1. Cell Cycle/DNA Damage
  2. Sirtuin
  3. SRT 1720

SRT 1720 

Cat. No.: HY-10532
Handling Instructions

SRT 1720 is a selective activator of human SIRT1 with an EC1.5 of 0.16 μM, and shows less potent activities agaiinst SIRT2 and SIRT3 with EC1.5s of 37 μM and > 300 μM, respectively.

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

SRT 1720 Chemical Structure

SRT 1720 Chemical Structure

CAS No. : 925434-55-5

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Top Publications Citing Use of Products

    SRT 1720 purchased from MCE. Usage Cited in: Toxicol Lett. 2016 Dec 15;264:1-11.

    The HNF1α, FXR, Mrp2 and Bsep protein levels are decreased after EE administration and significantly increased by SRT1720 in a dose dependent manner, which is in accordance with the mRNA levels.

    SRT 1720 purchased from MCE. Usage Cited in: Hypertension. 2016 Nov;68(5):1191-1199.

    SRT1720 rescues the downregulation of SIRT1 activity and protein expression in the aortas of KL+/– mice. A, Representative Western blot bands of Acetyl-P53 and total P53 and the quantification of SIRT1 activity. Data are expressed as the ratio of acetyl-p53/total P53. B, Representative Western blot bands and quantitative analysis of SIRT1 protein expression in aortas. Protein expression is normalized to β-actin, and the relative expression calculated as the fold change relative

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    SRT 1720 is a selective activator of human SIRT1 with an EC1.5 of 0.16 μM, and shows less potent activities agaiinst SIRT2 and SIRT3 with EC1.5s of 37 μM and > 300 μM, respectively.

    IC50 & Target[1] [1]


    0.16 μM (EC1.5)


    37 μM (EC1.5)

    In Vitro

    SRT 1720 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].

    In Vivo

    SRT 1720 (10, 30, 100 mg/kg, p.o.) significantly reduces the hyperinsulinaemia after 4 weeks, partially normalizing elevated insulin levels similar to rosiglitazone treatment. SRT 1720 treatment significantly reduces fasting blood glucose to near normal levels in Lepob/ob mice[1]. SRT 1720 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]. SRT 1720 (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].

    Molecular Weight




    CAS No.





    Room temperature in continental US; may vary elsewhere


    Please store the product under the recommended conditions in the Certificate of Analysis.

    Solvent & Solubility
    In Vivo:
    • 1.

      SRT 1720 is prepared in 10% hydroxypropyl-beta-cyclodextrin in 500 mM phosphate, pH 7.0[4].

    Animal Administration

    Mice: Nine week old C57BL/6 male mice are fed a high fat diet (60% calories from fat) until their mean body weight reach approximately 40 g. The mice are then divided into test groups (6-10 per group). SRT1460 (100 mg/kg), SRT1720 (100 mg/kg), SRT501 (500 mg/kg) and rosiglitazone (5 mg/kg) are administered once daily via oral gavage. The vehicle used is 2% HPMC + 0.2% DOSS. Individual mouse body weights are measured twice weekly. At 2, 4, 6, 8 and 10 weeks of dosing a fed blood glucose measure is taken and after 5 weeks of treatment an IPGTT is conducted on all mice from each of the groups. After 10 weeks of treatment, an ITT is conducted. Statistical analysis is completed using the JMP program. Data are analyzed by a one way ANOVA with comparison to control using a Dunnett’s Test. A p value < 0.05 indicates a significant difference between groups.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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