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Allosteric glutaminase (GLS1) inhibitor (IC50 = 3.3 μM). Selective for GLS1 over GLS2 and γ-glutamyl transpeptidase. Induces cell death of P493 human lymphoma B cells in vitro and reduces tumor volume of P493 cell xenografts in mice.
|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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 524.68. 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|
|0.2 mM||9.53 mL||47.65 mL||95.3 mL|
|1 mM||1.91 mL||9.53 mL||19.06 mL|
|2 mM||0.95 mL||4.76 mL||9.53 mL|
|10 mM||0.19 mL||0.95 mL||1.91 mL|
References are publications that support the biological activity of the product.
Le et al (2012) Glucose-independent glutamine metabolism via TCA cycling for proliferation and survival in B cells. Cell.Metab. 15 110 PMID: 22225880
Shukla et al (2012) Design, synthesis, and pharmacological evaluation of bis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfide 3 (BPTES) analogs as glutaminase inhibitors. J.Med.Chem. 55 10551 PMID: 23151085
DeLaBarre et al (2011) Full-length human glutaminase in complex with an allosteric inhibitor. Biochemistry 50 10764 PMID: 22049910
If you know of a relevant reference for BPTES, please let us know.
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Keywords: BPTES, BPTES supplier, allosteric, glutaminases, gls1, inhibitors, inhibits, selective, Glutaminase, 5301, Tocris Bioscience
Citations for BPTES
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Reviews for BPTES
Average Rating: 4 (Based on 1 Review.)
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incubation, slight effect
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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.