Professional Information
Fenofibrate (Systemic)
VA CLASSIFICATION
Primary: CV359
Commonly used brand name(s): Tricor.
Note: For a listing of dosage forms and brand names by country availability, see Dosage Forms section(s).
Category:
Antihyperlipidemic. —
Indications
Accepted
Hyperlipidemia (treatment)—Fenofibrate is indicated as an adjunct to diet for the treatment of adult patients with very high serum triglyceride concentrations (types IV and V hyperlipidemia) who have not responded adequately to diet and who are at risk of pancreatitis {01}. A risk of pancreatitis is associated with a serum triglyceride concentration of over 2000 mg per dL and increases in very low–density lipoprotein (VLDL) cholesterol, as well as with fasting chylomicron (type V hyperlipidemia) concentrations {01}. A total serum or plasma triglyceride concentration below 1000 mg per dL is not associated with a risk of pancreatitis {01}. Fenofibrate therapy may be considered for those subjects with triglyceride concentrations between 1000 and 2000 mg per dL who have a history of pancreatitis or of recurrent abdominal pain typical of pancreatitis {01}. Fenofibrate has not been adequately studied to decrease the risk of pancreatitis in patients with a type IV lipoprotein pattern, with triglyceride concentrations below 1000 mg per dL, who (through dietary indiscretion or alcohol consumption) convert to a type V lipoprotein pattern with large triglyceride concentrations accompanied by fasting chylomicronemia {01}.
—For additional information on initial therapeutic guidelines related to the treatment of hyperlipidemia, see Appendix III .
—The effect of fenofibrate on coronary heart disease morbidity and mortality and noncardiovascular mortality has not been established {01}. Because fenofibrate has chemical, pharmacologic, and clinical similarities to the other fibrate drugs, clofibrate and gemfibrozil, the adverse findings in four large randomized, placebo-controlled clinical studies with these drugs may also apply to fenofibrate {01}. In one clofibrate study, there was no difference in mortality between the clofibrate-treated subjects and the placebo-treated subjects, but twice as many clofibrate-treated subjects developed cholelithiasis and cholecystitis requiring surgery {01}. Another clofibrate study resulted in a 44% higher age-adjusted total mortality in the clofibrate-treated group than in a comparable placebo-treated group {01}. The higher mortality rate was attributed to a 33% increase in noncardiovascular causes, including malignancy, postcholecystectomy complications, and pancreatitis {01}. A third study with gemfibrozil resulted in a 22% higher total mortality, primarily due to a higher cancer mortality, in the gemfibrozil-treated group, while cancers (excluding basal cell carcinoma) were diagnosed in 2.5% of patients in both gemfibrozil- and placebo-treated patients {01}. In a fourth study with gemfibrozil, cardiac deaths tended to be higher and gallbladder surgery and appendectomy were more frequent in the gemfibrozil-treated group than in the placebo-treated group {01}.
Unaccepted
Fenofibrate is not indicated for the treatment of either primary or secondary hyperlipoproteinemia as a form of prevention to reduce the risk of developing coronary heart disease {01}.
Pharmacology/Pharmacokinetics
Physicochemical characteristics:
Molecular weight—
360.83 {01}
Mechanism of action/Effect:
Fenofibrate is a lipid-regulating agent that has chemical, pharmacologic, and clinical similarities to the other fibrate drugs, clofibrate and gemfibrozil {01}. Although the exact mechanism of action of fenofibrate is not completely understood, fenofibric acid, the active metabolite of fenofibrate, is thought to lower plasma triglyceride concentrations by inhibiting triglyceride synthesis (resulting in a lower level of very low–density lipoproteins [VLDL] released into the circulation) and by stimulating the catabolism of triglyceride-rich lipoproteins (i.e., VLDL) {01}. In clinical trials, patients with hypertriglyceridemia and normal cholesterolemia, with or without hyperchylomicronemia (type IV or V hyperlipidemia), treated with doses of 201 mg of fenofibrate per day had decreases in VLDL triglycerides and VLDL cholesterol {01}. Treatment of patients with type IV hyperlipoproteinemia and elevated triglyceride concentrations often results in an increase in low-density lipoprotein (LDL) cholesterol {01}.
