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Catalog No.: 52007
Cas No.: 1001645-58-4
Purity : 98% 

SRT1720 is a selective SIRT1 activator with EC50 of 0.16 M, but is >230-fold less potent for SIRT2 and SIRT3. 

For research use only. We do not sell to patients.

Chemical Information

Iupac Chemical NameN-(2-(3-(piperazin-1-ylmethyl)imidazo[2,1-b]thiazol-6-yl)phenyl)quinoxaline-2-carboxamide hydrochloride 
SynonymsSRT1720 ; SRT-1720 ; SRT 1720 
Molecular FormulaC25H23N7OS.HCl 
Molecular Weight506.02 
CAS Number1001645-58-4
Related CAS925434-55-5 (free base) 1001645-58-4 (HCl)

Ordering Information

PackagingPriceAvailabilityPurityShipping Time
Request Bulk Quote Download MSDS Tel : +86-27-65522453   Email : sales@sun-shinechem.com
Formulationyellow solid,being red exposed in air. 
Storage3 years -20ºCpowder 
Solubility2mg/ml in DMSO 
Shipping ConditionShipped under ambient temperature 
HS Code
Cell study
Animal study
Clinical study

1. Tyler J. Lahusen and Chu-Xia Deng, SRT1720 Induces Lysosomal-Dependent Cell Death of Breast Cancer Cells. Cancer Biology and Signal Transduction DOI: 10.1158/1535-7163.MCT-14-0584 Published January 2015



SRT1720 is an activator of SIRT1, a NAD+-dependent protein and histone deacetylase that plays an important role in numerous biologic processes. Several studies have illustrated that SRT1720 treatment could improve metabolic conditions in mouse models and in a study in cancer SRT1720 caused increased apoptosis of myeloma cells. However, the effect of SRT1720 on cancer may be complex, as some recent studies have demonstrated that SRT1720 may not directly activate SIRT1 and another study showed that SRT1720 treatment could promote lung metastasis. To further investigate the role of SRT1720 in breast cancer, we treated SIRT1 knockdown and control breast cancer cell lines with SRT1720 both in vitro and in vivo. We showed that SRT1720 more effectively decreased the viability of basal-type MDA-MB-231 and BT20 cells as compared with luminal-type MCF-7 breast cancer cells or nontumorigenic MCF-10A cells. We demonstrated that SRT1720 induced lysosomal membrane permeabilization and necrosis, which could be blocked by lysosomal inhibitors. In contrast, SRT1720-induced cell death occurred in vitro irrespective of SIRT1 status, whereas in nude mice, SRT1720 exhibited a more profound effect in inhibiting the growth of allograft tumors of SIRT1 proficient cells as compared with tumors of SIRT1-deficient cells. Thus, SRT1720 causes lysosomal-dependent necrosis and may be used as a therapeutic agent for breast cancer treatment. Mol Cancer Ther; 14(1); 183–92. ©2014 AACR.

Chemical Structure

52007 - SRT1720 | CAS 1001645-58-4

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