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Beschreibung

A cell-permeable phenylpyrazine derivative that acts as a potent, ATP-competitive (Ki= 13 nM, IC50/[ATP] = 70 nM/50 µ,M and 128 nM/100 µ,M), ATR-selective inhibitor with much reduced or little potency against 4 related PIKKs (Ki= 2.2, 3.9, 16, and >1 µ,M, respectively, against DNA-PK, PI 3-Kgamma, ATM, and mTOR) and 50 other kinases. Shown to selectively inhibit ATR-dependent H2AX Ser139 & Chk1 Ser345 phosphorylation (complete inhibition at 10 µ,M in HT29 and HFL1 cultures) without affecting ATM- and DNA-PK-mediated H2AX or ATM-mediated Chk2 phosphorylation. Short-term (24 h) VE-821 treatment, either alone or in synergy with Cisplatin (Cat. No. 232120), results in reversible cytostatic growth arrest regardless of cellular ATM-p53 pathway activity, while cytotoxicity and Cisplatin synergism in cell death induction is reported to occur only upon long-term VE-821 exposure (>=72 h) in cultures with ATM-p53 pathway defects.Please note that the molecular weight for this compound is batch-specific due to variable water content., A cell-permeable phenylpyrazine derivative that acts as a potent, ATP-competitive (Ki= 13 nM, IC50/[ATP] = 70 nM/50 µ,M and 128 nM/100 µ,M), ATR-selective inhibitor with much reduced or little potency against 4 related PIKKs (Ki= 2.2, 3.9, 16, and >1 µ,M, respectively, against DNA-PK, PI 3-Kgamma, ATM, and mTOR) and 50 other kinases. Shown to selectively inhibit ATR-dependent H2AX Ser139 & Chk1 Ser345 phosphorylation (complete inhibition at 10 µ,M in HT29 and HFL1 cultures) without affecting ATM- and DNA-PK-mediated H2AX or ATM-mediated Chk2 phosphorylation. Short-term (24 h) VE-821 treatment, either alone or in synergy with Cisplatin (Cat. No. 232120), results in reversible cytostatic growth arrest regardless of cellular ATM-p53 pathway activity, while cytotoxicity and Cisplatin synergism in cell death induction is reported to occur only upon long-term VE-821 exposure (>=72 h) in cultures with ATM-p53 pathway defects.