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Fenofibric acid 135 mg Capsule, Delayed Release, 90-count — NDC 42571-348-90 (Billing 42571-0348-90)

by Micro Labs Limited · 90 CAPSULE, DELAYED RELEASE in 1 BOTTLE

This is a package of 90 capsules of Fenofibric acid 135 mg Capsule, Delayed Release from Micro Labs Limited, no longer marketed (first marketed Sep 2020), no longer in the FDA NDC Directory; retail pharmacies pay about $0.2863 per capsule (NADAC). It is the main listing for this product, which comes in 3 package sizes.

NDC 42571-0348-90
🏷️ FDA NDC (as labeled) 42571-348-90 billing pads the product segment with a zero
This package
Contains90-count Cost per ea$0.2863 NADAC Per package$25.77 / 90 capsules Pack sizes3 compare ↓
Also priced by: Part D plans $0.5579/unit — full pricing hub ↓
Main listing for product 42571-348 · Also comes in: 30 capsules 42571-348-30 500 capsules 42571-348-05
Rx only Generic Discontinued Non-controlled ⚠ Discontinued by firm ⇄ 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

NDC database record

One package, one record: these facts belong to NDC 42571-348-90 alone.

Record
FDA NDC Directory package listing · Human prescription drug
Code segments
42571 labeler · 348 product · 90 package
Package marketed since
Sep 1, 2020
Sample package
No — commercial package
Listing certified through
Dec 31, 2026
Billing quantity
90 EA per package
Barcode (UPC)
0342571347901, 0342571348908
FDA record last changed
Jul 24, 2026
⚠️
Excluded from the active FDA NDC Directory. The labeler reported this product as discontinued, so it is excluded from the active NDC Directory. The listing was last certified through Aug 2026. A label may still appear on DailyMed, but the NDC is no longer in the current FDA NDC Directory. Search the FDA NDC Directory ↗

Identity & classification

Regulatory identifiers FDA, NLM and CMS codes for this package

FDA NDC (as labeled) 42571-348-90
Product NDC 42571-348
11-digit billing NDC 42571034890
NCPDP billing unit EA — each (per item)
RxCUI 828373, 828379
UNII BGF9MN2HU1
UPC 0342571347901, 0342571348908
Application # ANDA213450
SPL Set ID 9c87ff52-04d5-4833-8cec-c33bb646b7c7
Established class (EPC) Peroxisome Proliferator Receptor alpha Agonist
DEA schedule Non-controlled
Marketing category ANDA
Marketing status Discontinued
FDA listing status Discontinued by firm (certified through Aug 2026)
Marketing start 2020-09-01
Route ORAL
Dosage form CAPSULE, DELAYED RELEASE
Substance FENOFIBRIC ACID

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

GPI-14 39200006006540
GPI class Fenofibric Acid
GCN Seq No 064677
GCN 16105
HICL code 036019
Ingredient (HICL) Fenofibric Acid (Choline)
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 FENOFIBRIC ACID DR 135 MG CAP
FDB brand name Fenofibric Acid
Legend status F — Federal legend — prescription drug or device
Quick answers
  • GSN (GCN sequence number): 064677
  • GCN: 16105
  • GPI-14 (Medi-Span): 39200006006540
  • HICL (First Databank): 036019
  • AHFS class code: 24:06.06.00
  • RxCUI (RxNorm): 828373
Why two NDCs? The FDA registers this code as 42571-348-90 — a 5-3-2 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 product segment → 42571-0348-90. 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 FENOFIBRIC ACID DR 135 MG CAP Ingredient Fenofibric Acid (Choline)
📗 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 →

Supplement & herbal interactions

🌿 Drug–supplement interaction checker →
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 $0.286 $25.77 / 90 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 · Q2 2026 $0.5579 $50.21 / 90 capsules
NADAC price history (per ea) — tap or hover for the price & month
Mar 2022 Oct 2022 Feb 2026 Sep 2026 $0.692 $0.237
▼ Down 59% over the last 22 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 Per unit Per pack Marketing startMarketing endStatus
42571-0348-05 42571-348-05 500 CAPSULE, DELAYED RELEASE in 1 BOTTLE — — 2020-09-01 — Discontinued by firm
42571-0348-30 42571-348-30 30 CAPSULE, DELAYED RELEASE in 1 BOTTLE — — 2020-09-01 — Discontinued by firm
42571-0348-90 You're viewing this Main listing 90 CAPSULE, DELAYED RELEASE in 1 BOTTLE $0.2863 / ea $25.77 2020-09-01 — Discontinued by firm

You're viewing one of 3 pack sizes for this product.

Pack size FAQ

What quantity is in this package?
This is a 90-count package — 90 capsule, delayed release in 1 bottle.
How does this package differ from NDC 42571-0348-30?
Both are Fenofibric acid 135 mg Capsule, Delayed Release — the drug itself is identical. This page's package is the 90-count one, while NDC 42571-0348-30 is the 30 capsules package.
What NDC number is used to bill for this package of Fenofibric acid 135 mg Capsule, Delayed Release?
Use the 11-digit billing form listed in the identifiers section of this page. Pharmacy and medical claims use the 11-digit form; the FDA label may print a shorter form of the same code.

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.

