SRT1720 HCl

SRT1720 HCl is a selective SIRT1 activator with EC50 of 0.16 μM in a cell-free assay, but is >230-fold less potent for SIRT2 and SIRT3. SRT1720 induces autophagy.

SRT1720 HCl Chemical Structure

SRT1720 HCl Chemical Structure

CAS: 1001645-58-4

Selleck's SRT1720 HCl has been cited by 176 publications

Purity & Quality Control

Batch: Purity: 99.61%
99.61

Products often used together with SRT1720 HCl

Selisistat (EX 527)


SRT1720 increases endometriotic lesions in Pgrcre/+Rosa26mTmG/+ mice, while Selisistat significantly reduces the number of endometriotic lesions.

Kim TH, et al.J Clin Endocrinol Metab. 2022 Feb 17;107(3):788-800.

Resveratrol


SRT1720 enhances etoposide- and vincristine-induced cell death, while resveratrol inhibits it in ES cells.

Sonnemann J, et al. J Cancer Res Clin Oncol. 2016 Jan;142(1):17-26.

Quercetin


Quercetin is more efficacious than SRT1720 in combatting the cytotoxic effects of D-GalN/LPS in Male Wistar rats.

Kemelo MK, et al. Eur Rev Med Pharmacol Sci. 2016;20(2):363-71.

Astragaloside IV


SRT1720 HCl and Astragaloside exhibit similar effects in calpain-1 knockout on Vascular endothelial dysfunction (VED).

Zhao F, et al. Front Pharmacol. 2022 Aug 2;13:920977.

MDL-28170


SRT1720 HCl and MDL-28170 treatment, including As-IV, restores the increased level of mitoROS and the reduced membrane potential in human coronary artery endothelial cells (HCAECs).

Zhao F, et al. Front Pharmacol. 2022 Aug 2;13:920977.

