FenofibrateCAS# 49562-28-9 |
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Quality Control & MSDS
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Chemical structure
3D structure
Cas No. | 49562-28-9 | SDF | Download SDF |
PubChem ID | 3339 | Appearance | Powder |
Formula | C20H21ClO4 | M.Wt | 360.83 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | DMSO : 50 mg/mL (138.57 mM; Need ultrasonic) H2O : < 0.1 mg/mL (insoluble) | ||
Chemical Name | propan-2-yl 2-[4-(4-chlorobenzoyl)phenoxy]-2-methylpropanoate | ||
SMILES | CC(C)OC(=O)C(C)(C)OC1=CC=C(C=C1)C(=O)C2=CC=C(C=C2)Cl | ||
Standard InChIKey | YMTINGFKWWXKFG-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C20H21ClO4/c1-13(2)24-19(23)20(3,4)25-17-11-7-15(8-12-17)18(22)14-5-9-16(21)10-6-14/h5-13H,1-4H3 | ||
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. |
Description | PPARα agonist; hypolipidemic. Attenuates insulin resistance and increases high-density lipoprotein-cholesterol in db/db mice. |
Fenofibrate Dilution Calculator
Fenofibrate Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.7714 mL | 13.8569 mL | 27.7139 mL | 55.4278 mL | 69.2847 mL |
5 mM | 0.5543 mL | 2.7714 mL | 5.5428 mL | 11.0856 mL | 13.8569 mL |
10 mM | 0.2771 mL | 1.3857 mL | 2.7714 mL | 5.5428 mL | 6.9285 mL |
50 mM | 0.0554 mL | 0.2771 mL | 0.5543 mL | 1.1086 mL | 1.3857 mL |
100 mM | 0.0277 mL | 0.1386 mL | 0.2771 mL | 0.5543 mL | 0.6928 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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Fenofibrate is PPARα agonist with EC50 of 18 μM and 30 μM for mouse and human PPARα, respectively.
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Dodecylamine Template-Based Hexagonal Mesoporous Silica (HMS) as a Carrier for Improved Oral Delivery of Fenofibrate.[Pubmed:28353172]
AAPS PharmSciTech. 2017 Oct;18(7):2764-2773.
The aim of present investigation was the preparation of dodecylamine template-based hexagonal mesoporous silica (HMS) as a carrier for poorly water-soluble drug (Fenofibrate). HMS material has distinctive characteristics such as easy synthesis, high surface area and wormhole pores. These characteristics are highly admirable to make use of it as a carrier in drug delivery system. HMS was prepared by pH and temperature-independent process. Fenofibrate was loaded into the HMS by solvent immersion method using organic solvent. The BET surface area of HMS was evaluated by nitrogen adsorption/desorption analysis. HMS and drug-loaded HMS were characterized by differential scanning calorimetry (DSC), X-ray powder diffraction (XRPD), Fourier transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM), transmission electron microscopy (TEM) and contact angle study. The HMS-based system was also evaluated for in vitro and in vivo study as compared to plain drug. The BET surface area of HMS was found 974 m(2)/g with a narrow pore size average of 2.6 nm. The DSC and XRD study confirmed the amorphization of drug within the HMS. SEM and TEM study showed morphological features of HMS as well as revealed the wormhole porous structure. Contact angle study showed improvement in aqueous wetting property of drug within the HMS (contact angle 46 degrees ). The In vitro drug release study showed a remarkable dissolution enhancement in HMS-based system as compared to plain drug. In vivo pharmacodynamic study (hyperlipidaemia model) exhibited HMS-based formulation was significantly improved the bioavailability of Fenofibrate. Thus, HMS has admirable properties; makes it a potential carrier for delivery system of poorly water-soluble drugs.
Crystallization of supercooled fenofibrate studied at ambient and elevated pressures.[Pubmed:28357419]
Phys Chem Chem Phys. 2017 Apr 12;19(15):9879-9888.
