Fenofibric acid

Q: Who makes Fenofibric acid?

Fenofibric acid is listed by 7 labelers in the FDA NDC directory, including Alembic Pharmaceuticals Inc., Alembic Pharmaceuticals Limited, Amneal Pharmaceuticals of New York LLC, Aurobindo Pharma Limited.

Capsule, Delayed Release · Oral

Prescription (Rx) Peroxisome Proliferator Receptor alpha Agonist

Uses

Fenofibric acid delayed-release capsules are indicated as adjunctive therapy to diet: to reduce triglyceride (TG) levels in adults with severe hypertriglyceridemia (TG greater than or equal to 500 mg/dL). to reduce elevated low-density lipoprotein cholesterol (LDL-C) in adults with primary hyperlipidemia when use of recommended LDL-C lowering therapy is not possible. Limitations of Use Markedly elevated levels of serum TG (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 determined [see Warnings and Precautions (5.7) ] . Fenofibrate did not reduce coronary heart disease morbidity and mortality in two large, randomized controlled trials of patients with type 2 diabetes mellitus [see Warnings and Precautions (5.1) and Clinical Studies (14.4) ] . Fenofibric acid delayed-release capsules are peroxisome proliferator-activated receptor (PPAR) alpha agonist indicated as adjunct to diet: to reduce triglyceride (TG) levels in adults with severe hypertriglyceridemia (TG greater than or equal to 500 mg/dL) (1) . to reduce elevated low-density lipoprotein cholesterol (LDL-C) in adults with primary hyperlipidemia when use of recommended LDL-C lowering therapy is not possible (1) . Limitations of Use: Markedly elevated levels of serum TG (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 determined (1) . Fenofibrate did not reduce coronary heart disease morbidity and mortality in two large, randomized controlled trials of patients with type 2 diabetes mellitus (1) .

Dosage and administration

Severe hypertriglyceridemia: 45 to 135 mg orally once daily; the dosage should be adjusted according to patient response (2.2) . Primary hyperlipidemia: 135 mg orally once daily (2.2) . Administer as a single dose, at any time of day, with or without food (2.2) . Assess TG when clinically appropriate, as early as 4 to 8 weeks after initiating fenofibric acid. Discontinue fenofibric acid in patients who do not have an adequate response after 2 months of treatment (2.2) . Swallow capsules whole. Do not crush, break, dissolve, or chew (2.2) . Renal impairment: Initial dosage of 45 mg orally once daily (2.3) . Geriatric patients: Select the dosage on the basis of renal function (2.4) . 2.1 Prior to Initiation of fenofibric acid delayed-release capsules Assess lipid levels before initiating therapy. Identify other causes (e.g., diabetes mellitus, hypothyroidism, or medications) of high TG levels and manage as appropriate. Patients should be placed on an appropriate lipid-lowering diet before receiving fenofibric acid delayed-release capsules, and should continue this diet during treatment with fenofibric acid delayed-release capsules. In patients with diabetes and fasting chylomicronemia, improve glycemic control prior to considering starting fenofibric acid delayed-release capsules. 2.2 Recommended Dosage and Administration Severe hypertriglyceridemia: The recommended dosage of fenofibric acid delayed-release capsules are 45 mg or 135 mg orally once daily. Dosage should be individualized according to patient response, and should be adjusted if necessary following repeat lipid determinations at 4 to 8 week intervals. Primary hyperlipidemia: The recommended dosage of fenofibric acid delayed-release capsules are 135 mg orally once daily. Administer fenofibric acid delayed-release capsules as a single dose at any time of day, with or without food. Advise patients to swallow fenofibric acid delayed-release capsules whole. Do not crush, break, dissolve, or chew capsules. Assess TG when clinically appropriate, as early as 4 to 8 weeks after initiating fenofibric acid delayed-release capsules. Discontinue fenofibric acid delayed-release capsules in patients who do not have an adequate response after two months of treatment. If a dose is missed, advise patients not to take an extra dose. Resume treatment with the next dose. Advise patients to take fenofibric acid delayed-release capsules at least 1 hour before or 4 hours to 6 hours after a bile acid binding resin to avoid impeding its absorption. 2.3 Recommended Dosage in Patients with Renal Impairment Assess renal function prior to initiation of fenofibric acid delayed-release capsules and periodically thereafter [see Warnings and Precautions (5.4) ]. Treatment with fenofibric acid delayed-release capsules should be initiated at a dosage of 45 mg orally once daily in patients with mild to moderately impaired renal function (eGFR 30 to <60 mL/min/1.73m 2 ), and increased only after evaluation of the effects on renal function and TG levels at this dosage. Fenofibric acid delayed-release capsules are contraindicated in patients with severe renal impairment (eGFR <30 mL/min/1.73m 2 ), including those with end-stage renal disease (ESRD) and those receiving dialysis [see Use in Specific Populations (8.6) and Clinical Pharmacology (12.3) ]. 2.4 Recommended Dosage in Geriatric Patients Dosage selection for geriatric patients should be made on the basis of renal function [see Use in Specific Populations (8.6) and Clinical Pharmacology (12.3) ].

