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Fenofibrate 160 mg Tablet, 30-count — NDC 0904-7539-04 (Billing 00904-7539-04)

by Major Pharmaceuticals · 30 BLISTER PACK in 1 CARTON / 1 TABLET in 1 BLISTER PACK

This is a package of 30 tablets of Fenofibrate 160 mg Tablet from Major Pharmaceuticals, marketed since May 2025 and currently FDA-listed; retail pharmacies pay about $0.1033 per tablet (NADAC). It is this product's only package size.

NDC 00904-7539-04
🏷️ FDA NDC (as labeled) 0904-7539-04 billing pads the labeler segment with a zero
Rx only Generic On market Non-controlled ⇄ Compare with another NDC
🗂️ FDA directory synced Oct 1, 2026 · this listing last changed Jul 24, 2026 · sources: openFDA · FDA label (DailyMed) · FDA Orange & Purple Book · First Databank · CMS NADAC, ASP, Medicare & Medicaid · RxNorm
📋 All sources & update times →

This page is curated, coded, and maintained by

Compiled from public FDA, CMS, DailyMed, NADAC, and related drug data sources. Editorial policy

⚠️
Other active recalls for Fenofibrate (different manufacturers) — 2 · tap to view
These affect other manufacturers’ products for the same ingredient — not necessarily the exact NDC on this page.
Class II · May 28, 2026 — CGMP Deviations (Ajanta Pharma USA Inc) · FDA recall D-0611-2026
Class II · Mar 13, 2025 — CGMP Deviations (Glenmark Pharmaceuticals Inc., USA) · FDA recall D-0314-2025
Each entry is an official FDA enforcement report — look up any recall number in the FDA recall database ↗

Identity & classification

Regulatory identifiers FDA, NLM and CMS codes for this package

FDA NDC (as labeled) 0904-7539-04
Product NDC 0904-7539
11-digit billing NDC 00904753904
NCPDP billing unit EA — each (per item)
RxCUI 349287
UNII U202363UOS
Application # ANDA213864
SPL Set ID 3f4e5db8-5bfb-4b24-8465-9757cbaad2be
Established class (EPC) Peroxisome Proliferator Receptor alpha Agonist
Mechanism of action Peroxisome Proliferator-activated Receptor alpha Agonists
Chemical class Fibric Acids
DEA schedule Non-controlled
Marketing category ANDA
Marketing status On market
FDA listing status Listed (active directory)
Marketing start 2025-05-22
Route ORAL
Dosage form TABLET
Substance FENOFIBRATE
TE code (Orange Book) AB · RLD · RS

Drug-database identifiers Medi-Span GPI and First Databank GCN / HICL / AHFS classification

GPI-14 39200025000325
GCN Seq No 044915
GCN 12595
HICL code 006552
Ingredient (HICL) Fenofibrate
HIC1 code M
Therapeutic class — broad (HIC1) Blood
HIC2 code M4
Therapeutic class — intermediate (HIC2) Affect Blood Lipids/Sugar/Amino Acids
HIC3 code M4E
Therapeutic class — specific (HIC3) Lipotropics
AHFS code 24:06.06.00
AHFS class Fibric Acid Derivatives
FDB label name FENOFIBRATE 160 MG TABLET
FDB brand name Fenofibrate
Legend status F — Federal legend — prescription drug or device
Quick answers
  • GSN (GCN sequence number): 044915
  • GCN: 12595
  • GPI-14 (Medi-Span): 39200025000325
  • HICL (First Databank): 006552
  • AHFS class code: 24:06.06.00
  • RxCUI (RxNorm): 349287
Why two NDCs? The FDA registers this code as 0904-7539-04 — a 4-4-2 layout, and that's what's printed on the package and shown on DailyMed. For insurance claims, every NDC is standardized to a uniform 11-digit 5-4-2 format by adding a zero to the labeler segment → 00904-7539-04. Same drug, same package — only the format differs.
Where does this data come from?
Identifiers from the FDA openFDA NDC Directory and Structured Product Labeling; RxCUI from RxNorm (NLM); GPI from Medi-Span; GCN / HIC / AHFS / legend from First Databank.

RxNorm drug class

This medicine belongs to the Peroxisome Proliferator-activated Receptor alpha Agonist class.

Pharmacologic class Peroxisome Proliferator-activated Receptor alpha Agonist
Drug family (ATC) Fibrates
How it works Peroxisome Proliferator-activated Receptor alpha Agonists
Where does this data come from?
Therapeutic classes from RxNorm RxClass (U.S. National Library of Medicine) — Established Pharmacologic Class (FDA), ATC drug family (WHO) and mechanism of action, matched by this product’s RxCUI.

Clinical

Label name FENOFIBRATE 160 MG TABLET Ingredient Fenofibrate
📗 Our plain-language guide HelloPharmacist
  • It helps lower triglycerides, and in some products LDL cholesterol, while raising HDL in some cases. It works alongside a healthy diet, not instead of one. Which uses apply depends...
  • It depends on the product. Tricor tablets and some capsules like Antara can be taken with or without food, while Lipofen should be taken with food. Check your label or ask me, and...
  • Common ones include abdominal pain, back pain, headache, nausea, constipation and a stuffy nose. It can also raise liver enzymes, which is why you will need blood tests.
  • Call right away for muscle pain or weakness, dark urine, yellow skin or eyes, severe belly pain, or leg swelling and chest pain. Seek emergency help for facial swelling, trouble br...
📖 Read our full Fenofibrate guide →
Where does this data come from?
Plain-language summary from MedlinePlus (U.S. National Library of Medicine); supplement & herbal interactions and nutrient depletion data from the Natural Medicines database; our full guide is HelloPharmacist editorial content.

