Fenofibrate 130 mg Capsule, 30-count
Other active recalls for Fenofibrate (different manufacturers) — 2 · tap to view
🆔 Identity & classification
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🏷️ RxNorm drug class
This medicine belongs to the Peroxisome Proliferator-activated Receptor alpha Agonist class.
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🏭 Manufacturer & labeler
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🩺 Clinical
Fenofibrate is used to reduce the amount of cholesterol (a fat-like substance that can build up in blood vessels leading to heart attack or strokes or other medical conditions) and triglycerides (other fatty substances) in the blood. Fenofibrate is in a class of medications called fibrates. It works by speeding the natural processes that remove cholesterol from the body.
Read the full MedlinePlus article ↗- Fenofibrate helps bring your blood lipid levels into a healthier range. Depending on your situation, that might mean lowering your triglycerides, bringing down your LDL (bad) chole...
- What exactly is fenofibrate supposed to do for me?
- It depends on which form you have. Lipofen capsules should be taken with food. Antara capsules and most fenofibrate tablets can be taken with or without food. Some film-coated feno...
- Does it matter if I take this with food or on an empty stomach?
Patient education
Supplement & herbal interactions
Some supplements/herbs that may interact with Fenofibrate — tap one for details:
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🧪 Inactive Ingredients / Excipients
Inactive ingredients, also called excipients, are components of the drug product other than the active ingredient. They may include fillers, dyes, coatings, preservatives, flavors, or other formulation ingredients.
💡 Tap an ingredient (hover on desktop) to see what it is and why it’s used.
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UNII 92RU3N3Y1O
Dimethicone is a silicone-based oil that acts as an anti-foaming agent and lubricant in medicines. It reduces gas bubbles in liquid formulations and helps coat and protect the stomach lining when ingested.
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A dark iron oxide compound that gives medicines their black or dark color. It's used as a colorant in tablets and capsules to help identify the product and make it visually distinctive.
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Gelatin is a protein derived from animal collagen, commonly used in medicines as a gelling agent and capsule material. It helps create soft or hard capsule shells that hold and release medication, and can also thicken liquid formulations.
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Hypromellose is a plant-based thickener made from cellulose. It's used in medicines as a binder to hold ingredients together, a coating for tablets, and a thickener for liquids.
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Methylcellulose is a thickening and binding ingredient made from cellulose, a plant fiber. It helps control how fast the medicine dissolves and gives tablets or capsules the right texture and consistency.
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Polysorbate 65 is a synthetic emulsifier derived from sorbitol and fatty acids. It helps mix oil and water in medications, keeping ingredients evenly distributed throughout the product.
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Potassium hydroxide is a strong alkaline chemical used in medicines to adjust and maintain the pH level of liquid formulations, helping keep the product stable and the active ingredients effective.
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Propylene glycol is a clear liquid derived from petroleum or vegetable sources. It acts as a solvent, humectant, and preservative in medicines, helping dissolve active ingredients and maintain product stability.
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Shellac is a natural resin secreted by the lac beetle. It's used as a coating on tablets and capsules to control how quickly the medicine dissolves and to improve appearance and stability.
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Silicon dioxide is a naturally occurring mineral used as a glidant and anti-caking agent. It helps powder ingredients flow smoothly and prevents clumping during manufacturing and storage.
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A detergent and foaming agent derived from coconut or palm oil. In medications, it helps break down and mix oil and water-based ingredients, aids in tablet disintegration, and improves how the drug dissolves and spreads in the mouth or digestive system.
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UNII 7CV7WJK4UI
Sodium stearyl fumarate is a synthetic compound made from stearyl alcohol and fumaric acid. It acts as a lubricant and glidant in tablets and capsules, helping ingredients flow smoothly during manufacturing and preventing sticking.
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UNII O8232NY3SJ
A plant-based carbohydrate derived from corn kernels. It acts as a filler to add bulk, a binder to hold ingredients together, and a disintegrant to help the tablet break apart in your stomach for absorption.
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UNII 7SEV7J4R1U
A powder made from a naturally occurring mineral. In medicines, talc works as a glidant and anti-caking agent, helping tablets and capsules flow smoothly during manufacturing and preventing clumping.