Dosage forms and strengths

Contraindications

Fenofibric acid delayed-release capsules are contraindicated in patients with: Severe renal impairment, including those with end-stage renal disease (ESRD) and those receiving dialysis [see Clinical Pharmacology (12.3) ] . Active liver disease, including those with unexplained persistent liver function abnormalities [see Warnings and Precautions (5.2) ] . Pre-existing gallbladder disease [see Warnings and Precautions (5.5) ]. Hypersensitivity to fenofibric acid, fenofibrate, or any of the excipients in fenofibric acid delayed-release capsules. Serious hypersensitivity reactions including anaphylaxis and angioedema have been reported with fenofibrate [see Warnings and Precautions (5.9) ] . Severe renal impairment, including those with end-stage renal disease (ESRD) and those receiving dialysis (4) . Active liver disease including those with unexplained persistent liver function abnormalities (4) . Pre-existing gallbladder disease (4) . Hypersensitivity to fenofibric acid, fenofibrate, or any of the excipients in fenofibric acid delayed-release capsules (4) .

Warnings and precautions

Hepatotoxicity: Serious drug-induced liver injury, including liver transplantation and death, has been reported with fenofibrates, including fenofibric acid. Monitor patient's liver function, including serum ALT, AST, and total bilirubin, at baseline and periodically for the duration of therapy. Discontinue if signs or symptoms of liver injury develop or if elevated enzyme levels persist ( 5.2 ). Myopathy and Rhabdomyolysis: Have been reported in patients taking fenofibrates. Risks are increased during co-administration with a statin, in geriatric patients, and in patients with renal impairment or hypothyroidism. Discontinue fenofibric acid if markedly elevated CK levels occur or if myopathy is either diagnosed or suspected. Temporarily discontinue fenofibric acid in patients experiencing an acute or serious condition at high risk of developing renal failure secondary to rhabdomyolysis. Inform patients of the risk of myopathy and rhabdomyolysis when starting or increasing the fenofibric acid dosage. Instruct patients to promptly report any unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever (5.3) . Increases in Serum Creatinine: Monitor renal function in patients with renal impairment taking fenofibric acid. Consider monitoring renal function in patients at risk for renal impairment (5.4) . Cholelithiasis: Fenofibrate may increase cholesterol excretion into the bile, leading to cholelithiasis. If cholelithiasis is suspected, gallbladder studies are indicated (5.5) . Hypersensitivity Reactions: 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 fenofibric acid and treat appropriately if reactions occur (5.9) . 5.1 Mortality and Coronary Heart Disease Morbidity Fenofibrate did not reduce cardiovascular disease morbidity or mortality in two large, randomized controlled trials of patients with type 2 diabetes mellitus [see Clinical Studies (14.4) ] . Because of chemical, pharmacological, and clinical similarities between fenofibrates, including fenofibric acid; pemafibrate; clofibrate; and gemfibrozil; the findings in 5 large randomized, placebo-controlled clinical trials with these other fibrate drugs may also apply