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 systemPer eaPer package
Retail pharmacies payNADAC · weekly $0.103 $3.10 / 30 tablet
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 · Q2 2026 $0.2520 $7.56 / 30 tablet
NADAC price history (per ea) — tap or hover for the price & month
Dec 2025 Mar 2026 Jun 2026 Sep 2026 $0.126 $0.089
▲ Up 16% over the last 10 months.
Where does this data come from?
NADAC (National Average Drug Acquisition Cost) is the CMS weekly pharmacy-acquisition-cost survey — what pharmacies pay. ASP (Average Sales Price) is the CMS Medicare Part B drug-payment file, published quarterly. Medicaid pays is computed by us from CMS State Drug Utilization Data (total reimbursed ÷ units, trailing 12 months) — gross of rebates and inclusive of dispensing fees, so it reflects what Medicaid paid, not an acquisition cost. Medicare drug plans pay is the median negotiated point-of-sale unit cost across plans listing this NDC in the CMS quarterly Prescription Drug Plan pricing files, before rebates. The VA pays is the federal contract price (FSS, and the statutory Big 4 ceiling where listed) from the VA National Acquisition Center pharmaceutical price file. All are free public government data; each measures a different payer, so the figures are not directly comparable.

Packaging — all sizes for this product

Package NDCDescription Marketing startMarketing endStatus
00904-7539-04 You're viewing this Main listing 30 BLISTER PACK in 1 CARTON / 1 TABLET in 1 BLISTER PACK 2025-05-22 — Active

Therapeutic equivalents

ProductLabelerPackNADAC/unitTEStatusPrice vs. this
Fenofibrate 160 mgthis 00904-7539-04 Major 30 tablets $0.103 AB Availability likely —
fenofibrate 160 mg 27241-0117-03 Ajanta 90 tablets $0.103 AB Availability likely —
Fenofibrate 160 mg 42858-0660-45 Rhodes 90 tablets $0.103 AB Availability likely —
Fenofibrate 160 mg 50268-0313-15 AvPAK 50 tablets $0.103 AB Availability likely —
Fenofibrate 160 mg 59651-0576-90 Aurobindo 90 tablets $0.103 AB Availability likely —
Fenofibrate 160 mg 60219-5522-05 Amneal 500 tablets $0.103 AB Availability likely —
Fenofibrate 160 mg 60687-0864-21 American 1 tablet $0.103 AB Availability likely —
Fenofibrate 160 mg 62135-0838-90 Chartwell 90 tablets $0.103 AB Availability likely —
Fenofibrate 160 mg 62332-0555-90 Alembic 90 tablets $0.103 AB Availability likely —
Fenofibrate 160 mg 69367-0254-05 Westminster 500 tablets $0.103 AB Discontinued —
Fenofibrate 160 mg 70756-0215-51 Lifestar 500 tablets $0.103 AB Availability likely —
Fenofibrate 160 mg 72603-0841-01 NorthStar 90 tablets $0.103 AB Availability likely —
Fenofibrate 160 mg 43598-0910-05 Dr. 500 tablets $0.108 AB FDA listed +5%
Fenofibrate 160 mg 69315-0290-05 Leading 500 tablets $0.108 AB FDA listed +5%
Fenofibrate 160 mg 42385-0936-05 Laurus 500 tablets $0.170 AB FDA listed +65%
Fenofibrate 160 mg 00115-5522-01 Amneal 100 tablets — AB FDA listed —
fenofibrate 160 mg 00615-8270-39 NCS 30 tablets — AB FDA listed —
Fenofibrate 160 mg 33342-0348-10 Macleods 90 tablets — AB FDA listed —
Fenofibrate 160 mg 35561-0344-00 Bostal 21631 tablets — AB FDA listed —
Fenofibrate 160 mg 42291-0427-50 AvKARE 500 tablets — AB FDA listed —
Fenofibrate 160 mg 46708-0351-30 Alembic 30 tablets — — FDA listed —
Fenofibrate 160 mg 46708-0555-90 Alembic 90 tablets — AB FDA listed —
Fenofibrate 160 mg 50090-5854-00 A-S 30 tablets — AB FDA listed —
Fenofibrate 160 mg 50090-6973-00 A-S 30 tablets — AB FDA listed —
Fenofibrate 160 mg 50090-6974-00 A-S 90 tablets — AB FDA listed —
Fenofibrate 160 mg 50090-7208-00 A-S 30 tablets — AB FDA listed —
Fenofibrate 160 mg 50090-7209-00 A-S 90 tablets — AB FDA listed —
Fenofibrate 160 mg 50090-7926-00 A-S 30 tablets — AB FDA listed —
Fenofibrate 160 mg 50090-7927-00 A-S 90 tablets — AB FDA listed —
Fenofibrate 160 mg 51655-0009-52 Northwind 30 tablets — AB FDA listed —
Fenofibrate 160 mg 51655-0856-52 Northwind 30 tablets — AB FDA listed —
fenofibrate 160 mg 55700-0876-30 Quality 30 tablets — AB FDA listed —
Fenofibrate 160 mg 60760-0318-30 St. 30 tablets — AB FDA listed —
Fenofibrate 160 mg 62332-0351-30 Alembic 30 tablets — — FDA listed —
Fenofibrate 160 mg 62332-0539-90 Alembic 90 tablets — AB FDA listed —
Fenofibrate 160 mg 63629-9474-01 Bryant 90 tablets — AB FDA listed —
Fenofibrate 160 mg 68071-3542-09 NuCare 90 tablets — AB FDA listed —
fenofibrate 160 mg 68071-4991-09 NuCare 90 tablets — AB FDA listed —
Fenofibrate 160 mg 68180-0232-02 Lupin 500 tablets — AB FDA listed —
Fenofibrate 160 mg 68788-7816-03 Preferred 30 tablets — AB FDA listed —
Fenofibrate 160 mg 68788-8861-03 Preferred 30 tablets — AB FDA listed —
Fenofibrate 160 mg 69238-1263-09 Amneal 90 tablets — AB FDA listed —
Fenofibrate 160 mg 70518-2907-00 REMEDYREPACK 90 tablets — AB Discontinued —
Fenofibrate 160 mg 70518-4326-00 REMEDYREPACK 90 tablets — AB FDA listed —
fenofibrate 160 mg 71205-0190-30 Proficient 30 tablets — AB FDA listed —
Fenofibrate 160 mg 71205-0949-30 Proficient 30 tablets — AB FDA listed —
Fenofibrate 160 mg 71335-0741-01 Bryant 30 tablets — AB FDA listed —
fenofibrate 160 mg 71335-1286-01 Bryant 30 tablets — AB FDA listed —
Fenofibrate 160 mg 71335-1756-01 Bryant 30 tablets — AB FDA listed —
Fenofibrate 160 mg 71335-3086-01 Bryant 30 tablets — AB FDA listed —
Fenofibrate 160 mg 72162-2170-09 Bryant 90 tablets — AB FDA listed —
Fenofibrate 160 mg 72789-0410-30 PD-Rx 30 tablets — AB FDA listed —
About this product: this is a generic version of the medicine. FDA equivalence ratings are shown when available, and other versions are listed above, least expensive first.
Where does this data come from?
Equivalents are other NDCs of the same ingredient, form and route from the openFDA NDC Directory, ranked least-expensive-first by NADAC. Therapeutic-equivalence (AB) ratings come from the FDA Orange Book; biologics use the FDA Purple Book for biosimilar & interchangeable status.

