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Dual-specificity PPARα/γ agonist (IC50 values are 0.35 and 3.8 μM for PPARγ and PPARα respectively). Prevents atherosclerosis progression in E3L.CETP transgenic mice. Also reduces insulin resistance in obese Zucker rats. Orally active.
Sold with the permission of AstraZeneca UK Ltd.
|Storage||Desiccate 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|
Preparing Stock Solutions
The following data is based on the product molecular weight 408.47. 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||2.45 mL||12.24 mL||24.48 mL|
|5 mM||0.49 mL||2.45 mL||4.9 mL|
|10 mM||0.24 mL||1.22 mL||2.45 mL|
|50 mM||0.05 mL||0.24 mL||0.49 mL|
References are publications that support the biological activity of the product.
Cronet et al (2001) Structure of the PPARβ and -γ ligand binding domain in complex with AZ 242; ligand selectivity and agonist activation in the PPAR family. Structure 9 699 PMID: 11587644
Ljung et al (2002) AZ 242, a novel PPARα/γ agonist with beneficial effects on Ins resistance and carbohydrate and lipid metabolism in ob/ob mice and obese Zucker rats. J.Lipid Res. 43 1855 PMID: 12401884
Ebdrup et al (2003) Synthesis and biological and structural characterization of the dual-acting peroxisome proliferator-activated receptor α/γ agonist ragaglitazar. J.Med.Chem. 46 1306 PMID: 12672231
van der Hoorn et al (2009) The dual PPARα/γ agonist tesaglitazar blocks progression of pre-existing atherosclerosis in APOE*3Leiden.CETP transgenic mice. Br.J.Pharmacol. 156 1067 PMID: 19220285
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Keywords: Tesaglitazar, Tesaglitazar supplier, AZ242, peroxisome, proliferator, activated, receptors, ppars, ppara, pparalpha, pparα, pparg, ppargamma, pparγ, agonists, astrazeneca, AZ, 242, Non-selective, PPAR, 3965, Tocris Bioscience
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HL-1 cardiomyocytes were incubated with Tesaglitazar (10 µM) for 30 min prior to addition of 15 µM 15d-PGJ2 for 30 min. Preincubation of cells with Tesaglitazar completely abolished activation of p42/44 MAPK indicating involvement of PPAR gamma in cellular signalling in response to 15d-PGJ2.
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