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GW 9578

目录号 : GC43800

A potent, selective PPARα agonist

GW 9578 Chemical Structure

Cas No.:247923-29-1

规格 价格 库存 购买数量
500μg
¥394.00
现货
1mg
¥754.00
现货
5mg
¥3,152.00
现货
10mg
¥5,517.00
现货

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Sample solution is provided at 25 µL, 10mM.

产品文档

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产品描述

Peroxisome proliferator-activated receptor α (PPARα) is a ligand-activated transcription factor found predominantly in the liver that is involved in the regulation of lipid homeostasis. Activation of PPARα results in expression of a variety of genes, particularly those involved in fatty acid β-oxidation, binding, and transport. GW 9578 is a potent agonist of PPARα that activates the murine and human receptors with EC50 values of 0.005 and 0.05 µM, respectively. GW 9578 is highly selective for PPARα compared to PPARγ and PPARδ, which it activates in murine at EC50 values of 0.15 and 2.6 µM, respectively and in human at 1.0 and 1.4 µM, respectively. GW 9578 is a potent lipid lowering agent that may reduce insulin resistance. When 0.2 mg/kg GW 9578 was given orally once daily for three days, serum total LDL cholesterol was decreased 40-60% in male Sprague-Dawely rats. Obese Zucker rats treated with 5 mg/kg GW 9578 for nine days had markedly reduced serum insulin concentrations compared to controls.

Chemical Properties

Cas No. 247923-29-1 SDF
Canonical SMILES CCCCCCCN(CCc1ccc(cc1)SC(C)(C)C(=O)O)C(=O)Nc1ccc(F)cc1F
分子式 C26H34F2N2O3S 分子量 492.6
溶解度 DMF: 10 mg/ml,DMSO: 10 mg/ml,DMSO:PBS (pH 7.2) (1:2): 0.3 mg/ml,Ethanol: 2.5 mg/ml 储存条件 Store at -20°C
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.03 mL 10.1502 mL 20.3004 mL
5 mM 0.406 mL 2.03 mL 4.0601 mL
10 mM 0.203 mL 1.015 mL 2.03 mL
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Research Update

PPAR-alpha and -gamma but not -delta agonists inhibit airway inflammation in a murine model of asthma: in vitro evidence for an NF-kappaB-independent effect

Br J Pharmacol 2003 May;139(1):163-71.PMID:12746235DOI:10.1038/sj.bjp.0705232.

1. Peroxisome proliferator-activated receptors (PPARs) are ligand-activated transcription factors that have been proposed to regulate inflammation by antagonising the nuclear factor-kappaB (NF-kappaB) signalling pathway. We investigated the role of PPARs using synthetic agonists in murine models of airway inflammation, and addressed the possible effect on NF-kappaB signalling in vitro using a human epithelial cell line, A549. 2. Sensitised BALB/c mice exposed to an aerosol solution of ovalbumin had an increased number of airway eosinophils, neutrophils and lymphocytes. When given intranasally an hour before the aerosol challenge, a PPAR-alpha (GW 9578) and PPAR-gamma (GI 262570) selective agonist as well as a dual PPAR-alpha/gamma (GW 2331) agonist selectively inhibited allergen-induced bronchoalveolar lavage eosinophil and lymphocyte but not neutrophil influx. In contrast, a PPAR-delta agonist (GW 501516) was inactive. 3. When given intranasally an hour before challenge, PPAR-alpha and PPAR-gamma selective agonists as well as a dual PPAR-alpha/gamma agonist did not inhibit lipopolysaccharide-induced bronchoalveolar lavage neutrophil influx or tumour necrosis factor-alpha (TNF-alpha) and KC production. 4. In A549 cells, selective agonists for PPAR-alpha, -gamma and -delta did not inhibit intracellular adhesion molecule-1 expression following stimulation with proinflammatory cytokines. In addition, IL-8 release and the activation of an NF-kappaB-responsive reporter gene construct were inhibited only at micromolar concentrations, suggesting that these effects were not PPAR-mediated. 5. Our in vivo data show that agonists of PPAR-alpha and -gamma, but not -delta, inhibit allergen-induced bronchoalveolar lavage eosinophil and lymphocyte influx. In vitro data suggest that this effect might not be mediated by antagonism of the NF-kappaB pathway.