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Identification
- Summary
Fenofibric acid is a fibrate used to treat severe hypertriglyceridemia, primary hypercholesterolemia, or mixed dyslipidemia.
- Brand Names
- Fibricor, Trilipix
- Generic Name
- Fenofibric acid
- DrugBank Accession Number
- DB13873
- Background
Fenofibric acid is a lipid-lowering agent that is used in severe hypertriglyceridemia, primary hyperlipidemia, and mixed dyslipidemia. It works to decrease elevated low-density lipoprotein cholesterol, total cholesterol, triglycerides, apolipoprotein B, while increasing high-density lipoprotein cholesterol.1,5 Due to its high hydrophilicity and poor absorption profile,1 prodrug ,fenofibrate, and other conjugated compounds of fenofibric acid, such as choline fenofibrate, have been developed for improved solubility, gastrointestinal absorption, and bioavailability, and more convenient administration.1,3
- Type
- Small Molecule
- Groups
- Approved
- Structure
Structure for Fenofibric acid (DB13873)
- Weight
- Average: 318.75
Monoisotopic: 318.0658867 - Chemical Formula
- C17H15ClO4
- Synonyms
- Not Available
Pharmacology
- Indication
For use as an adjunctive therapy to diet to: (a) reduce triglyceride levels in adult patients with severe hypertriglyceridemia, and (b) reduce elevated total cholesterol, low-density-lipoprotein (LDL-C), triglycerides, and apolipoprotein B, and to increase high-density-lipoprotein (HDL-C) in adult patients with primary hypercholesterolemia or mixed dyslipidemia (Fredrickson Types IIa and IIb). Label
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Indication Type Indication Combined Product Details Approval Level Age Group Patient Characteristics Dose Form Adjunct therapy in management of Dyslipidemia (fredrickson type Ⅱa) •••••••••••• ••••• •••••• Adjunct therapy in management of Hypertriglyceridemias •••••••••••• ••••• •••••• ••••••••••••• •••• ••••• •••••• Adjunct therapy in management of Mixed dyslipidemias •••••••••••• ••••• •••••• - Contraindications & Blackbox Warnings
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Various clinical studies have shown that elevated levels of total cholesterol, low-desnsity-lipoprotein (LDL-C), and apolipoprotein B (apo B) - an LDL membrane complex - are associated with human atherosclerosis Label. Concurrently, decreased levels of high-density-lioprotein (HDL-C) and its transport complex, apolipoproteins apo AI and apo AII, are associated with the development of atherosclerosis Label. Furthermore, epidemiological investigations demonstrate that cardiovascular morbidity and mortality vary directly with the levels of total cholesterol, LDL-C, and triglycerides, and inversely with the level of HDL-C Label.
Fenofibric acid, the active metabolite of fenofibrate, subsequently produces reductions in total cholesterol, LDL-C, apo B, total triglycerides, and triglyceride rich lipoprotein (VLDL) in treated patients Label. Moreover, such treatment with fenofibrate also results in increases in HDL-C and apo AI and apo AII Label.
- Mechanism of action
Having performed clinical studies with in vivo transgenic mice and in vitro human hepatocyte cultures, it is believed that the principal mechanism of action of fenofibric acid is demonstrated through its capability to activate peroxisome proliferator receptor alpha (PPAR-alpha) Label.
By activating PPAR-alpha, fenofibric acid increases lipolysis and the elimination of triglyceride-rich particles from plasma by actuating lipoprotein lipase and reducing production of apoprotein C-III, which acts as an inhibitor of lipoprotein lipase activity Label. The resultant decrease in triglycerides causes an alteration in the size and composition of low-density-lipoprotein from small, dense particles to large, buoyant ones Label. The size of these larger low-density-lipoprotein particles have a greater affinity for cholesterol receptors and are therefore catabolized more rapidly Label. Additionally, fenofibric acid's activation of PPAR-alpha also induces an increase in the synthesis of apoproteins apo A-I, apo A-II, and high-density-lipoprotein Label.
Moreover, the use of fenofibric acid can also act to reduce serum uric acid levels in ordinary or hyperuricemic individuals by increasing the urinary excretion of uric acid Label.
