Identification

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Name
Fenofibric acid
Accession Number
DB13873
Type
Small Molecule
Groups
Approved
Description

Fenofibrate is a third generation fibric acid derivative that is predominantly administered as monotherapy to decrease elevated low-density lipoprotein cholesterol, total cholesterol, triglycerides, apolipoprotein B and alternatively to increase high-density lipoprotein cholesterol in patients diagnosed with primary hyperlipidemia or mixed dyslipidemia and to reduce triglycerides in patients with severe hypertriglyceridemia Label,1. Fenofibrate however is generally extremely lipophilic, largely insoluble in water, and poorly absorbed 1. As the primary active metabolite of fenofibrate however, various hydrophilic salt formulations of fenofibric acid have since been developed, resulting in therapeutic agents that demonstrate far greater solubility, absorption throughout the gastrointestinal tract, bioavailability, and capability to be administered irrespective of patient food intake Label,1.

Structure
Thumb
Synonyms
Not Available
Product Ingredients
IngredientUNIICASInChI Key
Choline fenofibrate4BMH7IZT98856676-23-8JWAZHODZSADEHB-UHFFFAOYSA-M
Product Images
Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Fenofibric AcidTablet105 mg/1OralHalton Laboratories2015-07-30Not applicableUs
Fenofibric AcidTablet35 mg/1OralHalton Laboratories2015-07-30Not applicableUs
FibricorTablet105 mg/1OralAR Scientific, Inc.2009-08-14Not applicableUs
FibricorTablet35 mg/1OralAthena Bioscience, LLC2017-08-05Not applicableUs
FibricorTablet105 mg/1OralTribute Pharmaceuticals2015-07-30Not applicableUs
FibricorTablet35 mg/1OralAR Scientific, Inc.2009-08-14Not applicableUs
FibricorTablet35 mg/1OralTribute Pharmaceuticals2015-07-30Not applicableUs
FibricorTablet105 mg/1OralCaraco Pharma, Inc.2009-08-14Not applicableUs
FibricorTablet105 mg/1OralAralez Pharmaceuticals Us Inc.2017-08-05Not applicableUs
FibricorTablet35 mg/1OralCaraco Pharma, Inc.2009-08-14Not applicableUs
Additional Data Available
  • Application Number
    Application Number

    A unique ID assigned by the FDA when a product is submitted for approval by the labeller.

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  • Product Code
    Product Code

    A governmentally-recognized ID which uniquely identifies the product within its regulatory market.

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Generic Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Fenofibric AcidCapsule, delayed release135 mg/1OralAlembic Pharmaceuticals Inc.2017-05-15Not applicableUs
Fenofibric AcidCapsule, delayed release135 mg/1OralAmneal Pharmaceuticals of New York Llc2008-12-152019-03-11Us00115 1460 10 nlmimage10 37459bdc
Fenofibric AcidCapsule, delayed release135 mg/1OralAlembic Pharmaceuticals Limited2017-05-18Not applicableUs
Fenofibric AcidCapsule, delayed release45 mg/1OralZydus Pharmaceuticals USA Inc2016-09-12Not applicableUs
Fenofibric AcidCapsule, delayed release135 mg/1OralAmneal Pharmaceuticals of New York Llc2016-09-12Not applicableUs
Fenofibric acidCapsule, delayed release135 mg/1OralLupin Pharmaceuticals2013-12-17Not applicableUs
Fenofibric AcidCapsule, delayed release45 mg/1OralAlembic Pharmaceuticals Inc.2017-05-15Not applicableUs
Fenofibric AcidCapsule, delayed release45 mg/1OralAmneal Pharmaceuticals of New York Llc2008-12-152019-01-06Us
Fenofibric AcidTablet105 mg/1OralMutual Pharmaceutical2009-08-31Not applicableUs
Fenofibric AcidCapsule, delayed release45 mg/1OralAlembic Pharmaceuticals Limited2017-05-15Not applicableUs
Additional Data Available
  • Application Number
    Application Number

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  • Product Code
    Product Code

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Categories
UNII
BGF9MN2HU1
CAS number
42017-89-0
Weight
Average: 318.75
Monoisotopic: 318.0658867
Chemical Formula
C17H15ClO4
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

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

Pharmacodynamics

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.