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UNII 15FIX9V2JP
Titanium dioxide is a bright white mineral powder commonly used as a colorant and opacifying agent. It makes pills and tablets white or lighter in color and helps make coatings non-transparent.
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UNII 059QF0KO0R
Water is a liquid solvent that dissolves and mixes ingredients together in liquid medicines, syrups, and injections. It helps distribute the active drug evenly throughout the product.
16 inactive ingredients listed in the exact product block matched to this NDC.
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ingredient classCode="IACT" elements from the exact product block matched by this NDC. Label-section narrative from DailyMed / the openFDA label index is shown separately when available.Inactive ingredient FAQ
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💲 Pricing
A drug doesn't have one price. Each row is a different public payment system, and none is what you'd pay at the counter — that depends on your insurance. The ⓘ on each row explains what it measures.
| Price system | Per ea | Per package |
|---|---|---|
| Retail pharmacies payNADAC · weekly | $0.680 | $20.39 / 30 capsules |
| Medicaid paysCMS SDUD · 12 mo | No recent Medicaid claims on file for this NDC — rare and low-volume NDCs are suppressed in the public data. | |
| Medicare drug plans payPart D · quarterly | No Part D plan price is available for this NDC in our data. | |
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🔁 Therapeutic equivalents
| Product | Labeler | Pack | NADAC/unit | TE | Status | Price vs. this |
|---|---|---|---|---|---|---|
| Fenofibrate 130 mgthis 63304-0444-30 | Sun | 30 capsules | $0.680 | — | Discontinued | — |
| Fenofibrate 130 mg 68180-0131-06 | Lupin | 30 capsules | $0.680 | AB | Availability likely | — |
| Antara 130 mg 27437-0110-01 | Lupin | 100 capsules | — | AB | Discontinued | — |
| Fenofibrate 130 mg 55111-0395-01 | Dr. | 100 capsules | — | AB | FDA listed | — |
| Fenofibrate 130 mg 60505-3121-01 | Apotex | 100 capsules | — | AB | FDA listed | — |
| Fenofibrate 130 mg 72789-0310-30 | PD-Rx | 30 capsules | — | — | FDA listed | — |
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⏳ Availability & generic status
This product is an FDA-approved generic. Other versions of the same drug are listed under Therapeutic equivalents, least expensive first.
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💊 Medicaid utilization by pack size
📊 Medicare Part D spend CMS · PART D · 2026 (Q1)
🔬 Reported adverse events (FAERS)
Top reported reactions
Age at onset
Reporter sex
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📦 Packaging — all sizes for this product
| Package NDC | Description | Per unit | Per pack | Marketing start | Status |
|---|---|---|---|---|---|
| 63304-0444-05 | 500 CAPSULE in 1 BOTTLE (63304-444-05) | — | — | 2015-03-02 | Active |
| 63304-0444-30 You're viewing this | 30 CAPSULE in 1 BOTTLE (63304-444-30) | $0.6795 / ea | $20.39 | 2015-03-02 | Discontinued by firm |
| 63304-0444-90 | 90 CAPSULE in 1 BOTTLE (63304-444-90) | $0.6795 / ea | $61.16 | 2015-03-02 | Discontinued by firm |
You're viewing the smallest of 3 pack sizes for this product.
This pack has the lowest per-ea cost of the 2 priced pack sizes ($0.6795 NADAC).
Pack size FAQ
What quantity is in NDC 63304-0444-30?
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Prices are the latest CMS NADAC pharmacy acquisition cost per NDC; per-pack figures are per-unit × pack quantity, shown only when the pack is denominated in the same measure NADAC prices.
🧭 About this NDC listing & data coverage
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| NDC identity (package / product / labeler codes) | ✓ Available |
| Labeler | ✓ Available |
| Product & package description | ✓ Available |
| Marketing category & status | ✓ Available |
| Active ingredient / dosage form / route | ✓ Available |
| FDA label (SPL via DailyMed) | ✓ Available |
| Package photos | ✓ Available |
| Inactive ingredients (structured) | ✓ Available |
| NADAC pharmacy acquisition price (CMS) | ✓ Available |
| Orange Book / therapeutic-equivalence data | — Not published for this NDC Applies only to products approved under an NDA/ANDA; many listings are out of scope. |
| HCPCS J-code billing crosswalk | — Not published for this NDC Most self-administered / retail products have no J-code — that is normal. |
| Medicaid utilization (CMS SDUD) | — Not published for this NDC CMS reports utilization only for NDCs with Medicaid claims above its privacy threshold. |
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📄 Full prescribing information FDA SPL
🎯 Indications and Usage ▾
1 INDICATIONS AND USAGE Fenofibrate capsules, USP are peroxisome proliferator-activated receptor (PPAR) alpha agonist indicated as an 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). Fenofibrate 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)] .
