research purposes under agreement from AstraZeneca
|Storage||Store at -20°C|
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 398.88. 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||2.51 mL||12.54 mL||25.07 mL|
|5 mM||0.5 mL||2.51 mL||5.01 mL|
|10 mM||0.25 mL||1.25 mL||2.51 mL|
|50 mM||0.05 mL||0.25 mL||0.5 mL|
References are publications that support the biological activity of the product.
Zabludoff et al (2008) AZD7762, a novel checkpoint kinase inhibitor, drives checkpoint abrogation and potentiates DNA-targeted therapies. Mol. Cancer Ther. 7 2955 PMID: 18790776
Morgan et al (2010) Mechanism of radiosensitization by the Chk1/2 inhibitor AZD7762 involves abrogation of the G2 checkpoint and inhibition of homologous recombinational DNA repair. Cancer Res. 70 4972 PMID: 20501833
Ma et al (2018) Small molecules promote CRISPR-Cpf1-mediated genome editing in human pluripotent stem cells. Nat Commun. 9 1303 PMID: 29610531
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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.