TargetActionsOrganism
APeroxisome proliferator-activated receptor alpha
agonist
Humans
UMatrix metalloproteinase-25
unknown
Humans
UPeroxisome proliferator-activated receptor gammaNot AvailableHumans
UPeroxisome proliferator-activated receptor delta
unknown
Humans
UNuclear receptor subfamily 1 group I member 2
partial agonist
Humans
Additional Data Available
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Contraindications

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Blackbox Warnings

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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.

Toxicity

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,3.

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 3.

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,3.

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,3.

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,3. 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,3.

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,3.

No well controlled studies regarding the use of fenofibric acid in pregnant women have been established Label,3. 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,3.

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,3.

The safety and effectiveness of fenofibric acid in paediatric patients has not been formally established Label,3.

Fenofibric acid is predominantly excreted by the kidney system unchanged or as fenofibric acid glucuronide Label,3. The risk of experiencing adverse reactions associated with exposure to fenofibric acid may consequently be greater in patients with impaired renal function Label,3. 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,3. Renal function monitoring in elderly patients taking fenofibric acid is recommended Label,3.

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,3. Monitoring renal function in patients with renal impairment is recommended Label,3.

The use of fenofibric acid has not been evaluated in patients with hepatic impairment Label,3.

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,3. 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,3. 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,3.

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,3. Clofibrate increased hepatocellular carcinoma and pancreatic acinar adenomas in males and hepatic neoplastic nodules in females Label,3. And finally, gemfibrozil increased hepatic neoplastic nodules in males and females, while all three drugs increased testicular interstitial cell tumours in males Label,3.

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,3. 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,3.

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,3

Fenofibrate was shown to be devoid of mutagenic potential in the Ames and micronucleus tests in vivo/rat Label,3. 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,3.

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,3.

Affected organisms
  • Humans and other mammals
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.
DrugInteraction
(R)-warfarinThe risk or severity of bleeding can be increased when Fenofibric acid is combined with (R)-warfarin.
(S)-WarfarinThe risk or severity of bleeding can be increased when Fenofibric acid is combined with (S)-Warfarin.
4-hydroxycoumarinThe risk or severity of bleeding can be increased when Fenofibric acid is combined with 4-hydroxycoumarin.
AbacavirAbacavir may decrease the excretion rate of Fenofibric acid which could result in a higher serum level.
AcarboseAcarbose may decrease the excretion rate of Fenofibric acid which could result in a higher serum level.
AceclofenacAceclofenac may decrease the excretion rate of Fenofibric acid which could result in a higher serum level.
AcemetacinAcemetacin may decrease the excretion rate of Fenofibric acid which could result in a higher serum level.
AcenocoumarolThe risk or severity of bleeding can be increased when Fenofibric acid is combined with Acenocoumarol.
AcetaminophenAcetaminophen may decrease the excretion rate of Fenofibric acid which could result in a higher serum level.
AcetazolamideAcetazolamide may increase the excretion rate of Fenofibric acid which could result in a lower serum level and potentially a reduction in efficacy.
Additional Data Available
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Food Interactions
Not Available

References

General References
  1. 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. [PubMed:28352420]
  2. 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. [PubMed:21117499]
  3. DailyMed Trilipix (fenofibric acid) delayed release capsule monogram [Link]
External Links
PubChem Compound
64929
PubChem Substance
347829325
ChemSpider
58457
BindingDB
28700
ChEBI
83469
ChEMBL
CHEMBL981
Wikipedia
Fenofibrate
ATC Codes
C10AB11 — Choline fenofibrate
FDA label
Download (468 KB)
MSDS
Download (24.2 KB)