Therapeutic equivalents

ProductLabelerPackNADAC/unitTEStatusPrice vs. this
Fenofibric Acid 135 mg 00115-1325-10 Amneal 90 capsules $0.286 AB Availability likely —
Fenofibric Acid 135 mg 00115-1555-10 Amneal 90 capsules $0.286 — Discontinued —
Fenofibric acid 135 mgthis 42571-0348-90 Micro 90 capsules $0.286 — Discontinued —
Fenofibric Acid 135 mg 59651-0217-90 Aurobindo 90 capsules $0.286 AB Availability likely —
Fenofibric Acid 135 mg 69315-0282-09 Leading 90 capsules $0.286 AB Availability likely —
Fenofibric acid 135 mg 33342-0295-10 Macleods 90 capsules — — FDA listed —
Fenofibric Acid Delayed-Release 135 mg 42385-0945-11 Laurus 1000 capsules — AB Discontinued —
Fenofibric Acid 135 mg 46708-0245-30 Alembic 30 capsules — AB FDA listed —
Fenofibric Acid 135 mg 62332-0245-30 Alembic 30 capsules — 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

🏛️
2020
On the market since
Sep 2020
📍
2026
Currently FDA-listed
6 years 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.

🧪 Avoiding an ingredient? See Fenofibrate inactive ingredients by manufacturer: every current product's list side by side, so you can ask your pharmacy for the version that does not list it.

We could not link this NDC to a current FDA Structured Product Label. An inactive-ingredient list is therefore not available from this source.
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

LabelerMicro Labs Limited
Application holderMICRO LABS LTD
FDA applicationANDA213450 (ANDA)
Labeler code42571
First marketedSep 2020
Product typeHuman Prescription Drug
Portfolio190 products on file

More NDCs from Micro Labs Limited labeler code 42571

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 Fenofibricacid delayed-release capsules are indicated as adjunctive therapy to diet: toreduce triglyceride (TG) levels in adults with severe hypertriglyceridemia (TG greater than or equal to 500 mg/dL). toreduce elevated low-density lipoprotein cholesterol (LDL-C) in adults with primary hyperlipidemia when use of recommended LDL-C lowering therapy isnot possible. Limitations of Use Markedlyelevated levels of serum TG (e.g., > 2,000 mg/dL) may increase the risk of developing pancreatitis. The effect of fenofibrate therapy on reducingthis risk has not been determined [see Warnings and Precautions (5.7) ] .

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

Limitations of Use: Markedly elevated levels of serum TG (e.g., >2,000 mg/dL) may increase the risk of developing pancreatitis. The effect of fenofibrate therapy on reducing this risk has not been determined ( 1 ). Fenofibrate did not reduce coronary heart disease morbidity and mortality in two large, randomized controlled trials of patients with type 2 diabetes mellitus ( 1 ).

⏱️ Dosage and Administration ~2 min read ▾

2 DOSAGE AND ADMINISTRATION Severe hypertriglyceridemia: 45 to 135 mg orally once daily; the dosage should be adjusted according to patient response ( 2.2 ). Primary hyperlipidemia: 135 mg orally once daily ( 2.2 ). Administer as a single dose, at any time of day, with or without food ( 2.2 ).

Assess TG when clinically appropriate, as early as 4 to 8 weeks after initiating fenofibric acid delayed-release capsules. Discontinue fenofibric acid delayed-release capsules in patients who do not have an adequate response after 2 months of treatment ( 2.2 ). Swallow capsules whole.

Do not crush, break, dissolve, or chew ( 2.2 ). Renal impairment: Initial dosage of 45 mg orally once daily ( 2.3 ). Geriatric patients: Select the dosage on the basis of renal function ( 2.4 ).

2.1Prior to Initiation of Fenofibric Acid Delayed-Release Capsules Assess lipid levels before initiating therapy. Identify other causes (e.g., diabetes mellitus, hypothyroidism, or medications) of high TG levels and manage as appropriate. Patients should be placed on an appropriate lipid-lowering diet before receiving fenofibric acid delayed-release capsules, and should continue this diet during treatment with fenofibric acid delayed-release capsules.

Inpatients with diabetes and fasting chylomicronemia, improve glycemic control prior to considering starting fenofibric acid delayed-releasecapsules.

2.2Recommended Dosage and Administration Severe hypertriglyceridemia: The recommended dosage of fenofibric acid delayed-release capsules are 45 mg or 135 mg orally once daily. Dosage should be individualized according to patient response, and should be adjusted if necessary following repeat lipid determinations at 4 to 8 week intervals. Primary hyperlipidemia: The recommended dosage of fenofibric acid delayed-release capsule is 135 mg orally once daily.

Administer fenofibric acid delayed-release capsules as a single dose at any time of day, with or without food. Advise patients to swallow fenofibric acid delayed-release capsules whole. Do not crush, break, dissolve, or chew capsules.

Assess TGwhen clinically appropriate, as early as 4 to 8 weeks after initiating fenofibric acid delayed-release capsules. Discontinue fenofibric acid delayed-releasecapsules in patients who do not have an adequate response after two months of treatment. If adose is missed, advise patients not to take an extra dose.

Resume treatment with the next dose. Advisepatients to take fenofibric acid delayed-release capsules at least 1 hour before or 4 hours to 6 hours after a bile acid binding resin to avoidimpeding its absorption.

2.3Recommended Dosage in Patients with Renal Impairment Assessrenal function prior to initiation of fenofibric acid delayed-release capsules and periodically thereafter [see Warnings and Precautions (5.4) ] . Treatment with fenofibric acid delayed-release capsules should be initiated at a dosage of 45 mg orally once daily in patients with mild to moderately impaired renal function (eGFR 30 to <60 mL/min/1.73m 2 ), and increased only after evaluation of the effects on renal function and TG levels at this dosage. Fenofibricacid delayed-release capsules are contraindicated in patients with severe renal impairment (eGFR <30 mL/min/1.73m 2 ), including those with end-stagerenal 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 87 words ▾

3 DOSAGE FORMS AND STRENGTHS Fenofibric acid delayed-release capsules 45 mg: Reddish brown opaque cap imprinted with “CDR” and yellow opaque body imprinted with “45”, size “3”, hard gelatin capsule contains 4 white to off-white, round, biconvex delayed release mini tablets. Fenofibric acid delayed-release capsules 135 mg: Blue opaque cap imprinted with “CDR” and yellow opaque body imprinted with “135”, size “0”, hard gelatin capsule contains 12 white to off-white, round, biconvex delayed release mini tablets. Delayed Release Capsules: 45 mg and 135 mg ( 3 ).

