Mediclarum
Medicine guide

Fenofibrate

160 mg · Tablet, Film Coated

  • Prescription only
  • Peroxisome Proliferator Receptor alpha Agonist
Active substance
Fenofibrate
Made by
Alembic Pharmaceuticals Limited

Quoted from the official source. Not yet reviewed by Mediclarum — the leaflet in your pack is authoritative.

At a glance

Quoted from the official label · 2023-01-30

What it is

Peroxisome Proliferator Receptor alpha Agonist

Used for
  • To reduce elevated LDL-C, Total-C, TG and Apo B, and to increase HDL-C in adult patients with primary hypercholesterolemia or mixed dyslipidemia (1.1).
The label’s usual adult dose

Initial dose of 160 mg once daily (2.2).

Therapy should be withdrawn in patients who do not have an adequate response after two months of treatment with the maximum recommended dose of 160 mg once daily.

Full directions ↓
Do not take it if

Fenofibrate tablet is contraindicated in:

All warnings ↓
Good to know
  • Prescription only
  • FDA enforcement reports list no ongoing recall, and none from the last two years, for this product code · checked 2026-10-02
182other products contain Fenofibrate — compare makers, forms and strengths

Every line above is selected, not written, from the official label. Nothing is reworded. DailyMed

What it is for

Fenofibrate is a peroxisome proliferator-activated receptor (PPAR) alpha agonist indicated as an adjunct to diet:

  • To reduce elevated LDL-C, Total-C, TG and Apo B, and to increase HDL-C in adult patients with primary hypercholesterolemia or mixed dyslipidemia (1.1).
  • For treatment of adult patients with severe hypertriglyceridemia (1.2).
  • Limitations of Use:
  • Fenofibrate was not shown to reduce coronary heart disease morbidity and mortality in patients with type 2 diabetes mellitus (5.1).
  • 1.1 Primary Hypercholesterolemia or Mixed Dyslipidemia Fenofibrate tablets are indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein cholesterol (LDL-C), total cholesterol (Total-C), Triglycerides and apolipoprotein B (Apo B), and to increase high-density lipoprotein cholesterol (HDL-C) in adult patients with primary hypercholesterolemia or mixed dyslipidemia.
  • 1.2 Severe Hypertriglyceridemia Fenofibrate tablets are also indicated as adjunctive therapy to diet for treatment of adult patients with severe hypertriglyceridemia.
  • Improving glycemic control in diabetic patients showing fasting chylomicronemia will usually obviate the need for pharmacologic intervention.
  • Markedly elevated levels of serum triglycerides (e.g. > 2,000 mg/dL) may increase the risk of developing pancreatitis.
  • The effect of fenofibrate therapy on reducing this risk has not been adequately studied.
  • 1.3 Important Limitations of Use Fenofibrate at a dose equivalent to 160 mg of fenofibrate tablet was not shown to reduce coronary heart disease morbidity and mortality in a large, randomized controlled trial of patients with type 2 diabetes mellitus [see Warnings and Precautions (5.1)] .

From the official label · 2023-01-30 · DailyMed

How it works

From this product’s own US prescribing label.

The active moiety of fenofibrate tablet is fenofibric acid.

The pharmacological effects of fenofibric acid in both animals and humans have been extensively studied through oral administration of fenofibrate.

Peak level after6–8 h
Half-life20 h
Mostly cleared after≈ 4 daysfive half-lives — our arithmetic
PeakHalf gone4 days0
The shape is a standard model drawn from the two times above, not a measurement. How fast a medicine acts and wears off also depends on the dose, the form and the person.
How the body breaks it down

Race The influence of race on the pharmacokinetics of fenofibrate has not been studied, however fenofibrate is not metabolized by enzymes known for exhibiting inter-ethnic variability.

How it leaves the body

Following oral administration in healthy volunteers, approximately 60% of a single dose of radiolabelled fenofibrate appeared in urine, primarily as fenofibric acid and its glucuronate conjugate, and 25% was excreted in the feces.

With food

The absorption of fenofibrate is increased when administered with food.

Quoted from the prescribing label, sections “Mechanism of Action” and “Pharmacokinetics”. DailyMed · 2023-01-30

Do not take it if

  • Fenofibrate tablet is contraindicated in:
  • patients with severe renal impairment, including those receiving dialysis [see Clinical Pharmacology (12.3)].
  • patients with active liver disease, including those with primary biliary cirrhosis and unexplained persistent liver function abnormalities [see Warnings and Precautions (5.3)].
  • patients with preexisting gallbladder disease [see Warnings and Precautions (5.5)].
  • nursing mothers [see Use in Specific Populations (8.2)]
  • patients with known hypersensitivity to fenofibrate or fenofibric acid [see Warnings and Precautions (5.9)]. Severe renal dysfunction, including dialysis patients (4, 8.6, 12.3). Active liver disease (4, 5.3). Gallbladder disease (4, 5.5). Known hypersensitivity to fenofibrate (4). Nursing mothers (4, 8.2).

