The active moiety of TRICOR is fenofibric acid. The pharmacological effects of fenofibric acid in both animals and humans have been extensively studied through oral administration of fenofibrate.

The lipid-modifying 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 apoprotein C-III (an inhibitor of lipoprotein lipase activity).

The resulting decrease in TG 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 apolipoproteins A-I, A-II and HDLcholesterol.

Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.

TRICOR is a peroxisome proliferator-activated receptor (PPAR) alpha agonist indicated as an adjunct to diet:

To reduce elevated LDL-C, Total-C, TG and Apo B, and to increase HDL-C in adult patients with primary hypercholesterolemia or mixed dyslipidemia.

For treatment of adult patients with severe hypertriglyceridemia.

Limitations of Use: Fenofibrate was not shown to reduce coronary heart disease morbidity and mortality in patients with type 2 diabetes mellitus.

• Primary hypercholesterolemia or mixed dyslipidemia: Initial dose of 145 mg once daily.
• Severe hypertriglyceridemia: Initial dose of 48 to 145 mg once daily. Maximum dose is 145 mg.
• Renally impaired patients: Initial dose of 48 mg once daily.
• Geriatric patients: Select the dose on the basis of renal function.
• Maybe taken without regard to meals.

Adverse reactions > 2% and at least 1% greater than placebo: Abnormal liver tests, increased AST, increased ALT, increased CPK, and rhinitis.

• Severe renal dysfunction, including dialysis patients.
• Active liver disease.
• Gallbladder disease.
• Known hypersensitivity to fenofibrate.
• Nursing mothers.

• Hepatotoxicity: Serious drug-induced liver injury, including liver transplantation and death, has been reported with TRICOR. Monitor patient’s liver function, including serum ALT, AST, and total bilirubin, at baseline and periodically for the duration of therapy.
• Discontinue if signs or symptoms of liver injury develop or if elevated enzyme levels persist.
• Myopathy and rhabdomyolysis: Have been reported in patients taking fenofibrate. Risks are increased during co-administration with a statin (with a significantly higher rate observed for gemfibrozil), particularly in elderly patients and patients with diabetes, renal failure, or hypothyroidism.
• Serum creatinine: TRICOR can reversibly increase serum creatinine levels (5.4). Monitor renal function periodically in patients with renal impairment.
• Cholelithiasis: TRICOR increases cholesterol excretion into the bile, leading to risk of cholelithiasis. If cholelithiasis is suspected, gallbladder studies are indicated.
• Coumarin anticoagulants: Use caution in concomitant treatment with oral coumarin anticoagulants.
• Adjust the dosage of coumarin anticoagulant to maintain the prothrombin time/INR at the desired level to prevent bleeding complications.