SRT1720 HCl
SIRT1 activator / SIRT1 activator (EC1.5 = 0.16 µM, max activation = 781%).1 It reduced glucose levels and hyperinsulinemia in DIO, Lepob/ob mice and Zucker fa/fa rats. SRT1720 enhanced endurance running and protected against diet-induced obesity and insulin resistance via enhancement of oxidative metabolism in skeletal muscle, liver, and brown adipose tissue.2 It induced mitochondrial biogenesis in oxidant-induced renal proximal tube cell injury.3 SRT1720 repressed circadian clock gene expression and decreased H3 K9/K14 acetylation in a time-specific manner.4 It attenuated angiotensin II-induced atherosclerosis by inhibiting the vascular inflammatory response.5
Biochemicals & reagents
1001645-58-4
SIRT 1933
Milne et al. (2007), Small molecule activators of SIRT1 as therapeutics for the treatment of type 2 diabetes; Nature 450 712 Feige et al. (2008), Specific SIRT1 activation mimics low energy levels and protects against diet-induced metabolic disorders by enhancing fat oxidation; Cell Metab. 8 347 Funk et al. (2010), SRT1720 induces mitochondrial biogenesis and rescues mitochondrial function after oxidant injury in renal proximal tubule cells; J. Pharmacol. Exp. Ther. 333 593 Bellet et al. (2013), Pharmacological modulation of circadian rhythms by synthetic activators of the deacetylase SIRT1; Proc. Natl. Acad. Sci. USA 110 3333 Chen et al. (2015), The Sirt1 activator SRT1720 attenuates angiotensin II-induced atherosclerosis in apoE-/- mice through inhibiting vascular inflammatory response; Biochem. Biophys. Res. Commun. 465 732
-20°C
TARGET: Protein deacetylase -- PATHWAY: Chromatin; Posttranslational modification; Apoptosis inhibitor; Redox; Mitochondrial function -- RESEARCH AREA: Epigenetics; Exercise; Circadian clock; Oxidative stress -- DISEASE AREA: Kidney disease; DiabetesObesity; Inflammation; Atherosclerosis