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Pharmacology: Pharmacodynamics: Fenofibric acid is an agonist for the nuclear transcription factor peroxisome proliferator activated receptor-alpha (PPAR-α).
Fenofibric acid downregulates apoprotein C-III (an inhibitor of lipoprotein lipase) and upregulates the synthesis of apolipoprotein A-I, fatty acid transport protein, and lipoprotein lipase resulting in an increase in VLDL catabolism, fatty acid oxidation, and elimination of triglyceride-rich particles; as a result of a decrease in VLDL levels, total plasma triglycerides are reduced by 30% to 60%; modest increase in HDL occurs in some hypertriglyceridemic patients.
Pharmacokinetics: Absorption: Increased when taken with meals. Peak concentrations and AUC were not significantly different when a single dose was administered under fasting and nonfasting conditions. Administer with or without food.
Distribution: Widely to most tissues, Protein binding: ~99%.
Metabolism: Fenofibric acid undergoes inactivation by glucuronidation.
Bioavailability: ~81%.
Half-life elimination: Mean: 20 hours (range: 10 to 35 hours); half-life prolonged in patients with renal impairment.
Time to peak: 2 to 8 hours.
Excretion: Urine (~60% as metabolites); feces (25%).
Hemodialysis has no effect on removal of fenofibric acid from plasma.
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