Other actions/effects:
Fenofibrate reduces serum uric acid concentrations in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid {01}.
Absorption:
Fenofibrate is well absorbed from the gastrointestinal tract {01}. Absorption of the micronized form of fenofibrate is increased by approximately 35% when administered with food, as compared with that in the fasting state {01}.
Distribution:
Volume of distribution (Vol D)—30 L {01}.
Protein binding:
Very high (approximately 99% in normal and hyperlipidemic individuals) {01}.
Biotransformation:
Fenofibrate undergoes rapid metabolism by esterase hydrolysis and is converted to the active metabolite, fenofibric acid {01}. Fenofibric acid undergoes conjugation with glucuronic acid and is excreted in urine {01}. A small amount of fenofibric acid undergoes reduction at the carbonyl moiety, resulting in a benzhydrol metabolite which is then conjugated with glucuronic acid and excreted in urine {01}.
Half-life:
Elimination:
20 hours {01}.
Time to peak concentration:
6 to 8 hours {01}.
Elimination:
Renal—60%, primarily as fenofibric acid and fenofibric acid glucuronide {01}.
Fecal—25% {01}.
In dialysis—
Hemodialysis is not expected to remove fenofibrate significantly because of its extensive binding to plasma proteins {01}.
Precautions to Consider
Cross-sensitivity and/or related problems
Fenofibrate has chemical, pharmacological, and clinical similarities to the other fibrate agents, clofibrate and gemfibrozil {01}.
Carcinogenicity
A 24-month study in rats, given fenofibrate doses of 10, 45, and 200 mg per kg of body weight (mg/kg), resulted in a significant increase in the incidence of liver carcinomas in both male and female rats given the 200-mg/kg dose {01}. These doses represent 0.3, 1, and 6 times the maximum recommended human dose (MRHD) of fenofibrate, respectively, on a mg per square meter of body surface area (mg/m 2) basis {01}. A significant increase in pancreatic carcinomas occurred in male rats given the 45- and 200-mg/kg doses of fenofibrate and increases in pancreatic adenomas and benign testicular interstitial cell tumors occurred in male rats given the 200-mg/kg fenofibrate dose {01}. In a second 24-month study in a different strain of rats given fenofibrate in doses of 10 mg/kg and 60 mg/kg, significant increases in the incidence of pancreatic acinar adenomas occurred in both sexes and increases in interstitial cell tumors of the testes occurred in rats given the 60-mg/kg dose of fenofibrate {01}. These doses represent 0.3 and 2 times the MRHD of fenofibrate, respectively, on a mg/m 2 basis {01}.
A comparative carcinogenicity study was done in rats comparing three drugs: fenofibrate, given in doses of 10 mg/kg and 70 mg/kg or 0.3 and 1.6 times the MRHD of fenofibrate on a mg/m 2 basis; clofibrate, given in doses of 400 mg/kg or 1.6 times the MRHD of clofibrate on a mg/m 2 basis; and gemfibrozil, given in doses of 250 mg/kg or 1.7 times the MRHD of gemfibrozil on a mg/m 2 basis {01}. An increased incidence of pancreatic acinar adenomas was observed in male and female rats given fenofibrate {01}. An increase in hepatocellular carcinoma and pancreatic acinar adenomas occurred in male rats, and hepatic neoplastic nodules occurred in female rats given clofibrate; hepatic neoplastic nodules were increased in male and female rats given gemfibrozil, while an increase in testicular interstitial cell tumors occurred in male rats given all three drugs {01}.
