Drug Monograph
Fenofibrate (TriCor)
fenofibrate
Pharmacokinetic Profile
Half-Life
20 h (fenofibric acid)
Metabolism
Ester hydrolysis; glucuronidation (no CYP450)
Protein Binding
~99%
Bioavailability
~60% (enhanced with food)
Volume of Distribution
0.89 L/kg
Clinical Information
Drug Class
Fibric acid derivative (PPARα agonist)
Available Doses
48 mg, 145 mg tablets (TriCor)
Route
Oral, once daily
Renal Adjustment
Yes — initiate at 48 mg/day; avoid in severe impairment
Hepatic Adjustment
Contraindicated in active liver disease
Pregnancy
May cause fetal harm — avoid
Lactation
Contraindicated
Schedule / Legal
Prescription only (not controlled)
Generic Available
Yes
Fenofibrate Indications
| Indication | Approved Population | Therapy Type | Status |
|---|---|---|---|
| Primary hypercholesterolemia or mixed dyslipidemia — to reduce elevated LDL-C, Total-C, TG, Apo B, and increase HDL-C | Adults | Adjunctive to diet | FDA Approved |
| Severe hypertriglyceridemia — treatment of elevated triglycerides (Fredrickson types IV and V) | Adults | Adjunctive to diet | FDA Approved |
Fenofibrate is a first-line fibrate option for patients whose primary lipid abnormality is elevated triglycerides or atherogenic dyslipidemia (high TG, low HDL-C, small dense LDL). It is used as adjunctive therapy to diet after secondary causes of hyperlipidemia have been excluded. Clinicians should note the important limitation of use: fenofibrate was not demonstrated to reduce coronary heart disease morbidity and mortality in patients with type 2 diabetes in the FIELD and ACCORD Lipid trials (FDA PI).
Off-Label Uses
Diabetic retinopathy (moderate evidence): The FIELD and ACCORD-Eye trials demonstrated that fenofibrate reduced the need for laser photocoagulation and slowed retinopathy progression in type 2 diabetes, though this is not an FDA-approved indication. Australia has approved fenofibrate for diabetic retinopathy in patients with type 2 diabetes and pre-existing retinopathy.
Hyperuricemia associated with gout (low evidence): Fenofibrate has a well-documented uricosuric effect, reducing serum uric acid levels by increasing urinary excretion. Some clinicians use it as adjunctive therapy in patients with gout who also have dyslipidemia, though formal evidence for gout outcomes is limited.
Dosing
Adult Dosing by Clinical Scenario (TriCor formulation)
| Clinical Scenario | Starting Dose | Maintenance Dose | Maximum Dose | Notes |
|---|---|---|---|---|
| Mixed dyslipidemia — statin-intolerant patient or primary TG/HDL target | 145 mg once daily | 145 mg once daily | 145 mg/day | May be taken without regard to meals (TriCor formulation) Reassess lipids at 4-8 weeks |
| Severe hypertriglyceridemia — TG > 500 mg/dL, pancreatitis risk reduction | 48-145 mg once daily | 145 mg once daily | 145 mg/day | Start lower if co-existing renal or hepatic concern; titrate by lipid response Withdraw if inadequate response after 2 months at max dose |
| Atherogenic dyslipidemia in type 2 diabetes — add-on to statin | 145 mg once daily | 145 mg once daily | 145 mg/day | Preferred fibrate for statin combination (safer than gemfibrozil) Monitor for myopathy; avoid gemfibrozil co-administration |
| Mild-to-moderate renal impairment (CrCl 30-80 mL/min) | 48 mg once daily | 48 mg once daily | 48 mg/day | Increase only after evaluating renal function and lipid response Avoid in severe renal impairment (CrCl <30 mL/min) or dialysis |
| Elderly patients (≥65 years) | 48 mg once daily | 48-145 mg once daily | 145 mg/day | Dose selection based on renal function Higher risk for myopathy; monitor CK and creatinine |
Clinical Pearl — Formulation Bioequivalence
Multiple fenofibrate formulations exist with different dose strengths due to varying bioavailability profiles. TriCor 145 mg (nanocrystal tablet) is bioequivalent to micronized capsule 200 mg, Lipofen 150 mg, and Triglide 160 mg. When switching formulations, dose conversion is essential. TriCor 48 mg corresponds to micronized 67 mg. TriCor tablets may be taken without regard to meals, but some other formulations require food for optimal absorption.
