Currently Enrolling Trials
TriCor tablets have been developed to assist patients in managing their cholesterol levels. The drug is indicated for use in reducing elevated LDL-C, Total-C, triglycerides and Apo-B and increasing HDL-C in patients with primary hypercholesterolemia or mixed lipidemia. The drug has also been approved as adjunctive therapy for the treatment of hypertriglyceridemia, a disorder characterized by elevated levels of very low density lipoprotein (VLDL) in the plasma.
TriCor (160 mg per day) was evaluated in four randomized, placebo-controlled, double-blind, parallel-group trials as a therapy for hypercholesterolemia and mixed dyslipidemia. Treatment with TriCor was shown to lower LDL-C, Total-C, the LDL-C/HDL-C ratio and triglycerides, in addition to raising HDL-C. Apo-B levels were also measured in a subset of subjects. Compared to placebo, treatment with TriCor significantly reduced Apo-B from baseline to endpoint.
The effect of TriCor on serum triglycerides was evaluated in two randomized, double-blind, placebo-controlled trials that included 147 hypertriglyceridemic subjects. Treatment was administered for eight weeks in both trials. The trials differed in terms of initial subject triglyceride (TG) levels; one entered subjects with baseline TG levels of 500 to 1500 mg/dL, and the other entered subjects with TG levels of 350 to 500 mg/dL. In subjects with hypertriglyceridemia and normal cholesterolemia with or without hyperchylomicronemia, treatment with TriCor decreased very low density lipoprotein (VLDL) triglycerides and VLDL cholesterol.
Adverse events reported by subjects treated with TriCor in clinical trials include (but are not limited to) the following:
- Respiratory symptoms
- Back pain
- Abdominal pain
- Abnormal liver function tests
Individuals with serious liver, kidney or gallbladder disease should not take TriCor.
Mechanism of Action
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.
The 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 alpha (PPAR alpha). 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 fall in triglycerides 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 PPAR alpha also induces an increase in the synthesis of apoproteins A-I, A-II and HDL-cholesterol.
Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid. (from TriCor tablets Prescribing Information)
For additional information on TriCor, please visit the product web site at www.tricortablets.com.