In a 21-month study in mice given fenofibrate in doses of 10, 45, and 200 mg/kg, significant increases in liver carcinoma occurred in both male and female mice given the 200-mg/kg dose of fenofibrate {01}. These doses represent approximately 0.2, 0.7, and 3 times the MRHD of fenofibrate on a mg/m 2 basis, respectively {01}. In a second 18-month study in mice given the same doses of fenofibrate, a significant increase in liver carcinoma in male mice and liver adenoma in female mice occurred when they were given the 200-mg/kg dose of fenofibrate {01}.
Peroxisomal proliferation, as determined by electron microscopy studies, has occurred following administration of fenofibrate to rats {01}. An adequate study to test for peroxisome proliferation in humans has not been done, but a comparison of liver biopsies before and after treatment of human subjects with other members of the fibrate class of medications has revealed changes in peroxisome morphology and numbers after treatment {01}.
Mutagenicity
Fenofibrate was not found to be mutagenic in the Ames test and mouse lymphoma, chromosomal aberration, and unscheduled DNA synthesis tests {01}.
Pregnancy/Reproduction
Pregnancy—
Adequate and well-controlled studies in pregnant women have not been done {01}. Fenofibrate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus {01}. Fenofibrate has been shown to be embryocidal and teratogenic in rats given 7 to 10 times the MRHD of fenofibrate on a mg/m 2 basis, and embryocidal in rabbits given 9 times the MRHD of fenofibrate on a mg/m 2 basis {01}.
A study in female rats given 9 times the MRHD of fenofibrate before and throughout gestation resulted in a delay of delivery in 100% of dams, a 60% increase in post implantation loss, a decrease in litter size, a decrease in birth weight, a 40% survival of pups at birth, a 4% survival of pups as neonates, a 0% survival of pups to weaning, and an increased occurrence of spina bifida {01}. A study in female rats given 10 times the MRHD of fenofibrate on days 6 through 15 of gestation resulted in an increase in gross, visceral, and skeletal findings in fetuses, manifested as a domed head, hunched shoulders, a rounded body, an abnormal chest, kyphosis, stunted fetuses, elongated sternal ribs, malformed sternebrae, extra foramen in palatine, misshapen vertebrae, and supernumerary ribs {01}.
A study in female rats given 7 times the MRHD of fenofibrate from day 15 of gestation through weaning resulted in a delay in delivery, a 40% decrease in live births, a 75% decrease in neonatal survival, and decreases in pup weight at birth, as well as on days 4 and 21 post partum {01}. A study of fenofibrate in female rabbits resulted in abortions in 10% of dams given 9 times and 25% of dams given 18 times the MRHD of fenofibrate, and death of 7% of fetuses given 18 times the MRHD of fenofibrate {01}.
FDA Pregnancy Category C {01}.
Breast-feeding
Because of the potential for tumorigenicity as seen in animal studies, fenofibrate should not be used in women who are breast-feeding {01}. A decision should be made whether to discontinue nursing or to discontinue fenofibrate {01}.
Pediatrics
No information is available on the relationship of age to the effects of fenofibrate in pediatric patients. Safety and efficacy have not been established {01}.
Geriatrics
Clearance of fenofibric acid following a single oral dose of fenofibrate in elderly volunteers, ages 77 through 87 years, was 1.2 L per hour (L/hr), compared to 1.1 L/hr in younger adults, indicating that a similar dosage regimen can be used in the elderly without resulting in an increase in accumulation of fenofibrate or its metabolites {01}.
Pharmacogenetics
Fenofibrate is not metabolized by enzymes known for exhibiting interethnic variability, therefore, interethnic pharmacokinetic differences are not expected {01}. Pharmacokinetic differences have not been observed between male and female individuals administered fenofibrate {01}.
Drug interactions and/or related problems
The following drug interactions and/or related problems have been selected on the basis of their potential clinical significance (possible mechanism in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):
Note: Combinations containing any of the following medications, depending on the amount present, may also interact with this medication.
