Fenofibrate 134 mg Capsule, 30-count — NDC 69097-895-02 (Billing 69097-0895-02)
This is a package of 30 capsules of Fenofibrate 134 mg Capsule from Cipla USA Inc.,, marketed since Mar 2017 and currently FDA-listed.
NDC database record
One package, one record: these facts belong to NDC 69097-895-02 alone.
- Record
- FDA NDC Directory package listing · Human prescription drug
- Code segments
- 69097 labeler · 895 product · 02 package
- Package marketed since
- Mar 30, 2017
- Sample package
- No — commercial package
- Listing certified through
- Dec 31, 2026
- Barcode (UPC)
- 0369097896072, 0369097895075
- FDA record last changed
- Jul 24, 2026
Other active recalls for Fenofibrate (different manufacturers) — 2 · tap to view
Identity & classification
Regulatory identifiers FDA, NLM and CMS codes for this package
Drug-database identifiers Medi-Span GPI and First Databank GCN / HICL / AHFS classification
- GSN (GCN sequence number): 044305
- GCN: 92504
- GPI-14 (Medi-Span): 39200025100115
- HICL (First Databank): 020377
- AHFS class code: 24:06.06.00
- RxCUI (RxNorm): 200311
Where does this data come from?
- FDA openFDA NDC Directory · synced Oct 1, 2026
- FDA label on DailyMed · label index refreshed Oct 5, 2026
- RxNorm (NLM RxNav) · catalog refreshed Oct 1, 2026
- Medi-Span GPI (licensed)
- First Databank (licensed) · refreshed Oct 1, 2026
RxNorm drug class
This medicine belongs to the Peroxisome Proliferator-activated Receptor alpha Agonist class.
Where does this data come from?
- RxClass (NLM) · catalog refreshed Oct 1, 2026
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 ↗- 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...
Patient education
Supplement & herbal interactions
Some supplements/herbs that may interact with Fenofibrate — tap one for details:
Where does this data come from?
- MedlinePlus (NLM) · refreshed Oct 1, 2026
- FDA label on DailyMed · label index refreshed Oct 5, 2026
Ask a licensed pharmacist directly — free, answered by our team.
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 | $0.2819 | $8.46 / 30 capsules |
Where does this data come from?
- CMS NADAC weekly file
- CMS ASP pricing files · refreshed Sep 20, 2026
- CMS Medicaid State Drug Utilization Data · refreshed Oct 5, 2026
- CMS Part D plan pricing files · refreshed Sep 24, 2026
- VA National Acquisition Center price file
Packaging — all sizes for this product
| Package NDC | Description | Per unit | Per pack | Marketing start | Marketing end | Status |
|---|---|---|---|---|---|---|
| 69097-0895-02 You're viewing this | 30 CAPSULE in 1 BOTTLE, PLASTIC | — | — | 2017-03-30 | — | Active |
| 69097-0895-07 69097-895-07 Main listing | 100 CAPSULE in 1 BOTTLE, PLASTIC | $0.1089 / ea | $10.89 | 2017-03-30 | — | Active |
| 69097-0895-12 69097-895-12 | 500 CAPSULE in 1 BOTTLE, PLASTIC | — | — | 2017-03-30 | — | Active |
You're viewing the smallest of 3 pack sizes for this product.
Pack size FAQ
What quantity is in this package?
How does this package differ from NDC 69097-0895-07?
What NDC number is used to bill for this package of Fenofibrate 134 mg Capsule?
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
| Product | Labeler | Pack | NADAC/unit | TE | Status | Price vs. this |
|---|---|---|---|---|---|---|
| Fenofibrate 134 mg 13668-0439-01 | Torrent | 100 capsules | $0.119 | AB | Availability likely | — |
| Fenofibrate 134 mg 27241-0119-04 | Ajanta | 100 capsules | $0.119 | AB | Availability likely | — |
| Fenofibrate 134 mg 42858-0134-01 | Rhodes | 100 capsules | $0.119 | AB | Discontinued | — |
| Fenofibrate 134 mg 43975-0305-10 | ANI | 100 capsules | $0.119 | AB | Availability likely | — |
| Fenofibrate 134 mg 59651-0202-01 | Aurobindo | 100 capsules | $0.119 | AB | Availability likely | — |
| fenofibrate 134 mg 62135-0894-90 | Chartwell | 90 capsules | $0.119 | AB | Availability likely | — |
| fenofibrate 134 mg 68462-0581-01 | Glenmark | 100 capsules | $0.119 | AB | Availability likely | — |
| Fenofibrate 134 mg 35561-0346-11 | Bostal | 90 capsules | — | AB | FDA listed | — |
| Fenofibrate 134 mg 46708-0085-30 | Alembic | 30 capsules | — | AB | FDA listed | — |
| fenofibrate 134 mg 50090-6120-00 | A-S | 90 capsules | — | AB | FDA listed | — |
| Fenofibrate 134 mg 62332-0085-30 | Alembic | 30 capsules | — | AB | FDA listed | — |
| Fenofibrate 134 mgthis 69097-0895-02 | Cipla | 30 capsules | — | — | FDA listed | — |
Where does this data come from?
- FDA openFDA NDC Directory · synced Oct 1, 2026
- FDA Orange Book · refreshed Oct 3, 2026
- CMS NADAC weekly file
Availability & generic status
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?
- FDA Orange Book · refreshed Oct 3, 2026
What it looks like
Where does this data come from?
