Muraglitazar - CAS 331741-94-7
Catalog number: 331741-94-7
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C29H28N2O7
Molecular Weight:
516.54
COA:
Inquire
Targets:
PPAR
Description:
Muraglitazar is a peroxisome proliferator-activated receptor (PPAR) α/γ dual agonist(EC50s = 320 and 110 nM in vitro).
Purity:
≥98%
Appearance:
Off-White Solid
Synonyms:
Pargluva; BMS 298585; BMS-298585; BMS298585; Muraglitazar;N-((4-methoxyphenoxy)carbonyl)-N-((4-(2-(5-methyl-2-phenyl-4-oxazolyl)ethoxy)phenyl)methyl)glycine;Muraglitazar;N-[(4-Methoxyphenoxy)carbonyl]-N-[[4-[2-(5-methyl-2-phenyl-4-oxazolyl)ethoxy]phenyl]methyl]glycine;Pargluva
Solubility:
Soluble in DMSO
Storage:
Store at -20 °C
MSDS:
Inquire
Application:
A peroxisome proliferator-activated receptor (PPAR) α/γ dual agonist.
Quality Standard:
Enterprise standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly.
Quantity:
Milligrams-Grams
Melting Point:
123-125 °C
InChIKey:
IRLWJILLXJGJTD-UHFFFAOYSA-N
InChI:
1S/C29H28N2O7/c1-20-26(30-28(37-20)22-6-4-3-5-7-22)16-17-36-24-10-8-21(9-11-24)18-31(19-27(32)33)29(34)38-25-14-12-23(35-2)13-15-25/h3-15H,16-19H2,1-2H3,(H,32,33)
Canonical SMILES:
c1c(cccc1)c1oc(c(n1)CCOc1ccc(CN(C(=O)Oc2ccc(cc2)OC)CC(=O)O)cc1)C
Current Developer:
Bristol-Myers Squibb
1.Anti-inflammatory properties of a dual PPARgamma/alpha agonist muraglitazar in in vitro and in vivo models.
Paukkeri EL, Leppänen T, Lindholm M, Yam MF, Asmawi MZ, Kolmonen A, Aulaskari PH, Moilanen E. Arthritis Res Ther. 2013 Apr 17;15(2):R51. doi: 10.1186/ar4211.
INTRODUCTION: Peroxisome proliferator-activated receptor (PPAR) agonists are widely used drugs in the treatment of diabetes and dyslipidemia. In addition to their metabolic effects, PPAR isoforms PPARα and PPARγ are also involved in the regulation of immune responses and inflammation. In the present study, we investigated the effects of a dual PPARγ/α agonist muraglitazar on inflammatory gene expression in activated macrophages and on carrageenan-induced inflammation in the mouse.
2.PPAR agonists reduce steatosis in oleic acid-overloaded HepaRG cells.
Rogue A1, Anthérieu S2, Vluggens A2, Umbdenstock T3, Claude N4, de la Moureyre-Spire C5, Weaver RJ5, Guillouzo A6. Toxicol Appl Pharmacol. 2014 Apr 1;276(1):73-81. doi: 10.1016/j.taap.2014.02.001. Epub 2014 Feb 15.
Although non-alcoholic fatty liver disease (NAFLD) is currently the most common form of chronic liver disease there is no pharmacological agent approved for its treatment. Since peroxisome proliferator-activated receptors (PPARs) are closely associated with hepatic lipid metabolism, they seem to play important roles in NAFLD. However, the effects of PPAR agonists on steatosis that is a common pathology associated with NAFLD, remain largely controversial. In this study, the effects of various PPAR agonists, i.e. fenofibrate, bezafibrate, troglitazone, rosiglitazone, muraglitazar and tesaglitazar on oleic acid-induced steatotic HepaRG cells were investigated after a single 24-hour or 2-week repeat treatment. Lipid vesicles stained by Oil-Red O and triglycerides accumulation caused by oleic acid overload, were decreased, by up to 50%, while fatty acid oxidation was induced after 2-week co-treatment with PPAR agonists. The greatest effects on reduction of steatosis were obtained with the dual PPARα/γ agonist muraglitazar.
3.Muraglitazar-eluting bioabsorbable vascular stent inhibits neointimal hyperplasia in porcine iliac arteries.
Uurto I1, Hämäläinen M2, Suominen V3, Laurila M4, Kotsar A3, Isotalo T5, Tammela TL3, Kellomäki M6, Salenius JP3. J Vasc Interv Radiol. 2015 Jan;26(1):124-30. doi: 10.1016/j.jvir.2014.10.005. Epub 2014 Nov 18.
PURPOSE: To evaluate the biocompatibility of a new muraglitazar-eluting polylactide copolymer stent and investigate its ability to prevent the formation of intimal hyperplasia.
4.Peroxisome proliferator-activated receptor agonists and bladder cancer: lessons from animal studies.
Tseng CH1, Tseng FH. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2012;30(4):368-402. doi: 10.1080/10590501.2012.735519.
This article reviews available animal studies on the possible link between the use of peroxisome proliferator-activated receptor (PPAR) agonists and bladder cancer, with further discussion on the possible implications to humans. Carcinogenicity studies suggest that the PPARγ agonist pioglitazone and dual PPARα/γ agonists such as ragaglitazar, muraglitazar, and naveglitazar may increase the risk of bladder cancer in a dose-responsive pattern in rats. It is interesting that bladder cancer related to PPAR agonists shows remarkable species- and sex-specificity and has a predilection to occur in the ventral dome of bladder in rodents. While male rats treated with pioglitazone or muraglitazar have a higher propensity to develop bladder cancer than female rats, mice of both sexes do not develop bladder cancer even when exposed to very high doses. Direct genotoxicity or cytotoxicity of PPAR agonists is unlikely to be the mode of action because most of the parent compounds or their metabolites of the PPAR agonists are neither mutagenic nor genotoxic, and they are rarely excreted in the urine; but a receptor-mediated PPAR effect cannot be excluded.
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CAS 331741-94-7 Muraglitazar

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