⛔ Contraindications 148 words ▾

4 CONTRAINDICATIONS Fenofibric acid delayed-release capsules are contraindicated in patients with: Severe renal impairment, including those with end-stage renal disease (ESRD) and those receiving dialysis [see Clinical Pharmacology (12.3) ] . Active liver disease, including those with unexplained persistent liver function abnormalities [see Warnings and Precautions (5.2) ] . Pre-existing gallbladder disease [see Warnings and Precautions (5.5) ] .

Hypersensitivity to fenofibric acid, fenofibrate, or any of the excipients in fenofibric acid delayed-release capsules. Serious hypersensitivity reactions including anaphylaxis and angioedema have been reported with fenofibrate [see Warnings and Precautions (5.9) ] . Severe renal impairment, including those with end-stage renal disease (ESRD) and those receiving dialysis ( 4 ).

Active liver disease including those with unexplained persistent liver function abnormalities ( 4 ). Pre-existing gallbladder disease ( 4 ). Hypersensitivity to fenofibric acid, fenofibrate, or any of the excipients in fenofibric acid delayed-release capsules ( 4 ).

⚠️ Warnings and Cautions ~2 min read ▾

5 WARNINGS AND PRECAUTIONS Hepatotoxicity: Serious drug-induced liver injury, including liver transplantation and death, has been reported with fenofibrates, including fenofibric acid delayed-release 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 or hypothyroidism. Discontinue fenofibric acid if markedly elevated CK levels occur or if myopathy is either diagnosed or suspected.

Temporarily discontinue fenofibric acid in patients experiencing an acute or serious condition at high risk of developing renal failure secondary to rhabdomyolysis. Inform patients of the risk of myopathy and rhabdomyolysis when starting or increasing the fenofibric acid delayed-release capsules dosage. Instruct patients to promptly report any unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever ( 5.3 ).

Increases in Serum Creatinine: Monitor renal function in patients with renal impairment taking fenofibric acid delayed-release 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 fenofibric acid delayed-release capsules and treat appropriately if reactions occur ( 5.9 ).

5.1Mortality and Coronary Heart Disease Morbidity Fenofibrate didnot reduce cardiovascular disease morbidity or mortality in two large, randomized controlled trials of patients with type 2 diabetesmellitus [see Clinical Studies (14.4) ] . Because of chemical, pharmacological, and clinical similarities between fenofibrates, including fenofibric acid delayed-release capsules; pemafibrate; clofibrate;and gemfibrozil; the findings in 5 large randomized, placebo-controlled clinical trials with these other fibrate drugs may alsoapply to fenofibric acid delayed-release capsules.

Pemafibratedid not reduce cardiovascular disease morbidity or mortality in a large, randomized, placebo-controlled trial of patients with type 2diabetes mellitus on background statin therapy [see Clinical Studies (14.4) ] . In theCoronary Drug Project, a large trial conducted from 1965 to 1985 in men post myocardial infarction, there was no difference in mortality ornonfatal myocardial infarction between the clofibrate group and the placebo group after 5 years of treatment (NCT00000482). In atrial conducted by the World Health Organization (WHO) from 1965 to 1976, men without known coronary artery disease were treated withplacebo 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 clofibrategroup 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 HelsinkiHeart Study, conducted from 1982 to 1987, was a large (N = 4,081) trial of middle-aged men without a history of coronary artery disease. Subjectsreceived either placebo or gemfibrozil for 5 years, with a 3.5-year open extension afterward. Total mortality was numerically but not statisticallyhigher in the gemfibrozil randomization group versus placebo [9… [Excerpted — this section continues on DailyMed.]

🤒 Adverse Reactions ~3 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) ] 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 Micro Labs USA, Inc. at 1-855-839-8195 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 fenofibric acid has been established in adults with hypertriglyceridemia or primary hyperlipidemia based on adequate and well-controlled trials of other formulations of fenofibrate, referenced below as “fenofibrate” [see Clinical Studies (14) ].

Dosages of fenofibrate used in these trials were comparable to fenofibric acid delayed-release capsule 135 mg per day [see Clinical Pharmacology (12.3) ]. Adverse reactions reported by 2% or more of patients treated with fenofibrate (and greater than placebo) during the double-blind, placebo-controlled trials are listed in Table 1. Adverse reactions led to discontinuation of treatment in 5% of patients treated with fenofibrate and in 3% treated with placebo.

Increases in liver function tests were the most frequent events, causing discontinuation of fenofibrate treatment in 1.6% of patients in double-blind trials. Table 1. Adverse Reactions Reported by 2% or More of Patients Treated with Fenofibrate and Greater than Placebo During the Double-Blind, Placebo-Controlled Trials Adverse Reaction Placebo (N =365) Fenofibrate (N = 439) Abnormal Liver Tests 1% 8% Abdominal Pain 4% 5% Increased ALT 2% 3% Increased AST 1% 3% Increased Creatine Phosphokinase 1% 3% Constipation 1% 2% Rhinitis 1% 2% Other Adverse Reactions Urticaria Urticaria was seen in 1.1% vs.

0%, and rash in 1.4% vs. 0.8% of fenofibrate and placebo patients respectively in controlled trials. Increases in Liver Enzymes In a pooled analysis of three 12-week, double-blind, controlled studies of fenofibric acid delayed-release capsules, increases in ALT and AST > 3 times the upper limit of normal on two consecutive occasions occurred in 1.9% and 0.2%, respectively, of patients receiving fenofibric acid delayed-release capsules 135 mg daily and placebo, without other lipid-altering drugs.

