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Seladelpar

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品牌名称:$brandModel.Title(进口品牌)型号: 原产地:美洲 发布时间:2021/7/26更新时间:2024/1/2

产品摘要:Seladelpar (MBX-8025) 是一种有效的,具有口服活性的, 特异性 PPAR-δ 激动剂,EC50 为 2 nM。

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Seladelpar

CAS No. : 851528-79-5

MCE 站:Seladelpar

产品活性:Seladelpar (MBX-8025) 是一种有效的,具有口服活性的, 特异性 PPAR-δ 激动剂,EC50 为 2 nM。

研究领域:Cell Cycle/DNA Damage

作用靶点:PPAR

In Vitro: Seladelpar (MBX-8025) is an orally active, potent (2 nM), and specific (>750-fold and >2500-fold compared with PPAR-α or PPAR-γ receptors, respectively) PPAR-δ agonist being developed as a lipid-altering agent. Seladelpar is a potent, and selective PPAR-δ agonist (50% effect concentration human PPAR-δ=2 nM, PPAR-α=1,600 nM) that demonstrates favorable effects on insulin resistance, diabetes, and atherogenic dyslipidemia.

In Vivo: From weaning, female Alms1 mutant (foz/foz) mice and wild-type littermates are fed an atherogenic diet for 16 weeks; groups (n=8-12) are then randomized to receive Seladelpar (10 mg/kg) or vehicle (1% methylcellulose) by gavage for 8 weeks. Despite minimally altering body weight, Seladelpar normalizes hyperglycemia, hyperinsulinemia, and glucose disposal in foz/foz mice. Serum alanine aminotransferase ranges 300-600 U/L in vehicle-treated foz/foz mice; Seladelpar reduces alanine aminotransferase by 50%. In addition, Seladelpar normalizes serum lipids and hepatic levels of free cholesterol and other lipotoxic lipids that are increased in vehicle-treated foz/foz versus wild-type mice. This abolished hepatocyte ballooning and apoptosis, substantially reduce steatosis and liver inflammation, and improve liver fibrosis. In vehicle-treated foz/foz mice, the mean nonalcoholic fatty liver disease activity score is 6.9, indicating nonalcoholic steatohepatitis (NASH); Seladelpar reverses NASH in all foz/foz mice (nonalcoholic fatty liver disease activity score 3.13). In atherogenic diet-fed Wt mice, administration of Seladelpar reduces body weight by ?18% (P<0.05). In contrast, Seladelpar produces minimal effect on body weight in atherogenic diet–fed foz/foz mice. These animals develope severe hyperglycemia, hyperinsulinemia, and whole-body insulin resistance after 16 weeks (P<0.05); Seladelpar strikingly improves these indices (P<0.05). After intraperitoneal glucose injection, blood glucose reaches ~32 mM in vehicle-treated versus ~14 mM in Seladelpar-treated foz/foz mice (P<0.05); the area under the blood glucose disappearance curve is correspondingly lower in Seladelpar-treated foz/foz mice (P<0.05). Seladelpar produces a proportionally similar effect on glucose handling in atherogenic diet–fed Wt mice (P<0.05).

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