Target Actions Organism APeroxisome proliferator-activated receptor alpha agonistHumans AFatty acid-binding protein, liver inhibitorHumans UMatrix metalloproteinase-25 unknownHumans UPeroxisome proliferator-activated receptor gamma Not Available Humans UPeroxisome proliferator-activated receptor delta unknownHumans UNuclear receptor subfamily 1 group I member 2 partial agonistHumans - Absorption
Some studies have demonstrated that the bioavailability of fenofibric acid (a sample administration of 130 mg oral suspension to healthy volunteers about 4 hours after a light breakfast) is approximately 81% in the stomach, 88% in the proximal small bowel, 84% in the distal small bowel, and 78% in the colon 1. Nevertheless, following the oral administration of fenofibric acid in healthy volunteers, median peak plasma levels for the drug occurred about 2.5 hours after administration Label. Moreover, exposure after administration of three 35 mg fenofibric acid tablets is largely comparable to that of one 105 mg tablet Label.
- Volume of distribution
The volume of distribution for fenofibric acid is demonstrated to be 70.9 +/- 27.5 L 2.
- Protein binding
Fenofibric acid demonstrates serum protein binding of approximately 99% in ordinary and hyperlipidemic subjects Label.
- Metabolism
In vitro and in vivo metabolism studies reveal that fenofibric acid does not experience significant oxidative metabolism via the cytochrome P450 isoenzymes Label. The CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 enzymes are not known to play a role in the metabolism of fenofibric acid Label.
Rather, fenofibric acid is predominantly conjugated with glucuronic acid and then excreted in urine Label. A small amount of fenofibric acid is reduced at the carbonyl moiety to benzhydrol metabolite which is, in turn, conjugated with glucuronic acid and excreted in urine Label.
- Route of elimination
Fenofibric acid metabolites are largely excreted in the urine Label.
- Half-life
Following once daily dosing, fenofibric acid demonstrates an elimination associated with a half-life of about 20 hours after absorption Label.
- Clearance
In five elderly volunteers aged 77 to 87, the oral clearance of fenofibric acid after a single oral dose of fenofibrate was 1.2 L/h, which compares to 1.1 L/h in young adults Label.
- Adverse Effects
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Oral LD50 (rat): 1242 mg/kg, Oral LD50 (mouse): 100 mg/kg, lntraperitoneal LD50 (mouse): 500 mg/kg MSDS
Fenofibric acid is contraindicated for: (a) patients with severe renal impairment, including those receiving dialysis, (b) patients with active liver disease, including those with primary biliary cirrhosis and unexplained persistent liver function abnormalities, (c) patients with preexisting gallbladder disease, (d) patients with known hypersensitivity to fenofibric acid or Fenofibrate, and (e) nursing mothers Label.
The relationship between the use of fenofibric acid and risk of mortality and coronary heart disease morbidity has not been formally established Label. However, a number of studies involving fenofibrate and agents that are chemically and pharmacologically similar to fenofibrate demonstrate inconclusive results. In the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study, a non-significant 11% (HR 1.11 [0.95, 1.29], p=0.18) and 19% (HR 1.19 [0.90, 1.57], p=0.22) increase in total and coronary heart disease mortality, respectively, with Fenofibrate as compared to placebo Label. For the Coronary Drug Project, a large study of post myocardial infarction of patients treated for 5 years with clofibrate, there was a difference in the rate of cholelithiasis and cholecystitis requiring surgery between the clofibrate and placebo groups of 3.0% vs. 1.8%, respectively Label. The World Health Organization (WHO) also conducted a study in which 5000 subjects without known coronary artery disease were treated with placebo or clofibrate for 5 years and followed for an additional year Label. The results involved a statistically significant, higher age-adjusted all-cause mortality in the clofibrate group compared with the placebo group (5.70% vs. 3.96%, p<0.01) in which excess mortality was due to a 33% increase in non-cardiovascular causes, including malignancy, post-cholecystectomy complications, and pancreatitis Label. With the Helsinki Heart Study, 4081 middle aged men without a history of coronary artery disease were given either placebo or gemfibrozil for 5 years, with a 3.5 year open extension afterward Label. Although total mortality was numerically higher in the gemfibrozil arm, it was statistically significant (p=0.19, 95% confidence interval for relative risk = 0.91-1.64). Finally, a secondary prevention component of the Helsinki Heart Study observed middle aged men not included in the primary prevention study because they had known or suspected coronary heart disease Label. When these subjects were administered gemfibrozil or placebo therapy for 5 years, cardiac deaths trended higher in the gemfibrozil group but was ultimately not statistically significant (HR 2.2, 95% confidence interval: 0.94-5.05) Label.
Fibrates facilitate the risk for myopathy and have been associated with rhabdomyolysis Label. The risk for serious muscle toxicity appears to be increased in elderly patients and in patients with diabetes, renal failure, or hypothyroidism Label. Myopathy should be considered in any patient with diffuse myalgia, muscle tenderness or weakness, and/or marked elevations of creatine phosphokinase levels Label.