» Anticoagulants, oral{01} (concurrent use with fenofibrate may potentiate coumarin-type anticoagulant prolongation of prothrombin time {01}; the dosage of the anticoagulant should be reduced to maintain the prothrombin time at the desired level in order to prevent bleeding complications {01})
Bile acid sequestrants{01} , such as:
Cholestyramine or
Colestipol (concurrent use with these agents may bind fenofibrate {01}; in order to avoid interfering with the absorption of fenofibrate, it should be taken at least 1 hour before or 4 to 6 hours after taking a bile acid binding agent {01})
» Cyclosporine{01} (because fenofibrate is primarily eliminated by renal excretion and cyclosporine when used alone is potentially nephrotoxic, causing decreases in creatinine clearance and increases in serum creatinine concentrations, concurrent use of these agents may potentiate renal function deterioration {01}; concurrent use of fenofibrate with immunosuppressants and other potentially nephrotoxic agents should be carefully considered, and the lowest effective dose should be used {01})
» HMG-CoA reductase inhibitors{01} , such as:
Lovastatin{01} or
Pravastatin{01} or
Simvastatin{01} (although no data exists on the concurrent use of these agents with fenofibrate, concurrent use of gemfibrozil, another fibrate agent, with lovastatin has been associated with rhabdomyolysis, significantly increased creatine kinase [CK] concentrations, and myoglobinuria, resulting in a high percentage of acute renal failure cases {01}; because the potential benefits of combined therapy do not outweigh the risks of severe myopathy, rhabdomyolysis, and acute renal failure, and because the use of fibrates alone, including fenofibrate, may occasionally be associated with myositis, myopathy, or rhabdomyolysis, their concurrent use with HMG-CoA reductase inhibitors is not recommended {01})
Laboratory value alterations
The following have been selected on the basis of their potential clinical significance (possible effect in parentheses where appropriate)—not necessarily inclusive (» = major clinical significance):
With physiology/laboratory test values
Creatine kinase (CK), serum{01} (myopathy should be considered in patients with marked elevations of CK concentrations accompanied by diffuse myalgias, muscle tenderness or weakness {01})
Hematocrit{01} and
Hemoglobin concentrations{01} and
Leukocyte counts{01} (mild to moderate decreases in hemoglobin and hematocrit concentrations, and leukocyte counts have occurred; however, these values stabilize with continued use of fenofibrate {01})
Aspartate aminotransferase (AST [SGOT]), serum{01} and/or
Alanine aminotransferase (ALT [SGPT]), serum{01} (in an 8-week dose-ranging study, increases in serum transaminase values to at least 3 times the upper limit of normal occurred in 13% of patients receiving fenofibrate in doses equivalent to 134 or 201 mg of fenofibrate per day and occurred in 0% of patients receiving doses equivalent to 33.5 or 67 mg per day, or placebo {01}; in two U.S. placebo-controlled studies, serum transaminase values increased to > 3 times the upper limit of normal in 8 to 10% of patients taking fenofibrate in doses equivalent to 201 mg of fenofibrate per day {01}; in controlled multiple-dose trials lasting 3 to 24 weeks, increases in serum transaminase values to > 3 times the upper limit of normal occurred in 28 of 442 patients [6.3%] taking fenofibrate in doses equivalent to 134 or 201 mg per day {01}; in the latter trial, in the patients whose serum transaminase values were followed, values usually returned to normal limits either with continued treatment or after discontinuation of treatment; however, values remained above normal limits in 2 of the 28 patients [7.1%] at the end of follow-up of treatment {01})
Uric acid, serum (concentrations may be decreased {01}; fenofibrate reduces serum uric acid concentrations in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid)
Medical considerations/Contraindications
The medical considerations/contraindications included have been selected on the basis of their potential clinical significance (reasons given in parentheses where appropriate)— not necessarily inclusive (» = major clinical significance).
