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Fenofibrate structure.svg
Clinical data
Trade namesFenoglide, Lipofen, others
License data
  • AU: B3
Routes of
By mouth
ATC code
Legal status
Legal status
  • UK: POM (Prescription only) [1]
  • US: ℞-only
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Protein binding99%
Elimination half-life20 h
Excretionurine (60%), feces (25%)
  • propan-2-yl 2-[4-(4-chlorobenzoyl)phenoxy]-2-methylpropanoate
CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard100.051.234 Edit this at Wikidata
Chemical and physical data
Molar mass360.83 g·mol−1
3D model (JSmol)
Melting point80 to 81 °C (176 to 178 °F)
  • O=C(c1ccc(Cl)cc1)c2ccc(OC(C(=O)OC(C)C)(C)C)cc2
  • InChI=1S/C20H21ClO4/c1-13(2)24-19(23)20(3,4)25-17-11-7-15(8-12-17)18(22)14-5-9-16(21)10-6-14/h5-13H,1-4H3 checkY

Fenofibrate (sold under the brand names Tricor, Fenobrat etc.), is a medication of the fibrate class used to treat abnormal blood lipid levels.[2] It is less preferred to statin medications as it does not appear to reduce the risk of heart disease or death.[2][3] Its use is recommended together with dietary changes.[2] It is taken by mouth.[2]

Common side effects include liver problems, breathing problems, abdominal pain, muscle problems, and nausea.[2] Serious side effects may include toxic epidermal necrolysis, rhabdomyolysis, gallstones, blood clots, and pancreatitis.[2] Use in pregnancy and breastfeeding is not recommended.[3][4] It works by a number of mechanisms.[2]

It was patented in 1969, and came into medical use in 1975.[5] It is available as a generic medication.[3] In 2018, it was the 73rd most commonly prescribed medication in the United States with more than 11 million prescriptions.[6][7]

Medical uses[edit]

Fenofibrate is mainly used for primary hypercholesterolemia or mixed dyslipidemia, and was firstly indicated for the reduction in the progression of diabetic retinopathy in patients with type 2 diabetes and existing diabetic retinopathy in Australia.[8] Fenofibrate has been demonstrated to reduce risk and progression of diabetic retinopathy in type 2 diabetic patients.[9] The large scale, international FIELD and ACCORD-Eye trials found that fenofibrate therapy reduced required laser treatment for diabetic retinopathy by 31%, as well as reducing progression by 3.7% over 4 years.[10][9] Although there were no statistically significant cardiovascular risk benefits identified in these trials, there may be benefits to add on therapy to patients with high triglyceride dyslipidaemia currently taking statin medications.[11][12]

Fenofibrate appears to reduce the risk of below ankle amputations in patients with Type 2 diabetes without microvascular disease.[13] The FIELD study also demonstrated fenofibrate at doses of 200mg daily, reduced the risk for any amputation by 37% independent of glycaemic control, presence or absence of dyslipidaemia and its lipid-lowering mechanism of action.[13][14] However, the cohort of participants who underwent amputations were more likely to have had previous cardiovascular disease (e.g. angina, myocardial infarction), longer duration of diabetes and had baseline neuropathy.[13][14]

Fenofibrate also has an off-label use as an added therapy of high blood uric acid levels in people who have gout.[15]

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.[16]

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.[16]

Statins remain the first line for treatment of blood cholesterol. AHA guidelines from 2013 did not find evidence for routine use of additional medications.[17]

Additionally, in 2016, the FDA filed "Withdrawal of Approval of Indications Related to the Coadministration With Statins in Applications for Niacin Extended-Release Tablets and Fenofibric Acid Delayed Release Capsules" noting "the Agency has concluded that the totality of the scientific evidence no longer supports the conclusion that a drug-induced reduction in triglyceride levels and/or increase in HDL cholesterol levels in statin-treated patients results in a reduction in the risk of cardiovascular events. Consistent with this conclusion, FDA has determined that the benefits of niacin ER tablets and fenofibric acid DR capsules for coadministration with statins no longer outweigh the risks, and the approvals for this indication should be withdrawn."[18]


Fenofibrate is contraindicated in:[16]

Adverse effects[edit]

The most common adverse events (>3% of patients with coadministered statins) are[19]


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.[20]






  • Exercise caution in concomitant treatment with oral Coumadin anticoagulants (e.g. warfarin). Adjust the dosage of Coumadin to maintain the prothrombin time/INR at desired level to prevent bleeding complications.[19]


"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.[19]


These drug interactions with fenofibrate are considered major and may need therapy modifications:

  • Bile acid sequestrants (e.g. cholestyramine, colestipol, etc.): If taken together, bile acid resins may bind to fenofibrate, resulting in a decrease in fenofibrate absorption. To maximize absorption, patients need to separate administration by at least 1 h before or 4 h to 6 h after taking the bile acid sequestrant.[19][21]
  • Immunosuppressants (e.g. ciclosporin or tacrolimus): An increased risk of renal dysfunction exists with concomitant use of immunosuppressants and fenofibrate. Approach with caution when coadministering additional medications that decrease renal function.[22]
  • Vitamin K antagonists (e.g. warfarin): As previously mentioned, fenofibrate interacts with coumadin anticoagulants to increase the risk of bleeding. Dosage adjustment of vitamin K antagonist may be necessary.[19]
  • Statins: Combination of statins and fenofibrate may increase the risk of rhabdomyolysis or myopathy.[23]

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."[24]

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.[24]

PPARα also increases apoproteins AI and AII, reduces VLDL- and LDL-containing apoprotein B, and increases 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, Lipantil micro and Supralip by Abbott Laboratories, Fenocor-67 by Ordain Health Care, Fibractiv 105/35 by Cogentrix Pharma( India), Fenogal by SMB Laboratories, Antara by Oscient Pharmaceuticals, Tricheck by Zydus (CND), Atorva TG by Zydus Medica, Golip by GolgiUSA and Stanlip 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.[25]

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.[19][26]


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,[27] and is the subject of antitrust litigation by generic drug manufacturer Teva.[27] 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.[28] 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.[29]

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 in the US and Mylan in Europe, Canada, Australia, New Zealand and Japan).



In July 2020, researchers from Israel and the U.S. suggested that fenofibrate might significantly slow down the replication of the SARS-CoV-2 virus in lung cells.[30] This hypothesis has been supported by a retrospective analysis of clinical data from 1500 patients in Israel [31] and awaits testing in larger clinical trials.