Clinical Trials

Clinical Trials
PhaseStatusPurposeConditionsCount
1CompletedNot AvailableHealthy Volunteers1
1CompletedBasic ScienceHealthy Volunteers6
1CompletedBasic SciencePharmacokinetic Variables1
1CompletedTreatmentAdverse Events / Pharmacokinetic Variables1
1CompletedTreatmentAdverse Events / Pharmacokinetics1
1CompletedTreatmentDyslipidemia, Renal Insufficiency1
1CompletedTreatmentDyslipidemias1
1CompletedTreatmentHealthy Volunteers6
1CompletedTreatmentPharmacokinetics1
1, 2CompletedTreatmentDyslipidemias1
1, 2RecruitingTreatmentPrimary Biliary Cholangitis1
2Active Not RecruitingTreatmentMultiple Myeloma (MM)1
2CompletedNot AvailableAlcohol Dependence1
2CompletedTreatmentDiabetic Macular Edema (DME)1
2CompletedTreatmentHyperlipidemias1
2RecruitingTreatmentMedulloblastomas1
3CompletedTreatmentCombined (Atherogenic) Dyslipidemia / Coronary Heart Disease (CHD) / Dyslipidemias / Mixed hypercholesterolemia1
3CompletedTreatmentCoronary Artery Disease / Coronary Heart Disease (CHD) / Dyslipidemias1
3CompletedTreatmentCoronary Heart Disease (CHD) / Dyslipidemias / Mixed hypercholesterolemia4
3CompletedTreatmentDyslipidemias / High Cholesterol1
3CompletedTreatmentDyslipidemias / Kidney Diseases1
3CompletedTreatmentMixed hypercholesterolemia1
3TerminatedDiagnosticCoronary Artery Atherosclerosis1
3WithdrawnTreatmentHypertriglyceridemias1
4RecruitingBasic ScienceType 2 Diabetes Mellitus1
4TerminatedPreventionDyslipidemias1
Not AvailableUnknown StatusTreatmentMixed hypercholesterolemia1

Pharmacoeconomics

Manufacturers
Not Available
Packagers
Not Available
Dosage forms
FormRouteStrength
Capsule, delayed releaseOral45 mg/1
Capsule, delayed release pelletsOral135 mg/1
Capsule, delayed release pelletsOral45 mg/1
TabletOral105 mg/1
TabletOral35 mg/1
Capsule, delayed releaseOral135 mg/1
Prices
Not Available
Patents
Patent NumberPediatric ExtensionApprovedExpires (estimated)
US7259186No2007-08-212025-01-07Us
US7569612No2009-08-042027-08-20Us
US7741373No2010-06-222027-08-20Us
US7741374No2010-06-222027-08-20Us
US7915247No2011-03-292027-08-20Us
Additional Data Available
  • Filed On
    Filed On

    The date on which a patent was filed with the relevant government.

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Properties

State
Solid
Experimental Properties
Not Available
Predicted Properties
PropertyValueSource
Water Solubility0.0051 mg/mLALOGPS
logP3.97ALOGPS
logP4.36ChemAxon
logS-4.8ALOGPS
pKa (Strongest Acidic)3.1ChemAxon
pKa (Strongest Basic)-4.9ChemAxon
Physiological Charge-1ChemAxon
Hydrogen Acceptor Count4ChemAxon
Hydrogen Donor Count1ChemAxon
Polar Surface Area63.6 Å2ChemAxon
Rotatable Bond Count5ChemAxon
Refractivity83.19 m3·mol-1ChemAxon
Polarizability32.42 Å3ChemAxon
Number of Rings2ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleNoChemAxon
MDDR-like RuleNoChemAxon
Predicted ADMET features
Not Available

