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GW 7647 is a potent and highly selective PPARα agonist (EC50 values are 6, 1100 and 6200 nM for human PPARα, PPARγ and PPARδ receptors respectively). Modulates oleate metabolism and mitochondrial enzyme gene expression in mature myotubules in vitro. Has lipid-lowering effects following oral administration in vivo. Reduces NO production in macrophages; exhibits anti-inflammatory properties.
Sold for research purposes under agreement from GlaxoSmithKline
GW 7647 is also offered as part of the Tocriscreen 2.0 Max. Find out more about compound libraries available from Tocris.
|Storage||Store at RT|
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|
The following data is based on the product molecular weight 502.75. 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|
|1 mM||1.99 mL||9.95 mL||19.89 mL|
|5 mM||0.4 mL||1.99 mL||3.98 mL|
|10 mM||0.2 mL||0.99 mL||1.99 mL|
|50 mM||0.04 mL||0.2 mL||0.4 mL|
References are publications that support the biological activity of the product.
Brown et al (2001) Identification of a subtype selective human PPARα agonist through parallel-array synthesis. Bioorg.Med.Chem.Lett. 11 1225 PMID: 11354382
Cunard et al (2002) Regulation of cytokine expression by ligands of peroxisome proliferator activated receptors. J.Immunol. 168 2795 PMID: 11884448
Muoio et al (2002) Peroxisome proliferator-activated receptor-α regulates fatty acid utilization in primary human skeletal muscle cells. Diabetes 51 901 PMID: 11916905
Paukkeri et al (2007) PPARalpha agonists inhibit nitric oxide production by enhancing iNOS degradation in LPS-treated macrophages. Br.J.Pharmacol. 152 1081 PMID: 17891158
If you know of a relevant reference for GW 7647, please let us know.
Keywords: GW 7647, GW 7647 supplier, selective, potent, PPARα, PPARalpha, agonists, Orally, active, Peroxisome, Proliferator-activating, Receptors, PPAR, GW7647, GlaxoSmithKline, GSK, anti-inflammatory, 1677, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for GW 7647 include:
Ropero et al (2009) Rapid non-genomic regulation of Ca2+ signals and Ins secretion by PPAR alpha ligands in mouse pancreatic islets of Langerhans. J Endocrinol 200 127 PMID: 19017711
Guo et al (2018) Antagonism of PPAR-γ signaling expands human hematopoietic stem and progenitor cells by enhancing glycolysis. Nat Med 24 360 PMID: 29377004
Moreno-Santos et al (2014) Computational and biological evaluation of N-octadecyl-N'-propylsulfamide, a selective PPARα agonist structurally related to N-acylethanolamines. PLoS One 9 e92195 PMID: 24651609
Mottillo et al (2012) Lipolytic products activate peroxisome proliferator-activated receptor (PPAR) α and δ in brown adipocytes to match fatty acid oxidation with supply. Bioorg Med Chem 287 25038 PMID: 22685301
Hatano et al (2010) Murine atopic dermatitis responds to peroxisome proliferator-activated receptors α and β/δ (but not γ) and liver X receptor activators. Cell Commun Signal 125 160 PMID: 19818482
Mattsson et al (2015) Metabolic Profiling of Chicken Embryos Exposed to Perfluorooctanoic Acid (PFOA) and Agonists to Peroxisome Proliferator-Activated Receptors. PLoS One 10 e0143780 PMID: 26624992
Yu et al (2013) Development of time resolved fluorescence resonance energy transfer-based assay for FXR antagonist discovery. J Allergy Clin Immunol 21 4266 PMID: 23688559
Fellous et al (2020) Phytocannabinoids promote viability and functional adipogenesis of bone marrow-derived mesenchymal stem cells through different molecular targets Biochemical Pharmacology 175 PMID: 32061773
Do you know of a great paper that uses GW 7647 from Tocris? Please let us know.
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GW7647 is the most potent PPARalpha agonist that reduces LPS-induced iNOS expression and NO production in macrophages by enhancing iNOS protein degradation through the proteasome pathway. Concentration 3, 10 and 30 uM showed dose-dependent inhibition.
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