to fenofibric acid. Pemafibrate did not reduce cardiovascular disease morbidity or mortality in a large, randomized, placebo-controlled trial of patients with type 2 diabetes mellitus on background statin therapy [see Clinical Studies (14.4) ] . In the Coronary Drug Project, a large trial conducted from 1965 to 1985 in men post myocardial infarction, there was no difference in mortality or nonfatal myocardial infarction between the clofibrate group and the placebo group after 5 years of treatment (NCT00000482). In a trial conducted by the World Health Organization (WHO) from 1965 to 1976, men without known coronary artery disease were treated with placebo or clofibrate for 5 years and followed for an additional 1 year. There was 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). Excess mortality was due to a 33% increase in non-cardiovascular causes, including malignancy, post-cholecystectomy complications, and pancreatitis. The Helsinki Heart Study, conducted from 1982 to 1987, was a large (N = 4,081) trial 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 but not statistically higher in the gemfibrozil randomization group versus placebo [95% confidence interval (CI) of the hazard ratio (HR) 0.91 to 1.64]. A secondary prevention component of the Helsinki Heart Study treated middle-aged men with gemfibrozil or placebo for 5 years. The HR for cardiac deaths was 2.2, 95% CI, 0.94 to 5.05. 5.2 Hepatotoxicity Serious drug-induced liver injury (DILI), including liver transplantation and death, has been reported with postmarketing use of fenofibrates, including fenofibric acid. DILI has been reported within the first few weeks of treatment or after several months of therapy and in some cases has reversed with discontinuation of fenofibric acid treatment. Patients with DILI have experienced signs and symptoms including dark urine, abnormal stool, jaundice, malaise, abdominal pain, myalgia, weight loss, pruritus, and nausea. Many patients had concurrent elevations of total bilirubin, serum alanine transaminase (ALT), and aspartate transaminase (AST). DILI has been characterized as hepatocellular, chronic active, and cholestatic hepatitis, and cirrhosis has occurred in association with chronic active hepatitis. In clinical trials, an intermediate daily dosage or the maximum recommended daily dosage of fenofibrate have been associated with increases in serum AST or ALT. The incidence of increases in transaminases may be dose related [see Adverse Reactions ( 6.1 )] . Fenofibric acid is contraindicated in patients with active liver disease, including those with unexplained persistent liver function abnormalities. Monitor patient’s liver function, including serum ALT, AST, and total bilirubin, at baseline and periodically for the duration of therapy with fenofibric acid. Discontinue fenofibric acid if signs or symptoms of liver injury develop or if elevated enzyme levels persist (ALT or AST > 3 times the upper limit of normal, or if accompanied by elevation of bilirubin). Do not restart fenofibric acid in these patients if there is no alternative explanation for the liver injury. 5.3 Myopathy and Rhabdomyolysis Fenofibric acid may cause myopathy [muscle pain, tenderness, or weakness associated with elevated creatine kinase (CK)] and rhabdomyolysis.