In this work, we have performed a detailed investigation on the crystallization tendency of the modeled glass-forming pharmaceutical compound, Fenofibrate. To do this, we have employed four different experimental techniques allowing following of the crystallization process. This has included dielectric spectroscopy, optical microscopy, X-ray diffraction and differential scanning calorimetry. From the crystallization kinetic studies carried out at atmospheric pressure, we have determined the temperature dependence of the crystal growth rate and the overall crystallization rate. It was found that the time scale of the molecular motions responsible for alpha-relaxation correlates much better with the crystal growth rate than with the overall crystallization rate. Experiments carried out under varying thermodynamic conditions while remaining on the same timescale of alpha-relaxation have demonstrated that the crystallization tendency of the supercooled Fenofibrate significantly slows down with increasing pressure. Lastly, we have also shown that the thermodynamic history of reaching crystallization conditions has a substantial impact on its overall progress.
PPAR-alpha Agonist Fenofibrate Reduces Insulin Resistance in Impaired Glucose Tolerance Patients with Hypertriglyceridemia: A Cross-Sectional Study.[Pubmed:28361462]
Diabetes Ther. 2017 Apr;8(2):433-444.
INTRODUCTION: Peroxisome proliferator-activated receptor-alpha (PPAR-alpha) agonists can regulate metabolism and protect the cardiovascular system. This study investigated the effects of PPAR-alpha agonist Fenofibrate on insulin resistance in patients with impaired glucose tolerance (IGT). METHODS: This research evaluated cross-sectional and interventional studies. 191 subjects with IGT were divided into a hypertriglyceridemia group (HTG group, n = 118) and a normal triglyceride (TG) group (NTG group, n = 73). 79 subjects with normal glucose tolerance were recruited as a control group. The HTG group was treated with Fenofibrate (200 mg/day) for 12 weeks. The homeostatic model assessment index 2 (HOMA2) and the McAuley index (McA) were calculated. RESULTS: HOMA2 for beta-cell function (HOMA2-%B) was 93.47 +/- 26.28, 68.47 +/- 21.29, and 79.92 +/- 23.15 in HTG, NTG, and control groups, respectively. HOMA2 for insulin sensitivity (HOMA2-%S) was 48.40 (39.70, 68.70), 110.20 (62.55, 141.95), and 101.20 (79.90, 140.10) in HTG, NTG, and control groups, respectively. HOMA2 for insulin resistance (HOMA2-IR) was 2.09 (1.46, 2.52), 0.92 (0.70, 1.61), and 0.99 (0.71, 1.25) in HTG, NTG, and control groups, respectively. McA was 5.05 +/- 0.76, 7.99 +/- 1.79, and 8.34 +/- 1.55 in HTG, NTG, and control groups, respectively. The HTG group had higher HOMA2-%B and HOMA2-IR, and lower HOMA2-%S and McA than NTG and control groups (P < 0.001 for all). Fenofibrate decreased HOMA2-%B and HOMA2-IR and increased HOMA2-%S and McA in the HTG group (HOMA2-%B: from 93.47 +/- 26.28 to 89.34 +/- 23.53, P = 0.018; HOMA2-%S: from 48.40 (39.70, 68.70) to 56.75 (44.88, 72.53), P < 0.001; HOMA2-IR: from 2.07 (1.46, 2.52) to 1.76 (1.38, 2.30), P < 0.001; McA: from 5.05 +/- 0.76 to 9.34 +/- 0.88, P < 0.001). CONCLUSION: PPAR-alpha agonists improve parameters of glucoregulation in IGT patients with hypertriglyceridemia.
Pleiotropic actions of fenofibrate on the heart.[Pubmed:21093591]
Pharmacol Res. 2011 Jan;63(1):8-12.
Fenofibrate is a third-generation fibric acid derivative employed clinically as a hypolipidemic agent to lessen the risk caused by atherosclerosis. Dyslipidemia is a condition associated with elevated levels of low-density lipoproteins (LDL), very low-density lipoproteins (VLDL) and triglycerides, and reduced levels of high-density lipoproteins (HDL) in the circulation. Fenofibrate has an ability to diminish LDL, VLDL and triglycerides and pertinently augment HDL, and thus it is used to manage dyslipidemia. The lipid lowering effects of Fenofibrate are classically mediated via an activation of peroxisome proliferator-activated receptor-alpha (PPAR-alpha). Recent studies demonstrated numerous pleiotropic effects of Fenofibrate on the heart that afford direct myocardial protection besides its lipid lowering effects. Fenofibrate has an additional potential to prevent the induction and progression of hypertensive heart damage, cardiac hypertrophy, heart failure, myocarditis, lipotoxic cardiomyopathy and vascular endothelial dysfunction-associated cardiovascular abnormalities. In this review, we critically discussed recently identified pleiotropic actions of Fenofibrate on the heart. Moreover, the novel cardioprotective effects of Fenofibrate against various cardiac disorders have been delineated.
