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Biological Activity for GSK 126
GSK 126 is a very high affinity and selective EZH2 inhibitor (Ki = 0.5 - 3 nM). Exhibits >150-fold selectivity for EZH2 over EZH1 and >1000-fold selectivity over 20 other human methyltransferases. Inhibits proliferation of B-cell lymphoma cell lines in vitro. Also inhibits H3K27Me3 and tumor growth in mice bearing BCL xenografts. Targeting p53 and histone methyltransferases restores exhausted CD8+ T cells in HCV infection. Promotes the transition of ESCs to feeder-free extended pluripotent stem (EPS) cells in combination with LCDM cocktail.
Technical Data for GSK 126
|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.
Solubility Data for GSK 126
|Solvent||Max Conc. mg/mL||Max Conc. mM|
|DMSO||2.63||5 with gentle warming|
Preparing Stock Solutions for GSK 126
The following data is based on the product molecular weight 526.67. 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|
|0.05 mM||37.97 mL||189.87 mL||379.74 mL|
|0.25 mM||7.59 mL||37.97 mL||75.95 mL|
|0.5 mM||3.8 mL||18.99 mL||37.97 mL|
|2.5 mM||0.76 mL||3.8 mL||7.59 mL|
References for GSK 126
References are publications that support the biological activity of the product.
McCabe et al (2012) EZH2 inhibition as a therapeutic strategy for lymphoma with EZH2-activating mutations. Nature 492 108 PMID: 23051747
Barili et al (2020) Targeting p53 and histone methyltransferases restores exhausted CD8+ T cells in HCV infection. Nat.Commun. 11 604 PMID: 32001678
Zheng et al (2021) Derivation of feeder-free human extended pluripotent stem cells. Stem Cell Rep 16 1686 PMID: 34214484
If you know of a relevant reference for GSK 126, please let us know.
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Citations for GSK 126
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Currently there are no citations for GSK 126. Do you know of a great paper that uses GSK 126 from Tocris? Please let us know.
Reviews for GSK 126
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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* 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.
Stem Cells Scientific Review
Written by Kirsty E. Clarke, Victoria B. Christie, Andy Whiting and Stefan A. Przyborski, this review provides an overview of the use of small molecules in the control of stem cell growth and differentiation. Key signaling pathways are highlighted, and the regulation of ES cell self-renewal and somatic cell reprogramming is discussed. 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
Cancer Metabolism Poster
Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the main targets for cancer metabolism researchers. Genetic changes and epigenetic modifications in cancer cells alter the regulation of cellular metabolic pathways. These distinct metabolic circuits could provide viable cancer therapeutic targets.
Epigenetics in Cancer Poster
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.