Side effects

The following serious adverse reactions are described below and elsewhere in the labeling: Mortality and coronary heart disease morbidity [see Warnings and Precautions (5.1) ] Hepatoxicity [see Warnings and Precautions (5.2) ] Myopathy and Rhabdomyolysis [see Warnings and Precautions (5.3) ] Increases in Serum Creatinine [see Warnings and Precautions (5.4) ] Cholelithiasis [see Warnings and Precautions (5.5) ] Increased Bleeding Risk with Coumarin Anticoagulants [see Warnings and Precautions (5.6) ] Pancreatitis [see Warnings and Precautions (5.7) ] Hematologic Changes [see Warnings and Precautions (5.8) ] Hypersensitivity reactions [see Warnings and Precautions (5.9) ] Venothromboembolic disease [see Warnings and Precautions (5.10) ] Paradoxical Decreases in HDL Cholesterol Levels [see Warnings and Precautions (5.11) ] Adverse reactions (≥ 2% and greater than placebo): abnormal liver tests, increased AST, increased ALT, increased CPK, and rhinitis ( 6.1 ). To report SUSPECTED ADVERSE REACTIONS, contact Leading Pharma, LLC at 1-844-740-7500 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch. 6.1 Clinical Trials Experience Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in clinical practice. The safety of fenofibric acid has been established in adults with hypertriglyceridemia or primary hyperlipidemia based on adequate and well-controlled trials of other formulations of fenofibrate, referenced below as “fenofibrate” [see Clinical Studies (14) ]. Dosages of fenofibrate used in these trials were comparable to fenofibric acid 135 mg per day [see Clinical Pharmacology (12.3) ]. Adverse reactions reported by 2% or more of patients treated with fenofibrate (and greater than placebo) during the double-blind, placebo-controlled trials are listed in Table 1. Adverse reactions 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 Adverse Reaction Placebo (N =365) Fenofibrate (N = 439) Abnormal Liver Tests 1% 8% Abdominal Pain 4% 5% Increased ALT 2% 3% Increased AST 1% 3% Increased Creatine Phosphokinase 1% 3% Constipation 1% 2% Rhinitis 1% 2% Other Adverse Reactions Urticaria 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. Increases in Liver Enzymes In a pooled analysis of three 12-week, double-blind, controlled studies of fenofibric acid, increases in ALT and AST > 3 times the upper limit of normal on two consecutive occasions occurred in 1.9% and 0.2%, respectively, of patients receiving fenofibric acid 135 mg daily and placebo, without other lipid-altering drugs. In a pooled analysis of 10 placebo-controlled trials, increases to > 3 times the upper limit of normal in ALT occurred in 5.3% of patients taking either an intermediate or maximum recommended daily dosage of fenofibrate versus 1.1% of patients treated with placebo. In an 8-week trial, the incidence of ALT or AST elevations ≥ 3 times the upper limit of normal was 13% in patients receiving an intermediate daily dosage or the maximum recommended daily dosage of fenofibrate and was 0% in those receiving the lowest recommended daily dosage of fenofibrate or placebo [see Warnings and Precautions (5.2) ] . Clinical trials with fenofibric acid did not include a placebo-control arm. However, the adverse reaction profile of fenofibric acid was generally consistent with that of fenofibrate. The following adverse reactions not listed above for fenofibrate were reported in ≥ 3% of patients taking fenofibric acid: Gastrointestinal: Diarrhea, dyspepsia General: Pain Infections : Nasopharyngitis, sinusitis, upper respiratory tract infection Musculoskeletal and Connective Tissue : Arthralgia, myalgia, pain in extremity Nervous System : Dizziness 6.2 Postmarketing Experience The following adverse reactions have been identified during post-approval 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. Blood: Anemia Gastrointestinal: Pancreatitis General: Asthenia Hepatobiliary: Increased total bilirubin, hepatitis, cirrhosis Immune System: Anaphylaxis, angioedema Lipid Disorders: Severely depressed HDL-cholesterol levels Musculoskeletal: Muscle spasms, rhabdomyolysis Renal and Urinary: Acute renal failure Respiratory: Interstitial lung disease Skin and Subcutaneous Tissue: Photosensitivity reactions days to months after initiation. This may occur in patients who report a prior photosensitivity reaction to ketoprofen.