- FDA label on DailyMed · label index refreshed Oct 5, 2026
Inactive Ingredients / Excipients
Inactive ingredients, also called excipients, are components of the drug product other than the active ingredient. They may include fillers, dyes, coatings, preservatives, flavors, or other formulation ingredients.
💡 Tap an ingredient (hover on desktop) to see what it is and why it’s used.
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UNII 2S7830E561
Crospovidone is a synthetic polymer derived from povidone. It acts as a disintegrant, helping the tablet or capsule break apart quickly in the stomach so the active ingredient can be absorbed.
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UNII 767IP0Y5NH
A synthetic red colorant used to give medicines their color. It helps patients identify their medication and makes the product visually appealing.
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UNII H3R47K3TBD
FD&C Blue No. 1 is a synthetic blue dye approved for use in foods and medicines. It serves as a colorant to give the medication its distinctive appearance and help with product identification.
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UNII 2G86QN327L
Gelatin is a protein derived from animal collagen, commonly used in medicines as a gelling agent and capsule material. It helps create soft or hard capsule shells that hold and release medication, and can also thicken liquid formulations.
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UNII EWQ57Q8I5X
Lactose monohydrate is a natural sugar derived from milk. It serves as a filler and binder in tablets and capsules, helping create the proper size, texture, and consistency of the medicine.
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UNII 70097M6I30
Magnesium stearate is a salt made from magnesium and stearic acid, a fatty substance. It's used in tablets and capsules as a lubricant and glidant to help ingredients flow smoothly during manufacturing and prevent sticking.
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UNII FZ989GH94E
Povidone is a synthetic polymer made from a plastic-like material. It acts as a binder to hold tablet ingredients together and as a disintegrant to help the tablet break apart in your stomach so the medicine can be absorbed.
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UNII ETJ7Z6XBU4
Silicon dioxide is a naturally occurring mineral used as a glidant and anti-caking agent. It helps powder ingredients flow smoothly and prevents clumping during manufacturing and storage.
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UNII 368GB5141J
A detergent and foaming agent derived from coconut or palm oil. In medications, it helps break down and mix oil and water-based ingredients, aids in tablet disintegration, and improves how the drug dissolves and spreads in the mouth or digestive system.
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UNII 15FIX9V2JP
Titanium dioxide is a bright white mineral powder commonly used as a colorant and opacifying agent. It makes pills and tablets white or lighter in color and helps make coatings non-transparent.
10 inactive ingredients listed in the exact product block matched to this NDC.
Where does this data come from?
ingredient classCode="IACT" elements from the exact product block matched by this NDC. Label-section narrative from DailyMed / the openFDA label index is shown separately when available.- FDA label on DailyMed · label index refreshed Oct 5, 2026
- FDA openFDA NDC Directory · synced Oct 1, 2026
Inactive ingredient FAQ
Are inactive ingredients the same for every manufacturer?
Why might an inactive ingredient be missing?
Can inactive ingredients matter?
Manufacturer & labeler
More NDCs from Cipla USA Inc., labeler code 69097
- Bupropion Hydrochloride (SR) 150 mg Tablet, Extended Release NDC 69097-878-02
- Bupropion Hydrochloride (SR) 200 mg Tablet, Extended Release NDC 69097-879-02
- Lanreotide Acetate 60 mg/.2mL Injection NDC 69097-880-67
- Lanreotide Acetate 90 mg/.3mL Injection NDC 69097-890-67
- Sevelamer carbonate 800 mg Tablet, Film Coated NDC 69097-893-93
- Fenofibrate 67 mg Capsule NDC 69097-894-02
- Fenofibrate 200 mg Capsule NDC 69097-896-02
- Atorvastatin Calcium 10 mg Tablet, Film Coated NDC 69097-897-05
- Atorvastatin Calcium 20 mg Tablet, Film Coated NDC 69097-898-05
- Atorvastatin Calcium 40 mg Tablet, Film Coated NDC 69097-899-05
- OSELTAMIVIR PHOSPHATE 6 mg/mL For Suspension NDC 69097-904-43
- LANREOTIDE ACETATE 120 mg/.5mL Injection NDC 69097-906-67
Where does this data come from?
- FDA openFDA NDC Directory · synced Oct 1, 2026
- Drugs@FDA
Full prescribing information FDA SPL
🎯 Indications and Usage ▾
INDICATIONS AND USAGE Treatment of Hypercholesterolemia Fenofibrate capsules, USP are indicated as adjunctive therapy to diet for the reduction of LDLC, total-C, Triglycerides and apo B in adult patients with primary hypercholesterolemia or mixed dyslipidemia (Fredrickson Types IIa and IIb). Lipid altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and non-pharmacological interventions alone has been inadequate (see National Cholesterol Education Program [NCEP] Treatment Guidelines , below).
Treatment of Hypertriglyceridemia Fenofibrate capsules, USP are also indicated as adjunctive therapy to diet for treatment of adult patients with hypertriglyceridemia (Fredrickson Types IV and V hyperlipidemia). Improving glycemic control in diabetic patients showing fasting chylomicronemia will usually reduce fasting triglycerides and eliminate chylomicronemia thereby obviating the need for pharmacologic intervention. Markedly elevated levels of serum triglycerides (e.g. > 2,000 mg/dL) may increase the risk of developing pancreatitis.
The effect of fenofibrate therapy on reducing this risk has not been adequately studied. Drug therapy is not indicated for patients with Type I hyperlipoproteinemia, who have elevations of chylomicrons and plasma triglycerides, but who have normal levels of very low density lipoprotein (VLDL). Inspection of plasma refrigerated for 14 hours is helpful in distinguishing Types I, IV and V hyperlipoproteinemia 2 .
