Head-to-head clinical analysis & difference comparison: details on mechanism of action, dosing, half-life, interactions, and maternal-fetal safety.
FENOFIBRIC ACID vs ATROMID-S
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.
Inhibits hepatic triglyceride synthesis and increases lipoprotein lipase activity, leading to reduced VLDL and triglycerides.
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)
Type III hyperlipoproteinemia,Hypertriglyceridemia (Fredrickson types IV and V) not responsive to diet
135 mg orally once daily
500 mg to 1 g orally twice daily. Maximum dose 2 g/day.
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.
Terminal elimination half-life is 6-8 hours in patients with normal renal function; may be prolonged to 12-24 hours in renal impairment.
Primarily hepatic via glucuronidation; minor CYP3A4 involvement. Excreted as glucuronide conjugates in urine and feces.
Hepatic via glucuronidation and oxidation; major metabolite is clofibric acid.
Primarily renal as unchanged drug and glucuronide conjugate (approximately 60-70% of dose); remainder eliminated via biliary/fecal routes (~25%).
Primarily renal excretion as glucuronide conjugates; approximately 60-70% of the dose is excreted in urine, 20-30% in feces via biliary elimination.
Highly bound to serum albumin (approximately 99%).
>95% bound to plasma proteins, primarily albumin.
Approximately 0.4 L/kg (range 0.2-0.6 L/kg), indicating distribution mainly in extracellular fluid.
0.11-0.14 L/kg; low Vd indicates limited extravascular distribution, consistent with high protein 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.
Oral: approximately 60-70% due to first-pass metabolism; administered as clofibrate (prodrug) which is hydrolyzed to active clofibric acid.
If e GFR 30-59 m L/min: reduce dose to 45 mg orally once daily. If e GFR <30 m L/min: contraindicated.
GFR 30-59 m L/min: 500 mg twice daily. GFR 15-29 m L/min: 250 mg twice daily. GFR <15 m L/min: avoid use.
Contraindicated in Child-Pugh class B or C; no dose adjustment defined for Child-Pugh A (use with caution).
Child-Pugh Class B or C: avoid use or reduce dose by at least 50%; not recommended in severe hepatic impairment.
Not approved for use in pediatric patients.
Not recommended; safety and efficacy not established in pediatric patients.
No specific dose adjustment required; consider renal function and potential for decreased renal clearance in elderly.
Start at lower end of dosing range (500 mg twice daily). Monitor renal function; adjust dose based on GFR.
None
None
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,Cholelithiasis,Renal impairment dose adjustment,Rhabdomyolysis risk with statins,Malignancy risk (hepatic, GI)
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.
Hypersensitivity to clofibrate,Active liver disease,Severe renal dysfunction,Primary biliary cirrhosis,Pregnancy
Take with food to enhance absorption and reduce gastrointestinal intolerance. Avoid high-fat meals as they may exacerbate hypertriglyceridemia and reduce drug efficacy.
High-fat meals may reduce absorption; consistent timing of administration with food is recommended. Grapefruit juice may increase drug levels; avoid excessive intake. Alcohol may exacerbate hepatotoxicity.
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.
FDA Pregnancy Category C. First trimester: Potential for teratogenicity based on animal studies showing skeletal and visceral anomalies. Human data limited; use only if benefit outweighs risk. Second and third trimesters: May cause fetal harm due to placental transfer and potential for reduced fetal growth.
Excreted in breast milk in rats; human data unknown. Use caution, especially in preterm or jaundiced infants. M/P ratio not established.
Excreted into breast milk in low amounts; M/P ratio not established. Due to potential for serious adverse effects in infants, a decision should be made to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother.
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 specific dosing adjustments recommended due to lack of data. However, pharmacokinetic changes in pregnancy (increased volume of distribution, altered metabolism) may necessitate careful monitoring and empiric dose adjustments based on clinical response and adverse effects.
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).
ATROMID-S (clofibrate) is a fibric acid derivative primarily indicated for hyperlipidemia but its use is now limited due to increased non-cardiovascular mortality and cholelithiasis risk. Monitor liver function and prothrombin time (potentiates warfarin). Not first-line; consider statins or fibrates like fenofibrate.
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 meals to reduce gastrointestinal upset.,Report unexplained muscle pain, tenderness, or weakness; may indicate myopathy.,Avoid alcohol as it may increase liver enzyme elevations.,Notify your doctor if you develop gallstones symptoms (e.g., right upper abdominal pain, nausea).,Use effective contraception as clofibrate may cause fetal harm.
"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 ATROMID-S, 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.. ATROMID-S is a Antilipemic Agent that works by Inhibits hepatic triglyceride synthesis and increases lipoprotein lipase activity, leading to reduced VLDL and triglycerides.. They differ in pharmacokinetic profiles, FDA-approved indications, and side effect profiles.
Potency comparisons between FENOFIBRIC ACID and ATROMID-S depend on the specific clinical indication. These are agents from distinct pharmacological classes 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 ATROMID-S is: 500 mg to 1 g orally twice daily. Maximum dose 2 g/day.. 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 ATROMID-S 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. ATROMID-S is classified as Category C. FDA Pregnancy Category C. First trimester: Potential for teratogenicity based on animal studies showing skeletal and visceral anomalies. Human data limited; use only if benefit out. Always consult a maternal-fetal medicine specialist before taking either drug during pregnancy or lactation.