Drug interactions

Table 2 presents clinically important drug interactions with fenofibric acid. Table 2. Clinically Important Drug Interactions with fenofibric acid Statins Clinical Impact: Fibrates may cause myopathy when given alone. The risk of myopathy and rhabdomyolysis is increased with concomitant use of fibrates with statins. Intervention: Consider if the benefit of using fenofibric acid concomitantly with statin therapy outweighs the increased risk of myopathy and rhabdomyolysis. If concomitant use is decided, monitor patients for signs and symptoms of myopathy, particularly during initiation of therapy and during upward dosage titration of statin therapy. Colchicine Clinical Impact: Cases of myopathy and rhabdomyolysis have been reported with concomitant use of colchicine with fenofibrates. Intervention: Consider if the benefit of using colchicine concomitantly with fenofibric acid outweighs the increased risk of myopathy and rhabdomyolysis. If concomitant use is decided, monitor patients for signs and symptoms of myopathy, particularly during initiation of therapy and during upward dosage titration of colchicine. Coumarin Anticoagulants Clinical Impact: Fibrates may cause potentiation of coumarin-type anticoagulant effects with prolongation of the PT/INR. Intervention: Caution should be exercised when coumarin anticoagulants are given in conjunction with fenofibric acid. 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 Immunosuppressants Clinical Impact: 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 fenofibric acid, there is a risk that an interaction will lead to deterioration of renal function. Intervention: The benefits and risks of using fenofibric acid with immunosuppressants and other potentially nephrotoxic agents should be carefully considered, and the lowest effective dosage employed and renal function monitored. Bile-Acid Binding Resins Clinical Impact: Bile-acid binding resins may bind other drugs given concurrently. Intervention: In patients taking a bile acid resin, administer fenofibric acid at least 1 hour before or 4 to 6 hours after the bile acid resin to avoid impeding its absorption. Consider if the benefit of concomitant use of statins or colchicine outweighs the increased risk of myopathy and rhabdomyolysis. Monitor patients for signs and symptoms of myopathy (7) . Exercise caution in concomitant treatment with coumarin anticoagulants. Reduce the dosage of coumarin to maintain the PT/INR at the desired level to prevent bleeding complications (7) . Consider the benefits and risks of concomitant use with immunosuppressants and other potentially nephrotoxic agents. Use the lowest effective dosage and monitor renal function (7) . Administer fenofibric acid at least 1 hour before or 4 to 6 hours after a bile acid resin to avoid impeding its absorption (7) .

Use in specific populations

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 comparable to the maximum recommended clinical dosage of 135 mg of fenofibric acid daily, based on body surface area (mg/m 2 ). Adverse reproductive outcomes occurred at higher doses in the presence of maternal toxicity (see Data). Fenofibric acid 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 mg/kg/day, 127 mg/kg/day, 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, comparable to 135 mg fenofibric acid 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 mg/kg/day, 150 mg/kg/day, and 300 mg/kg/day from gestation day 6 to 18 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 mg/kg/day, 75 mg/kg/day, 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 fenofibric acid and for 5 days after the final dose. 8.4 Pediatric Use The safety and effectiveness of fenofibric acid have not been established in pediatric patients with severe hypertriglyceridemia or primary hyperlipidemia. 8.5 Geriatric Use Assess renal function in geriatric patients and follow contraindications and dosing recommendations for patients with renal impairment [see Contraindications (4) , Warnings and Precautions (5.3 , 5.4) , and Use in Specific Populations (8.6) ] . While fenofibric acid exposure is not influenced by age, geriatric patients are more likely to have renal impairment, and fenofibric acid is substantially excreted by the kidney [see Clinical Pharmacology (12.3) ] . Consider monitoring renal function in geriatric patients taking fenofibric acid. 8.6 Renal Impairment Fenofibric acid are contraindicated in patients with severe renal impairment (eGFR <30 mL/min/1.73m 2 ), including those with end-stage renal disease (ESRD) and those receiving dialysis. Dosage reduction is required in patients with mild to moderate renal impairment [see Dosage and Administration (2.4) and Clinical Pharmacology (12.3) ] . Patients with severe renal impairment have 2.7-fold higher exposure of fenofibric acid and increased accumulation of fenofibric acid during chronic dosing compared with healthy volunteers. Renal impairment is a risk factor for myopathy and rhabdomyolysis [see Warnings and Precautions (5.3, 5.4) and Clinical Pharmacology (12.3 )]. 8.7 Hepatic Impairment The use of fenofibric acid has not been evaluated in patients with hepatic impairment. Fenofibric acid are contraindicated in patients with active liver disease, including those with unexplained persistent liver function abnormalities [see Clinical Pharmacology (12.3) ].