Availability & generic status

🏛️
2025
On the market since
May 2025
📍
2026
Currently FDA-listed
1 year listed
🔓
·
Generic on the market
this product is a generic
✅This is a generic drug

This product is an FDA-approved generic. Other versions of the same drug are listed under Therapeutic equivalents, least expensive first.

Where does this data come from?
Patents and exclusivity from the FDA Orange Book (small-molecule drugs), refreshed from public FDA data. Generic launch timing is an estimate, not a guarantee.

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.

Loading inactive ingredients from the official FDA label in the background. No external source is being called by this page request.
Where does this data come from?
Source: official FDA Structured Product Labeling (SPL) via DailyMed and the openFDA label index. Structured IACT rows and label-wide narrative are kept separate; availability and product-level specificity depend on the submitted label.

Inactive ingredient FAQ

Are inactive ingredients the same for every manufacturer?
No. Inactive ingredients can differ by manufacturer, dosage form, strength, and package / product version.
Why might an inactive ingredient be missing?
Some SPLs do not provide a complete structured inactive-ingredient list, and older or unusual labels may only include the information in narrative text.
Can inactive ingredients matter?
Yes. They can matter for allergies, intolerances, dyes, gluten / lactose concerns, preservatives, and formulation differences — but confirm with a pharmacist or the manufacturer when it’s clinically important.

Manufacturer & labeler

LabelerMajor Pharmaceuticals
Application holderMANKIND PHARMA LTD
FDA applicationANDA213864 (ANDA)
Labeler code00904
First marketedMay 2025
Product typeHuman Prescription Drug
Portfolio630 products on file
The labeler markets the product; the application holder owns the FDA approval. They’re often the same company but can differ (e.g. a repackager or an authorized generic). A mailing address / phone appears here when the manufacturer includes it in the product’s FDA label (not all do).
Where does this data come from?
Labeler, application holder and registered establishment from the FDA openFDA NDC Directory and Drugs@FDA; address/contact from the product’s FDA label.

Full prescribing information FDA SPL

The complete FDA label for this product — the official prescribing information, verbatim, section by section. Very long sections are excerpted here and marked; the full text is on DailyMed (linked in the sources below). Jump with a chip, search within the label, or expand everything.
🎯 Indications and Usage ⏱️ Dosage and Administration 💊 Dosage Forms and Strengths ⛔ Contraindications ⚠️ Warnings and Cautions 🤒 Adverse Reactions 🔄 Drug Interactions 👥 Use in Specific Populations 🤰 Pregnancy 🧒 Pediatric Use 🧓 Geriatric Use 🆘 Overdosage 🧬 Clinical Pharmacology 🧬 Mechanism of Action 📦 How Supplied / Storage and Handling 📋 Description 💬 Information for Patients 🧬 Pharmacokinetics 🧬 Pharmacodynamics 🔬 Clinical Studies 🧪 Nonclinical Toxicology 📄 Carcinogenesis, Mutagenesis, Impairment of Fertility 📄 Recent Major Changes 📄 Package Label / Principal Display Panel
🎯 Indications and Usage ~1 min read ▾

1 INDICATIONS AND USAGE Fenofibrate is 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 ).

1.1Primary 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.