SRT1720 HCl Related Products

Signaling Pathway

Choose Selective Sirtuin Inhibitors

Cell Data

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
CACs  Function Assay 4 μM 30 min DMSO induces acute SIRT1 activation  26254104
MC3T3-E1 Function Assay 10 µM  1 h reduces the TGF-β-stimulated VEGF release in dose- and time-dependent manner  26136978
MC3T3-E1 Function Assay 10 µM  12 h reduces the VEGF mRNA expression levels stimulated by TGF-β 26136978
MC3T3-E1 Function Assay 20 μM 1 h suppresses the TGF-β-induced phosphorylation of p44/p42 MAP kinase or SAPK/JNK 26136978
WE-68 Apoptosis Assay 0-24 μM 24 h induces cell death in dose dependently 26055805
SK-ES-1 Apoptosis Assay 0-10 μM 24 h induces cell death in dose dependently 26055805
SK-N-MC  Apoptosis Assay 0-2.5 μM 24 h induces cell death in dose dependently 26055805
WE-68 Function Assay 20 μM 0-24 h activates caspase 3/7 26055805
SK-ES-1 Function Assay 10 μM 0-24 h activates caspase 3/7 26055805
SK-N-MC  Function Assay 3 μM 0-24 h activates caspase 3/7 26055805
NRK-49F Function Assay 0–2 μM 36 h increases expression of α-SMA and fibronectin dose dependently 26022003
NRK-49F Function Assay 0–2 μM 36 h enhances phosphorylation of EGFR and PDGFRβ  26022003
NRK-49F Function Assay 0–2 μM 36 h enhances STAT3 phosphorylation 26022003
RAW264.7 Function Assay 1 μM 6 h upregulates the reduced SIRT1 protein or mRNA levels by high glucose 25793995
MCF10A Growth Inhibition Assay 0-20 μM 24 h reduces cell viability dose dependently 25411356
MCF-7 Growth Inhibition Assay 0-20 μM 24 h reduces cell viability dose dependently 25411356
T47D Growth Inhibition Assay 0-20 μM 24 h reduces cell viability dose dependently 25411356
SKBR3 Growth Inhibition Assay 0-20 μM 24 h reduces cell viability dose dependently 25411356
MDA-MB-231 Growth Inhibition Assay 0-20 μM 24 h reduces cell viability dose dependently 25411356
SUM149 Growth Inhibition Assay 0-20 μM 24 h reduces cell viability dose dependently 25411356
HS578T Growth Inhibition Assay 0-20 μM 24 h reduces cell viability dose dependently 25411356
BT20 Growth Inhibition Assay 0-20 μM 24 h reduces cell viability dose dependently 25411356
A459 Growth Inhibition Assay 0-20 μM 24 h reduces cell viability dose dependently 25411356
HCT116 Growth Inhibition Assay 0-20 μM 24 h reduces cell viability dose dependently 25411356
Neu Growth Inhibition Assay 0-20 μM 24 h reduces cell viability dose dependently 25411356
MDA-MB-231 Function Assay 5 μM 8 h increases the number of acidic vesicular organelles 25411356
MDA-MB-231 Function Assay 5 μM 16 h induces lysosomal membrane permeabilization 25411356
MC3T3-E1 Function Assay 10 μM 60 min  suppresses the FGF-2-stimulated osteoprotegerin release 25290095
MC3T3-E1 Function Assay 10 μM 60 min  attenuates the FGF-2-induced osteoprotegerin mRNA expression 25290095
MC3T3-E1 Function Assay 10 μM 60 min  attenuates the FGF-2-induced osteoprotegerin mRNA expression 25290095
MC3T3-E1 Function Assay 10 μM 60 min  suppresses the BMP-4-stimulated VEGF release 24435444
MC3T3-E1 Function Assay 10 μM 60 min  suppresses the PGF2α-stimulated OPG release 24333336
MC3T3-E1 Function Assay 10 μM 60 min  reduces the PGF2α-stimulated phosphorylation of p44/p42 MAP kinase 24333336
MC3T3-E1 Function Assay 10 μM 60 min  attenuates the PGF2α-induced phosphorylation of both MEK1/2 and Raf-1 24333336
RPE Cell Viability Assay 5 µM 1 h attenuates OAβ-induced decrease of cell viability 24036938
9607 Cell Viability Assay 1 μM 36 h increases the cell viability compared with melatonin alone 23726949
9607 Function Assay 1 μM 36 h increases SIRT1 and decreased acetylated-p53 expression 23726949
RPMI.8226 Cell Viability Assay 7/10 μM 24 h decreases viability concentration dependently 21950728
U266 Cell Viability Assay 7/10 μM 24 h decreases viability concentration dependently 21950728
MM.1S Cell Viability Assay 7/10 μM 24 h decreases viability concentration dependently 21950728
KMS12 Cell Viability Assay 7/10 μM 24 h decreases viability concentration dependently 21950728
LR5 Cell Viability Assay 7/10 μM 24 h decreases viability concentration dependently 21950728
MM.1R Cell Viability Assay 7/10 μM 24 h decreases viability concentration dependently 21950728
Ina6 Cell Viability Assay 7/10 μM 24 h decreases viability concentration dependently 21950728
RPMI-8226 Apoptosis Assay 7/10 μM 24 h induces a significant increase in the Annexin V+/PI− apoptosis 21950728
MM.1R  Apoptosis Assay 7/10 μM 24 h induces a significant increase in the Annexin V+/PI− apoptosis 21950728
H411EC3 Function Assay 50/100 nM 6 h increases SIRT1 activity in the presence of TSA, PEPCK activity, mRNA levels of Pck1 and Pgc1α, and elevating glucose production 21212096
hepatocytes Function Assay 10 nM 6 h increases SIRT1 activity in the presence of TSA, PEPCK activity, mRNA levels of Pck1 and Pgc1α, and elevating glucose production 21212096
hepatocytes Function Assay 10 nM 6 h increases Hmgcr and Acc gene expression 21212096
U2OS Function assay 0.10 uM Activation of SIRT1 in human U2OS cells assessed as decrease in p53 deacetylation level at 0.10 uM 18046409
A673 qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells 29435139
DAOY qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells 29435139
BT-37 qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells 29435139
RD qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells 29435139
MG 63 (6-TG R) qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells 29435139
NB1643 qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells 29435139
OHS-50 qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells 29435139
Rh41 qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells 29435139
Rh30 qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells 29435139
LAN-5 qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells 29435139
Rh18 qHTS assay qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells 29435139
Click to View More Cell Line Experimental Data