Overdosage

In the event of an overdose of fenofibric acid, consider contacting the Poison Help line (1-800-222-1222) or a medical toxicologist for additional overdosage management recommendations. There is no specific treatment for overdose with fenofibric acid. 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.

Description

Fenofibric acid delayed-release capsules are peroxisome proliferator-activated receptor (PPAR) alpha agonist available as delayed release capsules for oral administration. Each delayed release capsule contains choline fenofibrate, equivalent to 45 mg or 135 mg of fenofibric acid. The chemical name for choline fenofibrate is ethanaminium, 2-hydroxy-N,N,N-trimethyl, 2-{4-(4-chlorobenzoyl) phenoxy]-2-methylpropanoate (1:1) with the following structural formula: The molecular formula is C 22 H 28 ClNO 5 and the molecular weight is 421.9. Choline fenofibrate is very soluble in water and freely soluble in methanol. The melting point is approximately 210°C. Choline fenofibrate is a white to off-white crystalline powder. Each delayed release capsule contains enteric coated mini-tablets comprised of choline fenofibrate and the following inactive ingredients: Colloidal silicon dioxide, hydroxypropyl cellulose, hypromellose 2208, methacrylic acid and ethyl acrylate copolymer dispersion (sodium lauryl sulfate, polysorbate 80 and methacrylic acid and ethyl acrylate copolymer), povidone, sodium stearyl fumarate, talc and triethyl citrate. Capsule shell contains: gelatin, iron oxide black, iron oxide yellow, sodium lauryl sulfate and titanium dioxide. Additionally, 45 mg contains: iron oxide red. 135 mg contains: FD & C blue 1, FD & C red 3, FD & C red 40. The imprinting ink contains: black iron oxide, potassium hydroxide, propylene glycol, shellac and strong ammonia solution. Image

How supplied

Fenofibric acid delayed-release capsules 45 mg are the Size ‘3’ Hard gelatin capsules of opaque reddish brown color cap imprinted with ‘167’ in black ink, opaque yellow color body imprinted with ‘167’ in black ink and filled with white to off white round, biconvex coated mini tablets. Bottle of 90 capsules with child-resistant closure, NDC 69315-281-09 Fenofibric acid delayed-release capsules 135 mg are the Size ‘0’ Hard gelatin capsules of opaque blue color cap imprinted with ‘168’ in black ink, opaque yellow color body, imprinted with ‘168’ in black ink and filled with white to off white round, biconvex, coated mini tablets. Bottle of 90 capsules with child-resistant closure, NDC 69315-282-09 Store at 20º to 25ºC (68º to 77ºF); excursions permitted to 15° to 30°C (59° to 86°F) [See USP Controlled Room Temperature]. Keep out of the reach of children. Protect from moisture.

