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Fenofibric Acid Delayed-Release 45 mg Capsule, Delayed Release, 90-count — NDC 42385-944-90 (Billing 42385-0944-90)

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

This is a package of 90 capsules of Fenofibric Acid Delayed-Release 45 mg Capsule, Delayed Release from Laurus Labs Limited, no longer marketed (first marketed Aug 2020), no longer in the FDA NDC Directory; retail pharmacies pay about $0.1611 per capsule (NADAC). It is the main listing for this product, which comes in 3 package sizes.

NDC 42385-0944-90
🏷️ FDA NDC (as labeled) 42385-944-90 billing pads the product segment with a zero
This package
Contains90-count Cost per ea$0.1611 NADAC Per package$14.50 / 90 capsules Pack sizes3 compare ↓
Also priced by: Part D plans $0.5579/unit — full pricing hub ↓
Main listing for product 42385-944 · Also comes in: 30 capsules 42385-944-30 1000 capsules 42385-944-11
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 42385-944-90 alone.

Record
FDA NDC Directory package listing · Human prescription drug
Code segments
42385 labeler · 944 product · 90 package
Package marketed since
Aug 24, 2020
Sample package
No — commercial package
Listing certified through
Dec 31, 2026
Billing quantity
90 EA per package
Barcode (UPC-A, from the NDC)
3 4238594490 7
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 Jul 2024. 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) 42385-944-90
Product NDC 42385-944
11-digit billing NDC 42385094490
NCPDP billing unit EA — each (per item)
RxCUI 828373, 828379
UNII BGF9MN2HU1
Application # ANDA211626
SPL Set ID 302ffbf8-448e-4729-949f-40d457e30ab4
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 Jul 2024)
Marketing start 2020-08-24
Route ORAL
Dosage form CAPSULE, DELAYED RELEASE
Substance FENOFIBRIC ACID
TE code (Orange Book) AB · RLD · RS

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

GPI-14 39200006006520
GPI class Fenofibric Acid
GCN Seq No 064676
GCN 16104
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 45 MG CAP
FDB brand name Fenofibric Acid
Legend status F — Federal legend — prescription drug or device
Quick answers
  • GSN (GCN sequence number): 064676
  • GCN: 16104
  • GPI-14 (Medi-Span): 39200006006520
  • HICL (First Databank): 036019
  • AHFS class code: 24:06.06.00
  • RxCUI (RxNorm): 828373
Why two NDCs? The FDA registers this code as 42385-944-90 — 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 → 42385-0944-90. 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 45 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 $0.161 $14.50 / 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
Dec 2021 Aug 2022 Jan 2026 Sep 2026 $0.446 $0.144
▼ Down 64% over the last 23 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
42385-0944-11 42385-944-11 1000 CAPSULE, DELAYED RELEASE in 1 BOTTLE — — 2020-08-24 — Discontinued by firm
42385-0944-30 42385-944-30 30 CAPSULE, DELAYED RELEASE in 1 BOTTLE — — 2020-08-24 — Discontinued by firm
42385-0944-90 You're viewing this Main listing 90 CAPSULE, DELAYED RELEASE in 1 BOTTLE $0.1611 / ea $14.50 2020-08-24 — 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 42385-0944-30?
Both are Fenofibric Acid Delayed-Release 45 mg Capsule, Delayed Release — the drug itself is identical. This page's package is the 90-count one, while NDC 42385-0944-30 is the 30 capsules package.
What NDC number is used to bill for this package of Fenofibric Acid Delayed-Release 45 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 45 mg 00115-1554-10 Amneal 90 capsules $0.150 — Discontinued save 7%
Fenofibric Acid Delayed-Release 45 mgthis 42385-0944-90 Laurus 90 capsules $0.161 AB Discontinued —
Fenofibric Acid 45 mg 59651-0216-90 Aurobindo 90 capsules $0.161 AB Availability likely —
Fenofibric Acid 45 mg 69315-0281-09 Leading 90 capsules $0.161 AB Availability likely —
Fenofibric Acid 45 mg 00115-1324-10 Amneal 90 capsules — AB FDA listed —
Fenofibric acid 45 mg 33342-0294-10 Macleods 90 capsules — — FDA listed —
Fenofibric acid 45 mg 42571-0347-30 Micro 30 capsules — AB Discontinued —
Fenofibric Acid 45 mg 46708-0244-30 Alembic 30 capsules — AB FDA listed —
Fenofibric Acid 45 mg 62332-0244-30 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
Aug 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

