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BET bromodomain inhibitor (Kd values are 160, 170, 380, 490, 830 and 850 nM for BRD4(1), BRD2(1), BRD3(1), BRD3(2), BRD2(2) and BRD4(2) respectively). Also inhibits BRDT(1), CBP, p300 and BRDT(2) (Kd values are 1.2, 1.6, 2.6 and 3.7 μM respectively). Attenuates proliferation of HL-60 leukemia cells in vitro.
|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.
References are publications that support the biological activity of the product.
Lucas et al (2013) 4-Acyl pyrroles: mimicking acetylated lysines in histone code reading. Angew.Chem.Int.Ed.Engl. 52 14055 PMID: 24272870
Keywords: XD 14, XD 14 supplier, XD14, BET, bromodomain, inhibitors, inhibits, BRD4(1), BRD4(2), BRD3(1), BRD3(2), BRD2(1), BRD2(2), BRDT(1), BRDT(2), CREBBP, EP300, epigenetics, Bromodomains, 5489, 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!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
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.
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:
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.