Except under special circumstances, this medication should not be used when the following medical problems exist:
» Gallbladder disease, pre-existing{01} (use of fibrate agents, such as fenofibrate, has been associated with cholelithiasis and, therefore, is contraindicated in patients with pre-existing gallbladder disease {01})
» Hepatic function impairment, including primary biliary cirrhosis and unexplained persistent liver function abnormality{01} (use of fenofibrate has been associated with hepatotoxicity, which may further aggravate these conditions {01})
» Hypersensitivity to fenofibrate{01}
» Renal function impairment, severe{01} (the rate of clearance of fenofibric acid may be significantly reduced in patients with severe renal function impairment [creatinine clearance < 50 mL per minute (mL/min)], resulting in the medication's accumulation during chronic dosing {01}; use of fibrate agents, such as fenofibrate, has been associated with rhabdomyolysis in patients with impaired renal function {01})
Risk-benefit should be considered when the following medical problem exists
Renal function impairment, moderate{01} (in patients having moderate renal function impairment [creatinine clearance of 50 to 90 mL/min], clearance and volume of distribution of fenofibric acid are increased when compared to healthy adults [2.1 L/hr and 95 L versus 1.1 L/hr and 30 L, respectively]; however, no modification of dosage is required in patients having moderate renal function impairment {01}; use of fibrate agents, such as fenofibrate, has been associated with rhabdomyolysis in patients with impaired renal function {01})
Patient monitoring
The following may be especially important in patient monitoring (other tests may be warranted in some patients, depending on condition; » = major clinical significance):
Creatine kinase (CK), serum{01} (CK concentrations should be monitored in patients with symptoms of unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever {01}; if marked CK concentrations occur, fenofibrate therapy should be discontinued {01})
Hematocrit{01} and
Hemoglobin concentrations{01} and
Leukocyte counts{01} (periodic monitoring of blood counts are recommended during the first 12 months of fenofibrate therapy {01})
» Hepatic function determinations{01} , such as:
Alanine aminotransferase (ALT [SGPT]), serum{01} and
Aspartate aminotransferase (AST [SGOT]), serum{01} (regular periodic monitoring should be performed for the duration of fenofibrate therapy {01}; fenofibrate should be discontinued if serum transaminase values of > 3 times the upper limit of normal persist {01})
» Lipid concentrations, serum{01} (periodic monitoring should be done during initiation of therapy in order to establish the lowest effective dose of fenofibrate {01}; fenofibrate should be discontinued in patients who do not have an adequate response after 2 months of treatment with the maximum recommended dose [201 mg per day] {01})
Side/Adverse Effects
The following side/adverse effects have been selected on the basis of their potential clinical significance (possible signs and symptoms in parentheses where appropriate)—not necessarily inclusive:
Those indicating need for medical attention
Incidence less frequent
Influenza syndrome ( chills, fever, muscle aches and pains, or nausea and/or vomiting)
infections
pruritus {01} ( generalized itching)
skin rash and/or urticaria (hives )
Note: In clinical trials, skin rash was the most frequent side effect, requiring discontinuation of fenofibrate treatment in 2% of patients {01}. Acute hypersensitivity reactions, including severe skin rashes requiring patient hospitalization and treatment with steroids, have occurred very rarely during treatment with fenofibrate {01}. Urticaria was seen in 1.25% versus 0% and rash in 2.82% versus 1.23% of fenofibrate-treated and placebo-treated patients, respectively, in controlled trials {01}.
