Catalog No.S7102 Synonyms: VX970
Molecular Weight(MW): 463.55
VE-822 is an ATR inhibitor with IC50 of 19 nM in HT29 cells.
3 Customer Reviews
Flow cytometry analysis of E14.5 FL lineage negative cells from indicated genotypes treated with ATMi (KU-55933; 1nM), ATRi (VE-822; 1nM) or both inhibitors or DMSO as a negative control for 24 hours in culture before AnnexinV and PI levels were measured.
Sci Rep, 2016, 6:27379.. VE-822 purchased from Selleck.
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Choose Selective ATM/ATR Inhibitors
|Description||VE-822 is an ATR inhibitor with IC50 of 19 nM in HT29 cells.|
|Features||The first ATR-targeted drug candidate with high selectivity for ATR.|
VE-822 (80 nM) attenuates ATR signaling pathway and reduces survival in tumor cells in response to XRT and gemcitabine. VE-822 (80 nM) attenuates ATR signaling in normal cells without enhancing radiation and gemcitabine killing in normal cells. VE-822 (80 nM) increases XRT-induced residual γH2AX and 53BP1 foci compared with XRT in MiaPaCa-2 and PSN-1 cells. VE-822 (80 nM) pre-treatment decreases Rad51 foci after XRT in MiaPaCa-2 and PSN-1 cells. VE-822 (80 nM) alone increases the G1-phase-fraction in MiaPaCa-2 and PSN-1 cells. VE-822 (80 nM) abrogates XRT enriched G2/M-phase-fraction in MiaPaCa-2 and PSN-1 cells. VE-822 has little effect alone, while VE-822 (80 nM) combined with XRT and/or gemcitabine enhances early and late apoptosis in PSN-1 cells that is strongest in the triple combination.  VE-822 increases tumor response to DNA damaging agents associated with blockade of pChk1 Ser345. 
|In vivo||VE-822 (60 mg/kg) inhibits phospho-Ser-345-Chk1 in mice bearing PSN-1 tumors after DNA-damaging agents. VE-822 (60 mg/kg) combined with XTR doubles the time for tumors to grow to 600 mm3 of XRT alone in mice bearing both PSN-1 and MiaPaCa-2 tumors. VE-822 (60 mg/kg) added to the combination of gemcitabine and XRT substantially prolongs the tumor growth delay compared with the Gem+XRT1 group n mice bearing both PSN-1 tumors. VE-822 (60 mg/kg) combined with XRT1 increases uptake in tumors by 44% compared with XRT1, suggesting that addition of VE-822 increased γH2AX phosphorylation and persistence of DNA damage caused by XRT. |
|In vitro||DMSO||36 mg/mL (77.66 mM)|
|In vivo||Add solvents individually and in order:
5% DMSO+45% PEG 300+H2O
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Frequently Asked Questions
I want to have information to prepare VE-822 for mouse gavage. Thank you for your answer
VE-822 can be dissolved in 1% CMC Na at 30mg/ml as a suspension for oral gavage.