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indicationFor use as adjunctive therapy to diet to reduce elevated LDL-C, Total-C,Triglycerides and Apo B, and to increase HDL-C in adult patients with primary hypercholesterolemia or mixed dyslipidemia (Fredrickson Types IIa and IIb)
pharmacologyFenofibrate is a lipid regulating agent indicated as adjunctive therapy to diet to reduce elevated LDL-C, Total-C,Triglycerides and Apo B, and to increase HDL-C in adult patients with primary hypercholesterolemia or mixed dyslipidemia (Fredrickson Types IIa and IIb). Fenofibrate is also indicated as adjunctive therapy to diet for treatment of adult patients with hypertriglyceridemia (Fredrickson Types IV and V hyperlipidemia). 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 apoAI and apoAII.
mechanism of actionFenofibrate exerts its therapeutic effects through activation of peroxisome proliferator activated receptor a (PPARa). This increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III. The resulting fall in triglycerides produces an alteration in the size and composition of LDL from small, dense particles, to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly.
toxicityLD50=1600 mg/kg (Oral, in mice); Investigated as a teratogen and reproductive hazard.
absorptionFenofibrate is well absorbed from the gastrointestinal tract. After absorption, fenofibrate is mainly excreted in the urine in the form of metabolites, primarily fenofibric acid and fenofibric acid glucuronide
half life20 hours
route of eliminationFenofibric acid is primarily conjugated with glucuronic acid and then excreted in urine. 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.
drug interactionsAcenocoumarol: Fenofibrate may increase the anticoagulant effect of acenocoumarol.
Anisindione: Fenofibrate may increase the anticoagulant effect of anisindione.
Atorvastatin: Increased risk of myopathy/rhabdomyolysis
Cerivastatin: Increased risk of myopathy/rhabdomyolysis
Dicumarol: Fenofibrate may increase the anticoagulant effect of dicumarol.
Fluvastatin: Increased risk of myopathy/rhabdomyolysis
Lovastatin: Increased risk of myopathy/rhabdomyolysis
Pravastatin: Increased risk of myopathy/rhabdomyolysis
Rosuvastatin: May cause additive myotoxicity. Monitor for symptoms of muscle toxicity during concomitant therapy.
Simvastatin: Increased risk of myopathy/rhabdomyolysis
Ursodeoxycholic acid: The fibric acid derivative decreases the effect of ursodiol
Warfarin: Fenofibrate may increase the anticoagulant effect of warfarin. Monitor prothrombin time and therapeutic and adverse effects of warfarin if fenofibrate is initiated, discontinued or dose changed.