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Potent and selective ATM kinase inhibitor (IC50 = 0.6 nM in an enzyme inhibition assay). Exhibits > 600-fold selectivity for ATM over other kinases. Inhibits ATM kinase in an in vitro cellular assay (IC50 = 0.33 μM). Potentiates the antitumor effects of the topoisomerase 1 inhibitor irinotecan (CPT 11, Cat. No. 2688) in tumor bearing, immunocompromised mice. Orally bioavailable.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 434.47. Batch specific molecular weights may vary from batch to batch due to the degree 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||2.3 mL||11.51 mL||23.02 mL|
|5 mM||0.46 mL||2.3 mL||4.6 mL|
|10 mM||0.23 mL||1.15 mL||2.3 mL|
|50 mM||0.05 mL||0.23 mL||0.46 mL|
References are publications that support the biological activity of the product.
Degorce et al (2016) Discovery of novel 3-quinoline carboxamides as potent, selective and orally bioavailable inhibitors of ataxia telangiectasia mutated (ATM) kinase. J.Med.Chem. 59 6281 PMID: 27259031
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Keywords: AZ 5704, AZ 5704 supplier, AZ5704, orally, bioavailable, potent, selective, ATM, kinase, inhibitors, ataxia, telangiectasia, mutated, &, ATR, Kinase, Checkpoint, Control, Kinases, 6330, Tocris Bioscience
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Literature in this Area
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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.