1.2Severe 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.

1.3Important Limitations of Use Fenofibrate at a dose equivalent to 160 mg of fenofibrate tablets 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) ] .

⏱️ Dosage and Administration ~2 min read ▾

2 DOSAGE AND ADMINISTRATION • 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 ).

2.1General 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.

2.2Primary Hypercholesterolemia or Mixed Dyslipidemia The initial dose of fenofibrate tablets is 160 mg once daily.

2.3Severe 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.

2.4Impaired 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) ].

2.5Geriatric Patients Dose selection for the elderly should be made on the basis of renal function [see Use in Specific Populations (8.5) ] .

💊 Dosage Forms and Strengths 59 words ▾

3 DOSAGE FORMS AND STRENGTHS • 54 mg: Light yellow to yellow, oval shaped, film coated tablets debossed with "LS" on one side and "214" on the other side • 160 mg: White to off white, oval shaped, film coated tablets debossed with "LS" on one side and "215" on other side Oral Tablets: 54 mg and 160 mg

⛔ Contraindications 133 words ▾

4 CONTRAINDICATIONS 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 (5.2) ] • 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 ).

⚠️ Warnings and Cautions ~3 min read ▾

5 WARNINGS AND PRECAUTIONS • Hepatotoxicity : Serious drug-induced liver injury, including liver transplantation and death, has been reported with fenofibrate. 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 fenofibrate.

Risks are increased during coadministration with a statin (with a significantly higher rate observed for gemfibrozil), particularly in elderly patients and patients with diabetes, renal failure, or hypothyroidism ( 5.3 ). • Serum creatinine: Fenofibrate can reversibly increase serum creatinine levels ( 5.4 ). Monitor renal function periodically in patients with renal impairment ( 8.6 ). • Cholelithiasis: Fenofibrate increases cholesterol excretion into the bile, leading to risk of cholelithiasis. If cholelithiasis is suspected, gallbladder studies are indicated ( 5.5 ). • Coumarin anticoagulants: 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 ). • 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 patients appropriately if reactions occur ( 5.9 ).

5.1Mortality 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 0.79-1.08) (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 0.69-0.99), and the hazard ratio for MACE in women receiving combination therapy versus statin monotherapy was 1.38 (95% CI 0.98-1.94) (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 0.75-1.05, p = 0.16) and a significant 11% reduction in the secondary outcome of total cardiovascular disease events (HR 0.89 [0.80-0.99], p = 0.04).

There was a non-significant 11% (HR 1.11 [0.95, 1.29], p = 0.18) and 19% (HR 1.19 [0.90, 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… [Excerpted — this section continues on DailyMed.]

🤒 Adverse Reactions ~2 min read ▾

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) ] • Pancreatitis [see Warnings and Precautions (5.7) ] • Hypersensitivity reactions [see Warnings and Precautions (5.9) ] • Venothromboembolic disease [see Warnings and Precautions (5.10) ] Adverse reactions > 2% and at least 1% greater than placebo: Abnormal liver tests, increased AST, increased ALT, increased CPK, and rhinitis.

To report SUSPECTED ADVERSE REACTIONS, contact Lifestar Pharma LLC at 1-888-995-4337 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

6.1Clinical 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 5.0% of patients treated with fenofibrate and in 3.0% 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 Fenofibrate * Placebo Adverse Reaction (N = 439) (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 3.0% 1.6% Increased CPK 3.0% 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.

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 fenofibrate at doses equivalent to 107 mg to 160 mg fenofibrate daily versus 1.1% of patients treated with placebo. In an 8-week study, the incidence of ALT or AST elevations ≥ 3 times the upper limit of normal was 13% in patients receiving dosages equivalent to 107 mg to 160 mg fenofibrate daily and was 0% in those receiving dosages equivalent to 54 mg or less fenofibrate daily or placebo.

6.2Postmarketing 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, increased total bilirubin, 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.

🔄 Drug Interactions ~1 min read ▾

7 DRUG INTERACTIONS • Coumarin anticoagulants: ( 7.1 ). • Immunosuppressants: ( 7.2 ). • Bile acid resins: ( 7.3 ).

7.1Coumarin 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) ] .

7.2Immunosuppressants 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.

7.3Bile 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.

7.4Colchicine Cases of myopathy, including rhabdomyolysis, have been reported with fenofibrates co-administered with colchicine, and caution should be exercised when prescribing fenofibrate with colchicine.

👥 Use in Specific Populations ~3 min read ▾

8 USE 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 ).

8.1Pregnancy 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 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 2-4% and 15-20%, respectively.

Data AnimalData In pregnant rats given oral dietary doses of 14, 127, and 361 mg/kg/day from gestation day 6-15 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 6-18 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, 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.

8.2Lactation 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 tablets and for 5 days after the final dose [see Contraindications (4) ] .

8.4Pediatric Use Safety and effectiveness have not been established in pediatric patients.

8.5Geriatric 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… [Excerpted — this section continues on DailyMed.]

🤰 Pregnancy ~2 min read ▾

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 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 2-4% and 15-20%, respectively.