LabelerLaurus Labs Limited
Application holderRISING PHARMA HOLDINGS INC
FDA applicationANDA211626 (ANDA)
Labeler code42385
First marketedAug 2020
Product typeHuman Prescription Drug
Portfolio87 products on file

More NDCs from Laurus Labs Limited labeler code 42385

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 🆘 Overdosage 🧬 Clinical Pharmacology 📦 How Supplied / Storage and Handling 📋 Description 💬 Information for Patients 🔬 Clinical Studies 🧪 Nonclinical Toxicology 📄 Carcinogenesis, Mutagenesis, Impairment of Fertility 📄 Recent Major Changes 📄 Package Label / Principal Display Panel
🎯 Indications and Usage ~2 min read ▾

1 INDICATIONS AND USAGE Fenofibric acid delayed-release capsules are peroxisome proliferator-activated receptor (PPAR) alpha agonist indicated as adjunctive therapy to diet to: Reduce TG in patients with severe hypertriglyceridemia ( 1.1 ). Reduce elevated LDL-C, Total-C, TG and Apo B, and to increase HDL-C in patients with primary hypercholesterolemia or mixed dyslipidemia ( 1.2 ). Limitations of Use: Fenofibrate at a dose equivalent to 135 mg of fenofibric acid delayed-release capsules did not reduce coronary heart disease morbidity and mortality in patients with type 2 diabetes mellitus ( 5.1 ).

1.1Treatment of Severe Hypertriglyceridemia Fenofibric acid delayed-release capsules are indicated as adjunctive therapy to diet to reduce triglycerides (TG) in patients with severe hypertriglyceridemia. Improving glycemic control in diabetic patients showing fasting chylomicronemia will usually obviate the need for pharmacological intervention. Markedly elevated levels of serum triglycerides (e.g. > 2,000 mg/dL) may increase the risk of developing pancreatitis.

The effect of fenofibric acid delayed-release capsules therapy on reducing this risk has not been adequately studied.

1.2Treatment of Primary Hypercholesterolemia or Mixed Dyslipidemia Fenofibric acid delayed-release capsules are indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein cholesterol (LDL-C), total cholesterol (Total-C), triglycerides (TG), and apolipoprotein B (Apo B), and to increase high-density lipoprotein cholesterol (HDL-C) in patients with primary hypercholesterolemia or mixed dyslipidemia.

1.3Limitations of Use Fenofibrate at a dose equivalent to 135 mg of fenofibric acid delayed-release capsules did not reduce coronary heart disease morbidity and mortality in 2 large, randomized controlled trials of patients with type 2 diabetes mellitus [see Warnings and Precautions ( 5.1 )].

1.4General Considerations for Treatment Laboratory studies should be performed to establish that lipid levels are abnormal before instituting fenofibric acid delayed-release capsules therapy. Every reasonable attempt should be made to control serum lipids with non-drug methods including appropriate diet, exercise, weight loss in obese patients, and control of any medical problems such as diabetes mellitus and hypothyroidism that may be contributing to the lipid abnormalities. Medications known to exacerbate hypertriglyceridemia (beta-blockers, thiazides, estrogens) should be discontinued or changed if possible, and excessive alcohol intake should be addressed before triglyceride-lowering drug therapy is considered.

If the decision is made to use lipid-altering drugs, the patient should be instructed that this does not reduce the importance of adhering to diet. Drug therapy is not indicated for patients who have elevations of chylomicrons and plasma triglycerides, but who have normal levels of VLDL.

⏱️ Dosage and Administration ~1 min read ▾

2 DOSAGE AND ADMINISTRATION Hypertriglyceridemia: 45 mg to 135 mg once daily ( 2.2 ). Primary hypercholesterolemia or mixed dyslipidemia: 135 mg once daily ( 2.3 ). Renally impaired patients: 45 mg once daily ( 2.4 ). Maximum dose: 135 mg once daily ( 2.1 ). May be taken without regard to food ( 2.1 ).