Fenofibrate administered across a range of doses with the higher dose equivalent to 105 mg fenofibric acid has been associated with increases in serum transaminases like AST (SGOT) and ALT (SGPT) Label. In a pooled analysis of 10 placebo-controlled trials, increases to more than 3 times the upper limit of normal of ALT occurred in 5.3% of patients taking Fenofibrate versus 1.1% of patients treated with placebo Label. If enzyme levels persist above three times the normal limit, therapy is to be discontinued Label. After discontinuing fenofibrate treatment or during continued treatment a return to normal transaminase limits was usually observed Label. The incidence of increases in transaminases observed with fenofibrate therapy appear to be dose related Label. From an 8 week dose-ranging study, the incidence of ALT or AST elevations to at least three times the upper limit of normal was 13% in patients receiving dosages equivalent to 35 mg to 105 mg fenofibric acid per day and was comparatively 0% in those receiving placebo or doses equivalent to 35 mg or less fenofibric acid per day Label. Hepatocellular, chronic active and cholestatic hepatitis associated with Fenofibrate therapy have been reported after exposures of weeks to several years Label. In extremely rare cases, cirrhosis has been reported in associated with chronic active hepatitis Label.
Increases in serum creatinine have been reported in patients on Fenofibrate Label. These elevations tend to return to baseline following discontinuation of the drug Label. Although the clinical significance of these observations is unknown, renal monitoring should be considered for patients with renal impairment and for patients at risk for renal insufficiency, perhaps like patients with diabetes or the elderly Label.
Fenofibric acid may increase cholesterol excretion into the bile, leading to cholelithiasis Label. If gallstones are found, fenofibric acid should be discontinued Label.
Caution must be exercised over the ability of fenofibric acid to potentiate the anticoagulant effects of coumarin anticoagulants, resulting in prolongation of the prothrombin time/International Normalized Ratio (PT/INR) Label.
Pancreatitis has also been reported in patients taking Fenofibrate Label. This effect may be caused by the failure of efficacy in patients with severe hypertriglyceridemia, a direct drug effect, or a secondary phenomenon mediated through biliary tract stone or sludge formation with obstruction of the common bile duct Label.
Mild to moderate hemoglobin, hematocrit, and white blood cell decreases have been observed in patients following the start of fenofibrate therapy Label. However, although these levels tend to stabilize during long-term administration of the medication Label, thrombocytopenia and agranulocytosis have been observed in patients treated with fenofibrates as well Label. Scheduled monitoring of red and white blood cell counts during the first 12 months of fenofibric acid administration is subsequently recommended Label.
Acute hypersensitivity reactions including Stevens-Johnson syndrome and toxic epidermal necrolysis requiring patient hospitalization and treatment with steroids have been reported in patients treated with fenofibrates Label.
In the fenofibrate arm during the FIELD trial, occurrences of pulmonary embolus (PE) and deep vein thrombosis (DVT) were recorded at higher rates when compared to the placebo group Label. In particular, the placebo group had N=4900 and the fenofibrate group N=4895 Label. For DVT there were 48 events (1%) in the placebo group and 67 (1%) in the fenofibrate group with p=0.074 Label. While for PE, there were 32 (0.7%) events in the placebo group and 53 (1%) in the fenofibrate group with p=0.022 Label. Likewise, in the Coronary Drug Project, a higher proportion of the clofibrate group reported definite or suspected fatal or nonfatal PE or thrombophlebitis when compared to the placebo group (5.2% vs 3.3% at 5 years with p<0.01) Label.
Additionally there have been postmarketing and clinical trial reports of serious paradoxical decreases in HDL cholesterol levels to as low as 2 mg/dL happening in diabetic and non-diabetic patients initiated on fibrate therapy Label. This decrease in HDL-C is accompanied by a decrease in apolipoprotein A1. Such decreases have been reported to occur within 2 weeks to years after initiation of fibrate therapy Label. The HDL-C levels remain depressed until fibrate therapy has been withdrawn; the response to withdrawal of fibrate therapy is in fact rapid and sustained Label. HDL-C levels are recommended to be checked within the first few months after initiation of fibrate therapy. In the case of severely depressed HDL-C levels being detected, fibrate therapy should be withdrawn and HDL-C levels monitored until it has returned to baseline with no intention or plan to re-initiate fibrate therapy Label.
Adverse effects associated with the use of fenofibrate and fenofibric acid include abdominal pain, back pain, headache, nausea, constipation, abnormal liver tests, increased AST, increased ALT, increased creatine phosphokinase, respiratory disorder, rhinitis, diarrhea, dyspepsia, nasopharyngitis, sinusitis, upper respiratory tract infection, arthralgia, myalgia, pain in extremity, and/or dizziness Label,4.
