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Description

A cell-permeable quinolinecarboxamide compound that is shown to inhibit the mitochondrial SIRT3 in a substrate AceCS2-competitive (Ki = 0.56 µ,M, Km = 2.44 µ,M), but NAD+-uncompetitive (Ki = 0.34 µ,M, Km = 280 µ,M), manner. Also reported to decrease cellular p53 Lys382 acetylation (Effective conc. = 10 µ,M in U2OS and MEF cultures) and inhibit p300 HAT activity (IC50 = 9 µ,M) in vitro, as well as offer therapeutic benefits in several murine and rodent type 2 diabetes models (100 mg/kg/dayl p.o.) in vivo. Whether and how SRT1720 activates SIRT1 activity remains uncertain. Also available as a 25 mM solution in DMSO (Cat. No. 530748)., A cell-permeable quinolinecarboxamide compound that is shown to inhibit the mitochondrial SIRT3 in a substrate AceCS2- (Acetyl-CoA synthetase 2) competitive (Ki = 0.56 µ,M, Km = 2.44 µ,M, Vmax = 173.35 µ,M/min), but NAD+-uncompetitive (Ki = 0.34 µ,M, Km = 280 µ,M, Vmax = 0.86 µ,M/min), manner, indicative of NAD+ binding as a prerequisite for inhibitor binding. Also reported to decrease cellular p53 Lys382 acetylation (Effective conc. = 10 µ,M in U2OS and MEF cultures) and inhibit p300 HAT activity (IC50 = 9 µ,M) in vitro, as well as offer therapeutic benefits in several murine and rodent type 2 diabetes models (100 mg/kg/dayl p.o.) in vivo. Whether and how SRT1720 activates SIRT1 activity remains uncertain.