The initial treatment for dyslipidemia is dietary therapy specific for the type of lipoprotein abnormality. Excess body weight and excess alcoholic intake may be important factors in hypertriglyceridemia and should be addressed prior to any drug therapy. Physical exercise can be an important ancillary measure.
Diseases contributory to hyperlipidemia, such as hypothyroidism or diabetes mellitus should be looked for and adequately treated. Estrogen therapy, like thiazide diuretics and beta-blockers, is sometimes associated with massive rises in plasma triglycerides, especially in subjects with familial hypertriglyceridemia. In such cases, discontinuation of the specific etiologic agent may obviate the need for specific drug therapy of hypertriglyceridemia.
The use of drugs should be considered only when reasonable attempts have been made to obtain satisfactory results with non-drug methods. If the decision is made to use drugs, the patient should be instructed that this does not reduce the importance of adhering to diet (See WARNINGS and PRECAUTIONS ). Fredrickson Classification of Hyperlipoproteinemias C = cholesterol TG = triglycerides LDL = low density lipoprotein VLDL = very lot density lipoprotein IDL = intermediate density lipoprotein Lipid Elevation Type Lipoprotein Elevated Major Minor I (rare) IIa IIb III (rare) IV V (rare) Chylomicrons LDL LDL, VLDL IDL VLDL Chylomicrons, VLDL TG C C C, TG TG TG ↑ ↔ C - TG - ↑ ↔ C ↑ ↔ The NCEP Treatment Guidelines Definite Atherosclerotic Two or More Other LDL-Cholesterol mg/dL (mmol/L) Disease Coronary heart disease or peripheral vascular disease (including symptomatic carotid artery disease).
Risk Factors Other risk factors for coronary heart disease (CHD) include: age (males: ≥ 45 years; females: ≥ 55 years or premature menopause without estrogen replacement therapy); family history of premature CHD; current cigarette smoking; hypertension; confirmed HDL-C < 35 mg/dL (< 0.91 mmol/L); and diabetes mellitus. Subtract I risk favor if HDL-C is ≥ 60 mg/dL (≥ 1.6 mmol/L) Initiation Level Goal No No Yes No Yes Yes or No ≥ 190 (≥ 4.9) ≥ 160 (≥ 4.1) ≥ 130 In CHD patients with LDL-C levels 100 to 129 mg/dL, the physician should exercise clinical judgment in deciding whether to initiate drug treatment.
(≥ 3.4) < 160 (< 4.1) < 130 (< 3.4) < 100 (< 2.6)
⏱️ Dosage and Administration ▾
DOSAGE AND ADMINISTRATION Patients should be placed on an appropriate lipid-lowering diet before receiving fenofibrate capsules, and should continue this diet during treatment with fenofibrate capsules. Fenofibrate capsules should be given with meals, thereby optimizing the bioavailability of the medication. For the treatment of adult patients with primary hypercholesterolemia or mixed hyperlipidemia, the initial dose of fenofibrate capsules is 200 mg per day.
For adult patients with hypertriglyceridemia, the initial dose is 67 to 200 mg per day. Dosage should be individualized according to patient response, and should be adjusted if necessary following repeat lipid determinations at 4 to 8 week intervals. The maximum dose is 200 mg per day.
Treatment with fenofibrate capsules should be initiated at a dose of 67 mg/day in patients having impaired renal function, and increased only after evaluation of the effects on renal function and lipid levels at this dose. In the elderly, the initial dose should likewise be limited to 67 mg/day. Lipid levels should be monitored periodically and consideration should be given to reducing the dosage of fenofibrate capsules if lipid levels fall significantly below the targeted range.
⛔ Contraindications ▾
CONTRAINDICATIONS Fenofibrate capsules are contraindicated in patients who exhibit hypersensitivity to fenofibrate. Fenofibrate capsules are contraindicated in patients with hepatic or severe renal dysfunction, including primary biliary cirrhosis, and patients with unexplained persistent liver function abnormality. Fenofibrate capsules are contraindicated in patients with preexisting gallbladder disease (see WARNINGS ).
⚠️ Warnings ▾
WARNINGS Liver Function Fenofibrate capsules at doses equivalent to 134 mg to 200 mg fenofibrate per day has been associated with increases in serum transaminases [AST (SGOT) or ALT (SGPT)]. In a pooled analysis of 10 placebo controlled trials, increases to > 3 times the upper limit of normal occurred in 5.3% of patients taking fenofibrate versus 1.1% of patients treated with placebo. When transaminase determinations were followed either after discontinuation of treatment or during continued treatment, a return to normal limits was usually observed.
The incidence of increases in transaminase related to fenofibrate therapy appear to be dose related. In an 8 week dose-ranging study, the incidence of ALT or AST elevations to at least three times the upper limit of normal was 13% in patients receiving dosages equivalent to 134 mg to 200 mg fenofibrate per day and was 0% in those receiving dosages equivalent to 34 mg or 67 mg of fenofibrate per day or placebo. Hepatocellular, chronic active and cholestatic hepatitis associated with fenofibrate therapy have been reported after exposures of weeks to several years.
In extremely rare cases, cirrhosis has been reported in association with chronic active hepatitis. Regular periodic monitoring of liver function, including serum ALT (SGPT) should be performed for the duration of therapy with fenofibrate, and therapy discontinued if enzyme levels persist above three times the normal limit. Cholelithiasis Fenofibrate, like clofibrate and gemfibrozil, may increase cholesterol excretion into the bile, leading to cholelithiasis.