Adverse effects identified during the post-approval use period of fenofibrate include rhabdomyolysis, panrcreatitis, renal failure, muscle spasms, acute renal failure, hepatitis, cirrhosis, anemia, asthenia, and severely depressed HDL-cholesterol levels 4.
As Fenofibric acid has the capability to potentiate the anticoagulant effect of coumarin anticoagulants (and subsequently prolong the PT/INR of patients), caution should be exercised when oral coumarin anticoagulants are given in conjunction with fenofibric acid. Frequent PT/INR determinations are therefore advisable until stabilized PT/INR readings are obtained Label,4.
Fenofibric acid should be administered to patients at least 1 hour before or 4 to 6 hours after a bile acid resin is given as such drugs may bind other agents being given concurrently and impede their absorption Label,4.
Immunosuppressant medications like cyclosporine and tacrolimus can cause nephrotoxicity with decreases in creatinine clearance and rises in serum creatinine, and because renal excretion is the main elimination route for fenofibric acid, there exists a risk that an interaction could lead to deterioration of renal function Label,4. As a consequence, the benefits and risks of using fenofibric acid with any other potentially nephrotoxic agents should be carefully considered and the lowest effective dose employed Label,4.
Cases of myopathy, including rhabdomyolysis, have been reported with fenofibrates co-administered with colchicine, and caution should be exercised when considering the combination use of fenofibrates with colchicine Label,4.
No well controlled studies regarding the use of fenofibric acid in pregnant women have been established Label,4. Since the safety of fenofibric acid in pregnant women has not been formally elucidated, fenofibric acid should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus Label,4.
Moreover, fenofibric acid should not be used in nursing mothers. Under the circumstances, a decision should be made between having to discontinue nursing or to discontinue the use of fenofibric acid, taking into perspective the importance of the drug therapy to the mother Label,4.
The safety and effectiveness of fenofibric acid in paediatric patients has not been formally established Label,4.
Fenofibric acid is predominantly excreted by the kidney system unchanged or as fenofibric acid glucuronide Label,4. The risk of experiencing adverse reactions associated with exposure to fenofibric acid may consequently be greater in patients with impaired renal function Label,4. Subsequently, because elderly patients may have a higher incidence of renal impairment, the dosage of fenofibric acid for geriatric patients should be based upon renal function, with normal renal function requiring no dosage modifications Label,4. Renal function monitoring in elderly patients taking fenofibric acid is recommended Label,4.
In patients with severe renal impairment, the use of fenofibric acid is to be avoided while dose reductions is necessary in patients with mild to moderate renal impairment Label,4. Monitoring renal function in patients with renal impairment is recommended Label,4.
The use of fenofibric acid has not been evaluated in patients with hepatic impairment Label,4.
In a 24 month study, Wistar rats were dosed at various levels of fenofibrate. At a dose of 200mg/kg/day (6 times the maximum recommended human dose [MRHD] based on body surface area comparisons mg/m2), the incidence of liver carcinomas was significantly increased in both sexes of the rats Label,4. At doses of 10 (0.3 times the MRHD) and 200 mg/kg/day, a statistically significant increase in pancreatic carcinomas was observed in males, and an increase in pancreatic adenomas and benign testicular interstitial cell tumours were observed at 200 mg/kg/day in males Label,4. In a second 24 month study on the Sprague-Dawley strain of rats, doses of 10 and 60 mg/kg/day produced significant increases in the incidence of pancreatic acinar adenomas in both sexes of the rats and increases in interstitial cell tumours of the testes at 2 times the MRHD Label,4.
In addition, fenofibrate 10 and 60 mg/kg/day, clofibrate 400 mg/kg/day (2 times the MRHD), and gemfibrozil 250 mg/kg/day (2 times the MRHD) are studied in a 117 week study in rats. Fenofibrate increased pancreatic acing adenomas in both sexes of the rats Label,4. Clofibrate increased hepatocellular carcinoma and pancreatic acinar adenomas in males and hepatic neoplastic nodules in females Label,4. And finally, gemfibrozil increased hepatic neoplastic nodules in males and females, while all three drugs increased testicular interstitial cell tumours in males Label,4.
In a 21 month study with CF-1 mice, fenofibrate 10, 45, and 200 mg/kg/day (approximately 0.2, 1, and 3 times the MRHD) significantly increased the liver carcinomas in both sexes at 3 times the MRHD Label,4. With a second 18 month study at 10, 60, and 200 mg/kg/day, fenofibrate significantly increased the liver carcinomas in male and female mice 3 times the MRHD Label,4.