Quoted from the official label, section “Contraindications”.

How to take it

These directions are for this exact strength and form. Another one is different.

  • Primary hypercholesterolemia or mixed dyslipidemia:
  • Initial dose of 160 mg once daily (2.2).
  • Severe hypertriglyceridemia: Initial dose of 54 to 160 mg once daily.
  • Maximum dose is 160 mg (2.3).
  • Renally impaired patients: Initial dose of 54 mg once daily (2.4).
  • Geriatric patients: Select the dose on the basis of renal function (2.5).
  • Should be given with meals (2.1).
  • 2.1 General Considerations Patients should be placed on an appropriate lipid-lowering diet before receiving fenofibrate tablets, and should continue this diet during treatment with fenofibrate tablets.
  • Fenofibrate tablets should be given with meals, thereby optimizing the bioavailability of the medication.
  • The initial treatment for dyslipidemia is dietary therapy specific for the type of lipoprotein abnormality.
  • Excess body weight and excess alcoholic intake may be important factors in hypertriglyceridemia and should be addressed prior to any drug therapy.
  • Physical exercise can be an important ancillary measure.
  • Diseases contributory to hyperlipidemia, such as hypothyroidism or diabetes mellitus should be looked for and adequately treated.
  • Estrogen therapy, thiazide diuretics and beta-blockers, are sometimes associated with massive rises in plasma triglycerides, especially in subjects with familial hypertriglyceridemia.
  • In such cases, discontinuation of the specific etiologic agent may obviate the need for specific drug therapy of hypertriglyceridemia.
  • Lipid levels should be monitored periodically and consideration should be given to reducing the dosage of fenofibrate tablets if lipid levels fall significantly below the targeted range.
  • Therapy should be withdrawn in patients who do not have an adequate response after two months of treatment with the maximum recommended dose of 160 mg once daily.
  • 2.2 Primary Hypercholesterolemia or Mixed Dyslipidemia The initial dose of fenofibrate tablet is 160 mg once daily.
  • 2.3 Severe Hypertriglyceridemia The initial dose is 54 to 160 mg per day.
  • Dosage should be individualized according to patient response, and should be adjusted if necessary following repeat lipid determinations at 4 to 8 week intervals.
  • The maximum dose is 160 mg once daily.
  • 2.4 Impaired Renal Function Treatment with fenofibrate tablets should be initiated at a dose of 54 mg per day in patients having mild to moderately impaired renal function, and increased only after evaluation of the effects on renal function and lipid levels at this dose.
  • The use of fenofibrate tablets should be avoided in patients with severe renal impairment [see Use in Specific Populations (8.6) and Clinical Pharmacology (12.3)].
  • 2.5 Geriatric Patients Dose selection for the elderly should be made on the basis of renal function [see Use in Specific Populations (8.5)].

Quoted from the official label, section “Dosage & Administration”.