Patient information

Hepatotoxicity Inform patients that fenofibric acid delayed-release capsules may cause liver enzyme elevations and possibly liver failure. Advise patients to promptly report fatigue, anorexia, right upper abdominal discomfort, dark urine or jaundice [see Contraindications (4) and Warnings and Precautions (5.2) ]. Myopathy and Rhabdomyolysis Advise patients that fenofibric acid delayed-release capsules may cause myopathy and rhabdomyolysis. Inform patients that the risk is also increased when taking certain types of medication and they should discuss all medication, both prescription and over the counter, with their healthcare provider. Instruct patients to inform other healthcare providers prescribing a new medication or increasing the dosage of an existing medication that they are taking fenofibric acid delayed-release capsules. Instruct patients to promptly report any unexplained muscle pain, tenderness, or weakness particularly if accompanied by malaise or fever [see Warnings and Precautions (5.3) and Drug Interactions (7) ]. Increased Bleeding Risk with Coumarin Anticoagulants Inform patients that the concomitant use of fenofibric acid delayed-release capsules with coumarin-type anticoagulants may increase the risk of bleeding. Advise patients if they are taking or planning to take coumarin-type anticoagulants to inform their healthcare providers and that increased monitoring may be necessary [see Warnings and Precautions (5.6) and Drug Interactions (7) ] . Hypersensitivity Reactions Inform patients that serious hypersensitivity reactions, such as anaphylaxis and angioedema, have been reported with fenofibrates. Advise patients to report immediately any signs or symptoms suggesting allergic reaction, and to discontinue drug until they have consulted prescribing physicians [see Warnings and Precautions (5.9) ] . Pregnancy Advise patients to inform their healthcare provider of a known or suspected pregnancy to discuss if fenofibric acid delayed-release capsules should be discontinued [see Use in Specific Populations (8.1) ] . Lactation Advise patients that breastfeeding during treatment with fenofibric acid delayed-release capsules is not recommended [see Use in Specific Populations (8.2) ]. Missed Doses If a dose is missed, advise patients to not take an extra dose and to resume treatment with the next dose. The brand names listed are trademarks of their respective owners and are not trademark of the Graviti Pharmaceuticals Private Limited. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088. For more information call Leading Pharma, LLC at 1-844-740-7500 Manufactured by: Graviti Pharmaceuticals Pvt. Ltd. Telangana-502307, INDIA. Manufactured for: Leading Pharma, LLC Fairfield, NJ 07004, USA Revised : 07/2025

Label text from the FDA structured product label by Leading Pharma, LLC (revised Aug 22, 2025). Long sections are shortened; the complete label is on DailyMed.

Active ingredients

Fenofibric Acid in 10 products
Choline Fenofibrate in 4 products

Fenofibric acid NDC products (14)

NDC	Strength & form	Labeler	Type
62332-244	Fenofibric Acid 45 mg/1 Capsule, Delayed Release	Alembic Pharmaceuticals Inc.	ANDA
62332-245	Fenofibric Acid 135 mg/1 Capsule, Delayed Release	Alembic Pharmaceuticals Inc.	ANDA
46708-244	Fenofibric Acid 45 mg/1 Capsule, Delayed Release	Alembic Pharmaceuticals Limited	ANDA
46708-245	Fenofibric Acid 135 mg/1 Capsule, Delayed Release	Alembic Pharmaceuticals Limited	ANDA
0115-1324	Fenofibric Acid 45 mg/1 Capsule, Delayed Release	Amneal Pharmaceuticals of New York LLC	ANDA
0115-1325	Fenofibric Acid 135 mg/1 Capsule, Delayed Release	Amneal Pharmaceuticals of New York LLC	ANDA
59651-216	Fenofibric Acid 45 mg/1 Capsule, Delayed Release	Aurobindo Pharma Limited	ANDA
59651-217	Fenofibric Acid 135 mg/1 Capsule, Delayed Release	Aurobindo Pharma Limited	ANDA
69315-281	Fenofibric Acid 45 mg/1 Capsule, Delayed Release	Leading Pharma, LLC	ANDA
69315-282	Fenofibric Acid 135 mg/1 Capsule, Delayed Release	Leading Pharma, LLC	ANDA
68180-128	Choline Fenofibrate 45 mg/1 Capsule, Delayed Release	Lupin Pharmaceuticals, Inc.	ANDA
68180-129	Choline Fenofibrate 135 mg/1 Capsule, Delayed Release	Lupin Pharmaceuticals, Inc.	ANDA
33342-294	Choline Fenofibrate 45 mg/1 Capsule, Delayed Release	Macleods Pharmaceuticals Limited	ANDA
33342-295	Choline Fenofibrate 135 mg/1 Capsule, Delayed Release	Macleods Pharmaceuticals Limited	ANDA

Frequently asked questions

What is Fenofibric acid used for?

What are the side effects of Fenofibric acid?

Who makes Fenofibric acid?

Fenofibric acid is listed by 7 labelers in the FDA NDC directory, including Alembic Pharmaceuticals Inc., Alembic Pharmaceuticals Limited, Amneal Pharmaceuticals of New York LLC, Aurobindo Pharma Limited.