2.1General Considerations Patients should be placed on an appropriate lipid-lowering diet before receiving fenofibric acid delayed-release capsules and should continue this diet during treatment. Fenofibric acid delayed-release capsules can be taken without regard to meals. Patients should be advised to swallow fenofibric acid delayed-release capsules whole. Do not open, crush, dissolve, or chew capsules. Serum lipids should be monitored periodically.

2.2Severe Hypertriglyceridemia The initial dose of fenofibric acid delayed-release capsules are 45 mg to 135 mg 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. The maximum dose is 135 mg once daily.

2.3Primary Hypercholesterolemia or Mixed Dyslipidemia The dose of fenofibric acid delayed-release capsules are 135 mg once daily.

2.4Impaired Renal Function Treatment with fenofibric acid delayed-release capsules should be initiated at a dose of 45 mg once daily in patients with mild to moderate renal impairment and should only be increased after evaluation of the effects on renal function and lipid levels at this dose. The use of fenofibric acid delayed-release capsules should be avoided in patients with severely impaired renal function [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 110 words ▾

3 DOSAGE FORMS AND STRENGTHS Fenofibric acid delayed-release capsules 45 mg are the Size '3' Hard gelatin capsules of opaque reddish brown color cap imprinted with '167' in black ink, opaque yellow color body imprinted with '167' in black ink and filled with white to off white round, biconvex coated mini tablets. Fenofibric acid delayed release capsules 135 mg are the Size '0' Hard gelatin capsules of opaque blue color cap imprinted with '168' in black ink, opaque yellow color body imprinted with '168' in black ink and filled with white to off white round, biconvex coated mini tablets.

Oral Delayed-Release Capsules: 45 mg and 135 mg ( 3 ).

⛔ Contraindications 136 words ▾

4 CONTRAINDICATIONS Fenofibric acid delayed-release capsules are 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 hypersensitivity to fenofibric acid or fenofibrate [see Warnings and Precautions ( 5.9 )] .

Severe renal dysfunction, including patients receiving dialysis ( 4 , 12.3 ). Active liver disease ( 4 , 5.2 ). Gallbladder disease ( 4 , 5.5 ).

Nursing mothers ( 4 , 8.2 ). Known hypersensitivity to fenofibric acid or fenofibrate ( 4 , 5.9 ).

⚠️ 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 fenofibric acid. Monitor patient's liver function, including serum ALT, AST, and total bilirubin, at baseline and periodically for the duration of therapy. Discontinue if signs or symptoms of liver injury develop or if elevated enzyme levels persist ( 5.2 ).

Myopathy and rhabdomyolysis: Have been reported in patients taking fenofibrate. Risks are increased in elderly patients and patients with diabetes, renal failure, hypothyroidism, or statin co-administration ( 5.3 ). Serum creatinine: Fenofibric acid can reversibly increase serum creatinine levels ( 5.4 ).

Monitor renal function periodically in patients with renal insufficiency ( 8.6 ). Cholelithiasis: Fenofibric acid increases cholesterol excretion into the bile, leading to risk of cholelithiasis. If 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 fenofibric acid on coronary heart disease morbidity and mortality and non-cardiovascular mortality has not been established. Because of similarities between fenofibric acid and fenofibrate, clofibrate, and gemfibrozil, the findings in the following large randomized, placebo-controlled clinical studies with these fibrate drugs may also apply to fenofibric acid. The Action to Control Cardiovascular Risk in Diabetes Lipid (ACCORD Lipid) trial was a randomized placebo-controlled study of 5,518 patients with type 2 diabetes mellitus on background statin therapy treated with fenofibrate.