PPARalpha agonist fenofibrate improves diabetic nephropathy in db/db mice.[Pubmed:16672921]
Kidney Int. 2006 May;69(9):1511-7.
Peroxisome proliferator-activated receptor alpha (PPARalpha) is a member of the ligand-activated nuclear receptor superfamily, and plays an important role in lipid metabolism and glucose homeostasis. The purpose of this study is to determine whether the activation of PPARalpha by fenofbrate would improve diabetes and its renal complications in type II diabetes mellitus. Male C57 BLKS db/db mice and db/m controls at 8 weeks of age were divided to receive either a regular diet chow (db/db, n=8; db/m, n=6) or a diet containing Fenofibrate (db/db, n=8; db/m, n=7). Mice were followed for 8 weeks. Fenofibrate treatment dramatically reduced fasting blood glucose (P<0.001) and HbA1c levels (P<0.001), and was associated with decreased food intake (P<0.01) and slightly reduced body weight. Fenofibrate also ameliorated insulin resistance (P<0.001) and reduced plasma insulin levels (P<0.05) in db/db mice. Hypertrophy of pancreatic islets was decreased and insulin content markedly increased (P<0.05) in Fenofibrate-treated diabetic animals. In addition, Fenofibrate treatment significantly reduced urinary albumin excretion (P<0.001). This was accompanied by dramatically reduced glomerular hypertrophy and mesangial matrix expansion. Furthermore, the addition of Fenofibrate to cultured mesangial cells, which possess functional active PPARalpha, decreased type I collagen production. Taken together, the PPARalpha agonist Fenofibrate dramatically improves hyperglycemia, insulin resistance, albuminuria, and glomerular lesions in db/db mice. The activation of PPARalpha by Fenofibrate in mesangial cells may partially contribute to its renal protection. Thus, Fenofibrate may serve as a therapeutic agent for type II diabetes and diabetic nephropathy.
The direct peroxisome proliferator-activated receptor target fasting-induced adipose factor (FIAF/PGAR/ANGPTL4) is present in blood plasma as a truncated protein that is increased by fenofibrate treatment.[Pubmed:15190076]
J Biol Chem. 2004 Aug 13;279(33):34411-20.
The fasting-induced adipose factor (FIAF, ANGPTL4, PGAR, HFARP) was previously identified as a novel adipocytokine that was up-regulated by fasting, by peroxisome proliferator-activated receptor agonists, and by hypoxia. To further characterize FIAF, we studied regulation of FIAF mRNA and protein in liver and adipose cell lines as well as in human and mouse plasma. Expression of FIAF mRNA was up-regulated by peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARbeta/delta agonists in rat and human hepatoma cell lines and by PPARgamma and PPARbeta/delta agonists in mouse and human adipocytes. Transactivation, chromatin immunoprecipitation, and gel shift experiments identified a functional PPAR response element within intron 3 of the FIAF gene. At the protein level, in human and mouse blood plasma, FIAF was found to be present both as the native protein and in a truncated form. Differentiation of mouse 3T3-L1 adipocytes was associated with the production of truncated FIAF, whereas in human white adipose tissue and SGBS adipocytes, only native FIAF could be detected. Interestingly, truncated FIAF was produced by human liver. Treatment with Fenofibrate, a potent PPARalpha agonist, markedly increased plasma levels of truncated FIAF, but not native FIAF, in humans. Levels of both truncated and native FIAF showed marked interindividual variation but were not associated with body mass index and were not influenced by prolonged semistarvation. Together, these data suggest that FIAF, similar to other adipocytokines such as adiponectin, may partially exert its function via a truncated form.