Pharmacology
Mechanism of Action
Fenofibrate is a prodrug that is rapidly converted to its active metabolite, fenofibric acid, by tissue and plasma esterases. Fenofibric acid activates peroxisome proliferator-activated receptor alpha (PPARα), a nuclear transcription factor that regulates genes involved in lipid and lipoprotein metabolism. PPARα activation upregulates lipoprotein lipase expression while suppressing apolipoprotein C-III production, resulting in enhanced clearance of triglyceride-rich particles from plasma. This process also shifts LDL particle composition from small, dense atherogenic forms toward larger, more buoyant particles with greater receptor affinity. PPARα activation simultaneously increases synthesis of apolipoproteins A-I and A-II, which elevates HDL-C concentrations. Separately, fenofibrate promotes uric acid excretion through the kidneys, producing a clinically relevant uricosuric effect.
ADME Profile
| Parameter | Value | Clinical Implication |
|---|---|---|
| Absorption | Well absorbed (~60%); Tmax 6-8 h; food enhances absorption for some formulations; TriCor can be taken without regard to meals | Onset of lipid effects over days; steady-state fenofibric acid levels reached in approximately 9 days with twice the single-dose concentrations |
| Distribution | Vd 0.89 L/kg; protein binding ~99% (albumin) | Highly protein-bound; hemodialysis is ineffective for drug removal in overdose; limited extravascular distribution |
| Metabolism | Rapid ester hydrolysis to fenofibric acid (active); fenofibric acid conjugated with glucuronic acid via UGT; no significant CYP450 metabolism | Low CYP-mediated drug interaction risk; mild-to-moderate CYP2C9 inhibition; no unchanged fenofibrate detected in plasma |
| Elimination | t½ 20 h; 60% excreted in urine (as fenofibric acid and glucuronide conjugate); 25% in feces | Once-daily dosing is supported; dose reduction required in renal impairment (2.7-fold AUC increase in severe impairment) |
Side Effects
≥10%
Very Common
| Adverse Effect | Incidence | Clinical Note |
|---|---|---|
| No individual adverse effect reaches ≥10% incidence in pivotal trials | N/A | Fenofibrate has a relatively favorable tolerability profile; the most frequent effects cluster in the 2-8% range |
1-10%
Common
| Adverse Effect | Incidence | Clinical Note |
|---|---|---|
| Abnormal liver function tests | 7.5% vs 1.4% placebo | Dose-related; transaminases >3x ULN in 5.3% (pooled data); usually reversible on discontinuation |
| Respiratory disorder | 6.2% vs 5.5% placebo | Upper respiratory symptoms; modest excess over placebo |
| Abdominal pain | 4.6% vs 4.4% placebo | Similar to placebo; consider biliary causes if persistent |
| Back pain | 3.4% vs 2.5% placebo | Distinguish from myalgia; assess CK if associated with muscle weakness |
| Increased AST | 3.4% vs 0.5% placebo | Statistically significant excess; monitor periodically |
| Headache | 3.2% vs 2.7% placebo | Generally mild and self-limiting |
| Increased CPK | 3.0% vs 1.4% placebo | Warrants evaluation for myopathy, particularly with statin co-use |
| Increased ALT | 3.0% vs 1.6% placebo | Dose-related; incidence 13% at high doses vs 0% at ≤48 mg equivalent in dose-ranging study |
| Nausea | 2.3% vs 1.9% placebo | Typically transient; take with food if bothersome |
| Rhinitis | 2.3% vs 1.1% placebo | May represent upper respiratory tract irritation |
| Constipation | 2.1% vs 1.4% placebo | Manage with dietary fibre and hydration |
| Rash / Urticaria | 1.4% / 1.1% vs 0.8% / 0% placebo | Photosensitivity reactions reported postmarketing, sometimes occurring months after initiation; prior ketoprofen photosensitivity may be a risk factor |
