SRT 1720

SRT 1720 is a selective activator of human SIRT1 with an EC_1.5 of 0.16 μM, and shows less potent activities for SIRT2 and SIRT3 with EC_1.5s of 37 μM and > 300 μM, respectively. IC50 & Target:EC1.5: 0.16 μM (SIRT1), 37 μM (SIRT2), > 300 μM (SIRT3)^[1] In Vitro:SRT 1720 effectively decreases the acetylation of p53 in cells even in the absence of SIRT1, and this is attributed to inhibition of histone acetyltransferase p300^[2]. In Vivo:SRT 1720 (10, 30, 100 mg/kg, p.o.) significantly reduces the hyperinsulinaemia after 4 weeks, partially normalizing elevated insulin levels similar to rosiglitazone treatment. SRT 1720 treatment significantly reduces fasting blood glucose to near normal levels in Lep^ob/ob mice^[1]. SRT 1720 has ability to protect against the negative effects of diet-induced obesity in mice, and has a connection to metabolic adaptation in fatty acid and oxidative metabolism through downstream targets of SIRT1 such as PGC1α and FOXO1^[2]. SRT 1720 (50-100 mg/kg, p.o.), during emphysema development attenuates elastase-induced airspace enlargement and lung function impairment as well as reduces arterial oxygen saturation in WT mice^[3].