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SRT1720 HCl

  Cat. No.:  DC7300   Featured
Chemical Structure
1001645-58-4
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Field of application
SRT1720 is a selective SIRT1 activator with EC50 of 0.16 μM, but is >230-fold less potent for SIRT2 and SIRT3.
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].
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
2018-0101
Cat. No. Product name Field of application
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DC8900 SRT1720 SRT1720 is a selective activator of human SIRT1 (EC1.5 = 0.16 μM) versus the closest sirtuin homologues, SIRT2 and SIRT3 (SIRT2: EC1.5 = 37 μM;SIRT3: EC1.5 > 300 μM).
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DC10002 Salermide Salermide is an inhibitor of SIRT1 and SIRT2, causing tumor-specific apoptotic cell death. In MOLT4 leukemia cells, salermide causes 90% apoptosis within 72 hours (IC50 ~ 20 μM) by reactivating proapototic genes that are repressed by SIRT1.
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