Cas No.: | 1001645-58-4 |
Chemical Name: | SRT-1720 HCl |
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: | 542.48 |
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]. |