⏱️ Dosage and Administration ▾
2 DOSAGE AND ADMINISTRATION Severe hypertriglyceridemia : 43 mg to 130 mg orally once daily; the dosage should be adjusted according to patient response (2.2). Primary hyperlipidemia : 130 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 fenofibrate capsules. Discontinue fenofibrate capsules in patients who do not have an adequate response after 2 months of treatment (2.2). Renal impairment : Initial dosage of 43 mg orally once daily (2.3).
Geriatric patients : Select the dosage on the basis of renal function (2.4).
2.1Prior to Initiation of Fenofibrate 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 fenofibrate capsules and should continue this diet during treatment with fenofibrate capsules. • In patients with diabetes and fasting chylomicronemia, improve glycemic control prior to considering starting fenofibrate capsules.
2.2Recommended Dosage and Administration • Severe hypertriglyceridemia: o The recommended dosage of fenofibrate capsules is 43 mg or 130 mg orally once daily. o 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: o The recommended dosage of fenofibrate capsule is 130 mg orally once daily. • Administer fenofibrate capsules as a single dose at any time of day, with or without food. • Advise patients to swallow fenofibrate capsules whole.
Do not crush, break, dissolve, or chew capsules. • Assess TG when clinically appropriate, as early as 4 to 8 weeks after initiating fenofibrate capsules. Discontinue fenofibrate capsules in patients who do not have an adequate response after 2 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 fenofibrate capsules at least 1 hour before or 4 hours to 6 hours after a bile acid binding resin to avoid impeding its absorption.
2.3Recommended Dosage in Patients with Renal Impairment Assess renal function prior to initiation of fenofibrate capsules and periodically thereafter [see Warnings and Precautions (5.4)] . Treatment with fenofibrate capsules should be initiated at a dosage of 43 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. Fenofibrate 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)] .
2.4Recommended 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 ▾
3 DOSAGE FORMS AND STRENGTHS Fenofibrate capsules, 43 mg are white to off-white granular powder filled in size ‘4’ white opaque cap and white opaque body hard gelatin capsule imprinted with ‘ RG78 ’ on cap and body in black ink. Fenofibrate capsules, 130 mg are white to off-white granular powder filled in size ‘0’ white opaque cap and white opaque body hard gelatin capsule imprinted with ‘ RG79 ’ on cap and body in black ink. • Capsules: 43 mg and 130 mg (3)
⛔ Contraindications ▾
4 CONTRAINDICATIONS Fenofibrate is 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 fenofibrate, fenofibric acid, or any of the excipients in fenofibrate 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 fenofibrate fenofibric acid, or any of the excipients in fenofibrate capsules (4)
⚠️ Warnings and Cautions ▾
5 WARNINGS AND PRECAUTIONS Hepatotoxicity: Serious drug-induced liver injury, including liver transplantation and death, has been reported with fenofibrates including fenofibrate capsules. 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 hypothyroidism. Discontinue fenofibrate capsules if markedly elevated CK levels occur or if myopathy is either diagnosed or suspected.
Temporarily discontinue fenofibrate capsules 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 fenofibrate 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 fenofibrate capsules. 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 fenofibrate and treat appropriately if reactions occur (5.9).
5.1Mortality 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 fenofibrate, pemafibrate; clofibrate; and gemfibrozil; the findings in 5 large randomized, placebo-controlled clinical trials with these other fibrate drugs may also apply to fenofibrate.
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 middleaged 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…
🤒 Adverse Reactions ▾
6 ADVERSE REACTIONS 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 Sun Pharmaceutical Industries, Inc. at 1-800-818-4555 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch .
6.1Clinical 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 fenofibrate 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 fenofibrate 90 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 below. 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 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 the 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)] .