The mean duration of follow-up was 4.7 years. Fenofibrate plus statin combination therapy showed a non-significant 8% relative risk reduction in the primary outcome of major adverse cardiovascular events (MACE), a composite of non-fatal myocardial infarction, non-fatal stroke, and cardiovascular disease death (hazard ratio [HR] 0.92, 95% CI 0.79 to 1.08) (p=0.32) as compared to statin monotherapy. In a gender subgroup analysis, the hazard ratio for MACE in men receiving combination therapy versus statin monotherapy was 0.82 (95% CI 0.69 to 0.99), and the hazard ratio for MACE in women receiving combination therapy versus statin monotherapy was 1.38 (95% CI 0.98 to 1.94) (interaction p=0.01).

The clinical significance of this subgroup finding is unclear. The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study was a 5-year randomized, placebo-controlled study of 9,795 patients with type 2 diabetes mellitus treated with fenofibrate. Fenofibrate demonstrated a non-significant 11% relative reduction in the primary outcome of coronary heart disease events (hazard ratio [HR] 0.89, 95% CI 0.75 to 1.05, p = 0.16) and a significant 11% reduction in the secondary outcome of total cardiovascular disease events (HR 0.89 [0.80 to 0.99], p = 0.04).

There was a non-significant 11% (HR 1.11 [0.95, 1.29], p = 0.18) and 19% (HR 1.19 [0.90, 1.57], p = 0.22) increase in total and coronary heart disease mortality, respectively, with fenofibrate as compared to placebo. In the Coronary Drug Project, a large study of post-myocardial infarction patients treated for 5 years with clofibrate, there was no difference in mortality seen between the clofibrate group and the placebo group. There was, however, a difference in the rate of cholelithiasis… [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 )] Pancreatitis [see Warnings and Precautions ( 5.7 )] Hypersensitivity reactions [see Warnings and Precautions ( 5.9 )] Venothromboembolic disease [see Warnings and Precautions ( 5.10 )] The most common adverse events reported during clinical trials with fenofibrate (≥ 2% and at least 1% greater than placebo) were abnormal liver tests, increased AST, increased ALT, increased CPK, and rhinitis ( 6.1 ).

To report SUSPECTED ADVERSE REACTIONS, contact Laurus Generics Inc. at 1-833-3-LAURUS (1-833-352-8787) 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. Fenofibric acid is the active metabolite of fenofibrate. Adverse events reported by 2% or more of patients treated with fenofibrate and greater than placebo during double-blind, placebo-controlled trials are listed in Table 1.

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 tests were the most frequent events, causing discontinuation of fenofibrate treatment in 1.6% of patients in double-blind trials. Table 1.

Adverse Events Reported by 2% or More of Patients Treated with Fenofibrate and Greater than Placebo During the Double-Blind, Placebo-Controlled Trials BODY SYSTEM Adverse Event Fenofibrate* (N = 439) Placebo (N = 365) BODY AS A WHOLE Abdominal Pain 4.6% 4.4% Back Pain 3.4% 2.5% Headache 3.2% 2.7% DIGESTIVE Nausea 2.3% 1.9% Constipation 2.1% 1.4% INVESTIGATIONS Abnormal Liver Tests 7.5% 1.4% Increased AST 3.4% 0.5% Increased ALT 3.0% 1.6% Increased Creatine Phosphokinase 3.0% 1.4% RESPIRATORY Respiratory Disorder 6.2% 5.5% Rhinitis 2.3% 1.1% * Dosage equivalent to 135 mg fenofibric acid 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. Clinical trials with fenofibric acid did not include a placebo-control arm.

However, the adverse event profile of fenofibric acid was generally consistent with that of fenofibrate. The following adverse events not listed above were reported in ≥ 3% of patients taking fenofibric acid alone: Gastrointestinal Disorders: Diarrhea, dyspepsia General Disorders and Administration Site Conditions: Pain Infections and Infestations: Nasopharyngitis, sinusitis, upper respiratory tract infection Musculoskeletal and Connective Tissue Disorders: Arthralgia, myalgia, pain in extremity Nervous System Disorders: Dizziness Increases in Liver Enzymes In a pooled analysis of three 12-week, double-blind, controlled studies of fenofibric acid, increases in ALT and AST > 3 times the upper limit of normal on two consecutive occasions occurred in 1.9% and 0.2%, respectively, of patients receiving fenofibric acid 135 mg daily and placebo, without other lipid-altering drugs.