Incidence rare
Agranulocytosis {01} ( chills; fever; sore throat)
alveolitis, allergic {01} ( cough; shortness of breath or troubled breathing)
cholecystitis {01} (abdominal pain, vague; indigestion, chronic; nausea)
cholelithiasis (abdominal fullness, gaseous ; abdominal pain, recurrent; fever; yellow eyes or skin)
eczema {01}
hepatotoxicity {01} (abdominal fullness; dark urine; fever; general ill feeling; generalized itching ; loss of appetite; unusual fatigue; yellow eyes or skin)
musculoskeletal symptoms, such as myalgia {01} (muscle pain), myasthenia {01} (muscle weakness), myositis (inflammation or swelling of skeletal muscle), and/or rhabdomyolysis {01} ( fever; muscle cramps, pain, stiffness, or weakness; unusual tiredness)
pancreatitis {01} (abdominal pain and distention; fever; nausea; vomiting)
thrombocytopenia {01} ( unusual bleeding or bruising)
Note: Rare cases of agranulocytosis and thrombocytopenia have been reported during postmarketing surveillance outside of the U.S. {01}
Fenofibrate, like clofibrate and gemfibrozil, may increase cholesterol excretion into the bile, leading to cholelithiasis {01}. A gallstone prevalence sub-study of a placebo-controlled trial with gemfibrozil revealed a trend toward a greater prevalence of gallstones in gemfibrozil-treated patients {01}. If cholelithiasis is suspected, gallbladder studies should be performed and fenofibrate should be discontinued if gallstones are found {01}.
Hepatotoxicity associated with fenofibrate therapy appears to be dose-related {01}. Hepatocellular, chronic active, and cholestatic hepatitis have been reported after weeks to several years of exposure to fenofibrate {01}. Rarely, cirrhosis has been reported in association with chronic active hepatitis {01}.
Treatment with fibrate agents, such as fenofibrate, may occasionally be associated with myositis {01}. Rhabdomyolysis has also been associated rarely with this class of agents, usually in patients with impaired renal function {01}. Degradation of muscle occurs in rhabdomyolysis, resulting in the release of myoglobin into the urine, which can lead to acute renal failure {01}. Myopathy and/or rhabdomyolysis should be considered in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevations of creatine kinase (CK) in serum {01}. Patients receiving fenofibrate and complaining of muscle pain, tenderness, or weakness, especially if accompanied by malaise or fever, should have a prompt medical evaluation for myopathy, including serum CK determinations {01}. If myopathy or myositis is suspected or diagnosed, or if serum CK concentrations are significantly elevated, fenofibrate therapy should be discontinued {01}.
Pancreatitis has been reported in patients taking fenofibrate, gemfibrozil, and clofibrate and may be associated with a failure in fenofibrate efficacy or a blockage of the common bile duct by biliary tract stone or sludge formation {01}.
Those indicating need for medical attention only if they continue or are bothersome
Incidence less frequent
Dizziness
eye irritation
gastrointestinal symptoms, such as belching
constipation
flatulence {01} (gas)
libido, decreased {01}
photosensitivity (increased sensitivity of the skin to sunlight)
rhinitis {01} (stuffy nose)
Overdose
For more information on the management of overdose or unintentional ingestion, contact a Poison Control Center (see Poison Control Center Listing ).
Treatment of overdose
Treatment should be symptomatic and supportive {01}.
Specific treatment—Hemodialysis should not be considered in the treatment of fenofibrate overdosage because fenofibrate is extensively bound to plasma proteins {01}.
Supportive care—Patients in whom intentional overdose is confirmed or suspected should be referred for psychiatric consultation.
Patient Consultation
As an aid to patient consultation, refer to Advice for the Patient, Fenofibrate (Systemic) .