Other warnings

  • Myopathy and rhabdomyolysis have been reported in patients taking fenofibrate.
  • Risks are increased during co-administration with a statin (with a significantly higher rate observed for gemfibrozil), particularly in elderly patients and patients with diabetes, renal failure, or hypothyroidism (5.2).
  • Fenofibrate can increase serum transaminases.
  • Monitor liver tests, including ALT, periodically during therapy (5.3).
  • Fenofibrate can reversibly increase serum creatinine levels (5.4).
  • Monitor renal function periodically in patients with renal impairment (8.6).
  • Fenofibrate increases cholesterol excretion into the bile, leading to risk of cholelithiasis.
  • If cholelithiasis is suspected, gallbladder studies are indicated (5.5).
  • Use caution in concomitant treatment with oral coumarin anticoagulants.
  • Adjust the dosage of coumarin anticoagulant to maintain the prothrombin time/INR at the desired level to prevent bleeding complications (5.6).
  • Acute hypersensitivity reactions, including anaphylaxis and angioedema, and delayed hypersensitivity reactions, including severe cutaneous adverse drug reactions have been reported postmarketing.
  • Some cases were life- threatening and required emergency treatment.
  • Discontinue fenofibrate and treat patients appropriately if reactions occur (5.9).
  • 5.1 Mortality and Coronary Heart Disease Morbidity The effect of fenofibrate on coronary heart disease morbidity and mortality and non-cardiovascular mortality has not been established.
  • The Action to Control Cardiovascular Risk in Diabetes Lipid (ACCORD Lipid) trial was a randomized placebo-controlled study of 5518 patients with type 2 diabetes mellitus on background statin therapy treated with fenofibrate.
  • The mean duration of follow-up was 4.7 years.
  • Fenofibrate plus statin combination therapy showed a non-significant 8% relative risk reduction in the primary outcome of major adverse cardiovascular events (MACE), a composite of non-fatal myocardial infarction, non-fatal stroke, and cardiovascular disease death (hazard ratio [HR] 0.92, 95% CI 0.79 to 1.08) (p=0.32) as compared to statin monotherapy.
  • In a gender subgroup analysis, the hazard ratio for MACE in men receiving combination therapy versus statin monotherapy was 0.82 (95% CI 0.69 to 0.99), and the hazard ratio for MACE in women receiving combination therapy versus statin monotherapy was 1.38 (95% CI 0.98 to 1.94) (interaction p=0.01).
  • The clinical significance of this subgroup finding is unclear.
  • The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study was a 5-year randomized, placebo-controlled study of 9795 patients with type 2 diabetes mellitus treated with fenofibrate.
  • Fenofibrate demonstrated a non-significant 11% relative reduction in the primary outcome of coronary heart disease events (hazard ratio [HR] 0.89, 95% CI 0.75 to 1.05, p=0.16) and a significant 11% reduction in the secondary outcome of total cardiovascular disease events (HR 0.89 [0.8 to 0.99], p=0.04).
  • There was a non-significant 11% (HR 1.11 [0.95, 1.29], p=0.18) and 19% (HR 1.19 [0.9, 1.57], p=0.22) increase in total and coronary heart disease mortality, respectively, with fenofibrate as compared to placebo.
  • Because of chemical, pharmacological, and clinical similarities between fenofibrate, clofibrate, and gemfibrozil, the adverse findings in 4 large randomized, placebo-controlled clinical studies with these other fibrate drugs may also apply to fenofibrate.
  • In the Coronary Drug Project, a large study of post myocardial infarction of patients treated for 5 years with clofibrate, there was no difference in mortality seen between the clofibrate group and the placebo group.
  • There was however, a difference in the rate of cholelithiasis and cholecystitis requiring surgery between the two groups (3% vs. 1.8%).
  • In a study conducted by the World Health Organization (WHO), 5000 subjects without known coronary artery disease were treated with placebo or clofibrate for 5 years and followed for an additional one year.
  • There was a statistically significant, higher age − adjusted all-cause mortality in the clofibrate group compared with the placebo group (5.7% vs. 3.96%, p = < 0.01).
  • Excess mortality was due to a 33% increase in non-cardiovascular causes, including malignancy, post-cholecystectomy complications, and pancreatitis.
  • This appeared to confirm the higher risk of gallbladder disease seen in clofibrate-treated patients studied in the Coronary Drug Project.
  • The Helsinki Heart Study was a large (n=4081) study of middle-aged men without a history of coronary artery disease.
  • Subjects received either placebo or gemfibrozil for 5 years, with a 3.5 year open extension afterward.
  • Total mortality was numerically higher in the gemfibrozil randomization group but did not achieve statistical significance (p = 0.19, 95% confidence interval for relative risk G:P = 0.91 to 1.64).
  • Although cancer deaths trended higher in the gemfibrozil group (p = 0.11), cancers (excluding basal cell carcinoma) were diagnosed with equal frequency in both study groups.
  • Due to the limited size of the study, the relative risk of death from any cause was not shown to be different than that seen in the 9 year follow-up data from World Health Organization study (RR=1.29).
  • A secondary prevention component of the Helsinki Heart Study enrolled middle-aged men excluded from the primary prevention study because of known or suspected coronary heart disease.
  • Subjects received gemfibrozil or placebo for 5 years.
  • Although cardiac deaths trended higher in the gemfibrozil group, this was not statistically significant (hazard ratio 2.2, 95% confidence interval:
  • 0.94 to 5.05).
  • The rate of gallbladder surgery was not statistically significant between study groups, but did trend higher in the gemfibrozil group, (1.9% vs. 0.3%, p = 0.07).
  • 5.2 Skeletal Muscle Fibrates increase the risk for myopathy and have been associated with rhabdomyolysis.
  • The risk for serious muscle toxicity appears to be increased in elderly patients and in patients with diabetes, renal insufficiency, or hypothyroidism.
  • Myopathy should be considered in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevations of creatine phosphokinase (CPK) levels.
  • Patients should be advised to report promptly unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever.
  • CPK levels should be assessed in patients reporting these symptoms, and fenofibrate therapy should be discontinued if markedly elevated CPK levels occur or myopathy/myositis is suspected or diagnosed.