If cholelithiasis is suspected, gallbladder studies are indicated. Fenofibrate therapy should be discontinued if gallstones are found. Concomitant Oral Anticoagulants Caution should be exercised when anticoagulants are given in conjunction with fenofibrate because of the potentiation of coumarin-type anticoagulants in prolonging the prothrombin time/INR.
The dosage of the anticoagulant should be reduced to maintain the prothrombin time/lNR at the desired level to prevent bleeding complications. Frequent prothrombin time/INR determinations are advisable until it has been definitely determined that the prothrombin time/INR has stabilized. Concomitant HMG-CoA Reductase Inhibitors The combined use of fenofibrate and HMG-CoA reductase inhibitors should be avoided unless the benefit of further alterations in lipid levels is likely to outweigh the increased risk of this drug combination.
Concomitant administration of fenofibrate (equivalent to fenofibrate 200 mg) and pravastatin (40 mg) once daily for 10 days increased the mean C max and AUC values for pravastatin by 36% (range from 69% decrease to 321% increase) and 28% (range from 54% decrease to 128% increase), respectively, and for 3α-hydroxy-iso-pravastatin by 55% (range from 32% decrease to 314% increase) and 39% (range from 24% decrease to 261% increase), respectively. (See also CLINICAL PHARMACOLOGY, Drug-drug interactions .) The combined use of fibric acid derivatives and HMG-CoA reductase inhibitors has been associated, in the absences of a marked pharmacokinetic interaction, in numerous case reports, with rhabdomyolysis, markedly elevated creatine kinase (CK) levels and myoglobinuria, leading in a high proportion of cases to acute renal failure.
The use of fibrates alone, including fenofibrate capsules may occasionally be associated with myositis, myopathy, or rhabdomyolysis. Patients receiving fenofibrate and complaining of muscle pain, tenderness, or weakness should have prompt medical evaluation for myopathy, including serum creatine kinase level determination. If myopathy/myositis is suspected or diagnosed, fenofibrate therapy should be stopped.
Mortality The effect of fenofibrate on coronary heart disease morbidity and mortality and noncardiovascular mortality has not been established. Other Considerations The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study was a 5 year randomized, placebo… [Excerpted — this section continues on DailyMed.]
🤒 Adverse Reactions ▾
ADVERSE REACTIONS Clinical Trials Experience Because clinical studies are conducted under widely varying conditions, adverse reaction rates observed in the clinical studies of a drug cannot be directly compared to rates in the clinical studies of another drug and may not reflect the rates observed in practice. Adverse events reported by 2% or more of patients treated with fenofibrate (and greater than placebo) during the double-blind, placebo-controlled trials, regardless of causality, are listed in Table 3 below. Adverse events led to discontinuation of treatment in 5.0% of patients treated with fenofibrate and in 3.0% treated with placebo.
Increases in liver function tests were the most frequent events, causing discontinuation of fenofibrate treatment in 1.6% of patients in double-blind trials. Table 3. Adverse Reactions Reported by 2% or More of Patients Treated with Fenofibrate and Greater than Placebo During the Double-Blind, Placebo-Controlled Trials BODY SYSTEM Fenofibrate Dosage equivalent to 145 mg fenofibrate.
PLACEBO Adverse Reaction (N = 439) (N = 365) BODY AS A WHOLE Abdominal Pain 4.6% 4.4% Back Pain 3.4% 2.5% Headache 3.2% 2.7% DIGESTIVE Abnormal Liver Function Tests 7.5% Significantly different from Placebo. 1.4% Nausea 2.3% 1.9% Constipation 2.1% 1.4% METABOLIC AND NUTRITIONAL DISORDERS Increased ALT 3% 1.6% Increased CPK 3% 1.4% Increased AST 3.4% 0.5% RESPIRATORY Respiratory Disorder 6.2% 5.5% Rhinitis 2.3% 1.1% Post-Marketing Experience The following adverse reactions have been identified during post-approval use of fenofibrate:myalgia, rhabdomyolysis, pancreatitis, acute renal failure, muscle spasm, hepatitis, cirrhosis,anemia, arthralgia, decreases in hemoglobin, decreases in hematocrit, white blood cell decreases, asthenia and interstitial lung diseases.
Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure. Photosensitivity reactions have occurred days to months after initiation; in some of these cases, patients reported a prior photosensitivity reaction to ketoprofen.
🔄 Drug Interactions ▾
Drug Interactions Oral Anticoagulants CAUTION SHOULD BE EXERCISED WHEN COUMARIN ANTICOAGULANTS ARE GIVEN IN CONJUNCTION WITH FENOFIBRATE CAPSULES. THE DOSAGE OF THE ANTICOAGULANTS SHOULD BE REDUCED TO MAINTAIN THE PROTHROMBIN TIME/INR AT THE DESIRED LEVEL TO PREVENT BLEEDING COMPLICATIONS. FREQUENT PROTHROMBIN TIME/INR DETERMINATIONS ARE ADVISABLE UNTIL IT HAS BEEN DEFINITELY DETERMINED THAT THE PROTHROMBIN TIME/INR HAS STABILIZED.
HMG-CoA Reductase Inhibitors The combined use of fenofibrate and HMG-CoA reductase inhibitors should be avoided unless the benefit of further alterations in lipid levels is likely to outweigh the increased risk of this drug combination (see WARNINGS ). Resins Since bile acid sequestrants may bind other drugs given concurrently, patients should take fenofibrate capsules at least 1 hour before or 4 to 6 hours after a bile acid binding resin to avoid impeding its absorption. Cyclosporine Because cyclosporine can produce nephrotoxicity with decreases in creatinine clearance and rises in serum creatinine, and because renal excretion is the primary elimination route of fibrate drugs including fenofibrate, there is a risk that an interaction will lead to deterioration.
