Potent MTH1 inhibitor (IC50 = 5 nM). Induces oxidative DNA damage and reduces survival in cancer cells. Inhibits growth of breast and colorectal cancer xenografts in mice.
Sold under license from Thomas Helleday's Foundation for Medical Research and Oxcia AB.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 295.17. 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||3.39 mL||16.94 mL||33.88 mL|
|5 mM||0.68 mL||3.39 mL||6.78 mL|
|10 mM||0.34 mL||1.69 mL||3.39 mL|
|50 mM||0.07 mL||0.34 mL||0.68 mL|
References are publications that support the biological activity of the product.
Gad et al (2014) MTH1 inhibition eradicates cancer by preventing sanitation of the dNTP pool. Nature 508 215 PMID: 24695224
If you know of a relevant reference for TH 588, please let us know.
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Keywords: TH 588, TH 588 supplier, TH588, MTH1, MutT, homolog-1, inhibitors, inhibits, potent, (MTH1), 5334, Tocris Bioscience
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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!
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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.