In providing consultation, consider emphasizing the following selected information (» = major clinical significance):
Before using this medication
» Conditions affecting use, especially:
Hypersensitivity to fenofibrate
Carcinogenicity—
Liver carcinomas and pancreatic acinar adenomas have occurred in rats given long-term, high doses of fenofibrate
Pregnancy—Not recommended during pregnancy unless potential benefit outweighs the risk
Breast-feeding—Not recommended in women who are breast-feeding
Other medications, especially oral anticoagulants, cyclosporine, or HMG-CoA reductase inhibitors
Other medical problems, especially pre-existing gallbladder disease; hepatic function impairment, including primary biliary cirrhosis and unexplained persistent liver function abnormality; or severe renal function impairment
Proper use of this medication
» Compliance with therapy; taking medication at the same time each day to maintain the therapeutic effect; not taking more or less medication than the amount prescribed
» Compliance with prescribed diet during treatment
Taking medication with a meal to increase its bioavailability
» Proper dosing
Taking as soon as possible; not taking if almost time for next dose; not doubling doses
» Proper storage
Precautions while using this medication
» Regular visits to physician to check progress
» Notifying physician immediately if unexplained muscle pain, tenderness, or weakness occurs, especially if accompanied by unusual tiredness or fever
Notifying physician if pregnancy is suspected
Reporting any signs of infection (fever, sore throat, chills) to physician because of risk of agranulocytosis
Side/adverse effects
Signs of potential side effects, especially influenza-like syndrome; infections; pruritus; skin rash and/or urticaria; agranulocytosis; allergic alveolitis; cholecystitis; cholelithiasis; eczema; hepatotoxicity; musculoskeletal symptoms, such as myalgia, myasthenia, myositis, and/or rhabdomyolysis; pancreatitis; and thrombocytopenia
General Dosing Information
Prior to any drug therapy, an attempt should be made to treat hyperlipidemia with nondrug methods, such as dietary therapy specific for the type of lipoprotein abnormality, reduction of excess body weight, reduction of excess alcohol intake, and physical exercise {01}. Secondary causes of hyperlipidemia, such as hypothyroidism or diabetes mellitus, should be ruled out or adequately treated {01}. Treatment with estrogens, thiazide diuretics, and beta-adrenergic blocking agents may contribute to increases in plasma triglyceride levels, especially in individuals with familial hypertriglyceridemia {01}. In such cases, the medication should be changed or discontinued if it is considered medically appropriate to do so {01}. The use of lipid-lowering agents should be considered only when satisfactory results have not been obtained from using nondrug methods {01}.
Diet/Nutrition
Patients should be placed on an appropriate triglyceride-lowering diet before receiving fenofibrate and should continue this diet during treatment with fenofibrate {01}.
Fenofibrate should be given with a meal to optimize the bioavailability of the medication {01}.
Oral Dosage Forms
FENOFIBRATE CAPSULES (MICRONIZED)
Usual adult dose
Antihyperlipidemic
Oral, initially, 67 mg per day, depending on the physician's assessment of the patient's risk for pancreatitis {01}. Dosage should be individualized according to patient response, and should be increased sequentially, if necessary, following repeat serum triglyceride estimations at 4- to 8-week intervals {01}. Fenofibrate should be discontinued in patients who do not have an adequate response after two months of treatment with the maximum recommended dose (200 mg per day) {01}.
In patients with impaired renal function, treatment should be initiated at a dose of 67 mg per day and increased only after the effects of fenofibrate on renal function and triglyceride concentrations have been evaluated {01}.
Usual adult prescribing limits
200 mg per day {01}.
Usual pediatric dose
Safety and efficacy have not been established {01}.
Usual geriatric dose
Antihyperlipidemic
Oral, initially, 67 mg per day {01}. See Usual adult dose .
Strength(s) usually available
U.S.—
67 mg (Rx) [Tricor (lactose) (pregelatinized starch) (sodium lauryl sulfate) (crospovidone) ( magnesium stearate)]
200 mg (Rx) [Tricor (lactose) (pregelatinized starch) (sodium lauryl sulfate) ( crospovidone) (magnesium stearate)]
Packaging and storage:
Store at controlled room temperature, between 15 and 30 ºC (59 and 86 ºF) {01}. Protect from moisture {01}.
Auxiliary labeling:
• Take with a meal.
Developed: 05/18/1998
References
- Tricor package insert (Abbott—US), Rev 2/98, Rec 3/98.
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