In a pooled analysis of 10 placebo-controlled trials, increases to > 3 times the upper limit of normal in ALT occurred in 5.3% of patients taking either an intermediate or maximum recommended daily dosage of fenofibrate versus 1.1% of patients treated with placebo. In an 8-week trial, the incidence of ALT or AST elevations ≥ 3 times the upper limit of normal was 13% in patients receiving an intermediate daily dosage or the maximum recommended daily dosage of fenofibrate and was 0% in those receiving the lowest recommended daily dosage of fenofibrate or placebo [see Warnings and Precautions (5.2) ] .

Clinical trials with fenofibric acid delayed-release capsules did not include a placebo-control arm. However, the adverse reaction pr… [Excerpted — this section continues on DailyMed.]

🔄 Drug Interactions ~2 min read ▾

7 DRUG INTERACTIONS Table 2 presents clinically important drug interactions with fenofibric acid delayed-release capsules. Table 2. Clinically Important Drug Interactions with Fenofibric acid delayed-release capsules Statins Clinical Impact: Fibrates may cause myopathy when given alone.

The risk of myopathy and rhabdomyolysis is increased with concomitant use of fibrates with statins. Intervention: Consider if the benefit of using fenofibric acid delayed-release capsules concomitantly with statin therapy outweighs the increased risk of myopathy and rhabdomyolysis. If concomitant use is decided, monitor patients for signs and symptoms of myopathy, particularly during initiation of therapy and during upward dosage titration of statin therapy.

Colchicine Clinical Impact: Cases of myopathy and rhabdomyolysis have been reported with concomitant use of colchicine with fenofibrates. Intervention: Consider if the benefit of using colchicine concomitantly with fenofibric acid delayed-release capsules outweighs the increased risk of myopathy and rhabdomyolysis. If concomitant use is decided, monitor patients for signs and symptoms of myopathy, particularly during initiation of therapy and during upward dosage titration of colchicine.

Coumarin Anticoagulants Clinical Impact: Fibrates may cause potentiation of coumarin-type anticoagulant effects with prolongation of the PT/INR. Intervention: Caution should be exercised when coumarin anticoagulants are given in conjunction with fenofibric acid delayed-release capsules. The dosage of the anticoagulants should be reduced to maintain the PT/INR at the desired level to prevent bleeding complications.

Frequent PT/INR determinations are advisable until it has been definitely determined that the PT/INR has stabilized Immunosuppressants Clinical Impact: Immunosuppressants such as cyclosporine and tacrolimus can produce nephrotoxicity with decreases in creatinine clearance and rises in serum creatinine, and because renal excretion is the primary elimination route of fibrate drugs including fenofibric acid delayed-release capsules, there is a risk that an interaction will lead to deterioration of renal function. Intervention: The benefits and risks of using fenofibric acid delayed-release capsules with immunosuppressants and other potentially nephrotoxic agents should be carefully considered, and the lowest effective dosage employed and renal function monitored.

Bile-Acid Binding Resins Clinical Impact: Bile-acid binding resins may bind other drugs given concurrently. Intervention: In patients taking a bile acid resin, administer fenofibric acid delayed-release capsules at least 1 hour before or 4 to 6 hours after the bile acid resin to avoid impeding its absorption. Consider if the benefit of concomitant use of statins or colchicine outweighs the increased risk of myopathy and rhabdomyolysis.

Monitor patients for signs and symptoms of myopathy ( 7 ). Exercise caution in concomitant treatment with coumarin anticoagulants. Reduce the dosage of coumarin to maintain the PT/INR at the desired level to prevent bleeding complications ( 7 ).

Consider the benefits and risks of concomitant use with immunosuppressants and other potentially nephrotoxic agents. Use the lowest effective dosage and monitor renal function ( 7 ). Administer fenofibric acid delayed-release capsules at least 1 hour before or 4 to 6 hours after a bile acid resin to avoid impeding its absorption ( 7 ).

👥 Use in Specific Populations ~3 min read ▾

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 135 mg of fenofibric acid delayed-release capsules daily, based on body surface area (mg/m 2 ).

Adverse reproductive outcomes occurred at higher doses in the presence of maternal toxicity (see Data). Fenofibric acid delayed-release capsules should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown.

In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. Data Animal Data In pregnant rats given oral dietary doses of 14 mg/kg/day, 127 mg/kg/day, and 361 mg/kg/day from gestation day 6 to 15 during the period of organogenesis, no adverse developmental findings were observed at 14 mg/kg/day (less than the clinical exposure at the maximum recommended human dose [MRHD] of 300 mg fenofibrate daily, comparable to 135 mg fenofibric acid delayed-release capsules 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 fenofibric acid delayed-release capsules and for 5 days after the final dose.

8.4Pediatric Use The safety and effectiveness of fenofibric acid delayed-release capsules 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) ]… [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 comparable to the maximum recommended clinical dosage of 135 mg of fenofibric acid delayed-release capsules daily, based on body surface area (mg/m 2 ).

Adverse reproductive outcomes occurred at higher doses in the presence of maternal toxicity (see Data). Fenofibric acid delayed-release capsules should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown.

In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. Data Animal Data In pregnant rats given oral dietary doses of 14 mg/kg/day, 127 mg/kg/day, and 361 mg/kg/day from gestation day 6 to 15 during the period of organogenesis, no adverse developmental findings were observed at 14 mg/kg/day (less than the clinical exposure at the maximum recommended human dose [MRHD] of 300 mg fenofibrate daily, comparable to 135 mg fenofibric acid delayed-release capsules 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.

🧒 Pediatric Use 25 words ▾

8.4Pediatric Use The safety and effectiveness of fenofibric acid delayed-release capsules have not been established in pediatric patients with severe hypertriglyceridemia or primary hyperlipidemia.