  • Data from observational studies indicate that the risk for rhabdomyolysis is increased when fibrates, in particular gemfibrozil, are co-administered with an HMG-CoA reductase inhibitor (statin).
  • The combination should be avoided unless the benefit of further alterations in lipid levels is likely to outweigh the increased risk of this drug combination [see Clinical Pharmacology (12.3)].
  • Cases of myopathy, including rhabdomyolysis, have been reported with fenofibrates co- administered with colchicine, and caution should be exercised when prescribing fenofibrate with colchicine [see Drug Interactions (7.4)] .
  • 5.3 Liver Function Fenofibrate at doses equivalent to 107 mg to 160 mg fenofibrate per day has been associated with increases in serum transaminases [AST (SGOT) or ALT (SGPT)].
  • In a pooled analysis of 10 placebo-controlled trials, increases to > 3 times the upper limit of normal occurred in 5.3% of patients taking fenofibrate versus 1.1% of patients treated with placebo.
  • When transaminase determinations were followed either after discontinuation of treatment or during continued treatment, a return to normal limits was usually observed.
  • The incidence of increases in transaminases related to fenofibrate therapy appear to be dose related.
  • In 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 107 mg to 160 mg fenofibrate per day and was 0% in those receiving dosages equivalent to 54 mg or less fenofibrate per day, or placebo.
  • Hepatocellular, chronic active and cholestatic hepatitis associated with fenofibrate therapy have been reported after exposures of weeks to several years.
  • In extremely rare cases, cirrhosis has been reported in association with chronic active hepatitis.
  • Baseline and regular periodic monitoring of liver function, including serum ALT (SGPT) should be performed for the duration of therapy with fenofibrate, and therapy discontinued if enzyme levels persist above three times the normal limit.
  • 5.4 Serum Creatinine Elevations in serum creatinine have been reported in patients on fenofibrate.
  • These elevations tend to return to baseline following discontinuation of fenofibrate.
  • The clinical significance of these observations is unknown.
  • Monitor renal function in patients with renal impairment taking fenofibrate.
  • Renal monitoring should also be considered for patients taking fenofibrateat risk for renal insufficiency such as the elderly and patients with diabetes.
  • 5.5 Cholelithiasis Fenofibrate, like clofibrate and gemfibrozil, may increase cholesterol excretion into the bile, leading to cholelithiasis.
  • If cholelithiasis is suspected, gallbladder studies are indicated.
  • Fenofibrate therapy should be discontinued if gallstones are found.
  • 5.6 Coumarin Anticoagulants Caution should be exercised when coumarin anticoagulants are given in conjunction with fenofibrate because of the potentiation of coumarin-type anticoagulant effects in prolonging the Prothrombin Time/International Normalized Ratio (PT/INR).
  • To prevent bleeding complications, frequent monitoring of PT/INR and dose adjustment of the anticoagulant are recommended until PT/INR has stabilized [see Drug Interactions (7.1)].
  • 5.7 Pancreatitis Pancreatitis has been reported in patients taking fenofibrate, gemfibrozil, and clofibrate.
  • This occurrence may represent a 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.
  • 5.8 Hematologic Changes Mild to moderate hemoglobin, hematocrit, and white blood cell decreases have been observed in patients following initiation of fenofibrate therapy.
  • However, these levels stabilize during long-term administration.
  • Thrombocytopenia and agranulocytosis have been reported in individuals treated with fenofibrate.
  • Periodic monitoring of red and white blood cell counts are recommended during the first 12 months of fenofibrate administration.
  • 5.9 Hypersensitivity Reactions Acute Hypersensitivity Anaphylaxis and angioedema have been reported postmarketing with fenofibrate.
  • In some cases, reactions were life-threatening and required emergency treatment.
  • If a patient develops signs or symptoms of an acute hypersensitivity reaction, advise them to seek immediate medical attention and discontinue fenofibrate.
  • Delayed Hypersensitivity Severe cutaneous adverse drug reactions (SCAR), including Stevens-Johnson syndrome, toxic epidermal necrolysis, and Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS), have been reported postmarketing, occurring days to weeks after initiation of fenofibrate.
  • The cases of DRESS were associated with cutaneous reactions (such as rash or exfoliative dermatitis) and a combination of eosinophilia, fever, systemic organ involvement (renal, hepatic, or respiratory).
  • Discontinue fenofibrate and treat patients appropriately if SCAR is suspected.
  • 5.10 Venothromboembolic Disease In the FIELD trial, pulmonary embolus (PE) and deep vein thrombosis (DVT) were observed at higher rates in the fenofibrate- than the placebo-treated group.
  • Of 9,795 patients enrolled in FIELD, there were 4,900 in the placebo group and 4,895 in the fenofibrate group.
  • For DVT, there were 48 events (1%) in the placebo group and 67 (1%) in the fenofibrate group (p = 0.074); and for PE, there were 32 (0.7%) events in the placebo group and 53 (1%) in the fenofibrate group (p = 0.022).
  • In the Coronary Drug Project, a higher proportion of the clofibrate group experienced definite or suspected fatal or nonfatal pulmonary embolism or thrombophlebitis than the placebo group (5.2% vs. 3.3% at five years; p < 0.01).
  • 5.11 Paradoxical Decreases in HDL Cholesterol Levels There have been postmarketing and clinical trial reports of severe decreases in HDL cholesterol levels (as low as 2 mg/dL) occurring in diabetic and non-diabetic patients initiated on fibrate therapy.
  • The decrease in HDL-C is mirrored by a decrease in apolipoprotein A1.
  • This decrease has been reported to occur within 2 weeks to years after initiation of fibrate therapy.
  • The HDL-C levels remain depressed until fibrate therapy has been withdrawn; the response to withdrawal of fibrate therapy is rapid and sustained.
  • The clinical significance of this decrease in HDL-C is unknown.
  • It is recommended that HDL-C levels be checked within the first few months after initiation of fibrate therapy.
  • If a severely depressed HDL-C level is detected, fibrate therapy should be withdrawn, and the HDL-C level monitored until it has returned to baseline, and fibrate therapy should not be re-initiated.