The benefits and risks of using fenofibrate with immunosuppressants and other potentially nephrotoxic agents should be carefully considered, and the lowest effective dose employed.
🧒 Pediatric Use ▾
Pediatric Use Safety and efficacy in pediatric patients have not been established.
🧓 Geriatric Use ▾
Geriatric Use Fenofibric acid is known to be substantially excreted by the kidney, and the risk of adverse reactions to this drug may be greater in patients with impaired renal function. Fenofibric acid exposure is not influenced by age. However, elderly patients have a higher incidence of renal impairment, such that dose selection for the elderly should be made on the basis of renal function (see CLINICAL PHARMACOLOGY, Special Populations, Renal Insufficiency ).
Elderly patients with normal renal function should require no dose modifications.
🆘 Overdosage ▾
OVERDOSAGE There is no specific treatment for overdose with fenofibrate. General supportive care of the patient is indicated, including monitoring of vital signs and observation of clinical status, should an overdose occur. If indicated, elimination of unabsorbed drug should be achieved by emesis or gastric lavage; usual precautions should be observed to maintain the airway.
Because fenofibrate is highly bound to plasma proteins, hemodialysis should not be considered.
🧬 Clinical Pharmacology ▾
CLINICAL PHARMACOLOGY A variety of clinical studies have demonstrated that elevated levels of total cholesterol (total-C), low density lipoprotein cholesterol (LDL-C), and apolipoprotein B (apo B), an LDL membrane complex, are associated with human atherosclerosis. Similarly, decreased levels of high density lipoprotein cholesterol (HDL-C) and its transport complex, apolipoprotein A (apo AI and apo AII) are associated with the development of atherosclerosis. Epidemiologic investigations have established that cardiovascular morbidity and mortality vary directly with the level of total-C, LDL-C, and triglycerides, and inversely with the level of HDL-C.
The independent effect of raising HDL-C or lowering triglycerides (TG) on the risk of cardiovascular morbidity and mortality has not been determined. Fenofibric acid, the active metabolite of fenofibrate, produces reductions in total cholesterol, LDL cholesterol, apolipoprotein B, total triglycerides and triglyceride rich lipoprotein (VLDL) in treated patients. In addition, treatment with fenofibrate results in increases in high density lipoprotein (HDL) and apoproteins apo AI and apo AII.
The effects of fenofibric acid seen in clinical practice have been explained in vivo in transgenic mice and in vitro in human hepatocyte cultures by the activation of peroxisome proliferator activated receptor α (PPARα). Through this mechanism, fenofibrate increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoproteins C-III (an inhibitor of lipoprotein lipase activity). The resulting fall in triglycerides produces an alteration in the size and composition of LDL from small, dense particles (which are thought to be atherogenic due to their susceptibility to oxidation), to large buoyant particles.
These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly. Activation of PPARα also induces an increase in the synthesis of apoproteins A-I, A-II and HDL-cholesterol. Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.
Pharmacokinetics /Metabolism Clinical experience has been obtained with two different formulations of fenofibrate: a “micronized” and “non-micronized” formulation, which have been demonstrated to be bioequivalent. Comparisons of blood levels following oral administration of both formulations in healthy volunteers demonstrate that a single capsule containing 67 mg of the “micronized” formulation is bioequivalent to 100 mg of the “non-micronized” formulation. Three capsules containing 67 mg fenofibrate (micronized) are bioequivalent to a single 200 mg fenofibrate capsule (micronized).
Absorption The absolute bioavailability of fenofibrate cannot be determined as the compound is virtually insoluble in aqueous media suitable for injection. However, fenofibrate is well absorbed from the gastrointestinal tract. Following oral administration in healthy volunteers, approximately 60% of a single dose of radiolabelled fenofibrate appeared in urine, primarily as fenofibric acid and its glucuronate conjugate, and 25% was excreted in the feces.
Peak plasma levels of fenofibric acid occur within 6 to 8 hours after administration. The absorption of fenofibrate is increased when administered with food. With micronized fenofibrate, the absorption is increased by approximately 35% under fed as compared to fasting conditions.
Distribution In healthy volunteers, steady-state plasma levels of fenofibric acid were shown to be achieved within 5 days of dosing with single oral doses equivalent to 67 mg fenofibrate and did not demonstrate accumulation across time following multiple dose administration. Serum protein binding was approximately 99% in normal and hyperlipidemic subjects. Metabolism Following oral administration, fenofibrate is rapidly hydrolyzed by esterases to the active metabolite, feno… [Excerpted — this section continues on DailyMed.]
📦 How Supplied / Storage and Handling ▾
HOW SUPPLIED Fenofibrate capsules, USP (micronized), 67 mg are hard gelatin capsule shells with pink opaque cap and pink opaque body imprinted IG and 470 with black ink. They are supplied as follows: NDC 69097-894-02 Bottles of 30 capsules NDC 69097-894-07 Bottles of 100 capsules NDC 69097-894-15 Bottles of 1,000 capsules Fenofibrate capsules, USP (micronized), 134 mg are hard gelatin capsule shells with blue opaque cap and blue opaque body imprinted IG and 471 with black ink. They are supplied as follows: NDC 69097-895-02 Bottles of 30 capsules NDC 69097-895-07 Bottles of 100 capsules NDC 69097-895-12 Bottles of 500 capsules Fenofibrate capsules, USP (micronized), 200 mg are hard gelatin capsule shells with orange opaque cap and orange opaque body imprinted IG and 472 with black ink.