🧓 Geriatric Use 84 words ▾

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 substantially excreted by the kidney [see Clinical Pharmacology (12.3) ] . Consider monitoring renal function in geriatric patients taking fenofibric acid delayed-release capsules.

🆘 Overdosage 100 words ▾

10 OVERDOSAGE In the event of an overdose of fenofibric acid delayed-release capsules, consider contacting the Poison Help line (1-800-222-1222) or a medical toxicologist for additional overdosage management recommendations. There is no specific treatment for overdose with fenofibric acid delayed-release capsules. 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 fenofibric acid delayed-release capsules 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 Fenofibric acid delayed-release capsules contains fenofibric acid, which is the circulating pharmacologically active moiety in plasma after oral administration of fenofibric acid delayed-release capsules. Fenofibric acid is also the circulating pharmacologically active moiety in plasma after oral administration of fenofibrate, the ester of fenofibric acid. Absorption Fenofibric acid is well absorbed throughout the gastrointestinal tract.

The absolute bioavailability of fenofibric acid is approximately 81%. Peak plasma levels of fenofibric acid occur within 4 to 5 hours after a single dose administration of fenofibric acid delayed-release capsules capsule under fasting conditions. Effect of Food Fenofibric acid exposure in plasma, as measured by C max and AUC, is not significantly different when a single 135 mg dose of fenofibric acid delayed-release capsules are administered under fasting or nonfasting conditions.

Distribution Upon multiple dosing of fenofibric acid delayed-release capsules, fenofibric acid levels reach steady-state within 8 days. Plasma concentrations of fenofibric acid at steady-state are approximately double those following a single dose. Serum protein binding was approximately 99% in normal and dyslipidemic subjects.

Elimination Fenofibric acid is eliminated with a half-life of approximately 20 hours, allowing once daily administration of fenofibric acid delayed-release capsules. Metabolism 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 after fenofibrate administration indicate that fenofibric acid does not undergo oxidative metabolism (e.g., cytochrome P450) to a significant extent. Excretion After absorption, fenofibric acid delayed-release capsules are primarily excreted in the urine in the form of fenofibric acid and fenofibric acid glucuronide. Specific Populations Geriatric Patients In geriatric 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 geriatric patients with normal renal function, without increasing accumulation of the drug or metabolites [see Dosage and Administration (2.4) and Use in Specific Populations (8.5) ] . Pediatric Patients The pharmacokinetics of fenofibric acid delayed-release capsules has not been studied in pediatric populations.

Male and Female Patients No pharmacokinetic difference between males and females has been observed for fenofibric acid. Racial and Ethnic Groups The influence of race on the pharmacokinetics of fenofibric acid has not been studied; however, fenofibric acid is not metabolized by enzymes known for exhibiting inter-ethnic variability. Patients with Renal Impairment The pharmacokine… [Excerpted — this section continues on DailyMed.]

🧬 Mechanism of Action 96 words ▾

12.1Mechanism of Action The active moiety of fenofibric acid delayed-release capsules 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 129 words ▾

16 HOW SUPPLIED/STORAGE AND HANDLING Fenofibric acid delayed-release capsules 45 mg: Reddish brown opaque cap imprinted with “CDR” and yellow opaque body imprinted with “45”, size “3”, hard gelatin capsule contains 4 white to off-white, round, biconvex delayed release mini tablets. Bottles of 30 NDC 42571-347-30 Bottles of 90 NDC 42571-347-90 Fenofibric acid delayed-release capsules 135 mg: Blue opaque cap imprinted with “CDR” and yellow opaque body imprinted with “135”, size “0”, hard gelatin capsule contains 12 white to off-white, round, biconvex delayed release mini tablets.

Bottles of 30 NDC 42571-348-30 Bottles of 90 NDC 42571-348-90 Bottles of 500 NDC 42571-348-05 Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F) [See USP controlled room temperature]. Keep out of the reach of children. Protect from moisture.

📋 Description 210 words ▾

11 DESCRIPTION Fenofibric acid delayed-release capsules (fenofibric acid) are a peroxisome proliferator-activated receptor (PPAR) alpha agonist available as delayed release capsules for oral administration. Each delayed release capsule contains choline fenofibrate, equivalent to 45 mg or 135 mg of fenofibric acid. The chemical name for choline fenofibrate is ethanaminium, 2-hydroxy-N,N,N-trimethyl, 2-{4-(4-chlorobenzoyl)phenoxy] -2-methylpropanoate (1:1) with the following structural formula: The molecular formula is C 22 H 28 ClNO 5 and the molecular weight is 421.91.

Choline fenofibrate is freely soluble in methanol, sparingly soluble in ethanol and water, slightly soluble in DMSO and practically insoluble in dichloromethane. The melting point is approximately 210°C. Choline fenofibrate is a white to off white crystalline powder, which is stable under ordinary conditions.

Each delayed release capsule contains enteric coated mini-tablets comprised of choline fenofibrate and the following inactive ingredients: hypromellose, hydroxypropyl cellulose, methacrylic acid - ethyl acrylate copolymer (1:1) type A , microcrystalline cellulose, povidone K30, silicon dioxide, sodium stearyl fumarate, talc, triethyl citrate. The capsule shell of the 45 mg capsule contains the following inactive ingredients: ferrosoferric oxide, ferric oxide red, gelatin and titanium dioxide. The capsule shell of the 135 mg capsule contains the following inactive ingredients: FD&C blue no.1, FD&C red no.3, FD&C red no.

