Inhibits Class I and II histone deacetylases (HDACs); induces accumulation of acetylated histones H2A, H2B, H3 and H4 in transformed cultured cells. Suppresses cell growth in a range of cancer cell lines; induces apoptosis in cutaneous T cell lymphoma cells in vitro. Activates autophagy.
SAHA is also offered as part of the Tocriscreen Plus, Tocriscreen Epigenetics Toolbox, Tocriscreen Library of FDA-Approved Compounds and Tocriscreen Stem Cell Toolbox. Find out more about compound libraries available from Tocris.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 264.32. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||3.78 mL||18.92 mL||37.83 mL|
|5 mM||0.76 mL||3.78 mL||7.57 mL|
|10 mM||0.38 mL||1.89 mL||3.78 mL|
|50 mM||0.08 mL||0.38 mL||0.76 mL|
References are publications that support the biological activity of the product.
Butler et al (2000) Suberoylanilide hydroxamic acid, an inhibitor of histone deacetylase, suppresses the growth of prostate cancer cells in vitro and in vivo. Cancer Res. 60 5165 PMID: 11016644
Leoni et al (2002) The antitumor histone deacetylase inhibitor suberoylanilide hydroxamic acid exhibits antiinflammatory properties via suppression of cytokines. Proc.Natl.Acad.Sci.U.S.A 99 2995 PMID: 11867742
Marks and Breslow (2007) Dimethyl sulfoxide to vorinostat: development of this histone deacetylase inhibitor as an anticancer drug. Nat.Biotechnol. 25 84 PMID: 17211407
Huangfu et al (2008) Induction of pluripotent stem cells by defined factors is greatly improved by small-molecule compounds. Nat.Biotechnol. 26 795 PMID: 18568017
Galluzzi et al (2017) Pharmacological modulation of autophagy: therapeutic potential and persisting obstacles. Nat.Rev.Drug.Discov. PMID: 28529316
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Keywords: SAHA, SAHA supplier, histone, deacetylases, HDACs, inhibits, inhibitors, Class, I, II, vorinostat, anticancer, antiproliferatives, epigenetics, proapoptotic, Vorinostat, Autophagy, Non-selective, Non-Selective, 4652, Tocris Bioscience
2 Citations for SAHA
Citations are publications that use Tocris products. Selected citations for SAHA include:
Bhattacharya et al (2017) RAD51 interconnects between DNA replication, DNA repair and immunity. Nucleic Acids Res 45 4590 PMID: 28334891
Sarenac et al (2016) Single-cell analysis reveals IGF-1 potentiation of inhibition of the TGF-β/Smad pathway of fibrosis in humankeratocytes in vitro Scientific Reports 6 34373 PMID: 27687492
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Epigenetics Scientific Review
Written by Susanne Müller-Knapp and Peter J. Brown, this review gives an overview of the development of chemical probes for epigenetic targets, as well as the impact of these tool compounds being made available to the scientific community. In addition, their biological effects are also discussed. Epigenetic compounds available from Tocris are listed.
Epigenetics Research Bulletin
Produced by Tocris and updated in 2014, the epigenetics research bulletin gives an introduction into mechanisms of epigenetic regulation, and highlights key Tocris products for epigenetics targets including:
- DNA Methyltransferases
- Histone Deacetylases
- Histone Demethylases
- Histone Methyltransferases
Rheumatoid Arthritis Poster
Rheumatoid arthritis (RA) is a chronic destructive inflammatory autoimmune disease that results from a breakdown in immune tolerance, for reasons that are as yet unknown. This poster summarizes the pathology of RA and the inflammatory processes involved, as well as describing some of the epigenetic modifications associated with the disease and the potential for targeting these changes in the discovery of new treatments.