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Fenofibrate structure.svg
Systematic (IUPAC) name
propan-2-yl 2-{4-[(4-chlorophenyl)carbonyl]phenoxy}-2-methylpropanoate
Clinical data
Trade names Fenoglide, Lipofen
AHFS/Drugs.com monograph
MedlinePlus a601052
  • US: C
  • Legend
Pharmacokinetic data
Protein binding 99%
Metabolism glucuronidation
Half-life 20 hours
Excretion urine (60%), feces (25%)
49562-28-9 YesY
PubChem CID 3339
DrugBank DB01039 YesY
ChemSpider 3222 YesY
UNII U202363UOS YesY
KEGG D00565 YesY
Chemical data
Formula C20H21ClO4
360.831 g/mol
 YesY (what is this?)  (verify)

Fenofibrate (INN), marketed as Tricor and under several other brand names, is a drug of the fibrate class. It is mainly used to reduce cholesterol levels in patients at risk of cardiovascular disease. Like other fibrates, it reduces both low-density lipoprotein (LDL) and very low density lipoprotein (VLDL) levels, as well as increasing high-density lipoprotein (HDL) levels and reducing triglyceride levels.[1] It is used alone or along with statins in the treatment of hypercholesterolemia and hypertriglyceridemia.

Fenofibrate has been used since 1975, is one of the most commonly prescribed fibrates, and has a well known efficacy and tolerability profile.[1]

Medical uses[edit]

Fenofibrate is mainly used for primary hypercholesterolemia or mixed dyslipidemia. Fenofibrate appears to decrease the risk of cardiovascular disease and possibly diabetic retinopathy in those with diabetes mellitus.[2] It also appears to be helpful in decreasing amputations of the lower legs in this same group of people.[3] Fenofibrate also has an unlabeled use as an added therapy of high blood uric acid levels in people who have gout.[4]

It is used in addition to diet to reduce elevated low-density lipoprotein cholesterol (LDL), total cholesterol, triglycerides (TG), and apolipoprotein B (Apo B), and to increase high-density lipoprotein cholesterol (HDL) in adults with primary hypercholesterolemia or mixed dyslipidemia.[5]

It is used in addition to diet for treatment of adults with severe hypertriglyceridemia. Improving glycemic control in diabetics showing fasting chylomicronemia will usually decrease the need for pharmacologic intervention.[5]

Three randomized, double-blind trials have shown that treatment with fenofibric acid plus a statin improved HDL and triglyceride levels better than a statin alone and improved LDL levels better than fenofibric acid monotherapy.[1]

Additionally, in Europe, fenofibrate is indicated in mixed hyperlipidemia in those with high cardiovascular risk in addition to a statin when triglycerides and HDL are not adequately controlled.[citation needed]

Statins remain first line for treatment of blood cholesterol. As of now, “there are no data to show that adding a nonstatin drug(s) to high-intensity statin therapy will provide incremental ASCVD risk reduction with an acceptable margin of safety”. Therefore, fenofibrate may potentially be used as an adjunctive therapy to low or moderate-intensity statin only if the benefits of ASCVD risk reduction or lowering triglycerides for people with >500 mg/dL outweigh the possible increased risk of adverse effects.[6]


Fenofibrate is contraindicated in:[5]

Adverse effects[edit]

The most common adverse events (>3% of patients with coadministered statins) are[7]




  • Can increase serum transaminases; liver tests should be monitored periodically[7]


  • Can increase serum creatinine levels; renal function should be monitored periodically in patients with renal insufficiency[7]


  • Can increase cholesterol excretion into the bile, leading to risk of cholelithiasis; if suspected gallbladder studies are indicated. See "Interaction" section under Bile Acid Sequestrant[7]


  • Exercise caution in concomitant treatment with oral coumarin anticoagulants (e.g. Warfarin). Adjust the dosage of coumarin to maintain the prothrombin time/INR at desired level to prevent bleeding complications[7]


There is no specific treatment for overdose with fenofibric acid delayed-release capsules. General supportive care Is indicated, including monitoring of vital signs and observation of clinical status”. Additionally, hemodialysis should not be considered as an overdose treatment option because fenofibrate heavily binds to plasma proteins and does not dialyze well.[7]