40, gelatin and titanium dioxide. fenofibricacid-str.jpg

💬 Information for Patients ~2 min read ▾

17 PATIENT COUNSELING INFORMATION Hepatotoxicity Inform patients that fenofibric acid delayed-release capsules may cause liver enzyme elevations and possibly liver failure. Advise patients to promptly report fatigue, anorexia, right upper abdominal discomfort, dark urine or jaundice [see Contraindications (4) and Warnings and Precautions (5.2) ] . Myopathy and Rhabdomyolysis Advise patients that fenofibric acid delayed-release capsules may cause myopathy and rhabdomyolysis.

Inform patients that the risk is also increased when taking certain types of medication and they should discuss all medication, both prescription and over the counter, with their healthcare provider. Instruct patients to inform other healthcare providers prescribing a new medication or increasing the dosage of an existing medication that they are taking fenofibric acid delayed-release capsules. Instruct patients to promptly report any unexplained muscle pain, tenderness, or weakness particularly if accompanied by malaise or fever [see Warnings and Precautions (5.3) and Drug Interactions (7) ] .

Increased Bleeding Risk with Coumarin Anticoagulants Inform patients that the concomitant use of fenofibric acid delayed-release capsules with coumarin-type anticoagulants may increase the risk of bleeding. Advise patients if they are taking or planning to take coumarin-type anticoagulants to inform their healthcare providers and that increased monitoring may be necessary [see Warnings and Precautions (5.6) and Drug Interactions (7) ] . Hypersensitivity Reactions Inform patients that serious hypersensitivity reactions, such as anaphylaxis and angioedema, have been reported with fenofibrates.

Advise patients to report immediately any signs or symptoms suggesting allergic reaction, and to discontinue drug until they have consulted prescribing physicians [see Warnings and Precautions (5.9) ] . Pregnancy Advise patients to inform their healthcare provider of a known or suspected pregnancy to discuss if fenofibric acid delayed-release capsules should be discontinued [see Use in Specific Populations (8.1) ] . Lactation Advise patients that breastfeeding during treatment with fenofibric acid delayed-release capsules 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: Micro Labs Limited Goa-403 722, INDIA. Manufactured for: Micro Labs USA Inc.

Somerset, NJ 08873 Rev. 06/2025

🧬 Pharmacokinetics ~3 min read ▾

12.3Pharmacokinetics Fenofibric acid delayed-release capsules contains fenofibric acid, which is the circulating pharmacologically active moiety in plasma after oral administration of fenofibric acid delayed-release capsules. Fenofibric acid is also the circulating pharmacologically active moiety in plasma after oral administration of fenofibrate, the ester of fenofibric acid. Absorption Fenofibric acid is well absorbed throughout the gastrointestinal tract.

The absolute bioavailability of fenofibric acid is approximately 81%. Peak plasma levels of fenofibric acid occur within 4 to 5 hours after a single dose administration of fenofibric acid delayed-release capsules capsule under fasting conditions. Effect of Food Fenofibric acid exposure in plasma, as measured by C max and AUC, is not significantly different when a single 135 mg dose of fenofibric acid delayed-release capsules are administered under fasting or nonfasting conditions.

Distribution Upon multiple dosing of fenofibric acid delayed-release capsules, fenofibric acid levels reach steady-state within 8 days. Plasma concentrations of fenofibric acid at steady-state are approximately double those following a single dose. Serum protein binding was approximately 99% in normal and dyslipidemic subjects.

Elimination Fenofibric acid is eliminated with a half-life of approximately 20 hours, allowing once daily administration of fenofibric acid delayed-release capsules. Metabolism 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 after fenofibrate administration indicate that fenofibric acid does not undergo oxidative metabolism (e.g., cytochrome P450) to a significant extent. Excretion After absorption, fenofibric acid delayed-release capsules are primarily excreted in the urine in the form of fenofibric acid and fenofibric acid glucuronide. Specific Populations Geriatric Patients In geriatric 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 geriatric patients with normal renal function, without increasing accumulation of the drug or metabolites [see Dosage and Administration (2.4) and Use in Specific Populations (8.5) ] . Pediatric Patients The pharmacokinetics of fenofibric acid delayed-release capsules has not been studied in pediatric populations.

Male and Female Patients No pharmacokinetic difference between males and females has been observed for fenofibric acid. Racial and Ethnic Groups The influence of race on the pharmacokinetics of fenofibric acid has not been studied; however, fenofibric acid is not metabolized by enzymes known for exhibiting inter-ethnic variability. Patients with Renal Impairment The pharmacokinetics of fenofibric acid were examined in patients with mild, moderate, and severe renal impairment.

Patients with severe renal impairment (creatinine clearance [CrCl ≤30 mL/min] or estimated glomerular filtration rate [eGFR] <30 mL/min/1.73m 2 ) showed a 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 (CrCl 30 mL/min to 80 mL/min or eGFR 30 to 59 mL/min/1.73m 2 ) had similar exposure but an increase in the half-life for fenofibric acid compared to that of healthy subjects [see Dosage and Administration (2.3) ] .

Patients with Hepatic Impairment No pharmacokinetic studies have been conducted in patients with hepatic impairment. Drug Interaction Studies In vitro studies using human liver microsomes indicate that fenofibric acid is not an inhibitor of cytochrome (CYP) P450 isoforms CYP3A4, CYP2D6… [Excerpted — this section continues on DailyMed.]

🧬 Pharmacodynamics 28 words ▾

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.

🔬 Clinical Studies ~3 min read ▾

14 CLINICAL STUDIES

14.1Overview of Clinical Trials The effectiveness of fenofibric acid delayed-release capsules 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.” Dosages of fenofibrate used in these trials were comparable to fenofibric acid delayed-release capsule 135 mg per day [see Clinical Pharmacology (12.3) ].