Spectra

Mass Spec (NIST)
Not Available
Spectra
SpectrumSpectrum TypeSplash Key
Predicted MS/MS Spectrum - 10V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 20V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 40V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 10V, Negative (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 20V, Negative (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 40V, Negative (Annotated)Predicted LC-MS/MSNot Available
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-001i-0090000000-3649af6f9c4b41b005f1
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-001i-0090000000-32a876d779b641e3efe5
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-001i-0090000000-7f472b5dbad132612d0f
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-001i-0090000000-7d336fa21123052b7639
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-001i-0090000000-c719e39f8727bb7b4a81
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-001i-0090000000-d679eb2c4a1fd6add4da
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-001i-0090000000-315f65e0bc37c818bb8a
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-001i-0090000000-32a876d779b641e3efe5
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-001i-0090000000-32a876d779b641e3efe5
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-001i-0090000000-025493f1f9167267c269
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-001i-0090000000-6a4de28c55a429fcb2dc
LC-MS/MS Spectrum - LC-ESI-ITFT , negativeLC-MS/MSsplash10-001i-0090000000-3649af6f9c4b41b005f1
LC-MS/MS Spectrum - LC-ESI-QTOF , positiveLC-MS/MSsplash10-01c0-0049000000-4fde30c6366aaf26d77b
LC-MS/MS Spectrum - LC-ESI-QTOF , positiveLC-MS/MSsplash10-001i-0090000000-ef34ffdf5196e70b8a31
LC-MS/MS Spectrum - LC-ESI-QTOF , positiveLC-MS/MSsplash10-0019-0980000000-3ad6ba9802e2a2b7b641
LC-MS/MS Spectrum - LC-ESI-QTOF , positiveLC-MS/MSsplash10-000i-0910000000-b963e54c4d24ec26b369
LC-MS/MS Spectrum - LC-ESI-QTOF , positiveLC-MS/MSsplash10-000i-0900000000-048d283cdc91de474403
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-001i-0090000000-37c84c25e65d613b9ce6
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-014i-0039000000-9bde2b9a05392bcf9a07
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-001i-0090000000-4ca50e189c23da26c95f
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-001r-0890000000-0deb0153634d8254fbf7
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-000i-0900000000-a9899a3039e6e594019f
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-000i-0900000000-e09a6ff2195f97b9e36a
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-000i-0900000000-d3a8a6509bfc59986717
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-014i-0039000000-9877282b22141d22ef61
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-001i-0090000000-49eb13bf6ac8b940026a
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-001r-0980000000-b3128b9adac2ce9ef4a0
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-000i-0900000000-6957ae9ec970a7a430e7
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-000i-0900000000-e6ede86247f2a517f635
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-000i-0900000000-8018d16193aeeecc196c
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-001i-0090000000-ed51dbe03c7dbdb65df7

Taxonomy

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
Benzophenone / Aryl-phenylketone / Diphenylmethane / Phenoxyacetate / Phenoxy compound / Aryl ketone / Phenol ether / Benzoyl / Alkyl aryl ether / Chlorobenzene
show 16 more
Molecular Framework
Aromatic homomonocyclic compounds
External Descriptors
monocarboxylic acid, aromatic ketone, chlorobenzophenone (CHEBI:83469)

Targets

Kind
Protein
Organism
Humans
Pharmacological action
Yes
Actions
Agonist
General Function
Zinc ion binding
Specific 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 oleyleth...
Gene Name
PPARA
Uniprot ID
Q07869
Uniprot Name
Peroxisome proliferator-activated receptor alpha
Molecular Weight
52224.595 Da
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
  1. 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. [PubMed:17353509]
  2. 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. [PubMed:17606858]
Kind
Protein
Organism
Humans
Pharmacological action
Unknown
General Function
Zinc ion binding
Specific 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...
Gene Name
PPARG
Uniprot ID
P37231
Uniprot Name
Peroxisome proliferator-activated receptor gamma
Molecular Weight
57619.58 Da
References
  1. 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. [PubMed:11779144]
Kind
Protein
Organism
Humans
Pharmacological action
Unknown
Actions
Unknown
General Function
Zinc ion binding
Specific Function
Ligand-activated transcription factor. Receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Has a preference for poly-unsaturated fatty acids, such as gamma-lin...
Gene Name
PPARD
Uniprot ID
Q03181
Uniprot Name
Peroxisome proliferator-activated receptor delta
Molecular Weight
49902.99 Da
References
  1. 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. [PubMed:11779144]
Kind
Protein
Organism
Humans
Pharmacological action
Unknown
Actions
Partial agonist
General Function
Zinc ion binding
Specific 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 an...
Gene Name
NR1I2
Uniprot ID
O75469
Uniprot Name
Nuclear receptor subfamily 1 group I member 2
Molecular Weight
49761.245 Da
References
  1. 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. [PubMed:20024649]

Drug created on July 08, 2017 22:12 / Updated on November 02, 2019 04:32