Molecular Weight(MW): 394.47
Sirtinol is a specific SIRT1 and SIRT2 inhibitor with IC50 of 131 μM and 38 μM in cell-free assays, respectively.
Cited by 13 Publications
6 Customer Reviews
Effects of sirtinol on SIRT1 expression and HIF-1α. hMSCs were treated with sirtinol (100 uM) or equivalent concentration of DMSO (CTR) for 24 h and then exposed to 1% O2 for 6 h. All cells lysates were analyzed for SIRT1, HIF-1α, and tubulin by Western blot.
Biomed Res Int 2014 783459. Sirtinol purchased from Selleck.
SIRT1 is involved in GABA-mediated protection against apoptosis and induction of insulin secretion. INS-1 cells are protected from apoptosis induced by tacrolimus (FK506; panel A) or streptozotocin (STZ, panel B) by GABA, and the protective effect is reversed by EX527 (SIRT1 inhibitor) or sirtinol (SIRT1 and SIRT2 inhibitor). The cells were incubated with GABA (100 uM), EX527 (200 nM) or sirtinol (4 uM) as indicated, for 1 h before adding 1 uM FK506, and cell viability was tested after 48 h. Similarly, STZ (2 mM) was added after the cells were incubated with other reagents for 1 h, but was replaced with the original medium containing all additives and no STZ after 1 h incubation. Viable cells were counted after 24 h. The results are representative of two experiments.
Biochem Biophys Res Commun 2014 452(3), 649-54. Sirtinol purchased from Selleck.
Effects of Cap pretreatment with or without coadministration of sirtinol on the activities of caspase-3 in the rat primary cardiomyocytes after A/R. A/R induced a significant increase in the activities of caspase-3. Cap significantly decreased the change in the activities of caspase-3 caused by A/R, and sirtinol significantly blocked the effects of Cap. Values were expressed as the mean ± SEM (n = 6). ∗∗P < 0.01 versus the control group; ▲▲P < 0.01 versus the A/R group; ##P < 0.01 versus the Cap + A/R group.
Oxid Med Cell Longev, 2017, 2017:1035702. Sirtinol purchased from Selleck.
HG and PA decreases SIRT1 expression and the effects of resveratrol and sirtinol on the expression of SIRT1. (A) The mRNA expression of SIRT1 analyzed by real-time PCR. (B) The protein level of SIRT1 assayed by western blotting. RSV: resveratrol. N = 3, data are presented as mean ± SD, ∗P < 0.05 vs. control group, #P < 0.05 vs. HG + PA group.
Mol Cell Endocrinol, 2018, 474:97-104. Sirtinol purchased from Selleck.
SIRT1 inhibitor exacerbates TBI-induced mitochondrial damage, promotes neuronal apoptosis and activates p38 MAPK signaling. Rats were injected intraperitoneally with the SIRT1 inhibitor sirtinol (10 mg/kg) 30 min before LFP-induced TBI. After 12 h, rats were sacrificed. (A) The expression of SIRT1 and β-actin were detected by Western blot. β-Actin was used as loading control. (B) Quantification of Western blots for SIRT1. (C) The expression of SIRT1 was analyzed by immunohistochemical staining post-TBI.
Acta Pharmacol Sin, 2017, 38(2):168-181.. Sirtinol purchased from Selleck.
Purity & Quality Control
Choose Selective Sirtuin Inhibitors
|Description||Sirtinol is a specific SIRT1 and SIRT2 inhibitor with IC50 of 131 μM and 38 μM in cell-free assays, respectively.|
|Features||Sirtinol does not inhibit class I and class II HDACs.|
Sirtinol potently inhibits recombinant yeast Sir2p activity in vitro with IC50 of 68 μM. Unlike TSA, Sirtinol has shown no effect on human HDAC1, indicating that it is a selective sirtuin inhibitor. Unlike TSA, treatment of human primary fibroblasts with Sirtinol does not cause global changes in acetylation of histones and tubulin, nor does it induce a morphological change in the HeLa tumor cell line.  Sirtinol treatment at 100 μM for 24 hours causes a sustained growth arrest in MCF-7 and H1299 cells for up to 9 days after Sirtinol withdrawal. Sirtinol treatment induces increased SA-β-gal activity and expression of PAI-1 in both MCF-7 and H1299 cells, more potently than Splitomicin. Sirtinol inhibits colony formation at concentrations of 33 μM and higher in MCF-7 and H1299 cells, more effectively compared with Splitomicin. Sirtinol treatment (100 μM) significantly attenuates both basal and EGF- or IGF-I-stimulated phosphorylation of ERK, JNK/SAPK and p38 MAPK in MCF-7 and H1299 cells. Sirtinol blocks the basal and EGF-stimulated activation of Ras. Consistent, basal and EGF- or IGF-I-stimulated phosphorylation of Raf-1, MEK, SEK1/MKK4 and MKK7 is attenuated in Sirtinol-treated cells.  Inhibition of Sirt1 by Sirtinol enhances UV- and H2O2-induced p53 acetylation to enhance cell death in cultured skin keratinocytes.  Blocking of Sirt1 by Sirtinol treatment results in a significant inhibition in the growth and viability of human PCa cells while having no effect on normal prostate epithelial cells. 
|In vivo||Administration of Sirtinol at 1 mg/kg attenuates pro-inflammatory cytokine production and protects against hepatic injury following trauma-hemorrhage in male Sprague-Dawley rats. |
Inhibition in vitro of human Sirt2 activity:1.5 μg of recombinant human GST-Sirt2 (amino acids 18-340) are incubated at 30°C for 2 hours in 50 μL of assay buffer (50 mM Tris-HCl, pH 8.8, 4 mM MgCl2, 0.2 mM dithiothreitol with different concentrations of Sirtinol, 50 μM NAD, and tritiated acetylated HeLa histones (1000 cpm), purified by acid extraction. HDAC activity is determined by scintillation counting of the ethyl acetate-soluble [3H]acetic acid.
-  Grozinger CM, et al. J Biol Chem, 2001, 276(42), 38837-38843.
-  Mai A, et al. J Med Chem, 2005, 48(24), 7789-7795.
-  Ota H, et al. Oncogene, 2006, 25(2), 176-185.
-  Liu FC, et al. Acta Anaesthesiol Scand, 2008, 52(5), 635-640.
-  Kojima K, et al. Biochem Biophys Res Commun, 2008, 373(3), 423-428.
-  Cao C, et al. J Cell Mol Med, 2009, 13(9B), 3632-3643.
-  Jung-Hynes B, et al. J Biol Chem, 2009, 284(6), 3823-3832.
-  Sun JY, et al. Clin Lymphoma Myeloma Leuk, 2011, 11(1), 152-156.
|In vitro||DMSO||23 mg/mL (58.3 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+5% Tween 80+ddH2O
For best results, use promptly after mixing.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:
Mass (mg) = Concentration (mM) × Volume (mL) × Molecular Weight (g/mol)
*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).
Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )
* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
Molecular Weight Calculator
Enter the chemical formula of a compound to calculate its molar mass and elemental composition:
Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2
Instructions to calculate molar mass (molecular weight) of a chemical compound:
To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.
Definitions of molecular mass, molecular weight, molar mass and molar weight:
Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.
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.
Tel: +1-832-582-8158 Ext:3
If you have any other enquiries, please leave a message.