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Inhibitor of sterol regulatory element binding protein (SREBP); impairs the activation of SREBP-1 and SREBP-2. Exhibits antiproliferative effects in DU 145 cells independently of IGF-1 signaling (IC50 = 0.1 μM); reverses hyperglycemia in diabetic (ob/ob) mice. Cell permeable.
|Storage||Store at +4°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 375.33. 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||13.32 mL||66.61 mL||133.22 mL|
|1 mM||2.66 mL||13.32 mL||26.64 mL|
|2 mM||1.33 mL||6.66 mL||13.32 mL|
|10 mM||0.27 mL||1.33 mL||2.66 mL|
References are publications that support the biological activity of the product.
Kamisuki et al (2009) A small molecule that blocks fat synthesis by inhibiting the activation of SREBP. Chem.Biol. 16 882 PMID: 19716478
Choi et al (2003) Identification of bioactive molecules by adipogenesis profiling of organic compounds. J.Biol.Chem. 278 7320 PMID: 12496288
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Keywords: Fatostatin A, Fatostatin A supplier, sterol, regulatory, element, binding, proteins, SREBPs, SREBP1, SREBP2, inhibition, inhibitors, inhibits, antiproliferatives, 125B11, FatostatinA, SREBP, 4444, Tocris Bioscience
1 Citation for Fatostatin A
Citations are publications that use Tocris products. Selected citations for Fatostatin A include:
Roche et al (2018) Trafficking of cholesterol to the ER is required for NLRP3 inflammasome activation. J Cell Biol 217 3560 PMID: 30054450
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Literature in this Area
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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.