Serious
Serious (Regardless of Frequency)
| Adverse Effect | Estimated Frequency | Typical Onset | Required Action |
|---|---|---|---|
| Rhabdomyolysis | Rare | Weeks to months; risk increased with statin co-use | Immediate discontinuation; aggressive IV hydration; monitor CK, renal function, and electrolytes; risk markedly higher with gemfibrozil-statin than fenofibrate-statin combinations |
| Hepatotoxicity (hepatocellular, cholestatic, or chronic active hepatitis) | ~5.3% with transaminases >3x ULN | Weeks to years | Discontinue if ALT/AST persistently >3x ULN; monitor LFTs periodically throughout therapy |
| Cholelithiasis | Uncommon (~3% class effect from fibrate trials) | Months to years | Gallbladder studies if cholelithiasis suspected; discontinue if gallstones confirmed |
| Pancreatitis | Rare | Variable; may reflect treatment failure in severe hypertriglyceridemia or biliary obstruction | Discontinue fenofibrate; supportive care; investigate biliary causes |
| Venous thromboembolism (DVT/PE) | PE: 1.1% vs 0.7% placebo (FIELD trial); DVT: 1.4% vs 1.0% | Any time during therapy | Evaluate for VTE in patients presenting with relevant symptoms; standard anticoagulation if confirmed |
| Anaphylaxis / Angioedema | Very rare (postmarketing) | Any time; some cases life-threatening | Emergency treatment; permanent discontinuation of fenofibrate |
| Stevens-Johnson syndrome / TEN / DRESS | Very rare (postmarketing) | Days to weeks after initiation | Immediate discontinuation; dermatology and burn unit referral as appropriate; do not rechallenge |
| Acute renal failure | Very rare (postmarketing) | Variable; higher risk with nephrotoxic co-medications | Discontinue fenofibrate; nephrology consultation; distinguish from the benign, reversible serum creatinine rise seen with fenofibrate |
| Paradoxical severe decrease in HDL-C | Rare (postmarketing) | 2 weeks to years after initiation | Check HDL-C within first few months; withdraw fenofibrate if severely depressed HDL-C detected; HDL recovers rapidly after discontinuation |
Discontinuation
Discontinuation Rates
Adults (Placebo-Controlled Trials)
5.0% vs 3.0% placebo
Top reason: Elevated liver function tests (1.6% of all fenofibrate-treated patients)
Pediatric
N/A
Adequate and well-controlled trials in pediatric populations have not been conducted
| Reason for Discontinuation | Incidence | Context |
|---|---|---|
| Elevated liver function tests | 1.6% | Most common cause of treatment discontinuation; dose-related effect |
| Gastrointestinal symptoms | ~1.0% | Includes abdominal pain, nausea, and diarrhoea |
| All other causes combined | ~2.4% | Includes myalgia, rash, headache, and miscellaneous reasons |
Managing Transaminase Elevations
Transaminase elevations are the most clinically significant tolerability issue with fenofibrate. In a dose-ranging study, ALT/AST increases to at least three times ULN occurred in 13% of patients at higher doses (equivalent to 96-145 mg TriCor) but in 0% at 48 mg or lower. If elevations are detected, confirm with a repeat level within 1-2 weeks. Discontinue fenofibrate if transaminases remain persistently above three times the normal limit. Values typically normalise after drug withdrawal.
Drug Interactions
Fenofibrate does not undergo significant CYP450 oxidative metabolism. Its active metabolite, fenofibric acid, is conjugated via glucuronidation and excreted renally. While this profile results in relatively few pharmacokinetic drug interactions, clinically important pharmacodynamic interactions exist, particularly with anticoagulants, statins, and nephrotoxic agents.
