Seladelpar (MBX-8025) is an orally active, potent (50% effect concentrationEC₅₀2 nM), and specificPPAR-δagonist^[1][2].

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^[1]. 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^[2].

From weaning, femaleAlms1mutant (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 infoz/fozmice. Serum alanine aminotransferase ranges 300-600 U/L in vehicle-treatedfoz/fozmice; 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-treatedfoz/fozversus wild-type mice. This abolished hepatocyte ballooning and apoptosis, substantially reduce steatosis and liver inflammation, and improve liver fibrosis. In vehicle-treatedfoz/fozmice, the mean nonalcoholic fatty liver disease activity score is 6.9, indicating nonalcoholic steatohepatitis (NASH); Seladelpar reverses NASH in allfoz/fozmice (nonalcoholic fatty liver disease activity score 3.13). In atherogenic diet-fedWtmice, administration of Seladelpar reduces body weight by ~18% (P<0.05). In contrast, Seladelpar produces minimal effect on body weight in atherogenic diet–fedfoz/fozmice. 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-treatedfoz/fozmice (P<0.05); the area under the blood glucose disappearance curve is correspondingly lower in Seladelpar-treatedfoz/fozmice (P<0.05). Seladelpar produces a proportionally similar effect on glucose handling in atherogenic diet–fedWtmice (P<0.05)^[2].

444.46

Liquid

C₂₁H₂₃F₃O₅S

851528-79-5

Room temperature in continental US; may vary elsewhere.

DMSO : 100 mg/mL(224.99 mM;Need ultrasonic)

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80℃, 6 months; -20℃, 1 month。-80℃ 储存时，请在 6 个月内使用，-20℃ 储存时，请在 1 个月内使用。

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照In Vitro方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 10% DMSO    40%PEG300   5%Tween-80   45% saline

  Solubility: ≥ 2.5 mg/mL (5.62 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (5.62 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH2O 中，得到澄清透明的生理盐水溶液
• 2.

  请依序添加每种溶剂： 10% DMSO    90%corn oil

  Solubility: ≥ 2.5 mg/mL (5.62 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (5.62 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。