Fenofibric Acid (fenofibric acid (choline))

Fenofibrate and fenofibric acid are fibric acid-derivative antilipemic agents. Fenofibric acid is the pharmacologically active moiety of fenofibrate.

Fenofibrate and fenofibric acid are antilipemic agents. Fenofibrate is a prodrug; following oral administration, fenofibrate is rapidly hydrolyzed by esterases to its pharmacologically active metabolite fenofibric acid. No unchanged fenofibrate is detectable in plasma after administration.

Fenofibrate and fenofibric acid are structurally and pharmacologically related to clofibrate (no longer commercially available in the US) and gemfibrozil. Clofibrate, fenofibrate, fenofibric acid, and gemfibrozil have been referred to as fibric acid derivatives.

Fenofibrate has no antilipemic activity. Fenofibric acid, the active metabolite, decreases serum concentrations of total cholesterol, low-density lipoprotein (LDL)-cholesterol, apolipoprotein B (apo B), very low-density lipoprotein (VLDL)-cholesterol, and triglycerides. Fenofibric acid also increases serum concentrations of high-density lipoprotein (HDL)-cholesterol, apolipoprotein A-I (apo A-I), and apolipoprotein A-II (apo A-II).

The antilipemic effects of fenofibric acid appear to be related to the drug's effects on clearance of triglyceride-rich particles. Data from in vitro and in vivo studies indicate that fenofibric acid activates lipoprotein lipase and reduces production of apolipoprotein C-III (apo C-III), an inhibitor of lipoprotein lipase activity, thereby increasing lipolysis and clearance of triglyceride-rich particles. The reduction in triglyceride concentrations via this mechanism alters the size and composition of LDL-cholesterol from small, dense particles to larger, more buoyant particles that are less atherogenic and more rapidly catabolized.

Fenofibric acid also appears to activate a receptor (peroxisome proliferator activated receptor alpha) that induces the synthesis of HDL-cholesterol, apo A-I, and apo A-II. Limited data in patients with type 2 diabetes mellitus indicate that fenofibrate may slow the progression of coronary atherosclerosis; however, a corresponding clinical benefit (i.e., reduction in coronary heart disease (CHD)-related morbidity and mortality) has not been demonstrated.

Fenofibrate has been shown to reduce serum uric acid concentrations in healthy and hyperuricemic individuals by increasing the urinary excretion of uric acid.

Fenofibrate is commercially available as nonmicronized drug in capsules (e.g., Lipofen(R)) or tablets (e.g., Fenoglide(R) Lofibra(R)), micronized drug in capsules (e.g., Antara(R) ), ''nanocrystal'' drug in tablets (i.e., TriCor(R) ), or ''insoluble drug delivery-microparticle (IDD-P)'' drug in tablets (i.e., Triglide(R) ). Fenofibric acid is commercially available as delayed-release capsules containing choline fenofibrate (e.g., Trilipix(R)) or tablets (Fibricor(R) ). Plasma concentrations of fenofibric acid achieved following administration of three 48-mg or one 145-mg TriCor(R) tablet(s), one 160-mg Triglide(R) tablet, or one 135-mg Trilipix(R) delayed-release tablet are equivalent under fed conditions to those achieved with the 200-mg micronized fenofibrate capsule.

Plasma concentrations of fenofibric acid following administration of a single 120-mg Fenoglide(R) tablet are equivalent to those achieved with fenofibrate 130-mg capsules under fed (high-fat) conditions. Plasma concentrations of fenofibric acid following administration of 150-mg Lipofen(R) capsules are equivalent to those achieved with Tricor(R) 160-mg tablets. Pharmacokinetic data from single-dose studies in healthy individuals indicate that 100 mg of the nonmicronized capsule formulation of fenofibrate is bioequivalent to 67 mg of the micronized fenofibrate capsule; three capsules containing 67 mg of micronized fenofibrate are equivalent to a single 200-mg fenofibrate capsule.

Administration of some formulations (e.g., TriCor(R) tablets, Triglide(R) tablets) with food did not substantially alter the AUC of fenofibric acid. Administration of Antara(R) micronized capsules with a high-fat meal resulted in a 15 and 27% increase in peak plasma concentrations and AUC, respectively, of fenofibric acid compared with administration under fasting conditions. Administration of fenofibrate micronized capsules with food resulted in a 35% increase in the extent of absorption of the drug.

Administration of Lipofen(R) tablets with food increased the extent of absorption by approximately 58 or 25% under high-fat or low-fat conditions, respectively, compared with the fasting state. Administration of Fenoglide(R) tablets with a high-fat meal increased peak plasma concentrations of the drug by 44% but had no effect on systemic exposure.

USES: Fenofibric acid is used along with a proper diet to help lower "bad" cholesterol and fats (such as LDL, triglycerides) and raise "good" cholesterol (HDL) in the blood. It works by increasing the natural substance (enzyme) that breaks down fats in the blood. Fenofibric acid belongs to a group of drugs known as "fibrates." Lowering triglycerides in people with very high triglyceride blood levels may decrease the risk of pancreas disease (pancreatitis).

However, fenofibric acid might not lower your risk of a heart attack or stroke. Talk to your doctor about the risks and benefits of fenofibric acid. In addition to eating a proper diet (such as a low-cholesterol/low-fat diet), other lifestyle changes that may help this medication work better include exercising, losing weight if overweight, and stopping smoking.

Consult your doctor for more details.

Generic name: fenofibric acid (choline)
Pronunciation: (FEN-oh-FYE-brick AS-id)

The following indications are listed for Fenofibric Acid:

• Hyperlipidemia
• Hypertriglyceridemia

Also known as: Abnormally Increased Triglycerides In The Blood, Elevated Triglyceride Level, Hyperlipoidemia, Increased Triglyceride Levels, Lipemia, Lipidemia, Lipoidemia.

No ICD codes are available for this drug.