SRT 1720 dihydrochloride is a selective and orally active activator of SIRT1 with an EC 50 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. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo SRT 1720 (10, 30, 100 mg/kg, p.o.) dihydrochloride treatment significantly reduces fasting blood glucose to near normal levels in Lep ob/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. 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. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Form:Solid IC50& Target:SIRT1 0.10 μM (EC 50 )