Changes in peroxisome morphology and numbers have been observed in humans after treatment with other members of the fibrate class when liver biopsies were compared before and after treatment in the same individual Label,4
Fenofibrate was shown to be devoid of mutagenic potential in the Ames and micronucleus tests in vivo/rat Label,4. In addition, fenofibric acid, has bee.n demonstrated to be devoid of mutagenic potential in the following tests: Ames, mouse lymphoma, chromosomal aberration and sister chromatid exchange in human lymphocytes, and unscheduled DNA synthesis in primary rat hepatocytes Label,4.
In a fertility study, rats were given oral dietary doses of fenofibrate. Males received doses for 61 days prior to mating and females for 15 days prior to mating through weaning, which resulted in no adverse effect on fertility at doses up to 300 mg/kg/day (~10 times the MRHD, based on mg/m2 surface area comparisons) Label,4.
- Pathways
- Not Available
- Pharmacogenomic Effects/ADRs
- Not Available
Interactions
- Drug Interactions
- This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
Drug Interaction Integrate drug-drug
interactions in your softwareAbacavir Abacavir may decrease the excretion rate of Fenofibric acid which could result in a higher serum level. Aceclofenac Aceclofenac may decrease the excretion rate of Fenofibric acid which could result in a higher serum level. Acemetacin Acemetacin may decrease the excretion rate of Fenofibric acid which could result in a higher serum level. Acenocoumarol The risk or severity of bleeding can be increased when Fenofibric acid is combined with Acenocoumarol. Acetaminophen Acetaminophen may decrease the excretion rate of Fenofibric acid which could result in a higher serum level. - Food Interactions
- Take with or without food.
Products
Drug product information from 10+ global regionsOur datasets provide approved product information including:dosage, form, labeller, route of administration, and marketing period.Access drug product information from over 10 global regions.- Product Ingredients
Ingredient UNII CAS InChI Key Choline fenofibrate 4BMH7IZT98 856676-23-8 JWAZHODZSADEHB-UHFFFAOYSA-M - Product Images
- Brand Name Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Fenofibric Acid Tablet 105 mg/1 Oral Halton Laboratories 2015-07-30 Not applicable US 
Fenofibric Acid Tablet 35 mg/1 Oral Halton Laboratories 2015-07-30 Not applicable US Fibricor Tablet 35 mg/1 Oral Athena Bioscience, LLC 2017-08-05 Not applicable US Fibricor Tablet 105 mg/1 Oral Aralez Pharmaceuticals Us Inc. 2017-08-05 Not applicable US Fibricor Tablet 35 mg/1 Oral Tribute Pharmaceuticals 2015-07-30 Not applicable US - Generic Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Fenofibric Acid Capsule, delayed release 45 mg/1 Oral Slate Run Pharmaceuticals, Llc 2022-04-11 Not applicable US Fenofibric Acid Capsule, delayed release 135 mg/1 Oral A-S Medication Solutions 2019-07-25 Not applicable US Fenofibric Acid Capsule, delayed release 45 mg/1 Oral Amneal Pharmaceuticals of New York Llc 2016-09-12 Not applicable US Fenofibric Acid Capsule, delayed release 135 mg/1 Oral Alembic Pharmaceuticals Inc. 2017-05-15 Not applicable US Fenofibric Acid Capsule, delayed release pellets 135 mg/1 Oral Mylan Pharmaceuticals Inc. 2013-07-15 2019-05-31 US 
- Mixture Products
Name Ingredients Dosage Route Labeller Marketing Start Marketing End Region Image FENOVAS®10 MG Fenofibric acid (135 mg) + Rosuvastatin (10 mg) Capsule, liquid filled Oral PROCAPS S.A. 2016-10-10 2021-10-28 Colombia 
STAFEN® 135 / 20 MG CAPSULA Fenofibric acid (135 mg) + Rosuvastatin calcium (20 mg) Capsule, coated Oral LABORATORIO FRANCO COLOMBIANO LAFRANCOL S.A.S. 2013-02-28 Not applicable Colombia STAFEN® 135 / 20 MG CAPSULA Fenofibric acid (135 mg) + Rosuvastatin calcium (20 mg) Capsule, coated Oral LABORATORIO FRANCO COLOMBIANO LAFRANCOL S.A.S. 2013-02-28 Not applicable Colombia STAFEN®135 / 5 MG CAPSULAS Fenofibric acid (135 mg) + Rosuvastatin calcium (5 mg) Capsule, coated Oral LABORATORIO FRANCO COLOMBIANO LAFRANCOL S.A.S. 2013-07-31 Not applicable Colombia
Categories
- ATC Codes
- C10AB11 — Choline fenofibrate
- Drug Categories
- Acids, Acyclic
- Agents Causing Muscle Toxicity
- Anticholesteremic Agents
- Benzene Derivatives
- Benzophenones
- Butyrates
- Drugs that are Mainly Renally Excreted
- Ethers
- Fibric Acids
- Hypolipidemic Agents
- Hypolipidemic Agents Indicated for Hyperlipidemia
- Isobutyrates
- Ketones
- Lipid Modifying Agents
- Lipid Modifying Agents, Plain
- Lipid Regulating Agents
- Non-statin Hypolipidemic Agents Indicated for Hyperlipidemia
- Peroxisome Proliferator Receptor alpha Agonist
- Phenols
- Phenyl Ethers
- Chemical TaxonomyProvided by Classyfire
- Description
- This compound belongs to the class of organic compounds known as benzophenones. These are organic compounds containing a ketone attached to two phenyl groups.
