FENOFIBRIC ACID DELAYED-RELEASE 45 mg Capsule, Delayed Release, 1,000-count
🆔 Identity & classification
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🏷️ RxNorm drug class
This medicine belongs to the Peroxisome Proliferator-activated Receptor alpha Agonist class.
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🏭 Manufacturer & labeler
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🩺 Clinical
Fenofibrate is used to reduce the amount of cholesterol (a fat-like substance that can build up in blood vessels leading to heart attack or strokes or other medical conditions) and triglycerides (other fatty substances) in the blood. Fenofibrate is in a class of medications called fibrates. It works by speeding the natural processes that remove cholesterol from the body.
Read the full MedlinePlus article ↗- Fenofibrate helps bring your blood lipid levels into a healthier range. Depending on your situation, that might mean lowering your triglycerides, bringing down your LDL (bad) chole...
- What exactly is fenofibrate supposed to do for me?
- It depends on which form you have. Lipofen capsules should be taken with food. Antara capsules and most fenofibrate tablets can be taken with or without food. Some film-coated feno...
- Does it matter if I take this with food or on an empty stomach?
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🧪 Inactive Ingredients / Excipients
Inactive ingredients, also called excipients, are components of the drug product other than the active ingredient. They may include fillers, dyes, coatings, preservatives, flavors, or other formulation ingredients.
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💲 Pricing
A drug doesn't have one price. Each row is a different public payment system, and none is what you'd pay at the counter — that depends on your insurance. The ⓘ on each row explains what it measures.
| Price system | Per each | Per package |
|---|---|---|
| Retail pharmacies payNADAC · weekly | Not in the retail survey — common for institutional, discontinued, or low-volume packs. | |
| 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 | $557.90 / 1000 capsules |
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🔁 Therapeutic equivalents
| Product | Labeler | Pack | NADAC/unit | TE | Status | Price vs. this |
|---|---|---|---|---|---|---|
| Fenofibric Acid 45 mg 59651-0216-90 | Aurobindo | 90 capsules | $0.144 | AB | Availability likely | — |
| Fenofibric Acid 45 mg 69315-0281-09 | Leading | 90 capsules | $0.144 | AB | Availability likely | — |
| Fenofibric Acid 45 mg 00115-1554-10 | Amneal | 90 capsules | $0.150 | — | Discontinued | — |
| 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 Delayed-Release 45 mgthis 42385-0944-11 | Laurus | 1000 capsules | — | AB | Discontinued | — |
| 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 | — |
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⏳ Availability & generic status
This product is an FDA-approved generic. Other versions of the same drug are listed under Therapeutic equivalents, least expensive first.
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🔬 Reported adverse events (FAERS)
Top reported reactions
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📦 Packaging — all sizes for this product
| Package NDC | Description | Per unit | Per pack | Marketing start | Status |
|---|---|---|---|---|---|
| 42385-0944-11 You're viewing this | 1000 CAPSULE, DELAYED RELEASE in 1 BOTTLE (42385-944-11) | — | — | 2020-08-24 | Discontinued by firm |
| 42385-0944-30 | 30 CAPSULE, DELAYED RELEASE in 1 BOTTLE (42385-944-30) | — | — | 2020-08-24 | Discontinued by firm |
| 42385-0944-90 | 90 CAPSULE, DELAYED RELEASE in 1 BOTTLE (42385-944-90) | $0.1444 / ea | $13.00 | 2020-08-24 | Discontinued by firm |
You're viewing the largest of 3 pack sizes for this product.
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What quantity is in NDC 42385-0944-11?
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What NDC number is used to bill for this package of FENOFIBRIC ACID DELAYED-RELEASE 45 mg Capsule, Delayed Release?
Prices are the latest CMS NADAC pharmacy acquisition cost per NDC; per-pack figures are per-unit × pack quantity, shown only when the pack is denominated in the same measure NADAC prices.
🧭 About this NDC listing & data coverage
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| NDC identity (package / product / labeler codes) | ✓ Available |
| Labeler | ✓ Available |
| Product & package description | ✓ Available |
| Marketing category & status | ✓ Available |
| Active ingredient / dosage form / route | ✓ Available |
| FDA label (SPL via DailyMed) | ✓ Available |
| Package photos | — 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) | — Not published for this NDC CMS publishes NADAC only for NDCs reported in its retail-pharmacy survey. |
| Orange Book / therapeutic-equivalence data | ✓ Available |
| HCPCS J-code billing crosswalk | — Not published for this NDC Most self-administered / retail products have no J-code — that is normal. |
| Medicaid utilization (CMS SDUD) | — Not published for this NDC CMS reports utilization only for NDCs with Medicaid claims above its privacy threshold. |
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📄 Full prescribing information FDA SPL
🎯 Indications and Usage ▾
1 INDICATIONS AND USAGE 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 ▾
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 ▾
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 ▾
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 ▾
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…
🤒 Adverse Reactions ▾
6 ADVERSE REACTIONS The following serious adverse reactions are described below and elsewhere in the labeling: Mortality and coronary heart disease morbidity [see Warnings and Precautions ( 5.1 )] Hepatoxicity [see Warnings and Precautions ( 5.2 )] 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…
🔄 Drug Interactions ▾
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 ▾
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…
🆘 Overdosage ▾
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 ▾
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…
📦 How Supplied / Storage and Handling ▾
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 ▾
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.
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💬 Information for Patients ▾
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