6.2Postmarketing 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, white blood cell decreases Gastrointestinal: Pancreatitis General: Asthenia Hepatobiliary: Increased total bilirubin, hepatitis, cirrhosis Immune System: Anaphylaxis, angioedema Lipid Disorder…
🔄 Drug Interactions ▾
7 DRUG INTERACTIONS 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 fenofibrate capsules at least 1 hour before or 4 to 6 hours after a bile acid resin to avoid impeding its absorption (7). Table 2. presents clinically important drug interactions with fenofibrate. Table 2.
Clinically Important Drug Interactions with Fenofibrate 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 fenofibrate 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 fenofibrate 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 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 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 fenofibrate, there is a risk that an interaction will lead to deterioration of renal function.
Intervention: The benefits and risks of using fenofibrate 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 fenofibrate at least 1 hour before or 4 to 6 hours after the bile acid resin to avoid impeding its absorption.
👥 Use in Specific Populations ▾
8 USE IN SPECIFIC POPULATIONS
8.1Pregnancy 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 130 mg of fenofibrate 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 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 130 mg fenofibrate 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.
8.2Lactation 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 and for 5 days after the final dose.
8.4Pediatric Use The safety and effectiveness of fenofibrate have not been established in pediatric patients with severe hypertriglyceridemia or primary hyperlipidemia.
8.5Geriatric 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 subs…
🤰 Pregnancy ▾
8.1Pregnancy 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 130 mg of fenofibrate 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 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 130 mg fenofibrate 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.
🆘 Overdosage ▾
10 OVERDOSAGE In the event of an overdose of fenofibrate, consider contacting the Poison Help line (1-800-2221222) or a medical toxicologist for additional overdosage management recommendations. 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.
🧬 Clinical Pharmacology ▾
12 CLINICAL PHARMACOLOGY
12.1Mechanism of Action The active moiety of fenofibrate is fenofibric acid. The pharmacological effects of fenofibric acid in both animals and humans have been studied through oral administration of fenofibrate. The lipid-modifying effects of fenofibric acid seen in clinical practice have been explained in vivo in transgenic mice and in vitro in human hepatocyte cultures by the activation of PPAR alpha receptor.
Through this mechanism, fenofibric acid increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III (an inhibitor of lipoprotein lipase activity).
12.2Pharmacodynamics Fenofibric acid, the active metabolite of fenofibrate, produces reductions in total cholesterol (Total-C), total triglycerides, and triglyceride-rich lipoprotein (VLDL) in treated patients with severe hypertriglyceridemia.
12.3Pharmacokinetics Fenofibrate is a pro-drug of the active chemical moiety fenofibric acid. Fenofibrate is converted by ester hydrolysis in the body to fenofibric acid which is the active constituent measurable in the circulation. Absorption The absolute bioavailability of fenofibrate cannot be determined as the compound is virtually insoluble in aqueous media suitable for injection.
Fenofibrate is insoluble in water and its bioavailability is optimized when taken with meals. However, after fenofibrate is dissolved, fenofibrate is well absorbed from the gastrointestinal tract. Peak plasma levels of fenofibric acid from fenofibrate occur within 4 to 8 hours after administration.
There was less than dose-proportional increase in the systemic exposure of fenofibric acid from 43 mg and 130 mg of fenofibrate under fasting conditions. Doses of three-capsules of 43 mg fenofibrate given concurrently were dose equivalent to single-capsule doses of 130 mg. Effect of Food The extent of absorption of fenofibric acid was unaffected when fenofibrate was taken either in fasted state or with a low-fat meal.
However, the C max of fenofibrate increased in the presence of a low-fat meal. T max was unaffected in the presence of a low-fat meal. In the presence of a high-fat meal, there was a 26% increase in AUC and 108% increase in C max of fenofibric acid from fenofibrate relative to fasting state.
Distribution In healthy volunteers, steady-state plasma levels of fenofibric acid were shown to be achieved within a week of dosing and did not demonstrate accumulation across time following multiple dose administration. Serum protein binding was approximately 99% in normal and hyperlipidemic subjects. Elimination Fenofibric acid is eliminated with a half-life of 23 hours, allowing once daily administration of fenofibrate Metabolism Following oral administration, fenofibrate is rapidly hydrolyzed by esterases to the active metabolite, fenofibric acid; no unchanged fenofibrate is detected in plasma.