Quoted from the official label, section “Warnings”.

Pregnancy and breastfeeding

  • Risk Summary Limited available data with fenofibrate use in pregnant women are insufficient to determine a drug associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes.
  • In animal reproduction studies, no evidence of embryo-fetal toxicity was observed with oral administration of fenofibrate in rats and rabbits during organogenesis at doses less than or equivalent to the maximum recommended clinical dose of 160 mg daily, based on body surface area (mg/m 2 ).
  • Adverse reproductive outcomes occurred at higher doses in the presence of maternal toxicity (see Data).
  • Fenofibrate tablets should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
  • The estimated background risk of major birth defects and miscarriage for the indicated population is unknown.
  • In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively.
  • Data Animal Data In pregnant rats given oral dietary doses of 14, 127, and 361 mg/kg/day from gestation day 6 to 15 during the period of organogenesis, no adverse developmental findings were observed at 14 mg/kg/day (less than the clinical exposure at the maximum recommended human dose [MRHD] of 300 mg fenofibrate daily, equivalent to 160 mg fenofibrate tablets daily, based on body surface area comparisons).
  • Increased fetal skeletal malformations were observed at maternally toxic doses (361 mg/kg/day, corresponding to 12 times the clinical exposure at the MRHD) that significantly suppressed maternal body weight gain.
  • In pregnant rabbits given oral gavage doses of 15, 150, and 300 mg/kg/day from gestation day 618 during the period of organogenesis and allowed to deliver, no adverse developmental findings were observed at 15 mg/kg/day (a dose that approximates the clinical exposure at the MRHD, based on body surface area comparisons).
  • Aborted litters were observed at maternally toxic doses (≥ 150 mg/kg/day, corresponding to ≥ 10 times the clinical exposure at the MRHD) that suppressed maternal body weight gain.
  • In pregnant rats given oral dietary doses of 15, 75, and 300 mg/kg/day from gestation day 15 through lactation day 21 (weaning), no adverse developmental effects were observed at 15 mg/kg/day (less than the clinical exposure at the MRHD, based on body surface area comparisons), despite maternal toxicity (decreased weight gain).
  • Post-implantation loss was observed at ≥ 75 mg/kg/day (≥ 2 times the clinical exposure at the MRHD) in the presence of maternal toxicity (decreased weight gain).
  • Decreased pup survival was noted at 300 mg/kg/day (10 times the clinical exposure at the MRHD), which was associated with decreased maternal body weight gain/maternal neglect.
  • IN SPECIFIC POPULATIONS Geriatric Use:
  • Determine dose selection based on renal function (8.5).
  • Renal Impairment: Avoid use in severe renal impairment patients.
  • Dose reduction is required in mild to moderate renal impairment patients (8.6).
  • 8.1 Pregnancy Risk Summary Limited available data with fenofibrate use in pregnant women are insufficient to determine a drug associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes.
  • In animal reproduction studies, no evidence of embryo-fetal toxicity was observed with oral administration of fenofibrate in rats and rabbits during organogenesis at doses less than or equivalent to the maximum recommended clinical dose of 160 mg daily, based on body surface area (mg/m 2 ).
  • Adverse reproductive outcomes occurred at higher doses in the presence of maternal toxicity (see Data).
  • Fenofibrate tablets should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
  • The estimated background risk of major birth defects and miscarriage for the indicated population is unknown.
  • In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively.
  • Data Animal Data In pregnant rats given oral dietary doses of 14, 127, and 361 mg/kg/day from gestation day 6 to 15 during the period of organogenesis, no adverse developmental findings were observed at 14 mg/kg/day (less than the clinical exposure at the maximum recommended human dose [MRHD] of 300 mg fenofibrate daily, equivalent to 160 mg fenofibrate tablets daily, based on body surface area comparisons).
  • Increased fetal skeletal malformations were observed at maternally toxic doses (361 mg/kg/day, corresponding to 12 times the clinical exposure at the MRHD) that significantly suppressed maternal body weight gain.
  • In pregnant rabbits given oral gavage doses of 15, 150, and 300 mg/kg/day from gestation day 618 during the period of organogenesis and allowed to deliver, no adverse developmental findings were observed at 15 mg/kg/day (a dose that approximates the clinical exposure at the MRHD, based on body surface area comparisons).
  • Aborted litters were observed at maternally toxic doses (≥ 150 mg/kg/day, corresponding to ≥ 10 times the clinical exposure at the MRHD) that suppressed maternal body weight gain.
  • In pregnant rats given oral dietary doses of 15, 75, and 300 mg/kg/day from gestation day 15 through lactation day 21 (weaning), no adverse developmental effects were observed at 15 mg/kg/day (less than the clinical exposure at the MRHD, based on body surface area comparisons), despite maternal toxicity (decreased weight gain).
  • Post-implantation loss was observed at ≥ 75 mg/kg/day (≥ 2 times the clinical exposure at the MRHD) in the presence of maternal toxicity (decreased weight gain).
  • Decreased pup survival was noted at 300 mg/kg/day (10 times the clinical exposure at the MRHD), which was associated with decreased maternal body weight gain/maternal neglect.
  • 8.2 Lactation Risk Summary There is no available information on the presence of fenofibrate in human milk, effects of the drug on the breastfed infant, or the effects on milk production.
  • Fenofibrate is present in the milk of rats, and is therefore likely to be present in human milk.
  • Because of the potential for serious adverse reactions in breastfed infants, such as disruption of infant lipid metabolism, women should not breastfeed during treatment with fenofibrate tablets and for 5 days after the final dose [see Contraindications (4)].
  • 8.4 Pediatric Use Safety and effectiveness have not been established in pediatric patients.
  • 8.5 Geriatric Use Fenofibric acid is known to be substantially excreted by the kidney, and the risk of adverse reactions to this drug may be greater in patients with impaired renal function.
  • Fenofibric acid exposure is not influenced by age.
  • Since elderly patients have a higher incidence of renal impairment, dose selection for the elderly should be made on the basis of renal function [see Dosage and Administration (2.5) and Clinical Pharmacology (12.3)].
  • Elderly patients with normal renal function should require no dose modifications.
  • Consider monitoring renal function in elderly patients taking fenofibrate.
  • 8.6 Renal Impairment The use of fenofibrate should be avoided in patients who have severe renal impairment [see Contraindications (4)].
  • Dose reduction is required in patients with mild to moderate renal impairment [see Dosage and Administration (2.4) and Clinical Pharmacology (12.3)].
  • Monitoring renal function in patients with renal impairment is recommended.
  • 8.7 Hepatic Impairment The use of fenofibrate has not been evaluated in subjects with hepatic impairment [see Contraindications (4) and Clinical Pharmacology (12.3)].