- Kingdom
- Organic compounds
- Super Class
- Benzenoids
- Class
- Benzene and substituted derivatives
- Sub Class
- Benzophenones
- Direct Parent
- Benzophenones
- Alternative Parents
- Diphenylmethanes / Aryl-phenylketones / Phenoxyacetic acid derivatives / Phenoxy compounds / Phenol ethers / Benzoyl derivatives / Chlorobenzenes / Alkyl aryl ethers / Aryl chlorides / Monocarboxylic acids and derivatives show 4 more
- Substituents
- Alkyl aryl ether / Aromatic homomonocyclic compound / Aryl chloride / Aryl halide / Aryl ketone / Aryl-phenylketone / Benzophenone / Benzoyl / Carbonyl group / Carboxylic acid show 16 more
- Molecular Framework
- Aromatic homomonocyclic compounds
- External Descriptors
- monocarboxylic acid, aromatic ketone, chlorobenzophenone (CHEBI:83469)
- Affected organisms
- Humans and other mammals
Chemical Identifiers
- UNII
- BGF9MN2HU1
- CAS number
- 42017-89-0
- InChI Key
- MQOBSOSZFYZQOK-UHFFFAOYSA-N
- 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)
- IUPAC Name
- 2-[4-(4-chlorobenzoyl)phenoxy]-2-methylpropanoic acid
- SMILES
- CC(C)(OC1=CC=C(C=C1)C(=O)C1=CC=C(Cl)C=C1)C(O)=O
References
- General References
- Ling H, Luoma JT, Hilleman D: A Review of Currently Available Fenofibrate and Fenofibric Acid Formulations. Cardiol Res. 2013 Apr;4(2):47-55. doi: 10.4021/cr270w. Epub 2013 May 9. [Article]
- Vlase L, Popa A, Muntean D, Leucuta SE: Pharmacokinetics and comparative bioavailability of two fenofibrate capsule formulations in healthy volunteers. Arzneimittelforschung. 2010;60(9):560-3. doi: 10.1055/s-0031-1296325. [Article]
- Patel P, Barkate H: Comparison of efficacy and safety of choline fenofibrate (fenofibric acid) to micronized fenofibrate in patients of mixed dyslipidemia: A randomized, open-label, multicenter clinical trial in Indian population. Indian J Endocrinol Metab. 2016 Jan-Feb;20(1):67-71. doi: 10.4103/2230-8210.172243. [Article]
- DailyMed Trilipix (fenofibric acid) delayed release capsule monogram [Link]
- FDA Approved Drug Products: FIBRICOR (fenofibric acid) Tablets, for oral use [Link]
- External Links
- PubChem Compound
- 64929
- PubChem Substance
- 347829325
- ChemSpider
- 58457
- BindingDB
- 28700
- 24852
- ChEBI
- 83469
- ChEMBL
- CHEMBL981
- ZINC
- ZINC000000001984
- PDBe Ligand
- F5A
- Wikipedia
- Fenofibrate
- PDB Entries
- 6l36 / 6lx4 / 7bq0 / 7wgp
- FDA label
- Download (468 KB)
- MSDS
- Download (24.2 KB)
Clinical Trials
- Clinical Trials
Clinical Trial & Rare Diseases Add-on Data Package
Explore 4,000+ rare diseases, orphan drugs & condition pairs, clinical trial why stopped data, & more. Preview package Phase Status Purpose Conditions Count Start Date Why Stopped 100+ additional columns Unlock 175K+ rows when you subscribe.View sample data4 Completed Basic Science Type 2 Diabetes Mellitus 1 somestatus stop reason just information to hide 4 Recruiting Treatment Atherosclerosis / Dyslipidemia / Type 2 Diabetes Mellitus 1 somestatus stop reason just information to hide 4 Terminated Prevention Dyslipidemia 1 somestatus stop reason just information to hide 3 Completed Treatment Combined (Atherogenic) Dyslipidemia / Coronary Heart Disease (CHD) / Dyslipidemia / Mixed Dyslipidemias 1 somestatus stop reason just information to hide 3 Completed Treatment Coronary Artery Disease (CAD) / Coronary Heart Disease (CHD) / Dyslipidemia 1 somestatus stop reason just information to hide
Pharmacoeconomics
- Manufacturers
- Not Available
- Packagers
- Not Available
- Dosage Forms
Form Route Strength Capsule, coated Oral 135 mg Capsule Oral 59.600 mg Capsule, delayed release Oral 45 mg/1 Capsule, delayed release pellets Oral 135 mg/1 Capsule, delayed release pellets Oral 45 mg/1 Capsule, liquid filled Oral Tablet Oral 105 mg/1 Tablet Oral 35 mg/1 Capsule, coated Oral 45 mg Capsule, coated Oral 13500000 mg Capsule, coated Oral Capsule, coated Oral 20 mg Capsule, delayed release Oral 135 mg/1 Capsule, delayed release Oral 135 mg Capsule, delayed release pellets Oral 135 mg Capsule, delayed release pellets Oral 45 mg - Prices