In a pooled analysis of 10 placebo-controlled trials, increases to > 3 times the upper limit of normal in ALT occurred in 5.3% of patients taking fenofibrate 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 90 mg to 135 mg fenofibric acid daily and was 0% in those receiving dosages equivalent to 45 mg or less fenofibric acid 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 siz… [Excerpted — this section continues on DailyMed.]

🔄 Drug Interactions ~1 min read ▾

7 DRUG INTERACTIONS Coumarin Anticoagulants: ( 7.1 ). Bile Acid Binding Resins: ( 7.2 ). Immunosuppressants: ( 7.3 ).

7.1Coumarin Anticoagulants Potentiation of coumarin-type anticoagulant effect has been observed with prolongation of the PT/INR. Caution should be exercised when oral coumarin anticoagulants are given in conjunction with fenofibric acid. The dosage of the anticoagulant 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 )].

7.2Bile Acid Binding Resins Since bile acid binding resins may bind other drugs given concurrently, patients should take fenofibric acid at least 1 hour before or 4 to 6 hours after a bile acid resin to avoid impeding its absorption.

7.3Immunosuppressants 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 drugs of the fibrate class including fenofibric acid, there is a risk that an interaction will lead to deterioration of renal function. The benefits and risks of using fenofibric acid with immunosuppressants and other potentially nephrotoxic agents should be carefully considered, and the lowest effective dose employed.

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: Dose selection should be made based on renal function ( 8.5 ). Renal Impairment: Avoid use in severe renal impairment patients. Dose adjustment 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 135 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).

Fenofibric acid should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively.

Data Animal Data In pregnant rats given oral dietary doses of 14, 127, and 361 mg/kg/day from gestation day 6 to 15 during the period of organogenesis, no adverse developmental findings were observed at 14 mg/kg/day (less than the clinical exposure at the maximum recommended human dose [MRHD] of 300 mg fenofibrate daily, equivalent to 135 mg fenofibric acid daily, based on body surface area comparisons). Increased fetal skeletal malformations were observed at maternally toxic doses (361 mg/kg/day, corresponding to 12 times the clinical exposure at the MRHD) that significantly suppressed maternal body weight gain.

In pregnant rabbits given oral gavage doses of 15, 150, 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, 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 fenofibric acid and for 5 days after the final dose [see Contraindications ( 4 )] .

8.4Pediatric Use The safety and effectiveness of fenofibric acid in pediatric patients have not been established.

8.5Geriatric Use Fenofibric acid is substantially excreted by the kidney as fenofibric acid and fenofibric acid glucuronide, and the risk of adverse reactions to this drug may be greater in patients with impaired renal function. Fenofibric acid exposure is not influenc… [Excerpted — this section continues on DailyMed.]

🆘 Overdosage 71 words ▾

10 OVERDOSAGE There is no specific treatment for overdose with fenofibric acid. General supportive care of the patient is indicated, including monitoring of vital signs and observation of clinical status, should an overdose occur. If indicated, elimination of unabsorbed drug should be achieved by emesis or gastric lavage; usual precautions should be observed to maintain the airway.

Because fenofibric acid is highly bound to plasma proteins, hemodialysis should not be considered.

🧬 Clinical Pharmacology ~3 min read ▾

12 CLINICAL PHARMACOLOGY

12.1Mechanism of Action The active moiety of fenofibric acid delayed-release capsules are 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, fenofibric acid increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of Apo CIII (an inhibitor of lipoprotein lipase activity). Activation of PPARα also induces an increase in the synthesis of HDL-C and Apo AI and AII.

12.3Pharmacokinetics Fenofibric acid delayed-release capsules contains fenofibric acid, which is the only circulating pharmacologically active moiety in plasma after oral administration of fenofibric acid. Fenofibric acid is also the circulating pharmacologically active moiety in plasma after oral administration of fenofibrate, the ester of fenofibric acid. Plasma concentrations of fenofibric acid after administration of one 135 mg fenofibric acid delayed-release capsules are equivalent to those after one 200 mg capsule of micronized fenofibrate administered under fed conditions.

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 under fasting conditions.