Quoted from the official label, section “OTC — Pregnancy or Breast Feeding”.

Other medicines

  • Coumarin anticoagulants: (7.1).
  • Immunosuppressants: (7.2).
  • Bile acid resins: (7.3)
  • 7.1 Coumarin Anticoagulants Potentiation of coumarin-type anticoagulant effects has been observed with prolongation of the PT/INR.
  • Caution should be exercised when coumarin anticoagulants are given in conjunction with fenofibrate.
  • The dosage of the anticoagulants should be reduced to maintain the PT/INR at the desired level to prevent bleeding complications.
  • Frequent PT/INR determinations are advisable until it has been definitely determined that the PT/INR has stabilized [see Warnings and Precautions (5.6)].
  • 7.2 Immunosuppressants Immunosuppressants such as cyclosporine and tacrolimus can produce nephrotoxicity with decreases in creatinine clearance and rises in serum creatinine, and because renal excretion is the primary elimination route of fibrate drugs including fenofibrate, there is a risk that an interaction will lead to deterioration of renal function.
  • The benefits and risks of using fenofibrate with immunosuppressants and other potentially nephrotoxic agents should be carefully considered, and the lowest effective dose employed and renal function monitored.
  • 7.3 Bile Acid Binding Resins Since bile acid binding resins may bind other drugs given concurrently, patients should take Fenofibrate at least 1 hour before or 4 to 6 hours after a bile acid binding resin to
  • avoid impeding its absorption.
  • 7.4 Colchicine Cases of myopathy, including rhabdomyolysis, have been reported with fenofibrates co- administered with colchicine, and caution should be exercised when prescribing fenofibrate with colchicine.

Quoted from the official label, section “Drug Interactions”.

If you take too much

In an emergency, call your local emergency number or a poison control centre.

