SRT 1720 dihydrochloride is a selective and orally active activator of SIRT1 with an EC50 of 0.10 μM, and shows less potent activities on SIRT2 and SIRT3.In Vitro: SRT 1720 dihydrochloride 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.) dihydrochloride treatment significantly reduces fasting blood glucose to near normal levels in Lepob/ob mice. SRT 1720 dihydrochloride 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.) dihydrochloride, during emphysema development attenuates elastase-induced airspace enlargement and lung function impairment as well as reduces arterial oxygen saturation in WT mice.