Major
Gemfibrozil
MechanismGemfibrozil inhibits glucuronidation of statins and fenofibric acid; overlapping pharmacodynamic muscle toxicity
EffectDramatically increased risk of myopathy and rhabdomyolysis (up to 15-fold higher reporting rate vs fenofibrate alone with statins)
ManagementNever combine gemfibrozil with fenofibrate; if a fibrate-statin combination is needed, fenofibrate is the preferred fibrate
AHA Scientific Statement 2016
Major
Warfarin / Coumarin Anticoagulants
MechanismFenofibrate potentiates anticoagulant effect via protein-binding displacement and possible pharmacodynamic synergy
EffectProlonged PT/INR; increased risk of bleeding complications
ManagementReduce warfarin dose (often by 25-35%); monitor INR frequently at initiation and dose changes until stable
FDA PI
Moderate
Statins (HMG-CoA Reductase Inhibitors)
MechanismAdditive pharmacodynamic risk for myopathy; fenofibrate does not significantly alter statin plasma concentrations (unlike gemfibrozil)
EffectIncreased risk of myopathy and rhabdomyolysis, though substantially lower than with gemfibrozil-statin combinations
ManagementUse lowest effective statin dose; counsel patients on muscle symptom reporting; monitor CK if symptomatic; higher risk in elderly, diabetic, and renally impaired patients
FDA PI / ACCORD Trial
Moderate
Cyclosporine / Tacrolimus
MechanismAdditive nephrotoxicity; immunosuppressants may reduce fenofibric acid renal clearance
EffectIncreased risk of renal dysfunction and potential fenofibrate accumulation
ManagementUse lowest effective fenofibrate dose; monitor renal function closely; consider alternative lipid-lowering therapy
FDA PI
Moderate
Colchicine
MechanismBoth agents independently cause myopathy; possible additive muscle toxicity
EffectMyopathy and rhabdomyolysis reported with co-administration
ManagementUse with caution; monitor for muscle symptoms and CK; particularly relevant in patients with gout who also have dyslipidemia
FDA PI
Moderate
Bile Acid Sequestrants (Cholestyramine, Colesevelam)
MechanismBile acid resins bind fenofibrate in the GI tract, reducing absorption
EffectDecreased fenofibrate bioavailability and therapeutic effect
ManagementAdminister fenofibrate at least 1 hour before or 4-6 hours after the bile acid resin
FDA PIMonitoring
-
Lipid Panel
Baseline, 4-8 weeks, then periodically
Routine Total cholesterol, LDL-C, HDL-C, triglycerides, Apo B at baseline and for dose titration. Withdraw therapy if inadequate response after 2 months at maximum dose. Also check HDL-C within first few months to detect paradoxical severe decreases. -
Liver Function Tests
Baseline, then periodically throughout therapy
Routine ALT (SGPT) is the primary marker. Discontinue if transaminases persist above 3x ULN. Dose-related effect: 13% incidence of ≥3x ULN at higher doses vs 0% at ≤48 mg equivalent. -
Renal Function
Baseline, then periodically
Routine Serum creatinine and estimated GFR. Fenofibrate reversibly raises serum creatinine through a mechanism unrelated to kidney damage, but genuine nephrotoxicity can occur, especially with concomitant nephrotoxic drugs. Consider monitoring more frequently in elderly and diabetic patients. -
CBC
First 12 months of therapy
Routine Mild decreases in haemoglobin, haematocrit, and white blood cell count observed in early therapy and typically stabilise during long-term use. Thrombocytopenia and agranulocytosis reported rarely. -
Creatine Kinase (CK)
If muscle symptoms develop
Trigger-based Assess CK promptly in patients reporting unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever. Discontinue if markedly elevated or myopathy/myositis is diagnosed. -
PT / INR
Frequently when co-prescribed with warfarin
Trigger-based Fenofibrate potentiates the anticoagulant effect of coumarins. Monitor INR frequently at initiation, dose changes, and until stable. Warfarin dose reduction is usually necessary.
Contraindications & Cautions
Absolute Contraindications
- Severe renal impairment including patients receiving dialysis — 2.7-fold increase in fenofibric acid exposure with increased accumulation (FDA PI)
- Active liver disease including primary biliary cirrhosis and unexplained persistent liver function abnormalities
- Pre-existing gallbladder disease — fenofibrate increases biliary cholesterol excretion
- Known hypersensitivity to fenofibrate or fenofibric acid
- Breastfeeding — contraindicated during nursing
Relative Contraindications (Specialist Input Recommended)
- Concomitant statin therapy — requires documented risk-benefit assessment, particularly in elderly patients and those with diabetes, renal insufficiency, or hypothyroidism; fenofibrate is preferred over gemfibrozil if combination is necessary
- Concomitant anticoagulant therapy — requires close INR monitoring and warfarin dose adjustment
- Concomitant immunosuppressant use (cyclosporine, tacrolimus) — additive nephrotoxicity risk; lowest effective dose and renal monitoring required
- Pregnancy — may cause fetal harm based on mechanism of action; use only if potential benefit justifies the risk; safety not established in pregnant women
Use with Caution
- Mild to moderate renal impairment (CrCl 30-80 mL/min) — initiate at reduced dose (48 mg TriCor); monitor renal function
- Elderly patients — increased risk for myopathy, renal impairment; dose selection based on renal function
- History of prior photosensitivity reaction to ketoprofen — cross-reactivity photosensitivity reported
- Concomitant colchicine use — myopathy and rhabdomyolysis reported with this combination
- Patients with hypothyroidism — increased myopathy risk and secondary cause of dyslipidemia; optimise thyroid function first
FDA Regulatory Limitation of Use
No Demonstrated Cardiovascular Mortality Benefit
Fenofibrate was not shown to reduce coronary heart disease morbidity and mortality in a large, randomised controlled trial of patients with type 2 diabetes mellitus (FIELD trial, n=9795; ACCORD Lipid trial, n=5518). The FIELD trial showed a non-significant 11% relative reduction in CHD events (HR 0.89, 95% CI 0.75-1.05, p=0.16), and a non-significant 11% increase in total mortality (HR 1.11, 95% CI 0.95-1.29). ACCORD Lipid showed a non-significant 8% relative risk reduction for MACE with fenofibrate added to statin (HR 0.92, 95% CI 0.79-1.08, p=0.32). In addition, the FDA withdrew approval of the co-administration indication with statins in 2016, concluding that fenofibrate-induced changes in TG and HDL-C in statin-treated patients no longer demonstrated a reduction in cardiovascular events.
