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Class I HDAC inhibitor (IC50 values are 0.06, 0.1, 0.5 and 1.5 μM for HDACs 3, 2, 1 and 8, respectively). Exhibits >6-fold selectivity over other HDACs. Induces accumulation of acetylated histones in HCT116 cells in vitro. Inhibits proliferation of a range of cancer cell lines. Arrests cells at G1/S transition.
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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.
References are publications that support the biological activity of the product.
Wang et al (2015) Identification of histone deacetylase inhibitors with benzoylhydrazide scaffold that selectively inhibit class I histone deacetylases. Chem.Biol. 22 273 PMID: 25699604
Keywords: UF 010, UF 010 supplier, UF010, histone, deacetylase, inhibitors, inhibits, HDAC, classI, cancer, proliferation, cell, cycle, arrest, antiproliferative, epigenetics, Class, I, HDACs, 5588, Tocris Bioscience
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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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.
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.
Adapted from the 2015 Cancer Product Guide Edition 3, this poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.
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.