Fenofibric acidCAS# 42017-89-0 |
Quality Control & MSDS
3D structure
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| Cas No. | 42017-89-0 | SDF | Download SDF |
| PubChem ID | 64929 | Appearance | Powder |
| Formula | C17H15ClO4 | M.Wt | 318.8 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | FNF acid | ||
| Solubility | DMSO : ≥ 100 mg/mL (313.73 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 2-[4-(4-chlorobenzoyl)phenoxy]-2-methylpropanoic acid | ||
| SMILES | CC(C)(C(=O)O)OC1=CC=C(C=C1)C(=O)C2=CC=C(C=C2)Cl | ||
| Standard InChIKey | MQOBSOSZFYZQOK-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C17H15ClO4/c1-17(2,16(20)21)22-14-9-5-12(6-10-14)15(19)11-3-7-13(18)8-4-11/h3-10H,1-2H3,(H,20,21) | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
Fenofibric acid Dilution Calculator
Fenofibric acid Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.1368 mL | 15.6838 mL | 31.3676 mL | 62.7353 mL | 78.4191 mL |
| 5 mM | 0.6274 mL | 3.1368 mL | 6.2735 mL | 12.5471 mL | 15.6838 mL |
| 10 mM | 0.3137 mL | 1.5684 mL | 3.1368 mL | 6.2735 mL | 7.8419 mL |
| 50 mM | 0.0627 mL | 0.3137 mL | 0.6274 mL | 1.2547 mL | 1.5684 mL |
| 100 mM | 0.0314 mL | 0.1568 mL | 0.3137 mL | 0.6274 mL | 0.7842 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Fenofibric acid, an active metabolite of fenofibrate, is a PPAR activitor, with EC50s of 22.4 µM, 1.47 µM, and 1.06 µM for PPARα, PPARγ and PPARδ, respectively; Fenofibric acid also inhibits COX-2 enzyme activity, with an IC50 of 48 nM.
In Vitro:Fenofibric acid is a PPAR activitor, with EC50s of 22.4 µM, 1.47 µM, and 1.06 µM for PPARα, PPARγ and PPARδ, respectively[1]. Fenofibric acid (10, 25, 50, 75, and 100 nM) dose-dependently inhibits COX-2 enzyme, with IC50 of 48 nM[2]. Fenofibric acid (500 nM) reduces abundance of AOX1 protein in HepG2 cells[3]. Fenofibric acid (100 µM) decreases JNK1/2, c-Jun, and p38 MAPK phosphorylation, and prevents the accumulation of reactive oxygen species, endoplasmic reticulum (ER) stress and disruption of blood retinal barrier (BRB) in response to the combination of high-glucose (HG) and hypoxia in ARPE-19 cells. Fenofibric acid (100 µM) activates IGF-IR/Akt/ERK1/2-mediated survival signaling pathways in ARPE-19 cells under HG conditions and hypoxia[4].
In Vivo:Fenofibric acid (1, 5, 10 mg/kg, p.o.) shows anti-inflammatory activity in Wistar rats with acute inflammation induced by carrageenan[2].
References:
[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.
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Anti-inflammatory activity of anti-hyperlipidemic drug, fenofibrate, and its phase-I metabolite fenofibric acid: in silico, in vitro, and in vivo studies.[Pubmed:29238904]
Inflammopharmacology. 2018 Aug;26(4):973-981.
Fenofibrate, an anti-hyperlipidemic drug and its phase-I biotransformed metabolite Fenofibric acid, was studied for COX-1 (PDB ID: 3N8Y) and COX-2 (PDB ID: 1PXX) inhibition potentials in silico and in vitro for their effects on human recombinant COX-2 enzyme isolated from a Baculovirus expression system in sf21 cells (EC 1.14.99.1) using a conventional spectrophotometric assay. Furthermore, the compounds were also screened for their anti-inflammatory potentials in vivo using carrageenan-induced paw oedema method in Wistar rats. The test compounds Fenofibric acid, fenofibrate, and the standard drug diclofenac exhibited binding energies of - 9.0, - 7.2, and - 8.0 kcal mol(-1), respectively, against COX-2 and - 7.2, - 7.0, and - 6.5 kcal mol(-1), respectively, against COX-1. In in vitro studies, both the test compounds inhibited COX-2 enzyme activity. Fenofibric acid showed an IC50 value of 48 nM followed by fenofibrate (82 nM), while diclofenac showed an IC50 value of 58 nM. Furthermore, under in vivo conditions in carrageenan-induced paw oedema rodent model, Fenofibric acid exhibited relatively potent anti-inflammatory activity compared with fenofibrate. Hence, we conclude that Fenofibric acid and fenofibrate are not only anti-hyperlipidemic but also shows potent anti-inflammatory activity, which may have an additional impact in the treatment of diabetic complications, viz., hyperlipidemia and inflammation leading to atherosclerosis.