The following drug interactions with fenofibrate is considered major and may need therapy modifications:

  • Bile acid sequestrants (eg cholestyramine, colestipol, etc.): If taken together, bile acid resins may bind to fenofibrate, resulting in a decrease in fenofibrate absorption. In order to maximize absorption, patients need to separate administration by at least 1 hour before or 4-6 hours after taking the bile acid sequestrant.[7][8]
  • Immunosuppressants (eg cyclosporine or tacrolimus): There is an increased risk of renal dysfunction with concomitant use of immunosuppressants and fenofibrate. Please approach with caution when coadministering additional medications that decrease renal function. [9]
  • Vitamin K antagonists (eg warfarin): As previously mentioned, fenofibrate interacts with coumarin anticoagulants to increase the risk of bleeding. Dosage adjustment of Vitamin K antagonist may be necessary.[7]
  • Statins: Combination of statins and fenofibrate may increase the risk of rhabdomyolysis or myopathy.[10]

Mechanism of action[edit]

"In summary, enhanced catabolism of triglyceride-rich particles and reduced secretion of VLDL underlie the hypotriglyceridemic effect of fibrates, whereas their effect on HDL metabolism is associated with changes in HDL apolipoprotein expression."[11]

Fenofibrate is a fibric acid derivative, a prodrug comprising fenofibric acid linked to an isopropyl ester. It lowers lipid levels by activating Peroxisome proliferator-activated receptor alpha (PPARα). PPARα activates lipoprotein lipase and reduces apoprotein CIII, which increases lipolysis and elimination of triglyceride-rich particles from plasma.[11]

PPARα also increases apoproteins AI and AII, reduces very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) containing apoprotein B, and increases high-density lipoprotein (HDL) containing apoprotein AI and AII.


Fenofibrate is available in several formulations and is sold under several brand names, including Tricor by AbbVie, Lipofen by Kowa Pharmaceuticals America Inc, Lofibra by Teva, Lipanthyl, Lipidil, and Supralip by Abbott Laboratories, Fenocor-67 by Ordain Health Care, Fenogal by SMB Laboratories, Antara by Oscient Pharmaceuticals, Tricheck by Zydus (CND), Atorva TG by Zydus Medica, Golip by GolgiUSA and Storfib by Ranbaxy (India). Different formulations may differ in terms of pharmacokinetic properties, particularly bioavailability; some must be taken with meals, whereas others may be taken without regard to food.[12]

The active form of fenofibrate, fenofibric acid, is also available in the United States, sold as Trilipix. Fenofibric acid may be taken without regard to the timing of meals.[7][13]

When fenofibrate and a statin are given as combination therapy, it is recommended that fenofibrate be given in the morning and the statin at night, so that the peak dosages do not overlap.[14]


In the United States, Tricor was reformulated in 2005. This reformulation is controversial, as it is seen as an attempt to stifle competition from generic equivalents of the drug,[15] and is the subject of antitrust litigation by generic drug manufacturer Teva.[15] Also available in the United States, Lofibra is available in 54 and 160 mg tablets, as well as 67, 134, and 200;mg micronized capsules.[16] Generic equivalents of Lofibra capsules are currently available in all three strengths in the United States. In Europe, it is available in either coated tablet or capsule; the strength range includes 67, 145, 160 and 200 mg. The differences among strengths are a result of altered bioavailability (the fraction absorbed by the body) due to particle size. For example, 200 mg can be replaced by 160 mg micronized fenofibrate. The 145 mg strength is a new strength that appeared in 2005-2006 which also replaces 200 or 160 mg as the fenofibrate is nanonised (i.e. the particle size is below 400 nm).


Fenofibrate was first synthesized in 1974 as a derivative of clofibrate, and was launched on the French market shortly thereafter. It was initially known as procetofen, and was later renamed fenofibrate to comply with World Health Organization International Nonproprietary Name guidelines.[17]

Fenofibrate was developed by Groupe Fournier SA of France, which was acquired in 2005 by Solvay Pharmaceuticals, a business unit of the Belgian corporation Solvay S.A.. In 2009, Solvay was in turn acquired by Abbott Laboratories (now AbbVie).