Patient Counselling
Purpose of Therapy
Fenofibrate is a lipid-lowering medication prescribed to reduce elevated triglycerides and cholesterol levels in the blood. It works alongside diet and lifestyle changes — it is not a substitute for them. The goal is to reduce the risk of pancreatitis from very high triglycerides, improve overall lipid profile, and address atherogenic dyslipidemia. Patients should continue dietary modifications, regular exercise, and weight management throughout therapy.
How to Take
TriCor tablets should be taken once daily. The TriCor formulation can be taken with or without food. For other fenofibrate formulations, food may be required for adequate absorption — patients should follow the instructions specific to their product. If a dose is missed, skip it and resume with the next scheduled dose; do not double the dose. The medication should be swallowed whole.
Muscle Pain or Weakness
Tell patient
Fenofibrate can uncommonly cause muscle problems. The risk increases if you are also taking a statin, are elderly, have kidney problems, diabetes, or an underactive thyroid. Mild muscle soreness that resolves is generally not a concern, but persistent or unexplained symptoms require medical assessment.
Call prescriber
If you experience unexplained muscle pain, tenderness, or weakness — especially if accompanied by fever, malaise, dark-coloured urine, or general fatigue. These could indicate a rare but serious muscle condition requiring immediate attention.
Liver Health
Tell patient
Regular blood tests are needed to monitor your liver function while taking this medication. Liver enzyme elevations are the most common reason for dose adjustment or discontinuation. These changes are typically reversible once the medication is stopped.
Call prescriber
Report any symptoms of possible liver injury: yellowing of the skin or eyes (jaundice), unusually dark urine, light-coloured stools, persistent nausea, loss of appetite, unexplained fatigue, or abdominal pain in the upper right area.
Abdominal Pain
Tell patient
Mild abdominal discomfort may occur and is usually self-limiting. However, fenofibrate can increase the risk of gallstones by changing the composition of bile. Severe abdominal pain may indicate gallstones or, in rare cases, pancreatitis.
Call prescriber
Seek prompt medical attention for sudden, severe abdominal pain (especially right upper quadrant or radiating to the back), persistent vomiting, or pain worsening after eating fatty foods.
Allergic Reactions & Skin Changes
Tell patient
Allergic reactions and skin sensitivity to sunlight have been reported. Use sun protection (sunscreen, protective clothing) while on this medication. Patients who have previously had a photosensitivity reaction to ketoprofen (a pain reliever) may be at higher risk.
Call prescriber
Seek immediate medical attention for facial swelling, throat tightness, difficulty breathing, severe rash, blistering of the skin, or widespread skin peeling. These are rare but potentially life-threatening reactions.
Medication Interactions
Tell patient
Inform all healthcare providers (including dentists) that you take fenofibrate. This is especially important if you are prescribed blood thinners (warfarin), cholesterol medications (statins), gout medications (colchicine), or immunosuppressants. If taking a bile acid resin like cholestyramine, separate the doses by at least 1 hour before or 4-6 hours after.
Call prescriber
Before starting any new medication (including over-the-counter products), contact your prescriber to check for interactions.
Pregnancy & Breastfeeding
Tell patient
Fenofibrate may cause harm to a developing baby. Women of reproductive potential should discuss contraception with their prescriber. Breastfeeding is not recommended during treatment.
Call prescriber
If you become pregnant or plan to become pregnant while taking fenofibrate, contact your prescriber promptly to discuss whether the medication should be discontinued.