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, fenofibric acid levels reach steady state within 8 days. Plasma concentrations of fenofibric acid at steady state are approximately slightly more than double those following a single dose.

Serum protein binding is approximately 99% in normal and dyslipidemic subjects. 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. Elimination After absorption, fenofibric acid is primarily excreted in the urine in the form of fenofibric acid and fenofibric acid glucuronide. Fenofibric acid is eliminated with a half-life of approximately 20 hours, allowing once daily administration of fenofibric acid delayed-release capsules.

Specific Populations Geriatrics In five 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 an equivalent dose of fenofibric acid can be used in elderly subjects with normal renal function, without increasing accumulation of the drug or metabolites [see Use in Specific Populations ( 8.5 )] . Pediatrics The pharmacokinetics of fenofibric acid has not been studied in pediatric populations.

Gender No pharmacokinetic difference between males and females has been observed for fenofibric acid. Race 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. Renal Impairment The pharmacokinetics of fenofibric acid was examined in patients with mild, moderate, and severe renal im… [Excerpted — this section continues on DailyMed.]

📦 How Supplied / Storage and Handling 169 words ▾

16 HOW SUPPLIED/STORAGE AND HANDLING Fenofibric acid delayed-release capsules 45 mg are the Size '3' Hard gelatin capsules of opaque reddish brown color cap imprinted with '167' in black ink, opaque yellow color body imprinted with '167' in black ink and filled with white to off white round, biconvex coated mini tablets. Bottle of 30 capsules with child-resistant closure, NDC 42385-944-30 Bottle of 90 capsules with child-resistant closure, NDC 42385-944-90 Bottle of 1,000 capsules, NDC 42385-944-11 Fenofibric acid delayed-release capsules 135 mg are the Size '0' Hard gelatin capsules of opaque blue color cap imprinted with '168' in black ink, opaque yellow color body, imprinted with '168' in black ink and filled with white to off white round, biconvex, coated mini tablets.

Bottle of 30 capsules with child-resistant closure, NDC 42385-945-30 Bottle of 90 capsules with child-resistant closure, NDC 42385-945-90 Bottle of 1,000 capsules, NDC 42385-945-11 Store at 20° to 25°C (68° to 77°F) [see USP Controlled Room Temperature]. Keep out of the reach of children. Protect from moisture.

📋 Description 204 words ▾

11 DESCRIPTION Fenofibric acid delayed-release capsules are lipid regulating agent available as delayed release capsules for oral administration. Each delayed release capsule contains choline fenofibrate, equivalent to 45 mg or 135 mg of fenofibric acid. The chemical name for choline fenofibrate is ethanaminium, 2-hydroxy-N,N,N-trimethyl, 2-{4-(4-chlorobenzoyl)phenoxy] -2-methylpropanoate (1:1) with the following structural formula: The molecular formula is C 22 H 28 ClNO 5 and the molecular weight is 421.9.

Choline fenofibrate is very soluble in water and freely soluble in methanol. The melting point is approximately 210°C. Choline fenofibrate is a white to off-white crystalline powder.

Each delayed release capsule contains enteric coated mini-tablets comprised of choline fenofibrate and the following inactive ingredients: Colloidal silicon dioxide, hydroxypropyl cellulose, hypromellose 2208, methacrylic acid and ethyl acrylate copolymer dispersion (sodium lauryl sulfate, polysorbate 80 and methacrylic acid and ethyl acrylate copolymer), povidone, sodium stearyl fumarate, talc and triethyl citrate. Capsule shell contains: gelatin, iron oxide black, iron oxide yellow, sodium lauryl sulfate and titanium dioxide.

Additionally, 45 mg contains: iron oxide red. 135 mg contains: FD & C blue 1, FD & C red 3, FD & C red 40. The imprinting ink contains: black iron oxide, potassium hydroxide, propylene glycol, shellac and strong ammonia solution.