- Not Available
- Patents
Patent Number Pediatric Extension Approved Expires (estimated) Region US7259186 No 2007-08-21 2025-01-07 US US7569612 No 2009-08-04 2027-08-20 US US7741373 No 2010-06-22 2027-08-20 US US7741374 No 2010-06-22 2027-08-20 US US7915247 No 2011-03-29 2027-08-20 US
Properties
- State
- Solid
- Experimental Properties
- Not Available
- Predicted Properties
Property Value Source Water Solubility 0.0051 mg/mL ALOGPS logP 3.97 ALOGPS logP 4.36 Chemaxon logS -4.8 ALOGPS pKa (Strongest Acidic) 3.1 Chemaxon pKa (Strongest Basic) -4.9 Chemaxon Physiological Charge -1 Chemaxon Hydrogen Acceptor Count 4 Chemaxon Hydrogen Donor Count 1 Chemaxon Polar Surface Area 63.6 Å2 Chemaxon Rotatable Bond Count 5 Chemaxon Refractivity 83.19 m3·mol-1 Chemaxon Polarizability 32.42 Å3 Chemaxon Number of Rings 2 Chemaxon Bioavailability 1 Chemaxon Rule of Five Yes Chemaxon Ghose Filter Yes Chemaxon Veber's Rule No Chemaxon MDDR-like Rule No Chemaxon - Predicted ADMET Features
- Not Available
Spectra
- Mass Spec (NIST)
- Not Available
- Spectra
- Chromatographic Properties
Collision Cross Sections (CCS)
Adduct CCS Value (Å2) Source type Source [M-H]- 170.29146 predictedDeepCCS 1.0 (2019) [M+H]+ 172.64946 predictedDeepCCS 1.0 (2019) [M+Na]+ 178.74261 predictedDeepCCS 1.0 (2019)
Targets
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Agonist
- General Function
- Ligand-activated transcription factor. Key regulator of lipid metabolism. Activated by the endogenous ligand 1-palmitoyl-2-oleoyl-sn-glycerol-3-phosphocholine (16:0/18:1-GPC). Activated by oleylethanolamide, a naturally occurring lipid that regulates satiety. Receptor for peroxisome proliferators such as hypolipidemic drugs and fatty acids. Regulates the peroxisomal beta-oxidation pathway of fatty acids. Functions as a transcription activator for the ACOX1 and P450 genes. Transactivation activity requires heterodimerization with RXRA and is antagonized by NR2C2. May be required for the propagation of clock information to metabolic pathways regulated by PER2
- Specific Function
- Dna binding
- Gene Name
- PPARA
- Uniprot ID
- Q07869
- Uniprot Name
- Peroxisome proliferator-activated receptor alpha
- Molecular Weight
- 52224.595 Da
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Inhibitor
- General Function
- Plays a role in lipoprotein-mediated cholesterol uptake in hepatocytes (PubMed:25732850). Binds cholesterol (PubMed:25732850). Binds free fatty acids and their coenzyme A derivatives, bilirubin, and some other small molecules in the cytoplasm. May be involved in intracellular lipid transport (By similarity)
- Specific Function
- Antioxidant activity
- Gene Name
- FABP1
- Uniprot ID
- P07148
- Uniprot Name
- Fatty acid-binding protein, liver
- Molecular Weight
- 14208.34 Da
References
- Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Unknown
- General Function
- May activate progelatinase A
- Specific Function
- Metalloendopeptidase activity
- Gene Name
- MMP25
- Uniprot ID
- Q9NPA2
- Uniprot Name
- Matrix metalloproteinase-25
- Molecular Weight
- 62553.445 Da
References
- Duhaney TA, Cui L, Rude MK, Lebrasseur NK, Ngoy S, De Silva DS, Siwik DA, Liao R, Sam F: Peroxisome proliferator-activated receptor alpha-independent actions of fenofibrate exacerbates left ventricular dilation and fibrosis in chronic pressure overload. Hypertension. 2007 May;49(5):1084-94. Epub 2007 Mar 12. [Article]