  1. ^ "Fenofibrate 267mg Capsules - Summary of Product Characteristics (SmPC)". (emc). 12 February 2020. Retrieved 13 April 2020.
  2. ^ a b c d e f g "Fenofibric Acid/Fenofibrate Monograph for Professionals". Drugs.com. American Society of Health-System Pharmacists. Retrieved 3 March 2019.
  3. ^ a b c British national formulary : BNF 76 (76 ed.). Pharmaceutical Press. 2018. p. 198. ISBN 9780857113382.
  4. ^ "Fenofibrate Pregnancy and Breastfeeding Warnings". Drugs.com. Retrieved 3 March 2019.
  5. ^ Fischer, Jnos; Ganellin, C. Robin (2006). Analogue-based Drug Discovery. John Wiley & Sons. p. 474. ISBN 9783527607495.
  6. ^ "The Top 300 of 2021". ClinCalc. Retrieved 18 February 2021.
  7. ^ "Fenofibrate - Drug Usage Statistics". ClinCalc. Retrieved 18 February 2021.
  8. ^ "Australian Public Assessment Report for fenofibrate". TGA. TGA. Retrieved 27 June 2015.
  9. ^ a b Wong, Tien Yin; Simó, Rafael; Mitchell, Paul (July 2012). "Fenofibrate – A Potential Systemic Treatment for Diabetic Retinopathy?". American Journal of Ophthalmology. 154 (1): 6–12. doi:10.1016/j.ajo.2012.03.013.
  10. ^ Fazio, Sergio (June 2009). "More Clinical Lessons from the FIELD Study". Cardiovascular Drugs and Therapy. 23 (3): 235–241. doi:10.1007/s10557-008-6160-5. ISSN 0920-3206.
  11. ^ Elam, Marshall B.; Ginsberg, Henry N.; Lovato, Laura C.; Corson, Marshall; Largay, Joseph; Leiter, Lawrence A.; Lopez, Carlos; O’Connor, Patrick J.; Sweeney, Mary Ellen; Weiss, Daniel; Friedewald, William T. (2017-04-01). "Association of Fenofibrate Therapy With Long-term Cardiovascular Risk in Statin-Treated Patients With Type 2 Diabetes". JAMA Cardiology. 2 (4): 370. doi:10.1001/jamacardio.2016.4828. ISSN 2380-6583.
  12. ^ Kim, Nam Hoon; Han, Ki Hoon; Choi, Jimi; Lee, Juneyoung; Kim, Sin Gon (2019-09-27). "Use of fenofibrate on cardiovascular outcomes in statin users with metabolic syndrome: propensity matched cohort study". BMJ: l5125. doi:10.1136/bmj.l5125. ISSN 0959-8138. PMC 6763755. PMID 31562117.CS1 maint: PMC format (link)
  13. ^ a b c Rajamani, Kushwin; Colman, Peter G; Li, Li Ping; Best, James D; Voysey, Merryn; D'Emden, Michael C; Laakso, Markku; Baker, John R; Keech, Anthony C (May 2009). "Effect of fenofibrate on amputation events in people with type 2 diabetes mellitus (FIELD study): a prespecified analysis of a randomised controlled trial". The Lancet. 373 (9677): 1780–1788. doi:10.1016/S0140-6736(09)60698-X. PMC 2687887. PMID 19465233.CS1 maint: PMC format (link)
  14. ^ a b Steiner, George (October 2009). "How Can We Improve the Management of Vascular Risk in Type 2 Diabetes: Insights from FIELD". Cardiovascular Drugs and Therapy. 23 (5): 403–408. doi:10.1007/s10557-009-6190-7. ISSN 0920-3206.
  15. ^ Khanna D, Fitzgerald JD, Khanna PP, Bae S, Singh MK, Neogi T, Pillinger MH, Merill J, Lee S, Prakash S, Kaldas M, Gogia M, Perez-Ruiz F, Taylor W, Lioté F, Choi H, Singh JA, Dalbeth N, Kaplan S, Niyyar V, Jones D, Yarows SA, Roessler B, Kerr G, King C, Levy G, Furst DE, Edwards NL, Mandell B, Schumacher HR, Robbins M, Wenger N, Terkeltaub R (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.
  16. ^ a b c Package Insert: Abbot Laboratories (October 2010)
  17. ^ Stone NJ, Robinson JG, Lichtenstein AH, Bairey Merz CN, Blum CB, Eckel RH, Goldberg AC, Gordon D, Levy D, Lloyd-Jones DM, McBride P, Schwartz JS, Shero ST, Smith SC, Watson K, Wilson PW, Eddleman KM, Jarrett NM, LaBresh K, Nevo L, Wnek J, Anderson JL, Halperin JL, Albert NM, Bozkurt B, Brindis RG, Curtis LH, DeMets D, Hochman JS, Kovacs RJ, Ohman EM, Pressler SJ, Sellke FW, Shen WK, Smith SC, Tomaselli GF (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.
  18. ^ https://s3.amazonaws.com/public-inspection.federalregister.gov/2016-08887.pdf
  19. ^ a b c d e f g h i j Fenofibric Acid FDA Label Prescribing Information"FDA Label Information" (PDF). FDA.
  20. ^ Wierzbicki AS, Mikhailidis DP, Wray R, Schacter M, Cramb R, Simpson WG, Byrne CB (2003). "Statin-fibrate combination: therapy for hyperlipidemia: a review". Curr Med Res Opin. 19 (3): 155–68. doi:10.1185/030079903125001668. PMID 12814127. S2CID 35948128.
  21. ^ Product Information: TriCor(TM), fenofibrate. Abbott Laboratories, North Chicago, IL, 1998.
  22. ^ Product Information: Sandimmune(R) oral capsules, oral solution, intravenous injection, cyclosporine oral capsules, oral solution, intravenous injection. Novartis Pharmaceuticals Corporation, East Hanover, NJ, 2010.
  23. ^ Product Information: TRICOR(R) oral tablets, fenofibrate oral tablets. Abbott Laboratories, North Chicago, IL, 2007.
  24. ^ 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. CiteSeerX doi:10.1161/01.cir.98.19.2088. PMID 9808609.
  25. ^ Ling H, Luoma JT, Hilleman D (2013). "A review of currently available fenofibrate and fenofibric acid formulations". Cardiology Research. 4 (2): 47–55. doi:10.4021/cr270w. PMC 5358213. PMID 28352420.
  26. ^ Alagona P (2010). "Fenofibric acid: a new fibrate approved for use in combination with statin for the treatment of mixed dyslipidemia". Vascular Health and Risk Management. 6: 351–62. doi:10.2147/vhrm.s6714. PMC 2879297. PMID 20531954.
  27. ^ a b Abbott's request to dismiss the antitrust charge over Tricor was rejected. FDANews, Drug Daily Bulletin, (June 1, 2006) [1]
  28. ^ TEVA Pharmartsau6i8mkst7oceutical Lofibra Product Site
  29. ^ 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.
  30. ^ "Hebrew U. scientist: Drug could eradicate COVID-19 from lungs in days". The Jerusalem Post. Retrieved 2020-07-14.
  31. ^ "Promising clinical data for fenofibrate's ability to prevent lung damage in COVID patients". EurekAlert!. Retrieved 2021-03-03.

External links[edit]

  • "Fenofibrate". Drug Information Portal. U.S. National Library of Medicine.