Image

💬 Information for Patients ~1 min read ▾

17 PATIENT COUNSELING INFORMATION Patient Counseling Patients should be advised: of the potential benefits and risks of fenofibric acid delayed-release capsules. not to use fenofibric acid delayed-release capsules if there is a known hypersensitivity to fenofibrate or fenofibric acid. of medications that should not be taken in combination with fenofibric acid delayed-release capsules. that if they are taking coumarin anticoagulants, fenofibric acid delayed-release capsules may increase their anti-coagulant effect, and increased monitoring may be necessary. to continue to follow an appropriate lipid-modifying diet while taking fenofibric acid delayed-release capsules. to take fenofibric acid delayed-release capsules once daily, without regard to food, at the prescribed dose, swallowing each capsule 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 fenofibric acid delayed-release capsules. to inform their physician of symptoms of liver injury (e.g., jaundice, abdominal pain, nausea, malaise, dark urine, abnormal stool, pruritus); any muscle pain, tenderness, or weakness; or any other new symptoms. not to breastfeed during treatment with fenofibric acid delayed-release capsules and for 5 days after the final dose. The brand names listed are trademarks of their respective owners and are not trademarks of Graviti Pharmaceuticals Private Limited.

Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088. For more information call Laurus Generics Inc. at 1-833-3-LAURUS (1-833-352-8787).

Manufactured by: Graviti Pharmaceuticals Pvt. Ltd. Telangana-502307, INDIA.

Manufactured for: Laurus Generics Inc. 400 Connell Drive, Suite 5200 Berkeley Heights, NJ 07922 Revised: December, 2021

🔬 Clinical Studies ~3 min read ▾

14 CLINICAL STUDIES

14.1Severe 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 1,500 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 135 mg once daily of fenofibric acid decreased primarily VLDL-TG and VLDL-C.

Treatment of patients with elevated TG often results in an increase of LDL-C (Table 4). Table 4. Effects of Fenofibrate in Patients With Severe Hypertriglyceridemia Study 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 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 1,500 mg/dL N Baseline Mean (mg/dL) Endpoint Mean (mg/dL) Mean % Change N Baseline Mean (mg/dL) Endpoint Mean (mg/dL) Mean % Change 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* * = p < 0.05 vs.

Placebo

14.2Primary Hypercholesterolemia (Heterozygous Familial and Nonfamilial) and Mixed Dyslipidemia The effects of fenofibrate at a dose equivalent to fenofibric acid 135 mg once daily 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 therapy lowered LDL-C, Total-C, and the LDL-C/HDL-C ratio. Fenofibrate therapy also lowered triglycerides and raised HDL-C (Table 5).

Table 5. Mean Percent Change in Lipid Parameters at End of Treatment † Treatment Group Total-C (mg/dL) LDL-C (mg/dL) HDL-C (mg/dL) TG (mg/dL) Pooled Cohort Mean baseline lipid values (n = 646) 306.9 213.8 52.3 191.0 All Fenofibrate (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) 307.7 227.7 58.1 101.7 All Fenofibrate (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) 312.8 219.8 46.7 231.9 All Fenofibrate (n = 126) -16.8%* -20.1%* +14.6%* -35.9%* Placebo (n = 116) -3.0% -6.6% +2.3% +0.9% † Duration of study treatment was 3 to 6 months * p = < 0.05 vs.

Placebo 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).

🧪 Nonclinical Toxicology ~3 min read ▾

13 NONCLINICAL TOXICOLOGY

13.1Carcinogenesis, Mutagenesis, Impairment of Fertility 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 or fenofibrate.

Fenofibrate 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 135 mg fenofibric acid 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 ~3 min read ▾

13.1Carcinogenesis, Mutagenesis, Impairment of Fertility 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 or fenofibrate.

Fenofibrate 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 135 mg fenofibric acid 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 11 words ▾

RECENT MAJOR CHANGES Warnings and Precautions, Hepatotoxicity ( 5.2 ) 03/2021

📄 Package Label / Principal Display Panel 39 words ▾

PACKAGE LABEL PRINCIPAL DISPLAY PANEL NDC 42385- 944 -90 Fenofibric Acid Delayed-Release Capsules 45 mg* Rx only 90 Capsules Laurus Labs NDC 42385- 945 -90 Fenofibric Acid Delayed-Release Capsules 135 mg* Rx only 90 Capsules Laurus Labs Image image

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

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