Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
FENOFIBRIC ACID vs FENOGLIDE
Clinician-reviewed, head-to-head comparison of mechanism, dosing, pharmacokinetics, and safety profiles.
Last clinically reviewed: July 2026 · OpiCalc Medical Review Team
Fenofibric acid is a peroxisome proliferator-activated receptor alpha (PPARα) agonist that increases lipolysis and clearance of triglyceride-rich lipoproteins and reduces apolipoprotein C-III production, leading to decreased triglycerides and increased HDL cholesterol.
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.
Adjunct to diet for treatment of severe hypertriglyceridemia (Fredrickson types IV and V hyperlipidemia),Adjunct to diet for reduction of LDL-C, total-C, triglycerides, and Apo B in primary hypercholesterolemia or mixed dyslipidemia (Fredrickson types IIa and IIb)
Primary hypercholesterolemia,Mixed dyslipidemia,Severe hypertriglyceridemia
135 mg orally once daily
160 mg orally once daily, taken with or without food.
Terminal elimination half-life is approximately 20 hours (range 15-25 h) for fenofibric acid, supporting once-daily dosing. In renal impairment, half-life may be prolonged.
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.
Primarily hepatic via glucuronidation; minor CYP3A4 involvement. Excreted as glucuronide conjugates in urine and feces.
Hepatic metabolism via glucuronidation; minor CYP450 involvement (CYP3A4).
Primarily renal as unchanged drug and glucuronide conjugate (approximately 60-70% of dose); remainder eliminated via biliary/fecal routes (~25%).
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 bound to serum albumin (approximately 99%).
Fenofibric acid is extensively bound to plasma proteins, primarily albumin, with a binding rate greater than 99%.
Approximately 0.4 L/kg (range 0.2-0.6 L/kg), indicating distribution mainly in extracellular fluid.
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 bioavailability of fenofibric acid is approximately 100% when administered as the choline salt; the capsule formulation has high bioavailability relative to tablet. Food may reduce rate but not extent of absorption.
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.
If e GFR 30-59 m L/min: reduce dose to 45 mg orally once daily. If e GFR <30 m L/min: contraindicated.
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 Child-Pugh class B or C; no dose adjustment defined for Child-Pugh A (use with caution).
Contraindicated in severe hepatic impairment (Child-Pugh class C). Use caution in moderate impairment (Child-Pugh class B); consider dose reduction.
Not approved for use in pediatric patients.
Not approved for use in pediatric patients under 18 years of age.
No specific dose adjustment required; consider renal function and potential for decreased renal clearance in elderly.
No specific dose adjustment; monitor renal function due to age-related decline.
None
No FDA black box warning.
Hepatotoxicity: elevation of serum transaminases; contraindicated in active liver disease.,Myopathy/rhabdomyolysis risk, especially with statins or in patients with renal impairment, hypothyroidism, or alcohol abuse.,Cholelithiasis: risk of gallstones due to increased cholesterol excretion into bile.,Pancreatitis: reported in hypertriglyceridemia patients.,Renal impairment: dose adjustment required; avoid in severe renal disease.,Venothromboembolic events: increased risk in clinical trials.
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.
Active liver disease including primary biliary cirrhosis and unexplained persistent liver function abnormalities.,Known gallbladder disease (cholelithiasis).,Severe renal impairment (e GFR <30 m L/min/1.73 m²).,Hypersensitivity to fenofibrate or fenofibric acid.
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
Take with food to enhance absorption and reduce gastrointestinal intolerance. Avoid high-fat meals as they may exacerbate hypertriglyceridemia and reduce drug efficacy.
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.
Pregnancy Category C. First trimester: Data insufficient to assess risk; animal studies show embryotoxicity and teratogenicity at high doses. Second/third trimesters: Avoid use due to potential fetal harm; no well-controlled human studies.
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.
Excreted in breast milk in rats; human data unknown. Use caution, especially in preterm or jaundiced infants. M/P ratio not established.
Excreted in breast milk; M/P ratio unknown. Potential for neonatal β-receptor stimulation. Caution advised; manufacturer recommends discontinuing breastfeeding or drug.
Avoid use during pregnancy; no established safe dose. Pharmacokinetic changes (increased volume of distribution, clearance) may reduce efficacy; dose adjustments not recommended due to potential fetal risk.
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).
Fenofibric acid is a PPARα agonist that reduces triglycerides by 30-50% and increases HDL; monitor renal function as dose adjustment required for Cr Cl 30-59 m L/min; contraindicated in severe renal impairment (Cr Cl <30 m L/min) and active liver disease; may increase serum creatinine; use with caution in patients with gallbladder disease; can potentiate warfarin effect (monitor INR).
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 reduce GI side effects.,Report unexplained muscle pain, tenderness, or weakness, especially if accompanied by fever or malaise.,Avoid alcohol as it can increase triglyceride levels and worsen liver effects.,This medication is not a substitute for diet and exercise; continue lifestyle modifications.,Notify your doctor if you develop abdominal pain (possible gallstones).
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.
"Fenofibric acid, a peroxisome proliferator-activated receptor alpha (PPARα) agonist, may reduce the therapeutic efficacy of ursodeoxycholic acid (UDCA) by increasing the biliary excretion of cholesterol and altering bile acid composition, thereby counteracting the beneficial effects of UDCA in dissolving cholesterol gallstones and improving cholestatic liver diseases. This interaction can lead to reduced clinical response, including incomplete stone dissolution or worsening of liver function tests in conditions such as primary biliary cholangitis."
"Glisoxepide may increase the hypoglycemic activities of Fenofibric acid."
"Colchicine may increase the myopathic rhabdomyolysis activities of Fenofibric acid."
No interactions on record
Explore head-to-head clinical comparisons of other medications in the same therapeutic classes.
Common clinical questions about FENOFIBRIC ACID vs FENOGLIDE, answered by our medical review team.
FENOFIBRIC ACID is a Antilipemic that works by Fenofibric acid is a peroxisome proliferator-activated receptor alpha (PPARα) agonist that increases lipolysis and clearance of triglyceride-rich lipoproteins and reduces apolipoprotein C-III production, leading to decreased triglycerides and increased HDL cholesterol.. 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 FENOFIBRIC ACID 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 FENOFIBRIC ACID is: 135 mg orally once daily. 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 FENOFIBRIC ACID 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. FENOFIBRIC ACID is classified as Category C. Pregnancy Category C. First trimester: Data insufficient to assess risk; animal studies show embryotoxicity and teratogenicity at high doses. Second/third trimesters: Avoid use due. 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.