Data AnimalData In pregnant rats given oral dietary doses of 14, 127, and 361 mg/kg/day from gestation day 6-15 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 6-18 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, 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.

🧒 Pediatric Use 13 words ▾

8.4Pediatric Use Safety and effectiveness have not been established in pediatric patients.

🧓 Geriatric Use 95 words ▾

8.5Geriatric 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.

🆘 Overdosage 70 words ▾

10 OVERDOSAGE 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 ~3 min read ▾

12 CLINICAL PHARMACOLOGY

12.1Mechanism of Action The active moiety of fenofibrate tablets is fenofibric acid. The pharmacological effects of fenofibric acid in both animals and humans have been extensively 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 peroxisome proliferator activated receptor α (PPARα).

Through this mechanism, fenofibrate 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). The resulting decrease in TG produces an alteration in the size and composition of LDL from small, dense particles (which are thought to be atherogenic due to their susceptibility to oxidation), to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly.

Activation of PPARα also induces an increase in the synthesis of apolipoproteins A-I, A-II and HDL-cholesterol. Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.

12.2Pharmacodynamics A variety of clinical studies have demonstrated that elevated levels of total-C, LDL-C, and apo B, an LDL membrane complex, are associated with human atherosclerosis. Similarly, decreased levels of HDL-C and its transport complex, apolipoprotein A (apo AI and apo AII) are associated with the development of atherosclerosis. Epidemiologic investigations have established that cardiovascular morbidity and mortality vary directly with the level of total-C, LDL-C, and TG, and inversely with the level of HDL-C.

The independent effect of raising HDL-C or lowering triglycerides (TG) on the risk of cardiovascular morbidity and mortality has not been determined. Fenofibric acid, the active metabolite of fenofibrate, produces reductions in total cholesterol, LDL cholesterol, apolipoprotein B, total triglycerides and triglyceride rich lipoprotein (VLDL) in treated patients. In addition, treatment with fenofibrate results in increases in high-density lipoprotein (HDL) and apolipoproteins apoAI and apoAII.

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.

However, fenofibrate is well absorbed from the gastrointestinal tract. 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. Peak plasma levels of fenofibric acid occur within 6 to 8 hours after administration.

The absorption of fenofibrate is increased when administered with food. With fenofibrate tablets, the extent of absorption is increased by approximately 35% under fed as compared to fasting conditions. Distribution Upon multiple dosing of fenofibrate, fenofibric acid steady state is achieved within 5 days.

Plasma concentrations of fenofibric acid at steady state are approximately double of those following a single dose. Serum protein binding was approximately 99% in normal and hyperlipidemic subjects. 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… [Excerpted — this section continues on DailyMed.]

🧬 Mechanism of Action 182 words ▾

12.1Mechanism of Action The active moiety of fenofibrate tablets is fenofibric acid. The pharmacological effects of fenofibric acid in both animals and humans have been extensively 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 peroxisome proliferator activated receptor α (PPARα).

Through this mechanism, fenofibrate 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). The resulting decrease in TG produces an alteration in the size and composition of LDL from small, dense particles (which are thought to be atherogenic due to their susceptibility to oxidation), to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly.

Activation of PPARα also induces an increase in the synthesis of apolipoproteins A-I, A-II and HDL-cholesterol. Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.

📦 How Supplied / Storage and Handling 104 words ▾

16 HOW SUPPLIED/STORAGE AND HANDLING Fenofibrate tablets, USP are available in two strengths: 160 mg white to off white, oval shaped, film coated tablets debossed with "LS" on one side and "215" on the other side Cartons of 30 film coated tablets (10 film coated tablets each blister pack x 3), NDC 0904-7539-04 WARNING: This Unit Dose package is not child resistant and is Intended for Institutional Use Only. Keep this and all drugs out of the reach of children. Storage Store at 20°C to 25°C [68°F to 77°F] [See USP Controlled Room Temperature].

Keep out of the reach of children. Protect from moisture.

📋 Description 142 words ▾

11 DESCRIPTION Fenofibrate 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 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 is insoluble in water.

The melting point is 79-82°C. Fenofibrate, USP is a white solid which is stable under ordinary conditions. Meets USP Dissolution Test 2 Inactive Ingredients Each tablet contains colloidal silicon dioxide, crospovidone, hypromellose 2910, lactose monohydrate, lecithin, magnesium stearate, microcrystalline cellulose, polyvinyl alcohol-part hydrolyzed, sodium lauryl sulfate, talc, titanium dioxide, xanthan gum.

In addition, 54 mg individual tablets contain: D&C Yellow No. 10 Aluminium lake, FD&C Yellow No. 6 Aluminium lake, FD&C Blue No.

2 Aluminium lake Fenofibrate Structural Formula

💬 Information for Patients ~1 min read ▾

17 PATIENT COUNSELING INFORMATION 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 symptoms of liver injury (e.g., jaundice, abnormal pain, nausea, malaise, dark urine, abnormal stool, pruritus); 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. For more information, call Lifestar Pharma LLC at 1-888-995-4337. Manufactured for: Lifestar Pharma LLC 1200 MacArthur Blvd.

Mahwah, NJ 07430 USA Packaged and Distributed by: MAJOR® PHARMACEUTICALS Indianapolis, IN 46268 USA Refer to package label for Distributor's NDC Number Made in India Revised: February 2021, V-02

🧬 Pharmacokinetics ~3 min read ▾

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.