They are supplied as follows: NDC 69097-896-02 Bottles of 30 capsules NDC 69097-896-07 Bottles of 100 capsules NDC 69097-896-12 Bottles of 500 capsules STORAGE 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 ▾
DESCRIPTION Fenofibrate capsules, USP (micronized) are a lipid regulating agent available as capsules for oral administration. The chemical name for fenofibrate is 2-[4-(4-chlorobenzoyl) phenoxy]-2- methylpropanoic acid, 1-methylethyl ester with the following structural formula: The molecular formula is C 20 H 21 O 4 Cl and the molecular weight is 360.83; fenofibrate is insoluble in water. The melting point is 79° to 82°C.
Fenofibrate, USP is a white solid which is stable under ordinary conditions. Each 67 mg fenofibrate capsule contains the following inactive ingredients: lactose monohydrate, crospovidone, povidone, sodium lauryl sulfate, colloidal silicon dioxide, magnesium stearate, FD&C Blue No.1, FD&C Red No.3, D&C Yellow No.10, titanium dioxide and gelatin. Each 134 mg fenofibrate capsule contains the following inactive ingredients: lactose monohydrate, crospovidone, povidone, sodium lauryl sulfate, colloidal silicon dioxide, magnesium stearate, FD&C Blue No.1, D&C Red No.28, titanium dioxide and gelatin.
Each 200 mg fenofibrate capsule contains the following inactive ingredients: lactose monohydrate, crospovidone, povidone, sodium lauryl sulfate, colloidal silicon dioxide, magnesium stearate, FD&C Blue No.1, FD&C Red No.40, FD&C Yellow No.6, titanium dioxide and gelatin. The imprinting ink contains shellac, dehydrated alcohol, isopropyl alcohol, butyl alcohol, propylene glycol, strong ammonia solution, black iron oxide, potassium hydroxide and purified water. USP dissolution test is pending.
Fenofibrate Structural Formula
⚠️ Precautions ▾
PRECAUTIONS Initial Therapy Laboratory studies should be done to ascertain that the lipid levels are consistently abnormal before instituting fenofibrate therapy. Every attempt should be made to control serum lipids with appropriate diet, exercise, weight loss in obese patients, and control of any medical problems such as diabetes mellitus and hypothyroidism that are contributing to the lipid abnormalities. Medications known to exacerbate hypertriglyceridemia (beta-blockers, thiazides, estrogens) should be discontinued or changed if possible prior to consideration of triglyceride-lowering drug therapy.
Continued Therapy Periodic determination of serum lipids should be obtained during initial therapy in order to establish the lowest effective dose of fenofibrate capsules. Therapy should be withdrawn in patients who do not have an adequate response after two months of treatment with the maximum recommended dose of 200 mg per day. Pancreatitis Pancreatitis has been reported in patients taking fenofibrate, gemfibrozil, and clofibrate.
This occurrence may represent a failure of efficacy in patients with severe hypertriglyceridemia, a direct drug effect, or a secondary phenomenon mediated through biliary tract stone or sludge formation with obstruction of the common bile duct. Hypersensitivity Reactions Acute Hypersensitivity: Anaphylaxis and angioedema have been reported postmarketing with fenofibrate. In some cases, reactions were life-threatening and required emergency treatment.
If a patient develops signs or symptoms of an acute hypersensitivity reaction, advise them to seek immediate medical attention and discontinue fenofibrate. Delayed Hypersensitivity: Severe cutaneous adverse drug reactions (SCAR), including Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis, and Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS), have been reported postmarketing, occurring days to weeks after initiation of fenofibrate. The cases of DRESS were associated with cutaneous reactions (such as rash or exfoliative dermatitis) and a combination of eosinophilia, fever, systemic organ involvement (renal, hepatic, or respiratory).
Discontinue fenofibrate and treat patients appropriately if SCAR is suspected. Hematologic Changes Mild to moderate hemoglobin, hematocrit, and white blood cell decreases have been observed in patients following initiation of fenofibrate therapy. However, these levels stabilize during longterm administration.
Extremely rare spontaneous reports of thrombocytopenia and agranulocytosis have been received during postmarketing surveillance outside of the U.S. Periodic blood counts are recommended during the first 12 months of fenofibrate administration. Skeletal Muscle The use of fibrates alone, including fenofibrate, may occasionally be associated with myopathy.
Treatment with drugs of the fibrate class has been associated on rare occasions with rhabdomyolysis, usually in patients with impaired renal function. Myopathy should be considered in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevations of creatine phosphokinase levels. Patients should be advised to report promptly unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever.
CPK levels should be assessed in patients reporting these symptoms, and fenofibrate therapy should be discontinued if markedly elevated CPK levels occur or myopathy is diagnosed. Venothromboembolic Disease In the FIELD trial, pulmonary embolus (PE) and deep vein thrombosis (DVT) were observed at higher rates in the fenofibrate- than the placebo-treated group. Of 9,795 patients enrolled in FIELD, there were 4,900 in the placebo group and 4,895 in the fenofibrate group.
For DVT, there were 48 events (1%) in the placebo group and 67 (1%) in the fenofibrate group (p = 0.074); and for PE, there were 32 (0.7%) events in the placebo group and 53 (1%) in the fenofibrate group (p = 0.022). In the Coronary Drug Project, a… [Excerpted — this section continues on DailyMed.]