  • There is no specific treatment for overdose with fenofibrate.
  • General supportive care of the patient is indicated, including monitoring of vital signs and observation of clinical status, should an overdose occur.
  • If indicated, elimination of unabsorbed drug should be achieved by emesis or gastric lavage; usual precautions should be observed to maintain the airway.
  • Because fenofibric acid is highly bound to plasma proteins, hemodialysis should not be considered.

Quoted from the official label, section “Overdosage”.

Use in children

Safety and effectiveness have not been established in pediatric patients.

Quoted from the official label, section “Pediatric Use”.

Use in older people

  • Fenofibric acid is known to be substantially excreted by the kidney, and the risk of adverse reactions to this drug may be greater in patients with impaired renal function.
  • Fenofibric acid exposure is not influenced by age.
  • Since elderly patients have a higher incidence of renal impairment, dose selection for the elderly should be made on the basis of renal function [see Dosage and Administration (2.5) and Clinical Pharmacology (12.3)].
  • Elderly patients with normal renal function should require no dose modifications.
  • Consider monitoring renal function in elderly patients taking fenofibrate.

Quoted from the official label, section “Geriatric Use”.

Side effects

  • Adverse reactions > 2% and at least 1% greater than placebo:
  • Abnormal liver tests, increased AST, increased ALT, increased CPK, and rhinitis (6).
  • To report SUSPECTED ADVERSE REACTIONS, contact FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
  • 6.1 Clinical Trials Experience Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in the clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in practice.
  • Adverse events reported by 2% or more of patients treated with fenofibrate (and greater than placebo) during the double-blind, placebo-controlled trials, regardless of causality, are listed in Table 1 below.
  • Adverse events led to discontinuation of treatment in 5% of patients treated with fenofibrate and in 3% treated with placebo.
  • Increases in liver function tests were the most frequent events, causing discontinuation of fenofibrate treatment in 1.6% of patients in double- blind trials.
  • Table 1.
  • Adverse Reactions Reported by 2% or More of Patients Treated with Fenofibrate and Greater than Placebo During the Double-Blind, Placebo-Controlled Trials BODY SYSTEM Adverse Reaction Fenofibrate* (N=439) Placebo (N=365) BODY AS A WHOLE Abdominal Pain 4.6% 4.4% Back Pain 3.4% 2.5% Headache 3.2% 2.7% DIGESTIVE Nausea 2.3% 1.9% Constipation 2.1% 1.4% METABOLIC AND NUTRITIONAL DISORDERS Abnormal Liver Function Tests 7.5%** 1.4% Increased ALT 3% 1.6% Increased CPK 3% 1.4% Increased AST 3.4%** 0.5% RESPIRATORY Respiratory Disorder 6.2% 5.5% Rhinitis 2.3% 1.1% * Dosage equivalent to 160 mg fenofibrate. ** Significantly different from Placebo.
  • Urticaria was seen in 1.1% vs. 0%, and rash in 1.4% vs. 0.8% of fenofibrate and placebo patients respectively in controlled trials.
  • 6.2 Postmarketing Experience The following adverse reactions have been identified during postapproval use of fenofibrate.
  • Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure:
  • myalgia, rhabdomyolysis, pancreatitis, acute renal failure, muscle spasm, hepatitis, cirrhosis, anemia, arthralgia, decreases in hemoglobin, decreases in hematocrit, white blood cell decreases, asthenia, severely depressed HDL-cholesterol levels, and interstitial lung disease.
  • Photosensitivity reactions have occurred days to months after initiation; in some of these cases, patients reported a prior photosensitivity reaction to ketoprofen.

Quoted from the official label, section “Adverse Reactions”.

What to discuss with your doctor

  • Patients should be advised:
  • of the potential benefits and risks of fenofibrate tablets. not to use fenofibrate tablets if there is a known hypersensitivity to fenofibrate or fenofibric acid. of medications that should not be taken in combination with fenofibrate tablets. that if they are taking coumarin anticoagulants, fenofibrate tablets may increase their anti-coagulant effect, and increased monitoring may be necessary. to continue to follow an appropriate lipid-modifying diet while taking fenofibrate tablets. to take fenofibrate tablets once daily with a meal at the prescribed dose swallowing each tablet whole. to return to their physician’s office for routine monitoring. to inform their physician of all medications, supplements, and herbal preparations they are taking and any change to their medical condition.
  • Patients should also be advised to inform their physicians prescribing a new medication that they are taking fenofibrate tablets. to inform their physician of any muscle pain, tenderness, or weakness; onset of abdominal pain; or any other new symptoms. not to breastfeed during treatment with fenofibrate tablets and for 5 days after the final dose.
  • Call your doctor for medical advice about side effects.
  • You may report side effects to FDA at 1-800-FDA-1088.
  • Manufactured by:
  • Alembic Pharmaceuticals Limited (Formulation Division), Panelav 389350, Gujarat, India Revised:
  • 01/2020

Quoted from the official label, section “Patient Counseling Information”.

