Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
OMACOR vs FENOGLIDE
Clinician-reviewed, head-to-head comparison of mechanism, dosing, pharmacokinetics, and safety profiles.
Last clinically reviewed: July 2026 · OpiCalc Medical Review Team
Omega-3-acid ethyl esters (EPA and DHA) reduce hepatic triglyceride synthesis by inhibiting acyl-Co A:1,2-diacylglycerol acyltransferase and increasing beta-oxidation. They also decrease very-low-density lipoprotein (VLDL) secretion and enhance triglyceride clearance from circulating VLDL particles.
Fenofibrate is a peroxisome proliferator-activated receptor alpha (PPARα) agonist. It increases lipolysis and elimination of triglyceride-rich particles from plasma, reduces hepatic production of VLDL, and increases HDL cholesterol.
FDA: Adjunct to diet for reduction of triglyceride levels in adult patients with severe hypertriglyceridemia (≥500 mg/d L).,Off-label: Secondary prevention of cardiovascular events in patients with hypertriglyceridemia or high cardiovascular risk.
Primary hypercholesterolemia,Mixed dyslipidemia,Severe hypertriglyceridemia
4 g orally once daily or 2 g orally twice daily, taken with meals. Each capsule contains 1 g of omega-3-acid ethyl esters (approximately 465 mg eicosapentaenoic acid and 375 mg docosahexaenoic acid).
160 mg orally once daily, taken with or without food.
Terminal elimination half-life: ~55–75 hours for EPA and DHA (beta-phase). Clinical context: steady-state achieved after 4–8 weeks; half-life supports once-daily dosing.
The terminal elimination half-life of fenofibric acid is approximately 20 hours (range 15-25 hours). This long half-life allows once-daily dosing. Steady-state is reached within approximately 5 days.
Omega-3-acid ethyl esters are primarily hydrolyzed by pancreatic lipase to free fatty acids (EPA and DHA), which are then absorbed and incorporated into chylomicrons. They undergo hepatic metabolism via beta-oxidation. CYP450 involvement is minimal.
Hepatic metabolism via glucuronidation; minor CYP450 involvement (CYP3A4).
Primarily fecal as unchanged drug and metabolites; <5% renal. Biliary excretion accounts for ~90% of elimination via feces, with minimal urinary excretion (0.5–2%).
Fenoglide (fenofibrate) is primarily excreted in urine as fenofibric acid and its glucuronide conjugate, accounting for approximately 60-70% of the dose. About 20-25% is eliminated in feces via biliary excretion. Renal excretion is the major route.
Highly protein-bound (>99%) primarily to albumin.
Fenofibric acid is extensively bound to plasma proteins, primarily albumin, with a binding rate greater than 99%.
Vd: ~0.2–0.3 L/kg (EPA), ~2–3 L/kg (DHA). Clinical meaning: extensive tissue distribution, especially in adipose and cardiac tissues.
The apparent volume of distribution (Vd) of fenofibric acid is approximately 0.9 L/kg. This suggests distribution into total body water, with some tissue binding.
Oral: 50–100% (enhanced with fatty meal; absolute bioavailability not determined).
The absolute oral bioavailability of fenofibric acid from fenofibrate tablets is approximately 90% under fed conditions. Administration with food increases absorption by up to 35% compared to fasting.
No dose adjustment required for any degree of renal impairment. Use caution in patients with renal disease due to potential for increased bleeding risk.
No dose adjustment required for mild to moderate renal impairment (e GFR >30 m L/min/1.73 m2). Not recommended in severe renal impairment (e GFR <30 m L/min/1.73 m2) or dialysis.
Contraindicated in patients with Child-Pugh class C (severe) hepatic impairment. For Child-Pugh A or B, no dose adjustment is recommended, but monitor liver function tests periodically.
Contraindicated in severe hepatic impairment (Child-Pugh class C). Use caution in moderate impairment (Child-Pugh class B); consider dose reduction.
Safety and efficacy not established in pediatric patients. Not recommended for use in children.
Not approved for use in pediatric patients under 18 years of age.
No specific dose adjustment recommended. Monitor for potential drug interactions, especially with anticoagulants, due to increased bleeding risk. Start at lower end of dosing range if elderly patient has significant comorbidity or polypharmacy.
No specific dose adjustment; monitor renal function due to age-related decline.
No FDA black box warning.
No FDA black box warning.
Increased bleeding risk (monitor patients on anticoagulants).,Atrial fibrillation in patients with prior history or at high risk.,Persistent elevations of ALT or AST, especially with other hepatotoxic drugs.,Hypersensitivity reactions including anaphylaxis.,Fish allergy (capsules contain fish oil).
Hepatotoxicity: rare but severe; monitor liver enzymes.,Rhabdomyolysis: risk increased with renal impairment, hypothyroidism, statins.,Renal function: dose adjustment needed in mild-moderate impairment; contraindicated in severe renal disease.,Cholelithiasis: fenofibrate increases cholesterol excretion into bile.,Pancreatitis: associated with severe hypertriglyceridemia; monitor triglycerides.,Venous thromboembolism: increased risk with fenofibrate.
Hypersensitivity to omega-3-acid ethyl esters or any component.,Acute pancreatitis with marked hypertriglyceridemia (consider if triglycerides >500 mg/d L and chylomicronemia).
