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Selective and potent inhibitor of histone deacetylase (Ki = 3.4 nM). Active in vivo. Potential anti-cancer agent. Induces accelerated dedifferentiation of primordial germ cells (PGCs) into embryonic germ (EG) cells. Activates autophagy.
|Storage||Desiccate 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 302.37. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|0.5 mM||6.61 mL||33.07 mL||66.14 mL|
|2.5 mM||1.32 mL||6.61 mL||13.23 mL|
|5 mM||0.66 mL||3.31 mL||6.61 mL|
|25 mM||0.13 mL||0.66 mL||1.32 mL|
References are publications that support the biological activity of the product.
Durcova-Hills et al (2008) Reprogramming primordial germ cells into pluripotent stem cells. PloS ONE 3 e3531 PMID: 18953407
Yoshida et al (1990) Potent and specific inhibition of mammalian histone deacetylase both in vivo and in vitro by trichostatin A. J.Biol.Chem. 265 17174 PMID: 2211619
Vigushin et al (2001) Trichostatin A is a histone deacetylase inhibitor with potent antitumor activity against breast cancer in vivo. Clin.Cancer Res. 7 971 PMID: 11309348
Wharton et al (2000) Inhibition of mitogenesis in Balb/c-3T3 cells by trichostatin A. J.Biol.Chem. 275 33981 PMID: 10945992
Galluzzi et al (2017) Pharmacological modulation of autophagy: therapeutic potential and persisting obstacles. Nat.Rev.Drug.Discov. PMID: 28529316
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Keywords: Trichostatin A, Trichostatin A supplier, Histone, deacetylase, inhibitors, inhibits, HDAC, Deacetylases, TrichostatinA, stem, cells, epigenetics, Reprogramming, Autophagy, Non-selective, HDACs, Non-Selective, 1406, Tocris Bioscience
6 Citations for Trichostatin A
Citations are publications that use Tocris products. Selected citations for Trichostatin A include:
Franklin et al (2014) Increased long-term potentiation at medial-perforant path-dentate granule cell synapses induced by selective inhibition of histone deacetylase 3 requires Fragile X mental retardation protein. Neurobiol Learn Mem 114 193 PMID: 24956240
Li et al (2018) Epigenetic control of IL-23 expression in keratinocytes is important for chronic skin inflammation. Nat Commun 9 1420 PMID: 29650963
Kobori et al (2010) Butyrate stimulates IL-32α expression in human intestinal epithelial cell lines. Oncogene 16 2355 PMID: 20480520
Kurita et al (2012) HDAC2 regulates atypical antipsychotic responses through the modulation of mGlu2 promoter activity. Nat Neurosci 15 1245 PMID: 22864611
Xia et al (2013) Identification of repurposed small molecule drugs for chordoma therapy. Cancer Biol Ther 14 638 PMID: 23792643
Biernacka et al (2013) Hyperglycaemia-induced chemoresistance of prostate cancer cells due to IGFBP2. World J Gastroenterol 20 741 PMID: 23959956
Do you know of a great paper that uses Trichostatin A from Tocris? Please let us know.
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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.