However, fenofibrate is well absorbed from the gastrointestinal tract. 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. Peak plasma levels of fenofibric acid occur within 6 to 8 hours after administration.

The absorption of fenofibrate is increased when administered with food. With fenofibrate tablets, the extent of absorption is increased by approximately 35% under fed as compared to fasting conditions. Distribution Upon multiple dosing of fenofibrate, fenofibric acid steady state is achieved within 5 days.

Plasma concentrations of fenofibric acid at steady state are approximately double of those following a single dose. Serum protein binding was approximately 99% in normal and hyperlipidemic subjects. 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.

Elimination After absorption, fenofibrate is mainly excreted in the urine in the form of metabolites, primarily fenofibric acid and fenofibric acid glucuronide. After administration of radiolabelled fenofibrate, approximately 60% of the dose appeared in the urine and 25% was excreted in the feces. Fenofibric acid is eliminated with a half-life of 20 hours, allowing once daily dosing.

Special Populations Geriatrics In elderly volunteers 77 to 87 years of age, the 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 elderly with normal renal function, without increasing accumulation of the drug or metabolites [see Dosage and Administration (2.5) and Use in Specific Populations (8.5) ] . Pediatrics The pharmacokinetics of fenofibrate has not been studied in pediatric populations.

Gender No pharmacokinetic difference between males and females has been observed for fenofibrate. 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. Renal Impairment The pharmacokinetics of fenofibric acid was examined in patients with mild, moderate, and severe renal impairment.

Patients with severe renal impairment (estimated glomerular filtration rate [eGFR] < 30 mL/min/1.73 m 2 ) showed 2.7-fold increase in exposure for fenofibric acid and increased accumulation of fenofibric acid during chronic dosing compared to that of healthy subjects. Patients with mild to moderate renal impairment (eGFR 30-59 mL/min/1.73 m 2 ) had similar exposure but an increase in the half-life for fenofibric acid compared to that of healthy subjects. Based on these findings, the use of fenofibrate should be avoided in patients who have severe renal impairment and dose reduction is required in patients having mild to moderate renal impairment [see Dosage and Administration (2.4) ] .

Hepatic Impairment No pharmacokinetic studies have been conducted in patients with… [Excerpted — this section continues on DailyMed.]

🧬 Pharmacodynamics 141 words ▾

12.2Pharmacodynamics A variety of clinical studies have demonstrated that elevated levels of total-C, LDL-C, and apo B, an LDL membrane complex, are associated with human atherosclerosis. Similarly, decreased levels of HDL-C and its transport complex, apolipoprotein A (apo AI and apo AII) are associated with the development of atherosclerosis. Epidemiologic investigations have established that cardiovascular morbidity and mortality vary directly with the level of total-C, LDL-C, and TG, and inversely with the level of HDL-C.

The independent effect of raising HDL-C or lowering triglycerides (TG) on the risk of cardiovascular morbidity and mortality has not been determined. Fenofibric acid, the active metabolite of fenofibrate, produces reductions in total cholesterol, LDL cholesterol, apolipoprotein B, total triglycerides and triglyceride rich lipoprotein (VLDL) in treated patients. In addition, treatment with fenofibrate results in increases in high-density lipoprotein (HDL) and apolipoproteins apoAI and apoAII.

🔬 Clinical Studies ~3 min read ▾

14 CLINICAL STUDIES

14.1Primary Hypercholesterolemia (Heterozygous Familial and Nonfamilial) and Mixed Dyslipidemia The effects of fenofibrate at a dose equivalent to 160 mg fenofibrate tablets per day were assessed from four randomized, placebo-controlled, double-blind, parallel-group studies including patients with the following mean baseline lipid values: total-C 306.9 mg/dL; LDL-C 213.8 mg/dL; HDL-C 52.3 mg/dL; and triglycerides 191.0 mg/dL. Fenofibrate tablets therapy lowered LDL-C, Total-C, and the LDL-C/HDL-C ratio. Fenofibrate tablets therapy also lowered triglycerides and raised HDL-C (see Table 4).

Table 4. Mean Percent Change in Lipid Parameters at End of Treatment† †Duration of study treatment was 3 to 6 months. *p = < 0.05 vs. Placebo Treatment Group Total-C LDL-C HDL-C TG Pooled Cohort Mean baseline lipid values (n = 646) 306.9 mg/dL 213.8 mg/dL 52.3 mg/dL 191.0 mg/dL All FEN (n = 361) -18.7%* -20.6%* +11.0%* -28.9%* Placebo (n = 285) -0.4% -2.2% +0.7% +7.7% Baseline LDL-C > 160 mg/dL and TG < 150 mg/dL Mean baseline lipid values (n = 334) 307.7 mg/dL 227.7 mg/dL 58.1 mg/dL 101.7 mg/dL All FEN (n = 193) -22.4%* -31.4%* +9.8%* -23.5%* Placebo (n = 141) +0.2% -2.2% +2.6% +11.7% Baseline LDL-C >160 mg/dL and TG ≥ 150 mg/dL Mean baseline lipid values (n = 242) 312.8 mg/dL 219.8 mg/dL 46.7 mg/dL 231.9 mg/dL All FEN (n = 126) -16.8%* -20.1%* +14.6%* -35.9%* Placebo (n = 116) -3.0% -6.6% +2.3% +0.9% In a subset of the subjects, measurements of apo B were conducted.