🍼 Nursing Mothers ▾
Nursing Mothers It is not known whether fenofibrate is excreted into milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from fenofibrate, a decision should be made whether to discontinue nursing or administration of fenofibrate taking into account the importance of the drug to the lactating woman.
🧬 Pharmacokinetics ▾
Pharmacokinetics /Metabolism Clinical experience has been obtained with two different formulations of fenofibrate: a “micronized” and “non-micronized” formulation, which have been demonstrated to be bioequivalent. Comparisons of blood levels following oral administration of both formulations in healthy volunteers demonstrate that a single capsule containing 67 mg of the “micronized” formulation is bioequivalent to 100 mg of the “non-micronized” formulation. Three capsules containing 67 mg fenofibrate (micronized) are bioequivalent to a single 200 mg fenofibrate capsule (micronized).
Absorption The absolute bioavailability of fenofibrate cannot be determined as the compound is virtually insoluble in aqueous media suitable for injection. However, fenofibrate is well absorbed from the gastrointestinal tract. Following oral administration in healthy volunteers, approximately 60% of a single dose of radiolabelled fenofibrate appeared in urine, primarily as fenofibric acid and its glucuronate conjugate, and 25% was excreted in the feces.
Peak plasma levels of fenofibric acid occur within 6 to 8 hours after administration. The absorption of fenofibrate is increased when administered with food. With micronized fenofibrate, the absorption is increased by approximately 35% under fed as compared to fasting conditions.
Distribution In healthy volunteers, steady-state plasma levels of fenofibric acid were shown to be achieved within 5 days of dosing with single oral doses equivalent to 67 mg fenofibrate and did not demonstrate accumulation across time following multiple dose administration. Serum protein binding was approximately 99% in normal and hyperlipidemic subjects. Metabolism Following oral administration, fenofibrate is rapidly hydrolyzed by esterases to the active metabolite, fenofibric acid; no unchanged fenofibrate is detected in plasma.
Fenofibric acid is primarily conjugated with glucuronic acid and then excreted in urine. A small amount of fenofibric acid is reduced at the carbonyl moiety to a benzhydrol metabolite which is, in turn, conjugated with glucuronic acid and excreted in urine. In vivo metabolism data indicate that neither fenofibrate nor fenofibric acid undergo oxidative metabolism (e.g., cytochrome P450) to a significant extent.
Excretion After absorption, fenofibrate is mainly excreted in the urine in the form of metabolites, primarily fenofibric acid and fenofibric acid glucuronide. After administration of radiolabelled fenofibrate, approximately 60% of the dose appeared in the urine and 25% was excreted in the feces. Fenofibric acid is eliminated with a half-life of 20 hours, allowing once daily administration in a clinical setting.
Special Populations Geriatrics In elderly volunteers 77 to 87 years of age, the oral clearance of fenofibric acid following a single oral dose of fenofibrate was
1.2 L/h, which compares to
1.1L/h in young adults. This indicates that a similar dosage regimen can be used in the elderly, without increasing accumulation of the drug or metabolites. Pediatrics Fenofibrate has not been investigated in adequate and well-controlled trials in pediatric patients.
Gender No pharmacokinetic difference between males and females has been observed for fenofibrate. Race The influence of race on the pharmacokinetics of fenofibrate has not been studied however fenofibrate is not metabolized by enzymes known for exhibiting inter-ethnic variability. Therefore, inter-ethnic pharmacokinetic differences are very unlikely.
Renal Insufficiency The pharmacokinetics of fenofibric acid was examined in patients with mild, moderate, and severe renal impairment. Patients with severe renal impairment (creatinine clearance [CrCl] ≤ 30 mL/min) showed 2.7 fold increase in exposure for fenofibric acid and increased accumulation of fenofibric acid during chronic dosing compared to that of healthy subjects. Patients with mild to moderate renal impairment (CrCl 30 to 80 mL/min) had similar exposure but an increase in the… [Excerpted — this section continues on DailyMed.]
🔬 Clinical Studies ▾
Clinical Trials Hypercholesterolemia (Heterozygous Familial and Nonfamilial) and Mixed Dyslipidemia (Fredrickson Types IIa and IIb) The effects of fenofibrate at a dose equivalent to 200 mg fenofibrate per day were assessed from four randomized, placebo-controlled, double-blind, parallel-group studies including patients with the following mean baseline lipid values: total-C 306.9 mg/dL; LDL-C 213.8 mg/dL; HDL-C 52.3 mg/dL; and triglycerides 191.0 mg/dL. Fenofibrate therapy lowered LDL-C, total-C, and the LDL-C/HDL-C ratio.
Fenofibrate therapy also lowered triglycerides and raised HDL-C (see Table 1). Table 1: Mean Percent Change in lipid Parameters at End of Treatment Duration of study treatment was 3 to 6 months Treatment Group Total-C LDL-C HDL-C TG Pooled Cohort Mean baseline lipid values (n=646) 306.9 mg/dL 213.8 mg/dL 52.3 mg/dL 191.0mg/dL All FEN (n=361) -18.7% p = <0.05 vs. Placebo -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 (Type IIa) Mean baseline lipid values (n=334) 307.7 mg/dL 227.7 mg/dL 58.1 mg/dL 101.7 mg/dL All FEN (n=193) -22.4% -31.4% +9.8% -23.5% Placebo (n=141) +0.2% -2.2% +2.6% +11.7% Baseline LDL-C > 160 mg/dL and TG < 150 mg/dL (Type IIb) Mean baseline lipid values (n=242) 312.8 mg/dL 219.8 mg/dL 46.7 mg/dL 231.9 mg/dL All FEN (n=126) -16.8% -20.1% +14.6% -35.9% Placebo (n=116) -3.0% -6.6% +2.3% +0.9% In a subset of the subjects, measurements of apo B were conducted.