14.2Clinical Trials in Adults with Hypertriglyceridemia The effects of fenofibrate on serum TG were studied in two randomized, double-blind, placebo-controlled clinical trials of 147 patients with hypertriglyceridemia. Patients were treated for 8 weeks under protocols that differed only in that one entered patients with baseline TG levels of 500 to 1,500 mg/dL, and the other TG levels of 350 to 499 mg/dL. In patients with hypertriglyceridemia and normal cholesterolemia with or without hyperchylomicronemia, treatment with fenofibrate decreased primarily very low-density lipoprotein (VLDL) TG and VLDL cholesterol (VLDL-C).

Treatment of patients with elevated TG often results in an increase of LDL-C (see Table 5). Table 5. Effects of Fenofibrate in Patients with Hypertriglyceridemia Trial 1 Placebo Fenofibrate Baseline TG levels 350 to 499 mg/dL N Baseline Mean (mg/dL) Endpoint Mean (mg/dL) Mean % Change N Baseline Mean (mg/dL) Endpoint Mean (mg/dL) Mean % Change TG 28 449 450 -0.5 27 432 223 -46.2* VLDL-TG 19 367 350 2.7 19 350 178 -44.1* Total-C 28 255 261 2.8 27 252 227 -9.1* HDL-C 28 35 36 4 27 34 40 19.6* LDL-C 28 120 129 12 27 128 137

14.5VLDL-C 27 99 99 5.8 27 92 46 -44.7* Trial 2 Placebo Fenofibrate Baseline TG levels 500 to 1500 mg/dL N Baseline Mean (mg/dL) Endpoint Mean (mg/dL) Mean % Change N Baseline Mean (mg/dL) Endpoint Mean (mg/dL) Mean % Change TG 44 710 750 7.2 48 726 308 -54.5* VLDL-TG 29 537 571 18.7 33 543 205 -50.6* Total-C 44 272 271 0.4 48 261 223 -13.8* HDL-C 44 27 28 5.0 48 30 36 22.9* LDL-C 42 100 90 -4.2 45 103 131 45.0* VLDL-C 42 137 142 11.0 45 126 54 -49.4* * = p < 0.05 vs. Placebo

14.3Clinical Trials in Adults with Primary Hyperlipidemia The effects of fenofibrate were assessed in four randomized, placebo-controlled, double-blind, parallel-group trials in patients with hyperlipidemia and mixed dyslipidemia. Fenofibrate therapy reduced LDL-C, Total-C, and TG, and increased HDL-C (Table 6). Table 6.

Mean Percent Change in Lipid Parameters at End of Treatment † Treatment Group Total-C LDL-C HDL-C TG Mean baseline lipid values (n = 646) 306.9 mg/dL 213.8 mg/dL 52.3 mg/dL 191.0 mg/dL All fenofibrate (n = 361) -18.7%* -20.6%* +11.0%* -28.9%* Placebo (n = 285) -0.4% -2.2% +0.7% +7.7% † Duration of study treatment was 3 to 6 months * p = < 0.05 vs. Placebo

14.4Lack of Efficacy in Cardiovascular Outcomes Trials Fenofibrate did not reduce cardiovascular disease morbidity or mortality in two large, randomized controlled trials of patients with type 2 diabetes mellitus. The Action to Control Cardiovascular Risk in Diabetes Lipid (ACCORD Lipid) (NCT00000620) trial was a randomized placebo-controlled trial of 5,518 patients (2,765 assigned to receive fenofibrate) with type 2 diabetes mellitus on background statin therapy treated with fenofibrate. The mean age at baseline was 62 years and 31% were female.

Overall, 68% were White, 15% were Black or African American; 7% identified as Hispanic or Latino ethnicity. The mean duration of follow-up was 4.7 years. The primary outcome of major adverse cardiovascular events (MACE), a composite of non-fatal myocardial infarction, non-fatal stroke, and cardiovascular disease death was a HR of 0.92 (95% CI, 0.79 to 1.08) for fenofibrate plus statin combination therapy as compared to statin monotherapy.

The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial was a 5-year randomized, placebo-controlled trial of 9,795 patients (4,895 assigned to receive fenofibrate) with type 2 diabetes mellitus… [Excerpted — this section continues on DailyMed.]

🧪 Nonclinical Toxicology ~3 min read ▾

13 NONCLINICAL TOXICOLOGY

13.1Carcinogenesis, Mutagenesis, and Impairment of Fertility Fenofibric acid delayed-release capsules (fenofibric acid) No carcinogenicity and fertility studies have been conducted with choline fenofibrate or fenofibric acid. However, because fenofibrate is rapidly converted to its active metabolite, fenofibric acid, either during or immediately following absorption both in animals and humans, studies conducted with fenofibrate are relevant for the assessment of the toxicity profile of fenofibric acid. A similar toxicity spectrum is expected after treatment with either fenofibric acid delayed-release capsules or fenofibrate.

Fenofibrate Carcinogenesis 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 mg/kg/day, 45 mg/kg/day, and 200 mg/kg/day, approximately 0.3 times, 1 time, and 6 times the maximum recommended human dose (MRHD), based on body surface area comparisons (mg/m 2 ). 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 study in a different strain of rats (Sprague-Dawley), doses of 10 mg/kg/day 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 mg/kg/day and 60 mg/kg/day (0.3 and 2 times the MRHD), 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 mg/kg/day, 45 mg/kg/day, and 200 mg/kg/day (approximately 0.2 times, 1 time, and 3 times the MRHD on the basis of mg/m 2 surface area) significantly increased the liver carcinomas in both sexes at 3 times the MRHD. In a second 18-month study at 10 mg/kg/day, 60 mg/kg/day, 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. Mutagenesis 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.

Impairment of Fertility 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 (approximately 10 times the MRHD, based on mg/m 2 surface area comparisons).

