VE-821 | Potent and selective ATR inhibitor
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $80.00 | ||
| 25 mg | $290.00 |
VE-821 (1232410-49-9) is a potent and selective ATP-competitive ATR (Ataxia-telangiectasia and Rad3-related protein) inhibitor, Ki=13 nM.1 Increases the sensitivity of pancreatic2 and ovarian3 cancer cells to radiation and chemotherapy. Increased replication stress induced by PARP inhibitors or chemotherapeutic agents increases sensitivity to VE-821 in neuroblastoma cells.4 Enhances the cytotoxicity of DNA damaging agents.5
References/Citations:
- Reaper et al. (2011), Selective killing of ATM- or p53-deficient cancer cells through inhibition of ATR; Nat. Chem. Biol., 7 428
- Prevo et al. (2012), The novel ATR inhibitor VE-821 increases sensitivity of pancreatic cancer cells to radiation and chemotherapy; Cancer Biol. Ther., 13 1072
- Huntoon et al. (2013), ATR inhibition broadly sensitizes ovarian cancer cells to chemotherapy independent of BRCA status; Cancer Res., 73 3683
- King et al. (2021), Increased Replication Stress Determines ATR Inhibitor Sensitivity in Neuroblastoma Cells; Cancers (Basel), 13 6215
- Moolmuang and Ruchirawat (2021), The antiproliferative effects of ataxia-telangiectasia mutated and ATM- and Rad3-related inhibitions and their enhancements with the cytotoxicity of DNA damaging agents in cholangiocarcinoma cells; J. Pharm. Pharmacol., 73 40
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
VE-821 (1232410-49-9) is a potent and selective ATP-competitive ATR (Ataxia-telangiectasia and Rad3-related protein) inhibitor, Ki=13 nM.1 Increases the sensitivity of pancreatic2 and ovarian3 cancer cells to radiation and chemotherapy. Increased replication stress induced by PARP inhibitors or chemotherapeutic agents increases sensitivity to VE-821 in neuroblastoma cells.4 Enhances the cytotoxicity of DNA damaging agents.5
References/Citations:
- Reaper et al. (2011), Selective killing of ATM- or p53-deficient cancer cells through inhibition of ATR; Nat. Chem. Biol., 7 428
- Prevo et al. (2012), The novel ATR inhibitor VE-821 increases sensitivity of pancreatic cancer cells to radiation and chemotherapy; Cancer Biol. Ther., 13 1072
- Huntoon et al. (2013), ATR inhibition broadly sensitizes ovarian cancer cells to chemotherapy independent of BRCA status; Cancer Res., 73 3683
- King et al. (2021), Increased Replication Stress Determines ATR Inhibitor Sensitivity in Neuroblastoma Cells; Cancers (Basel), 13 6215
- Moolmuang and Ruchirawat (2021), The antiproliferative effects of ataxia-telangiectasia mutated and ATM- and Rad3-related inhibitions and their enhancements with the cytotoxicity of DNA damaging agents in cholangiocarcinoma cells; J. Pharm. Pharmacol., 73 40
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Focus Biomolecules • Plymouth Meeting, PA USA • 1-855-FOCUS21
Focus Biomolecules
Plymouth Meeting, PA USA
1-855-FOCUS21
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