The underlying mechanism of the ketogenic diet remains unknown, and involvement of PPARα has been suggested.[18] Fenofibrate exhibits anticonvulsant properties comparable to the ketogenic diet in adult rats, using pentylenetetrazol and lithium-pilocarpine models. These findings may be useful for future ketogenic diet study protocols.


  1. ^ a b c Yang LP, Keating GM (2009). "Fenofibric acid: in combination therapy in the treatment of mixed dyslipidemia". Am J Cardiovasc Drugs 9 (6): 401–9. doi:10.2165/11203920-000000000-00000. PMID 19929038. 
  2. ^ Fazio S (2009). "More clinical lessons from the FIELD study". Cardiovasc Drugs Ther 23 (3): 235–41. doi:10.1007/s10557-008-6160-5. PMID 19160032. 
  3. ^ Steiner G (2009). "How can we improve the management of vascular risk in type 2 diabetes: insights from FIELD". Cardiovasc Drugs Ther 23 (5): 403–8. doi:10.1007/s10557-009-6190-7. PMID 19757004. 
  4. ^ Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T et al. (2012). "2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia". Arthritis Care Res (Hoboken) 64 (10): 1431–46. doi:10.1002/acr.21772. PMC 3683400. PMID 23024028. 
  5. ^ a b c Package Insert: Abbot Laboratories (October 2010)
  6. ^ Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Blum CB, Eckel RH et al. (2014). "2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". Circulation 129 (25 Suppl 2): S1–45. doi:10.1161/01.cir.0000437738.63853.7a. PMID 24222016. 
  7. ^ a b c d e f g h i j Fenofibric Acid FDA Label Prescribing Information"FDA Label Information". FDA. 
  8. ^ Product Information: TriCor(TM), fenofibrate. Abbott Laboratories, North Chicago, IL, 1998.
  9. ^ Product Information: Sandimmune(R) oral capsules, oral solution, intravenous injection, cyclosporine oral capsules, oral solution, intravenous injection. Novartis Pharmaceuticals Corporation, East Hanover, NJ, 2010.
  10. ^ Product Information: TRICOR(R) oral tablets, fenofibrate oral tablets. Abbott Laboratories, North Chicago, IL, 2007.
  11. ^ a b Staels B, Dallongeville J, Auwerx J, Schoonjans K, Leitersdorf E, Fruchart JC (1998). "Mechanism of action of fibrates on lipid and lipoprotein metabolism". Circulation 98 (19): 2088–93. doi:10.1161/01.cir.98.19.2088. PMID 9808609. 
  12. ^ Ling H, Luoma JT, Hilleman D (2013). "A review of currently available fenofibrate and fenofibric acid formulations". Cardiol Res 4 (2): 47–55. doi:10.4021/cr270w. 
  13. ^ Alagona P (2010). "Fenofibric acid: a new fibrate approved for use in combination with statin for the treatment of mixed dyslipidemia". Vasc Health Risk Manag 6: 351–62. doi:10.2147/vhrm.s6714. PMC 2879297. PMID 20531954. 
  14. ^ Wierzbicki AS, Mikhailidis DP, Wray R, Schacter M, Cramb R, Simpson WG et al. (2003). "Statin-fibrate combination: therapy for hyperlipidemia: a review". Curr Med Res Opin 19 (3): 155–68. doi:10.1185/030079903125001668. PMID 12814127. 
  15. ^ a b Abbott's request to dismiss the antitrust charge over Tricor was rejected. FDANews, Drug Daily Bulletin, (June 1, 2006) [1]
  16. ^ TEVA Pharmartsau6i8mkst7oceutical Lofibra Product Site
  17. ^ Lalloyer F, Staels B (2010). "Fibrates, glitazones, and peroxisome proliferator-activated receptors". Arterioscler. Thromb. Vasc. Biol. 30 (5): 894–9. doi:10.1161/ATVBAHA.108.179689. PMC 2997800. PMID 20393155. 
  18. ^ Porta N, Vallée L, Lecointe C, Bouchaert E, Staels B, Bordet R et al. (2009). "Fenofibrate, a peroxisome proliferator-activated receptor-alpha agonist, exerts anticonvulsive properties". Epilepsia 50 (4): 943–8. doi:10.1111/j.1528-1167.2008.01901.x. PMID 19054409.  Vancouver style error (help)

External links[edit]