Drug reference

Fenofibrate

Fibrate (fibric acid derivative / PPAR-alpha agonist) · Antilipidemic

Also known as Fenofibric acid, Tricor, Lipanthyl, Lipicard

START

Baseline lipid panel, LFTs, creatinine, CK. Verify TG level indication. Counsel on taking with food. Avoid in severe renal or hepatic impairment.

TYPICAL MAX

200mg/day (micronized). Renal impairment limits max dose. Monitor LFTs and CK.

STOP IF

LFTs >3x ULN, CK >5-10x ULN with muscle symptoms, severe abdominal pain (gallstones/pancreatitis), AKI (rising creatinine >50% from baseline), severe rash.

WATCH

Lipid panel at 4-8 weeks, then every 3-6 months. LFTs and creatinine at 8-12 weeks, then every 6 months. FIELD and ACCORD trials showed no cardiovascular mortality benefit despite TG reduction. Gemfibrozil has more drug interactions with statins than fenofibrate. Fenofibrate is preferred fibrate for statin combination (lower myopathy risk than gemfibrozil).

CDSCO approvedSchedule HJan AushadhiNPPA price-controlledATC C10AB05

Dose laddermg/d

Renal dose adjustmenteGFR mL/min/1.73m²

KDIGO 2024 + manufacturer label

Pharmacokineticsplasma · t hours

ONSET: 1h · Onset ~1 hour
PEAK: 7h · Tmax 6-8 hours (micronized)
t½: 20h · t½ ~20 hours
DURATION: 1d · 24 hours (QD)

EXCRETION

Renal as fenofibric acid (~60%)

route + CYP

INTERACTIONS

12 major

SEVERE in our sources

PREGNANCY

Contraindicated in pregnancy—no benefit and potential fetal harm. Lipid-modifying drugs not recommended during pregnancy.

FDA category + note

Top interactionssee all 12 →

AnisindioneSevereDatabaseDDInter
AtorvastatinSevereDatabaseDDInter
CerivastatinSevereDatabaseDDInter
CitalopramSevereDatabaseDDInter

Available in India

63 branded formulations and 5 fixed-dose combinations. Look up specific brands in the Drugs workspace.

Jan Aushadhi — generic available at GoI pharmacies

Mechanism

Activates peroxisome proliferator-activated receptor alpha (PPAR-α), a nuclear transcription factor that regulates genes involved in lipid metabolism. Increases lipoprotein lipase activity, enhances fatty acid oxidation, reduces hepatic VLDL production, and increases HDL synthesis. Primarily lowers triglycerides and raises HDL-C.

Indications

Hypertriglyceridemia (Fredrickson types IV and V)Mixed dyslipidemia (Fredrickson types IIa, IIb, III)Primary hypercholesterolemia (adjunctive or monotherapy when statins contraindicated)Prevention of pancreatitis in severe hypertriglyceridemia (TG >500 mg/dL)

Dosing

Adult: Hypertriglyceridemia: 48-145mg daily (starting at 48-145mg based on formulation and TG level). Mixed dyslipidemia: 145mg daily (micronized) or 160mg daily (non-micronized). Take with food.
Pediatric: >9 years (Lofibra): 67-200mg daily. Adolescents: 48-145mg daily based on product.
Renal adjustment: CrCl 30-59: start 48mg daily (do not titrate above 145mg). CrCl <30: contraindicated.
Hepatic adjustment: Avoid in severe hepatic impairment; monitor LFTs.
Geriatric: Start at low end; monitor renal function and muscle symptoms.
Max dose: 200mg/day (micronized); 160mg/day (non-micronized tablet); 145mg/day (some formulations)

Pharmacokinetics

Onset

Lipid effects within 2-4 weeks; maximal effect 4-8 weeks

Peak effect

Tmax 6-8 hours (micronized); 4-6 hours (non-micronized) with food; steady-state in 5 days

Duration

24 hours (QD dosing)

Half-life

~20 hours (active metabolite fenofibric acid); parent compound ~20h

Bioavailability

~60% (varies by formulation; micronized has better absorption)

Protein binding

~99% (fenofibric acid; albumin)

Metabolism

Rapidly hydrolyzed by esterases in gut and plasma to active fenofibric acid; then glucuronidated

Excretion

~60% renal (fenofibric acid and glucuronides); ~25% fecal

Contraindications

Severe hepatic impairment (including primary biliary cirrhosis, unexplained persistent LFT elevation)
Severe renal impairment (CrCl <30 or eGFR <30)
Pre-existing gallbladder disease
Chronic or acute pancreatitis (unrelated to severe hypertriglyceridemia)
Hypersensitivity to fenofibrate
Breastfeeding

Side effects

Common

Elevated LFTsMyalgia (muscle pain)Increased creatinine (reversible)Abdominal painHeadacheNauseaBack painDiarrhea

Serious

Rhabdomyolysis (especially with statin co-therapy)
Hepatotoxicity (cholestatic hepatitis, cirrhosis rare)
Acute kidney injury (reversible with discontinuation)
Gallstones (increased cholesterol excretion in bile)
Pancreatitis (paradoxical—can occur with fibrate use)
Thromboembolic events (increased in FIELD and ACCORD trials)
Severe allergic reactions

Pregnancy & lactation

Pregnancy

Contraindicated in pregnancy—no benefit and potential fetal harm. Lipid-modifying drugs not recommended during pregnancy.

Lactation

Contraindicated. Fenofibric acid is excreted in the milk of lactating rats. Due to the potential for serious adverse reactions in nursing infants, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.

Drug interactions

Anisindione

Severe

Database

Drug interaction classified as: distribution

Source: DDInter

Atorvastatin

Severe

Database

Lower risk of statin myopathy compared to other fibrate-statin combinations.

Fenofibrate is the most suitable fibrate for combining with statins due to its minimal impact on statin metabolism and lower myopathy risk. However, continued vigilance for muscle symptoms is prudent.

Source: DDInter

Cerivastatin

Severe

Database

Drug interaction classified as: others

Source: DDInter

Citalopram

Severe

Database

Drug interaction classified as: metabolism.

Source: DDInter

Dicoumarol