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Tricor (fenofibrate)


Fibric acid derivative




Adjunctive therapy to diet to reduce elevated LDL, total cholesterol, TGs, and apolipoprotein B, and to increase HDL in adults with primary hypercholesterolemia or mixed dyslipidemia. Adjunctive therapy to diet for treatment of adults with severe hypertriglyceridemia.


Primary Hypercholesterolemia/Mixed Dyslipidemia

Initial/Max: 145mg qd
Titrate: May consider reducing dose if lipid levels fall significantly below the targeted range

D/C if no adequate response after 2 months of treatment w/ max dose

Severe Hypertriglyceridemia

Initial: 48-145mg/day
Titrate: Adjust dose if necessary following repeat lipid determinations at 4- to 8-week intervals; may consider reducing dose if lipid levels fall significantly below the targeted range
Max: 145mg qd

D/C if no adequate response after 2 months of treatment w/ max dose


Renal Impairment
Mild to Moderate:
Initial: 48mg/day
Titrate: Increase only after evaluation of effects on renal function and lipid levels


Oral route

May be taken w/o regard to meals
Swallow tab whole


Tab: 48mg, 145mg


Severe renal impairment (including dialysis), active liver disease (including primary biliary cirrhosis and unexplained persistent liver function abnormalities), preexisting gallbladder disease, and nursing mothers.


Not shown to reduce coronary heart disease morbidity and mortality in patients with type 2 diabetes mellitus (DM). Increased risk of myopathy and rhabdomyolysis; risk increased with DM, renal insufficiency, hypothyroidism, and in elderly. D/C therapy if marked CPK elevation occurs or myopathy/myositis is suspected or diagnosed. Increases in serum transaminases, hepatocellular, chronic active and cholestatic hepatitis, and cirrhosis (rare) reported; perform baseline and regular periodic monitoring of LFTs, and d/c therapy if enzyme levels persist >3X the normal limit. Elevations in SrCr reported; monitor renal function in patients with renal impairment or at risk for renal insufficiency. May cause cholelithiasis; d/c if gallstones are found. Acute hypersensitivity reactions and pancreatitis reported. Mild to moderate decreases in Hgb, Hct and WBCs, thrombocytopenia, and agranulocytosis reported; periodically monitor RBC and WBC counts during the first 12 months of therapy. May cause venothromboembolic disease. Severe decreases in HDL levels reported; check HDL levels within the 1st few months after initiation of therapy. If a severely depressed HDL level is detected, withdraw therapy, monitor HDL level until it has returned to baseline, and do not reinitiate therapy. Estrogen therapy, thiazide diuretics, and β-blockers may be associated with massive rises in plasma TG; discontinuation of these drugs may obviate the need for specific drug therapy of hypertriglyceridemia.


Abnormal LFTs, respiratory disorder, abdominal pain, back pain, increased AST/ALT/CPK, headache.


Increased risk of rhabdomyolysis with HMG-CoA reductase inhibitors (statins); avoid combination unless benefit outweighs risk. May potentiate anticoagulant effects of coumarin anticoagulants; use with caution, reduce anticoagulant dosage, and monitor PT/INR frequently. Immunosuppressants (eg, cyclosporine, tacrolimus) may produce nephrotoxicity; consider benefits and risks, use lowest effective dose, and monitor renal function with immunosuppressants and other potentially nephrotoxic agents. Bile acid-binding resins may bind other drugs given concurrently; take at least 1 hr before or 4-6 hrs after the bile acid-binding resin to avoid impeding its absorption. Cases of myopathy, including rhabdomyolysis, reported when coadministered with colchicine; caution when prescribing with colchicine.


Category C, not for use in nursing.


Fibric acid derivative; activates peroxisome proliferator-activated receptor α. Increases lipolysis and elimination of TG-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III (lipoprotein lipase activity inhibitor). Also, induces an increase in the synthesis of apolipoproteins A-I, A-II, and HDL.


Absorption: Well-absorbed. Tmax=6-8 hrs. Distribution: Plasma protein binding (99%). Metabolism: Rapid by ester hydrolysis to fenofibric acid (active metabolite); conjugation with glucuronic acid. Elimination: Urine (60%, fenofibric acid and glucuronate conjugate), feces (25%); T1/2=20 hrs.


Assess for renal impairment, active liver disease, preexisting gallbladder disease, other medical conditions (eg, DM, hypothyroidism), hypersensitivity to drug, pregnancy/nursing status, and possible drug interactions. Obtain baseline LFTs.


Monitor for signs/symptoms of myositis, myopathy, or rhabdomyolysis; measure CPK levels in patients reporting such symptoms. Monitor for cholelithiasis, pancreatitis, hypersensitivity reactions, pulmonary embolism, and deep vein thrombosis. Monitor renal function, LFTs, CBC, and lipid levels. Monitor PT/INR frequently with coumarin anticoagulants.


Advise of potential benefits and risks of therapy, and of medications to avoid during treatment. Instruct to follow appropriate lipid-modifying diet during therapy and to take drug qd, at the prescribed dose. Instruct to inform physician of all medications, supplements, and herbal preparations being taken, any changes in medical condition, development of muscle pain, tenderness, or weakness, and onset of abdominal pain or any other new symptoms. Advise to return for routine monitoring.


25°C (77°F); excursions permitted to 15-30°C (59-86°F). Protect from moisture.


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