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Fenofibric acid

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Chemical Structure| 42017-89-0 同义名 : FNF acid;NSC 281318;Procetofenic acid;Trilipix
CAS号 : 42017-89-0
货号 : A399267
分子式 : C17H15ClO4
纯度 : 98%
分子量 : 318.752
MDL号 : MFCD00792461
存储条件：

粉末 Sealed in dry,Room Temperature

液体 -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 105 mg/mL(329.41 mM)，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO
动物实验配方：
生物活性
靶点

  • PPARα
描述 Fenofibric acid serves as an activator for PPAR, exhibiting EC50s of 22.4 µM, 1.47 µM, and 1.06 µM for PPARα, PPARγ, and PPARδ, respectively[1]. At concentrations ranging from 10 to 100 nM, Fenofibric acid progressively inhibits the COX-2 enzyme, achieving an IC50 of 48 nM[2]. At a concentration of 500 nM, Fenofibric acid leads to a reduction in the levels of AOX1 protein in HepG2 cells[3]. Fenofibric acid at 100 µM reduces phosphorylation of JNK1/2, c-Jun, and p38 MAPK, and protects against the build-up of reactive oxygen species, endoplasmic reticulum (ER) stress, and damage to the blood retinal barrier (BRB) triggered by a combination of high-glucose and hypoxic conditions in ARPE-19 cells. Additionally, at this concentration, Fenofibric acid stimulates the IGF-IR/Akt/ERK1/2-mediated survival signaling pathways in ARPE-19 cells under these stress conditions[4].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

3.14mL

0.63mL

0.31mL

15.69mL

3.14mL

1.57mL

31.37mL

6.27mL

3.14mL
参考文献

[1]Dietz M, et al. Comparative molecular profiling of the PPARα/γ activator aleglitazar: PPAR selectivity, activity and interaction with cofactors. ChemMedChem. 2012 Jun;7(6):1101-11.

[2]Prasad GS, et al. Anti-inflammatory activity of anti-hyperlipidemic drug, fenofibrate, and its phase-I metabolite fenofibric acid: in silico, in vitro, and in vivo studies. Inflammopharmacology. 2017 Dec 13.

[3]Neumeier M, et al. Aldehyde oxidase 1 is highly abundant in hepatic steatosis and is downregulated by adiponectin and fenofibric acid in hepatocytes in vitro. Biochem Biophys Res Commun. 2006 Nov 24;350(3):731-5. Epub 2006 Sep 27.

[4]Miranda S, et al. Beneficial effects of fenofibrate in retinal pigment epithelium by the modulation of stress and survival signaling under diabetic conditions. J Cell Physiol. 2012 Jun;227(6):2352-62.