Severe renal impairment (e GFR <30 m L/min/1.73m²),Active liver disease including primary biliary cirrhosis,Known hypersensitivity to fenofibrate or excipients,Gallbladder disease,Nursing mothers
Avoid high-fat meals as they may increase triglyceride levels. No specific food interactions known, but consistency in timing with meals is recommended.
Take with food to enhance absorption. Avoid high-fat meals immediately before or after dose. Grapefruit juice may increase fenofibrate exposure (moderate interaction, monitor). Statin co-administration: avoid large amounts of grapefruit juice.
FDA Pregnancy Category C. No evidence of teratogenicity in animal studies at doses up to 10 times the human dose. There are no adequate and well-controlled studies in pregnant women. Use only if potential benefit justifies potential risk to fetus. Omega-3-acid ethyl esters may inhibit prostaglandin synthesis and delay labor. Third trimester use may increase risk of bleeding in mother and neonate.
First trimester: No adequate studies; animal data show no major malformations at clinically relevant doses. Second and third trimesters: Associated with adverse maternal and fetal outcomes (e.g., preterm birth, low birth weight) due to β-receptor agonist effects. Avoid use during pregnancy.
Not recommended during breastfeeding. Omega-3 fatty acids are excreted in human milk; M/P ratio not established. Potential for adverse effects in nursing infant. Consider alternative treatment or discontinue nursing.
Excreted in breast milk; M/P ratio unknown. Potential for neonatal β-receptor stimulation. Caution advised; manufacturer recommends discontinuing breastfeeding or drug.
No specific dose adjustments recommended for pregnancy-induced pharmacokinetic changes. Use with caution as pregnancy may alter lipid profiles; monitor triglyceride levels and adjust dose accordingly.
No established dose adjustments for pregnancy; use only if potential benefit outweighs risk. Consideration of lower doses due to altered pharmacokinetics (increased clearance, decreased plasma concentration).
Omacor (omega-3-acid ethyl esters) is indicated as an adjunct to diet for severe hypertriglyceridemia (≥500 mg/d L). Monitor LDL-C levels as they may increase during therapy; adjust statin dose if needed. Administer with meals to enhance absorption and reduce gastrointestinal side effects. Avoid use in patients with fish or shellfish allergy. May prolong bleeding time; monitor in patients on anticoagulants.
Fenofibrate is a fibric acid derivative used primarily for hypertriglyceridemia and mixed dyslipidemia. It activates PPAR-alpha, increasing lipoprotein lipase and reducing apolipoprotein C-III. Monitor renal function; dose adjustment required for Cr Cl 30-60 m L/min. Contraindicated in severe renal impairment (Cr Cl <30) and active liver disease. Can increase serum creatinine, but this is often reversible. Co-administration with statins increases risk of myopathy, especially in elderly or renal impairment. May increase homocysteine levels; monitor if at risk for thrombosis.
Take with food to improve absorption and reduce burping or fishy taste.,Do not take if you have an allergy to fish or shellfish.,Report unusual bleeding or bruising, especially if you are on blood thinners.,Do not substitute with over-the-counter fish oil supplements as they are not equivalent.,Continue dietary modifications and exercise as part of your treatment plan.
Take with food to improve absorption.,Avoid alcohol as it may worsen triglyceride levels.,Report unexplained muscle pain, tenderness, or weakness, especially if accompanied by fever or malaise.,Do not stop medication without consulting your doctor, even if you feel well.,Keep all appointments for blood tests to monitor liver function and lipid levels.
No interactions on record
No interactions on record
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about OMACOR vs FENOGLIDE, answered by our medical review team.
OMACOR is a Antilipemic that works by Omega-3-acid ethyl esters (EPA and DHA) reduce hepatic triglyceride synthesis by inhibiting acyl-Co A:1,2-diacylglycerol acyltransferase and increasing beta-oxidation. They also decrease very-low-density lipoprotein (VLDL) secretion and enhance triglyceride clearance from circulating VLDL particles.. FENOGLIDE is a Antilipemic that works by Fenofibrate is a peroxisome proliferator-activated receptor alpha (PPARα) agonist. It increases lipolysis and elimination of triglyceride-rich particles from plasma, reduces hepatic production of VLDL, and increases HDL cholesterol.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between OMACOR and FENOGLIDE depend on the specific clinical indication. These are both Antilipemic agents and are not directly interchangeable by dose. A physician or clinical pharmacist should guide any therapeutic switching decisions.
The standard adult dose of OMACOR is: 4 g orally once daily or 2 g orally twice daily, taken with meals. Each capsule contains 1 g of omega-3-acid ethyl esters (approximately 465 mg eicosapentaenoic acid and 375 mg docosahexaenoic acid).. The standard adult dose of FENOGLIDE is: 160 mg orally once daily, taken with or without food.. Dosing should always be individualized based on indication, renal and hepatic function, age, and other patient factors.
No direct drug-drug interaction has been formally documented between OMACOR and FENOGLIDE in current clinical databases. However, individual patient risk factors including other medications, organ function, and comorbidities should always be evaluated by a qualified healthcare provider.
The maternal-fetal safety profiles differ. OMACOR is classified as Category C. FDA Pregnancy Category C. No evidence of teratogenicity in animal studies at doses up to 10 times the human dose. There are no adequate and well-controlled studies in pregnant wome. FENOGLIDE is classified as Category C. First trimester: No adequate studies; animal data show no major malformations at clinically relevant doses. Second and third trimesters: Associated with adverse maternal and fetal . Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.