Fenofibric acid is primarily conjugated with glucuronic acid and then excreted in urine. A small amount of fenofibric acid is reduced at the carbonyl moiety to a benzhydrol metabolite which is, in turn, conjugated with glucuronic acid and excreted in urine. In vivo metabolism data indicate that neither fenofibrate nor fenofibric acid undergo oxidative metabolism (e.g., cytochrome P450) to a significant extent.
Excretion After absorption, fenofibrate is mainly excreted in the urine in the form of metabolites, primarily fenofibric acid and fenofibric acid glucuronide. After administration of radio-labeled fenofibrate, approximately 60% of the dose appeared in the urine and 25% was excreted in the feces. Specific Populations Geriatric Patients In geriatric volunteers 77 to 87 years of age, the apparent oral clearance of fenofibric acid following a single oral dose of fenofibrate was
1.2 L/h, which compares to
1.1L/h in young adults. This indicates that a similar dosage regimen can be used in geriatric patients with normal renal function, withou…
🧬 Mechanism of Action ▾
12.1Mechanism of Action The active moiety of fenofibrate is fenofibric acid. The pharmacological effects of fenofibric acid in both animals and humans have been studied through oral administration of fenofibrate. The lipid-modifying effects of fenofibric acid seen in clinical practice have been explained in vivo in transgenic mice and in vitro in human hepatocyte cultures by the activation of PPAR alpha receptor.
Through this mechanism, fenofibric acid increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III (an inhibitor of lipoprotein lipase activity).
📦 How Supplied / Storage and Handling ▾
16 HOW SUPPLIED/STORAGE AND HANDLING Fenofibrate capsules, USP are supplied as follows: Strength Description NDC Package Size (capsules per bottle) 43 mg white to off-white granular powder filled in size ‘4’ white opaque cap and white opaque body hard gelatin capsule imprinted with ‘ RG78 ’ on cap and body in black ink NDC 63304-443-30 30 NDC 63304-443-05 500 130 mg white to off-white granular powder filled in size ‘0’ white opaque cap and white opaque body hard gelatin capsule imprinted with ‘ RG79 ’ on cap and body in black ink NDC 63304-444-30 30 NDC 63304-444-90 90 NDC 63304-444-05 500 Storage Store at 20º - 25º C (68º - 77º F) [See USP Controlled Room Temperature] in a tightly closed container.
📋 Description ▾
11 DESCRIPTION Fenofibrate capsules, USP, is a peroxisome proliferator-activated receptor (PPAR) alpha agonist available as capsules for oral administration. Each capsule contains 43 mg or 130 mg of micronized fenofibrate, USP. The chemical name for fenofibrate is 2-[4-(4-chlorobenzoyl) phenoxy]-2-methyl-propanoic acid, l-methylethyl ester with the following structural formula: The molecular formula is C 20 H 21 O 4 Cl and the molecular weight is 360.83; fenofibrate (micronized), USP is practically insoluble in water, very soluble in methylene chloride, slightly soluble in alcohol.
The melting point is 79° to 82° C. Fenofibrate (micronized), USP is a white or almost white crystalline powder. Inactive Ingredients: Each gelatin capsule contains hypromellose, pregelatinized starch (maize), simethicone emulsion, sodium lauryl sulfate, sodium stearyl fumarate and talc.
The gelatin capsules also contain gelatin and titanium dioxide. The imprinting ink contains ferric oxide black, potassium hydroxide, propylene glycol, and shellac. Meets USP Dissolution Test 2.
Structure
💬 Information for Patients ▾
17 PATIENT COUNSELING INFORMATION Hepatotoxicity Inform patients that fenofibrate 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 fenofibrate 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 fenofibrate 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 Antara® 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 fenofibrate capsules should be discontinued [see Use in Specific Populations (8.1)] . Lactation Advise patients that breastfeeding during treatment with fenofibrate capsules are 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. Manufactured by: Ohm Laboratories Inc. New Brunswick, NJ 08901 Distributed by: Sun Pharmaceutical Industries, Inc.
Cranbury, NJ 08512 October 2025 FDA-11 Trademarks are property of their respective owners.