Fenofibrate treatment significantly reduced apo B from baseline to endpoint as compared with placebo (-25.1% vs. 2.4%, p < 0.0001, n = 213 and 143 respectively).

14.2Severe Hypertriglyceridemia The effects of fenofibrate on serum triglycerides were studied in two randomized, double-blind, placebo-controlled clinical trials of 147 hypertriglyceridemic patients. Patients were treated for eight weeks under protocols that differed only in that one entered patients with baseline TG levels of 500 to 1500 mg/dL, and the other TG levels of 350 to 500 mg/dL. In patients with hypertriglyceridemia and normal cholesterolemia with or without hyperchylomicronemia, treatment with fenofibrate at dosages equivalent to fenofibrate 160 mg per day decreased primarily very low-density lipoprotein (VLDL) triglycerides and VLDL cholesterol.

Treatment of patients with elevated triglycerides often results in an increase of LDL-C (see Table 5). Table 5. Effects of Fenofibrate in Patients With Severe Hypertriglyceridemia *= p < 0.05 vs.

Placebo Study 1 Placebo Fenofibrate Baseline TG levels 350 to 499 mg/dL N Baseline (Mean) Endpoint (Mean) % Change (Mean) N Baseline (Mean) Endpoint (Mean) % Change (Mean) Triglycerides 28 449 450 -0.5 27 432 223 -46.2* VLDL Triglycerides 19 367 350 2.7 19 350 178 -44.1* Total Cholesterol 28 255 261 2.8 27 252 227 -9.1* HDL Cholesterol 28 35 36 4 27 34 40 19.6* LDL Cholesterol 28 120 129 12 27 128 137

14.5VLDL Cholesterol 27 99 99 5.8 27 92 46 -44.7* Study 2 Placebo Fenofibrate Baseline TG levels 500 to 1500 mg/dL N Baseline (Mean) Endpoint (Mean) % Change (Mean) N Baseline (Mean) Endpoint (Mean) % Change (Mean) Triglycerides 44 710 750 7.2 48 726 308 -54.5* VLDL Triglycerides 29 537 571 18.7 33 543 205 -50.6* Total Cholesterol 44 272 271 0.4 48 261 223 -13.8* HDL Cholesterol 44 27 28 5.0 48 30 36 22.9* LDL Cholesterol 42 100 90 -4.2 45 103 131 45.0* VLDL Cholesterol 42 137 142 11.0 45 126 54 -49.4* The effect of fenofibrate on cardiovascular morbidity and mortality has not been determined.

🧪 Nonclinical Toxicology ~2 min read ▾

13 NONCLINICAL TOXICOLOGY

13.1Carcinogenesis and Mutagenesis and Impairment of Fertility Two dietary carcinogenicity studies have been conducted in rats with fenofibrate. In the first 24-month study, Wistar rats were dosed with fenofibrate at 10, 45, and 200 mg/kg/day, approximately 0.3, 1, and 6 times the maximum recommended human dose (MRHD) of 300 mg fenofibrate daily, equivalent to 160 mg fenofibrate daily, based on body surface area comparisons. At a dose of 200 mg/kg/day (at 6 times the MRHD), the incidence of liver carcinomas was significantly increased in both sexes.

A statistically significant increase in pancreatic carcinomas was observed in males at 1 and 6 times the MRHD; an increase in pancreatic adenomas and benign testicular interstitial cell tumors was observed at 6 times the MRHD in males. In a second 24-month rat carcinogenicity study in a different strain of rats (Sprague-Dawley), doses of 10 and 60 mg/kg/day (0.3 and 2 times the MRHD) produced significant increases in the incidence of pancreatic acinar adenomas in both sexes and increases in testicular interstitial cell tumors in males at 2 times the MRHD.

A 117-week carcinogenicity study was conducted in rats comparing three drugs: fenofibrate 10 and 60 mg/kg/day (0.3 and 2 times the MRHD, based on body surface area comparisons), clofibrate (400 mg/kg/day; 2 times the human dose), and gemfibrozil (250 mg/kg/day; 2 times the human dose, based on mg/m 2 surface area). Fenofibrate increased pancreatic acinar adenomas in both sexes. Clofibrate increased hepatocellular carcinoma and pancreatic acinar adenomas in males and hepatic neoplastic nodules in females.

Gemfibrozil increased hepatic neoplastic nodules in males and females, while all three drugs increased testicular interstitial cell tumors in males. In a 21-month study in CF-1 mice, fenofibrate 10, 45, and 200 mg/kg/day (approximately 0.2, 1, and 3 times the MRHD, based on body surface area comparisons) significantly increased the liver carcinomas in both sexes at 3 times the MRHD. In a second 18-month study at 10, 60, and 200 mg/kg/day, fenofibrate significantly increased the liver carcinomas in male mice and liver adenomas in female mice at 3 times the MRHD.

Electron microscopy studies have demonstrated peroxisomal proliferation following fenofibrate administration to the rat. An adequate study to test for peroxisome proliferation in humans has not been done, but changes in peroxisome morphology and numbers have been observed in humans after treatment with other members of the fibrate class when liver biopsies were compared before and after treatment in the same individual. Fenofibrate has been demonstrated to be devoid of mutagenic potential in the following tests: Ames, mouse lymphoma, chromosomal aberration and unscheduled DNA synthesis in primary rat hepatocytes.