Fenofibrate treatment significantly reduced apo B from baseline to endpoint as compared with placebo (-25.1% vs. 2.4%, p<0.0001, n=213 and 143 respectively). Hypertriglyceridemia (Fredrickson Type IV and V) The effects of fenofibrate on serum triglycerides were studied in two randomized, double-blind, placebo-controlled clinical trials of 147 hypertriglyceridemia patients (Fredrickson Type IV and V).
Patients were treated for eight weeks under protocols that differed only in that one entered patients with baseline triglyceride (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 (Type IV/V hyperlipidemia), treatment with fenofibrate at dosages equivalent to 200 mg fenofibrate per day decreased primarily very low density lipoprotein (VLDL) triglycerides and VLDL cholesterol. Treatment of patients with type IV hyperlipoproteinemia and elevated triglycerides often results in an increase of low density lipoprotein (LDL) cholesterol (see Table 2).
Table 2: Effects of Fenofibrate Capsules in Patients With Fredrickson Type IV/V Hyperlipidemia Study 1 Placebo Fenofibrate Capsules Baseline TG levels 350 to 499 mg/dL N Baseline (Mean) Endpoint (Mean) % Change (Mean) N Baseline (Mean) Endpoint (Mean) % Change (Mean) Triglycerides 28 449 450 -0.5 27 432 223 -46.2 = p<0.05 vs. Placebo 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 Capsules Baseline TG levels 350 to 499 mg/dL N Baseline (Mean) Endpoint (Mean) % Change (Mean) N Baseline (Mean) Endpoint (Mean) % Change (Mean) Triglycerides 44 710 750 7.2 48 726 308 -54.5 VLDL Triglycerides 29 537 571 18.7 33 543 205 -50.6 Total Cholesterol 44 272 271 0.4 48 261 223 -13.8 HDL Cholesterol 44 27 28 5.0 48 30 36
22.9LDL Cholesterol 42 100 90 -4.2 45 103 131
45.0VLDL Cholesterol 42 137 142 11.0 45 126 54 -49.4 The effect of fenofibrate on cardiovascular morbidity and mortality has not been determined.
📄 Carcinogenesis, Mutagenesis, Impairment of Fertility ▾
Carcinogenesis, Mutagenesis, Impairment of Fertility Two dietary carcinogenicity studies have been conducted in rats with fenofibrate. In the first 24 month study, 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), 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 rat carcinogenicity study in a different strain of rats, 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), 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 mice, fenofibrate 10, 45, and 200 mg/kg/day (approximately 0.2, 1, 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, 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 mg/m 2 surface area comparisons). Pregnancy Teratogenic Effects Pregnancy category C Safety in pregnant women has not been established. There are no adequate and well controlled studies of fenofibrate in pregnant women.
Fenofibrate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. In female rats given oral dietary doses of 15, 75, and 300 mg/kg/day of fenofibrate from 15 days prior to mating through weaning, maternal toxicity was observed at 0.3 times the MRHD, based on body surface area comparisons; mg/m 2 . 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, adverse developmental findings were not observed at 14 mg/kg/day (less than 1 times the MRHD, based on body surface area comparisons; mg/m 2 ).
At higher multiples of human doses evidence of maternal toxicity was observed. 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 or… [Excerpted — this section continues on DailyMed.]
📚 References ▾
REFERENCES 1.GOLDBERG AC, et al. Fenofibrate for the Treatment of Type IV and V Hyperlipoproteinemias: A Double-Blind, Placebo-Controlled Multicenter US Study. Clinical Therapeutics, 11, pp.
69-83, 1989.2.NIKKILA EA. Familial Lipoprotein Lipase Deficiency and Related Disorders of Chylomicron Metabolism. In Stanbury J.B., et al.
(eds.): The Metabolic Basis of Inherited Disease, 5th edition, McGraw-Hill, 1983, Chap. 30, pp. 622-642.3.BROWN WV, et al.
Effects of Fenofibrate on Plasma Lipids: Double-Blind, Multicenter Study In Patients with Type IIA or IIB Hyperlipidemia. Arteriosclerosis. 6, pp.
670-678, 1986. Manufactured by: InvaGen Pharmaceuticals, Inc. (a subsidiary of Cipla Ltd.) Hauppauge, NY 11788 Manufactured for: Cipla USA, Inc.
10 Independence Boulevard, Suite 300 Warren, NJ 07059 Revised: 05/2020
📄 Package Label / Principal Display Panel ▾
PRINCIPAL DISPLAY PANEL - 67 mg NDC 69097-894-07 Rx Only Fenofibrate Capsules, USP 67 mg 100 Capsules Cipla PRINCIPAL DISPLAY PANEL - 134 mg NDC 69097-895-07 Rx Only Fenofibrate Capsules, USP 134 mg 100 Capsules Cipla PRINCIPAL DISPLAY PANEL - 200 mg NDC 69097-896-07 Rx Only Fenofibrate Capsules, USP 200 mg 100 Capsules Cipla Fenofibrate Capsules, USP 200 mg Bottle Label Fenofibrate Capsules, USP 200 mg Bottle Label Fenofibrate Capsules, USP 200 mg Bottle Label
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