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Biological Activity for VE 821
VE 821 is a high affinity and selective ATP-competitive ATR inhibitor (Ki = 13 nM). Exhibits >75-fold selectivity for ATR over related kinases mTOR, DNA-PK, PI 3-Kγ and PIKKs (Ki values are >1, 2.2, 3.9 and 16 μM, respectively) and a panel of other kinases. Induces cell death in colon cancer cell lines in vitro and sensitizes tumor cells to treatment with DNA damaging anticancer agents.
Technical Data for VE 821
|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.
Solubility Data for VE 821
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions for VE 821
The following data is based on the product molecular weight 368.41. 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||2.71 mL||13.57 mL||27.14 mL|
|5 mM||0.54 mL||2.71 mL||5.43 mL|
|10 mM||0.27 mL||1.36 mL||2.71 mL|
|50 mM||0.05 mL||0.27 mL||0.54 mL|
References for VE 821
References are publications that support the biological activity of the product.
Reaper et al (2011) Selective killing of ATM- or p53-deficient cancer cells through inhibition of ATR. Nat.Chem.Biol. 7 428 PMID: 21490603
Williamson et al (2016) ATR inhibitors as a synthetic lethal therapy for tumours deficient in ARID1A. Nat.Commun. 7 13837 PMID: 27958275
If you know of a relevant reference for VE 821, please let us know.
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Citations for VE 821
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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.