Biological Activity

Description SRT1720 HCl is a selective SIRT1 activator with EC50 of 0.16 μM in a cell-free assay, but is >230-fold less potent for SIRT2 and SIRT3. SRT1720 induces autophagy.
Targets
SIRT1 [1]
(Cell-free assay)
0.16 μM(EC50)
In vitro
In vitro The maximum activation ratio of SRT1720 versus the closest sirtuin homologues, SIRT2 (EC1.5 = 37 μM) and SIRT3 (EC1.5 > 300 μM) is up to 781%. SRT1720 binds to the SIRT1 enzyme-peptide substrate complex at an allosteric site amino-terminal to the catalytic domain and lower the Michaelis constant for acetylated substrates. SRT1720 could reduce fed glucose levels. Glucose excursion during an intraperitoneal glucose tolerance test is also significantly reduced in the SRT1720 group, and comparable to rosiglitazone, a PPARγ activator that has been used to treat type 2 diabetes. SRT1720 does not have an effect on fasting glucose in chow-fed mice, revealing that pharmacological SIRT1 activation is unlikely to induce hypoglycaemia. SRT1720 significantly reduces the hyperinsulinaemia after 4 weeks, partially normalizing increased insulin levels similar to rosiglitazone treatment. SRT1720 treatment increases mitochondrial capacity by 15% in gastrocnemius muscle as measured by citrate synthase activity. [1] Higher concentrations of SRT1720 (15 μM) induces a modest (10-20%) decrease in normal cell viability. SRT1720 also significantly inhibits VEGF-dependent MM cell migration. [2]
Kinase Assay SIRT1 fluorescence polarization assay
In the SIRT1 FP assay, SIRT1 activity is monitored using a 20 amino acid peptide (Ac-Glu-Glu-Lys(biotin)-Gly-Gln-Ser-Thr-Ser-Ser-His-Ser-Lys(Ac)-Nle-Ser-Thr-Glu-Gly–Lys(MR121 or Tamra)-Glu-Glu-NH2) derived from the sequence of p53. The peptide is N-terminally linked to biotin and C-terminally modified with a fluorescent tag. The reaction for monitoring enzyme activity is a coupled enzyme assay where the first reaction is the deacetylation reaction catalyzed by SIRT1 and the second reaction is cleavage by trypsin at the newly exposed lysine residue. The reaction is stopped and streptavidin is added in order to accentuate the mass differences between substrate and product. The sensitivity of the FP assay allows identification of SRT1720. The fluorescence polarization reaction conditions are as follows: 0.5 μM peptide substrate, 150 μM βNAD+, 0-10 nM SIRT1, 25 mM Tris-acetate pH 8, 137 mM Na-Ac, 2.7 mM K-Ac, 1 mM Mg-Ac, 0.05% Tween-20, 0.1% Pluronic F127, 10 mM CaCl 2, 5 mM DTT, 0.025% BSA, and 0.15 mM nicotinamide. The reaction is incubated at 37 °C and stopped by addition of nicotinamide, and trypsin is added to cleave the deacetylated substrate. This reaction is incubated at 37 °C in the presence of 1 μM streptavidin. Fluorescent polarization is determined at excitation (650 nm) and emission (680 nm) wavelengths.
Cell Research Cell lines Human vascular endothelial cells (HUVECs)
Concentrations 5 μM
Incubation Time 2 hours
Method Transwell Insert Assays are utilized to measure migration. In vitro angiogenesis is assessed by Matrigel capillary-like tube structure formation assay. For endothelial tube formation assay, human vascular endothelial cells (HUVECs) are obtained from Clonetics and maintained in endothelial cell growth medium-2 containing 5% FBS. After three passages, HUVEC cell viability is measured with the trypan blue exclusion assay, and <5% of cell death is observed with SRT1720 treatment.
Experimental Result Images Methods Biomarkers Images PMID
Western blot Cleaved-PARP-1 / Cleaved-caspase-3 / LC3-II / p62 / SIRT1 26655844
Immunofluorescence Cathepsin B 26655844
Growth inhibition assay Cell viability 25411356
In Vivo
In vivo In DIO mice SRT1720 mimics several of the effects observed after calorie restriction including improved insulin sensitivity, normalized glucose and insulin levels, and increased mitochondrial capacity. In addition, in diet-induced obese and genetically obese mice, SRT1720 improves insulin sensitivity, lower plasma glucose, and increase mitochondrial capacity. Thus, SRT1720 is a promising new therapeutic agent for treating diseases of ageing such as type 2 diabetes. Consistent with improved glucose tolerance, the glucose infusion rate required to maintain euglycaemia is approximately 35% higher in SRT1720-treated fa/fa rats, and the total glucose disposal rate is increased by approximately 20%. [1] SRT1720 also prevents multiple myeloma tumor growth. SRT1720 increases the cytotoxic activity of bortezomib or dexamethasone. [2]
Animal Research Animal Models Chase-SCID mice with MM.1S cells
Dosages 200 mg/kg
Administration Orally

Chemical Information & Solubility

Molecular Weight 506.02 Formula

C25H23N7OS.HCl

CAS No. 1001645-58-4 SDF Download SRT1720 HCl SDF
Smiles C1CN(CCN1)CC2=CSC3=NC(=CN23)C4=CC=CC=C4NC(=O)C5=NC6=CC=CC=C6N=C5.Cl
Storage (From the date of receipt)

In vitro
Batch:

DMSO : 100 mg/mL ( (197.62 mM); Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Water : Insoluble

Ethanol : Insoluble


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In vivo
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

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Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Frequently Asked Questions

Question 1:
How can we prepare Srt1720 for in vivo mouse studies?

Answer:
SRT1720 HCl can be dissolved in 30% PEG 400+0.5% Tween 80+5% Propylene glycol at 30mg/ml as a suspension. It is fine for oral gavage. And we’ve also found that it can be dissolved in 2% DMSO+30% PEG 300+1%Tween 80+ddH2O at 3mg/ml clearly, which could be used for injection. When prepare the solution, please dissolve the compound in DMSO clearly first, then add PEG and Tween. After they mixed well, dilute with water.

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