Sources
Regulatory (PI / SmPC)
- TriCor (fenofibrate) tablets — Full Prescribing Information. AbbVie Inc. Revised 11/2018. FDA Label Primary source for all dosing, indications, contraindications, adverse reactions data, and pharmacokinetic parameters cited in this monograph.
- Fenofibrate Capsules (micronized) — Full Prescribing Information. Sun Pharmaceutical Industries. Revised August 2024. DailyMed Provides updated labeling language for hypersensitivity reactions (DRESS, SJS/TEN) and pregnancy/lactation counselling.
- Triglide (fenofibrate) tablets — Full Prescribing Information. Shionogi Inc. Revised 2013. FDA Label Alternative formulation label providing cross-reference for dose equivalence and renal dosing guidance.
Key Clinical Trials
- The FIELD Study Investigators. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet. 2005;366(9500):1849-1861. doi:10.1016/S0140-6736(05)67667-2 Landmark trial (n=9795) demonstrating non-significant 11% reduction in CHD events with fenofibrate monotherapy in type 2 diabetes; source for VTE signal data.
- ACCORD Study Group. Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med. 2010;362(17):1563-1574. doi:10.1056/NEJMoa1001282 ACCORD Lipid trial (n=5518) showing non-significant 8% MACE reduction with fenofibrate added to statin; gender subgroup interaction finding.
- Keech AC, Mitchell P, Summanen PA, et al. Effect of fenofibrate on the need for laser treatment for diabetic retinopathy (FIELD study): a randomised controlled trial. Lancet. 2007;370(9600):1687-1697. doi:10.1016/S0140-6736(07)61607-9 FIELD retinopathy sub-study showing fenofibrate reduced need for laser photocoagulation for diabetic retinopathy.
- ACCORD Study Group; ACCORD Eye Study Group. Effects of medical therapies on retinopathy progression in type 2 diabetes. N Engl J Med. 2010;363(3):233-244. doi:10.1056/NEJMoa1001288 ACCORD-Eye study demonstrating 40% reduction in retinopathy progression with fenofibrate plus simvastatin vs simvastatin alone.
Guidelines
- Wiggins BS, Saseen JJ, Page RL, et al. Recommendations for management of clinically significant drug-drug interactions with statins and select agents used in patients with cardiovascular disease: a scientific statement from the American Heart Association. Circulation. 2016;134(21):e468-e495. doi:10.1161/CIR.0000000000000456 Authoritative AHA guidance on statin-fibrate interaction management; source for rhabdomyolysis reporting rates comparing fenofibrate and gemfibrozil.
- Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol. Circulation. 2019;139(25):e1082-e1143. doi:10.1161/CIR.0000000000000625 Current ACC/AHA cholesterol guideline positioning fenofibrate as second-line adjunct for persistent hypertriglyceridemia despite statin therapy.
Mechanistic / Basic Science
- Staels B, Dallongeville J, Auwerx J, Schoonjans K, Leitersdorf E, Fruchart JC. Mechanism of action of fibrates on lipid and lipoprotein metabolism. Circulation. 1998;98(19):2088-2093. doi:10.1161/01.CIR.98.19.2088 Foundational review of PPARα-mediated mechanisms underlying fibrate effects on triglyceride metabolism, LDL particle size, and HDL synthesis.
Pharmacokinetics / Special Populations
- Balfour JA, McTavish D, Heel RC. Fenofibrate: a review of its pharmacodynamic and pharmacokinetic properties and therapeutic use in dyslipidaemia. Drugs. 1990;40(2):260-290. doi:10.2165/00003495-199040020-00007 Comprehensive pharmacokinetic review providing absorption, distribution, metabolism, and elimination data for fenofibrate formulations.
- Guay DRP. Micronized fenofibrate: a new fibric acid hypolipidemic agent. Ann Pharmacother. 1999;33(10):1083-1103. doi:10.1345/aph.18414 Detailed comparison of micronized vs non-micronized fenofibrate formulations including bioequivalence data and dose conversion tables.
- Hottelart C, El Esper N, Rose F, Achard JM, Fournier A. Fenofibrate increases creatininemia by increasing metabolic production of creatinine. Nephron. 2002;92(3):536-541. doi:10.1159/000064083 Mechanistic study demonstrating that fenofibrate-induced serum creatinine rises reflect increased creatinine production rather than impaired renal function.