In fertility studies rats were given oral dietary doses of fenofibrate, males received 61 days prior to mating and females 15 days prior to mating through weaning which resulted in no adverse effect on fertility at doses up to 300 mg/kg/day (10 times the MRHD, based on body surface area comparisons).

📄 Carcinogenesis, Mutagenesis, Impairment of Fertility ~2 min read ▾

13.1Carcinogenesis and Mutagenesis and Impairment of Fertility Two dietary carcinogenicity studies have been conducted in rats with fenofibrate. In the first 24-month study, Wistar rats were dosed with fenofibrate at 10, 45, and 200 mg/kg/day, approximately 0.3, 1, and 6 times the maximum recommended human dose (MRHD) of 300 mg fenofibrate daily, equivalent to 160 mg fenofibrate daily, based on body surface area comparisons. At a dose of 200 mg/kg/day (at 6 times the MRHD), the incidence of liver carcinomas was significantly increased in both sexes.

A statistically significant increase in pancreatic carcinomas was observed in males at 1 and 6 times the MRHD; an increase in pancreatic adenomas and benign testicular interstitial cell tumors was observed at 6 times the MRHD in males. In a second 24-month rat carcinogenicity study in a different strain of rats (Sprague-Dawley), doses of 10 and 60 mg/kg/day (0.3 and 2 times the MRHD) produced significant increases in the incidence of pancreatic acinar adenomas in both sexes and increases in testicular interstitial cell tumors in males at 2 times the MRHD.

A 117-week carcinogenicity study was conducted in rats comparing three drugs: fenofibrate 10 and 60 mg/kg/day (0.3 and 2 times the MRHD, based on body surface area comparisons), clofibrate (400 mg/kg/day; 2 times the human dose), and gemfibrozil (250 mg/kg/day; 2 times the human dose, based on mg/m 2 surface area). Fenofibrate increased pancreatic acinar adenomas in both sexes. Clofibrate increased hepatocellular carcinoma and pancreatic acinar adenomas in males and hepatic neoplastic nodules in females.

Gemfibrozil increased hepatic neoplastic nodules in males and females, while all three drugs increased testicular interstitial cell tumors in males. In a 21-month study in CF-1 mice, fenofibrate 10, 45, and 200 mg/kg/day (approximately 0.2, 1, and 3 times the MRHD, based on body surface area comparisons) significantly increased the liver carcinomas in both sexes at 3 times the MRHD. In a second 18-month study at 10, 60, and 200 mg/kg/day, fenofibrate significantly increased the liver carcinomas in male mice and liver adenomas in female mice at 3 times the MRHD.

Electron microscopy studies have demonstrated peroxisomal proliferation following fenofibrate administration to the rat. An adequate study to test for peroxisome proliferation in humans has not been done, but changes in peroxisome morphology and numbers have been observed in humans after treatment with other members of the fibrate class when liver biopsies were compared before and after treatment in the same individual. Fenofibrate has been demonstrated to be devoid of mutagenic potential in the following tests: Ames, mouse lymphoma, chromosomal aberration and unscheduled DNA synthesis in primary rat hepatocytes.

In fertility studies rats were given oral dietary doses of fenofibrate, males received 61 days prior to mating and females 15 days prior to mating through weaning which resulted in no adverse effect on fertility at doses up to 300 mg/kg/day (10 times the MRHD, based on body surface area comparisons).

📄 Recent Major Changes 21 words ▾

RECENT MAJOR CHANGES Warnings and Precautions, Heptatotoxicity ( 5.2 ) 02/2021 Warnings and Precautions, Myopathy and rhabdomyolysis ( 5.3 ) 02/2021

📄 Package Label / Principal Display Panel 23 words ▾

Package/Label Display Panel MAJOR® NDC 0904-7539-04 Unit Dose Fenofibrate Tablets, USP 160 mg 30 TABLETS (3 x 10) Rx only 160mg carton label

Source: FDA Structured Product Labeling, mirrored from DailyMed / openFDA. Prefer the government’s original formatting? View this label on DailyMed ↗

Medicare Part D spend CMS · PART D · 2026 (Q1)

Medicare Part D (outpatient prescription) spending for Fenofibrate — the program that covers self-administered drugs. 18 manufacturers.
⚠️ Drug-level data: CMS publishes Part D spending by drug, not by NDC — these figures combine every manufacturer, strength and package size sold under the name Fenofibrate. That’s a different level of aggregation than the Medicaid card above, which is specific to this exact 11-digit NDC (pack size included), so the two aren’t directly comparable.
Period
Total Part D spend
$14.59M
Claims incl. refills
510.2K
Beneficiaries
402.9K
Spend / beneficiary
$36.21
Spend / claim
$28.59
Trend by period
💵 About the dollar figures: spending is what Part D plans paid before confidential manufacturer rebates, so the program’s real net cost is lower. A blank patient count means fewer than 11 people — CMS hides counts that small to protect privacy. Source: CMS Medicare Quarterly Part D Spending by Drug (data.cms.gov), updated quarterly.
← 00904-7534-26 · Major 00904-7540-12 · Major →
For educational and professional reference only — not medical advice. Pricing reflects published NADAC and CMS ASP (free public data) and may differ from your acquisition cost; always verify before billing or dispensing.