SRT1720 HCl

Cas No.:	1001645-58-4
Chemical Name:	N-(2-(3-(piperazin-1-ylmethyl)imidazo[2,1-b]thiazol-6-yl)phenyl)quinoxaline-2-carboxamide dihydrochloride
Synonyms:	SRT-1720 HCl, SRT-1720 hydrochloride; SRT1720; SRT-1720; SRT 1720; CAY10559; CAY-10559; CAY 10559; SIRT-1933; SIRT 1933; SIRT1933.
SMILES:	C1CN(CCN1)CC2=CSC3=NC(=CN23)C4=CC=CC=C4NC(=O)C5=NC6=CC=CC=C6N=C5.Cl
Formula:	C25H25Cl2N7Os
M.Wt:	542.483
Sotrage:	2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO

Description:	SRT 1720 Hydrochloride is a selective activator of SIRT1 with an EC1.5 of 0.16 μM, and shows less potent activities on SIRT2 and SIRT3 with EC1.5s of 37 μM and 300 μM, respectively.
In Vivo:	SRT1720 (10, 30, 100 mg/kg, p.o.) significantly reduces the hyperinsulinaemia after 4 weeks, partially normalizing elevated insulin levels similar to rosiglitazone treatment. SRT1720 treatment significantly reduces fasting blood glucose to near normal levels in Lepob/ob mice[1]. SRT1720 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]. SRT1720 (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].
In Vitro:	SRT1720 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].