Dual site PPARγ inhibitor. Acts at orthosteric and allosteric sites in the ligand binding domain. Inhibits binding of endogenous ligands and transcriptional activity of PPARγ, more effectively than the orthosteric covalent antagonists GW 9662 (Cat. No. 1508) and T 0070907 (Cat. No. 2301).
|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 357.75. 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|
|0.5 mM||5.59 mL||27.95 mL||55.9 mL|
|2.5 mM||1.12 mL||5.59 mL||11.18 mL|
|5 mM||0.56 mL||2.8 mL||5.59 mL|
|25 mM||0.11 mL||0.56 mL||1.12 mL|
References are publications that support the biological activity of the product.
Brust et al (2017) Modification of the othosteric PPARγ covalent antagonist scaffold yields an improved dual-site allosteric inhibitor. ACS Chem.Biol. 12 969 PMID: 28165718
If you know of a relevant reference for SR 16832, please let us know.
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Keywords: SR 16832, SR 16832 supplier, SR16832, PPAR, gamma, peroxisome, proliferator, activated, receptor, inhibitors, inhibits, PPARgamma, Receptors, 6383, Tocris Bioscience
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Literature in this Area
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Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.