📄 Carcinogenesis, Mutagenesis, Impairment of Fertility ~3 min read ▾

13.1Carcinogenesis, Mutagenesis, and Impairment of Fertility Fenofibric acid delayed-release capsules (fenofibric acid) No carcinogenicity and fertility studies have been conducted with choline fenofibrate or fenofibric acid. However, because fenofibrate is rapidly converted to its active metabolite, fenofibric acid, either during or immediately following absorption both in animals and humans, studies conducted with fenofibrate are relevant for the assessment of the toxicity profile of fenofibric acid. A similar toxicity spectrum is expected after treatment with either fenofibric acid delayed-release capsules or fenofibrate.

Fenofibrate Carcinogenesis 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 mg/kg/day, 45 mg/kg/day, and 200 mg/kg/day, approximately 0.3 times, 1 time, and 6 times the maximum recommended human dose (MRHD), based on body surface area comparisons (mg/m 2 ). 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 study in a different strain of rats (Sprague-Dawley), doses of 10 mg/kg/day 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 mg/kg/day and 60 mg/kg/day (0.3 and 2 times the MRHD), 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 mg/kg/day, 45 mg/kg/day, and 200 mg/kg/day (approximately 0.2 times, 1 time, and 3 times the MRHD on the basis of mg/m 2 surface area) significantly increased the liver carcinomas in both sexes at 3 times the MRHD. In a second 18-month study at 10 mg/kg/day, 60 mg/kg/day, 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. Mutagenesis 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.

Impairment of Fertility 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 (approximately 10 times the MRHD, based on mg/m 2 surface area comparisons).

📄 Recent Major Changes 21 words ▾

Indications and Usage (1) 6/2025 Dosage and Administration (2) 6/2025 Warnings and Precautions, Mortality and Coronary Heart Disease Morbidity (5.1) 6/2025

📄 Package Label / Principal Display Panel 36 words ▾

PACKAGE LABEL.PRINCIPAL DISPLAY PANEL NDC 42571-347-90 Fenofibric acid Delayed-Release Capsules 45 mg* Rx Only 90 Capsules MICRO LABS LIMITED NDC 42571-348-90 Fenofibric acid Delayed-Release Capsules 135 mg* Rx Only 90 Capsules MICRO LABS LIMITED fenofibricacid-lbla.jpg fenofibricacid-lblb.jpg

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 Fenofibric Acid — the program that covers self-administered drugs. 6 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 Fenofibric Acid. 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
$1.62M
Claims incl. refills
37.2K
Beneficiaries
30.5K
Spend / beneficiary
$52.97
Spend / claim
$43.49
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.

Reported adverse events (FAERS)

Read carefully: FAERS reports are voluntary and unverified. Counts are not incidence, do not establish causation, are subject to reporting bias, and cannot be used to compare one drug to another. Shown for signal context only. Reports for Fenofibric Acid — the ingredient across all brands.

Top reported reactions

Fatigue67
Nausea56
Diarrhoea50
Pain42
Dyspnoea37
Headache37
Arthralgia34

Age at onset

Adult81
Elderly74

Reporter sex

776 reports
Male · 55%
Female · 45%

Serious outcomes

Hospitalization200
Death76
Life-threatening18
Disabling16
Reports over time (by year) — tap or hover for the count & year
2019 2021 2023 2026 67 0
Most recent year is provisional (FAERS lags ~3 months).
Where does this data come from?
Adverse-event reports from the FDA Adverse Event Reporting System (FAERS) via openFDA. FAERS reports are voluntary and unverified — counts are not incidence and don’t establish causation.

About this NDC listing & data coverage

Finished prescription product No longer marketed (per FDA listing data)
What data is (and isn’t) available for this NDC — tap to expand
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 — Not published for this NDC No photo available yet for this listing.
Inactive ingredients (structured) — Not published for this NDC The labeler did not submit a structured excipient list, or no SPL is 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.
“Not published” reflects what the public FDA / CMS / NLM sources provide for this exact package code — it is a property of the data feeds, not a judgment about the product.

Questions about this listing

What does the discontinued status mean for this NDC?
The labeler reported a marketing end date (or the listing was delisted), so this specific package is no longer actively marketed. Remaining stock may still be dispensed for a time, and the NDC stays valid for historical records and claims — but data feeds (pricing, labeling) typically stop updating for it. Other package sizes or other manufacturers' versions of the same medication may still be marketed — see the equivalents section where available.
Is the NDC printed on the package the same as the 11-digit billing NDC?
Yes, they identify this exact package in different formats. The form printed on the packaging and shown on DailyMed is the one the FDA registered. Insurance claims use a fixed 11-digit 5-4-2 format, so the short segment is padded with a leading zero and the dashes are dropped. The Identity section at the top of this page lists each form of this code.
Does this product come in other package sizes?
Yes — the FDA directory lists 2 other package presentations of this same product, including 30 capsules (42571-0348-30), 500 capsules (42571-0348-05). Each has its own NDC and its own page — see the package list near the top of this page.
Who lists this product with the FDA?
Micro Labs Limited is the labeler of record for this NDC — the company under whose FDA-assigned code the package is listed. The labeler may be the manufacturer itself or a distributor marketing the product under its own code.
Do I need a prescription for this product?
This NDC is listed with FDA as a prescription product, so it is dispensed under a prescriber's order. Your pharmacist can tell you whether any over-the-counter forms of the same medication exist.
This page identifies an FDA-listed package (the NDC) and reports public regulatory and pricing data about the listing. It is reference information, not a medical recommendation — talk to your pharmacist or prescriber about your own medication.
Where does this data come from?
Listing facts (marketing category, packager status, marketing dates) from the FDA openFDA NDC Directory; label availability from DailyMed; pricing coverage from CMS NADAC; equivalence scope from the FDA Orange Book.
← 42571-0347-30 · Micro 42571-0350-09 · Micro →
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.