Strengths and forms

  • FORMS AND STRENGTHS Fenofibrate tablets USP, 54 mg are yellow to light yellow colored, oval shape, film-coated tablets debossed with ‘L751’ on one side and plain on other side.
  • Fenofibrate tablets USP, 160 mg are white to off white, oval shape, film-coated tablets debossed with ‘L752’ on one side and plain on other side.
  • Oral Tablets: 54 mg and 160 mg (3).

Quoted from the official label, section “Dosage Forms & Strengths”.

What it looks like and how it is packed

  • Fenofibrate tablets, USP are available in two strengths:
  • 54 mg are yellow to light yellow colored, oval shape, film-coated tablets debossed with ‘L751’ on one side and plain on other side.
  • They are available as follows:
  • NDC 46708-350-30 bottle of 30 tablets NDC 46708-350-90 bottle of 90 tablets NDC 46708-350-71 bottle of 500 tablets 160 mg are white to off white, oval shape, film-coated tablets debossed with ‘L752’ on one side and plain on other side.
  • They are available as follows:
  • NDC 46708-351-30 bottle of 30 tablets NDC 46708-351-90 bottle of 90 tablets NDC 46708-351-71 bottle of 500 tablets Storage
  • Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F) [see USP Controlled Room Temperature].
  • Keep this and all medication out of reach of children.
  • Protect from moisture.

Quoted from the official label, section “How Supplied”.

What is in it

  • Fenofibrate, USP is a lipid regulating agent available as tablets for oral administration.
  • Each tablet contains 54 mg or 160 mg of fenofibrate, USP.
  • The chemical name for fenofibrate, USP is 2-[4-(4-chlorobenzoyl) phenoxy]-2-methyl-propanoic acid, 1-methylethyl ester with the following structural formula.
  • The empirical formula is C 20 H 21 O 4 Cl and the molecular weight is 360.83; fenofibrate, USP is very soluble in methylene chloride; slightly soluble in alcohol; practically insoluble in water.
  • The melting point is 79 to 82°C.
  • Fenofibrate, USP is a white or almost white crystalline powder which is stable under ordinary conditions.
  • Inactive Ingredients Each tablet contains microcrystalline cellulose, croscarmellose sodium, hypromellose, magnesium stearate, polydextrose, titanium dioxide, triacetin, polyethylene glycol 8000.
  • Additionally, fenofibrate tablets USP, 54 mg contains D&C Yellow No. 10 Aluminum Lake and FD&C Yellow No. 6 Aluminum Lake.
  • Fenofibrate tablets, USP meets USP Dissolution Test 3 . fenofibrate structure.jpg

Quoted from the official label, section “Description”.

Ingredients people check for

Lactose, gluten, dyes, sugars and other ingredients that matter with an allergy, intolerance or diet — as this product’s FDA label lists them.

  • Colour dyes54 mg contains D&C Yellow No. 10 Aluminum Lake; FD&C Yellow No. 6 Aluminum LakeSome people react to dyes such as tartrazine (Yellow 5) or carmine.
  • Titanium dioxidetitanium dioxideA whitening agent no longer allowed in food in the EU (E171).

Quoted from the FDA label. A label that does not name an ingredient is not a guarantee that the product is free of it, and formulations change. With an allergy, check the pack and ask a pharmacist.

Every version of this medicine (38)

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Same active substance, strength and form in other countries

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Every strength and form (21)

Details

Made byAlembic Pharmaceuticals Limited
Active substanceFenofibrate
Used inHeart, blood pressure and circulation
Strength160 mg
FormTablet, Film Coated
RouteOral
Packs30 TABLET, FILM COATED in 1 BOTTLE · 500 TABLET, FILM COATED in 1 BOTTLE · 90 TABLET, FILM COATED in 1 BOTTLE
NDC46708-351
NDC46708-555

Source: NDC Directory · 2026-09-13 · not reviewed by a clinician

Source: US Food and Drug Administration, NDC Directory. Reuse terms: US government work (FDA).

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Other strengths and forms

176 products are sold under this name. Grouped by form; a number on a strength means several companies make it.

Same active substance

These contain the same substance. That does not mean one can replace another — ask a pharmacist.

Antara30 mgPrescription onlyCapsule Lupin Pharmaceuticals, Inc. · FenofibrateAntara90 mgPrescription onlyCapsule Lupin Pharmaceuticals, Inc. · FenofibrateAntara43 mgPrescription onlyCapsule Lupin Pharmaceuticals, Inc. · FenofibrateAntara130 mgPrescription onlyCapsule Lupin Pharmaceuticals, Inc. · FenofibrateFenofibrate54 mgPrescription onlyTablet Amneal Pharmaceuticals of New York LLC · FenofibrateFenofibrate160 mgPrescription onlyTablet Amneal Pharmaceuticals of New York LLC · Fenofibrate

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