- Lebrasseur NK, Duhaney TA, De Silva DS, Cui L, Ip PC, Joseph L, Sam F: Effects of fenofibrate on cardiac remodeling in aldosterone-induced hypertension. Hypertension. 2007 Sep;50(3):489-96. Epub 2007 Jul 2. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- General Function
- Nuclear receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the nuclear receptor binds to DNA specific PPAR response elements (PPRE) and modulates the transcription of its target genes, such as acyl-CoA oxidase. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. ARF6 acts as a key regulator of the tissue-specific adipocyte P2 (aP2) enhancer. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated pro-inflammatory responses. Plays a role in the regulation of cardiovascular circadian rhythms by regulating the transcription of BMAL1 in the blood vessels (By similarity)
- Specific Function
- Alpha-actinin binding
- Gene Name
- PPARG
- Uniprot ID
- P37231
- Uniprot Name
- Peroxisome proliferator-activated receptor gamma
- Molecular Weight
- 57619.58 Da
References
- Inoue I, Itoh F, Aoyagi S, Tazawa S, Kusama H, Akahane M, Mastunaga T, Hayashi K, Awata T, Komoda T, Katayama S: Fibrate and statin synergistically increase the transcriptional activities of PPARalpha/RXRalpha and decrease the transactivation of NFkappaB. Biochem Biophys Res Commun. 2002 Jan 11;290(1):131-9. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Unknown
- General Function
- Ligand-activated transcription factor key mediator of energy metabolism in adipose tissues (PubMed:35675826). Receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Has a preference for poly-unsaturated fatty acids, such as gamma-linoleic acid and eicosapentanoic acid. Once activated by a ligand, the receptor binds to promoter elements of target genes. Regulates the peroxisomal beta-oxidation pathway of fatty acids. Functions as transcription activator for the acyl-CoA oxidase gene. Decreases expression of NPC1L1 once activated by a ligand
- Specific Function
- Dna binding
- Gene Name
- PPARD
- Uniprot ID
- Q03181
- Uniprot Name
- Peroxisome proliferator-activated receptor delta
- Molecular Weight
- 49902.99 Da
References
- Inoue I, Itoh F, Aoyagi S, Tazawa S, Kusama H, Akahane M, Mastunaga T, Hayashi K, Awata T, Komoda T, Katayama S: Fibrate and statin synergistically increase the transcriptional activities of PPARalpha/RXRalpha and decrease the transactivation of NFkappaB. Biochem Biophys Res Commun. 2002 Jan 11;290(1):131-9. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- Partial agonist
- General Function
- Nuclear receptor that binds and is activated by variety of endogenous and xenobiotic compounds. Transcription factor that activates the transcription of multiple genes involved in the metabolism and secretion of potentially harmful xenobiotics, drugs and endogenous compounds. Activated by the antibiotic rifampicin and various plant metabolites, such as hyperforin, guggulipid, colupulone, and isoflavones. Response to specific ligands is species-specific. Activated by naturally occurring steroids, such as pregnenolone and progesterone. Binds to a response element in the promoters of the CYP3A4 and ABCB1/MDR1 genes
- Specific Function
- Dna-binding transcription activator activity, rna polymerase ii-specific
- Gene Name
- NR1I2
- Uniprot ID
- O75469
- Uniprot Name
- Nuclear receptor subfamily 1 group I member 2
- Molecular Weight
- 49761.245 Da
References
- Creusot N, Kinani S, Balaguer P, Tapie N, LeMenach K, Maillot-Marechal E, Porcher JM, Budzinski H, Ait-Aissa S: Evaluation of an hPXR reporter gene assay for the detection of aquatic emerging pollutants: screening of chemicals and application to water samples. Anal Bioanal Chem. 2010 Jan;396(2):569-83. doi: 10.1007/s00216-009-3310-y. Epub 2009 Nov 29. [Article]
Drug created at July 09, 2017 04:12 / Updated at August 26, 2024 19:24