Fenofibrate: A Triglyceride Drug and Its Effect on Diabetic Eye Disease

Table of Contents

1. What Fenofibrate Is and When It Was Approved
2. How It Works on Blood Fats
3. Effects on Triglycerides and High-Density Lipoprotein Cholesterol
4. The Heart Trials in Diabetes
5. The Eye Signal Inside the Heart Trials
6. The LENS Trial in Scotland
7. What the Pooled Analyses Show
8. Proposed Explanations for the Eye Effect
9. The Label: Uses and Doses
10. Safety Findings in the Label and the Trials
11. Drug Interactions in the Label
12. What Is Not Known
13. Key Research Papers
14. Connections
15. Featured Videos

What Fenofibrate Is and When It Was Approved

Fenofibrate is a prodrug: the body turns it into fenofibric acid, which is the form that acts. It belongs to the fibrates, a drug class that also includes the older clofibrate and gemfibrozil and the newer pemafibrate. It is taken by mouth once a day.

The United States Food and Drug Administration records list the first fenofibrate approval, a capsule, on 31 December 1993. A 145-milligram tablet, the strength later used in the LENS eye trial, was approved on 5 November 2004. Several other tablet and capsule formulations followed in the 2000s, each with its own milligram numbers because the formulations are absorbed differently. Both of the original products named above are now listed by the agency as discontinued, with a recorded agency determination that they were not withdrawn for reasons of safety or effectiveness; generic fenofibrate tablets made by many manufacturers remain on the market.

A narrative review published in 2025 notes that fenofibrate is licensed for diabetic retinopathy in a few countries. In the United States the label covers blood fats only, and it says nothing about the eye.

How It Works on Blood Fats

Fenofibric acid switches on a protein inside cells called peroxisome proliferator-activated receptor alpha (PPAR-alpha). This receptor sits in the cell nucleus and turns sets of genes up or down, mainly in the liver, where it governs how fat is burned and packaged for export into the blood.

A 1998 review in Circulation by Staels and colleagues set out the main steps as the research then described them:

• More fat cleared from the blood. Fibrates raise the activity of lipoprotein lipase, the enzyme on blood-vessel walls that breaks down triglyceride-rich particles, and they lower the liver's output of apolipoprotein C-III, a protein that blocks that enzyme.
• Less fat sent out by the liver. They push the liver to take up fatty acids and burn them, and they reduce new fatty-acid and triglyceride production, so fewer very-low-density lipoprotein particles are released.
• More of the main high-density lipoprotein proteins. Through peroxisome proliferator-activated receptor alpha, fibrates raise production of apolipoproteins A-I and A-II, the main building blocks of high-density lipoprotein (HDL) particles.

The current label states the same mechanism more briefly: through this receptor, fenofibric acid increases the breakdown and removal of triglyceride-rich particles by activating lipoprotein lipase and reducing apolipoprotein C-III. The label adds that this was worked out in transgenic mice and in cultured human liver cells.

Effects on Triglycerides and High-Density Lipoprotein Cholesterol

The label reports two 8-week placebo-controlled trials in 147 people with high triglycerides, and a pooled set of four trials in people with high cholesterol or mixed blood-fat problems.

• Triglycerides 350 to 499 mg/dL at the start: triglycerides fell 46.2% on fenofibrate (from 432 to 223 mg/dL on average) against a 0.5% fall on placebo. High-density lipoprotein cholesterol rose 19.6%.
• Triglycerides 500 to 1,500 mg/dL at the start: triglycerides fell 54.5% (from 726 to 308 mg/dL) against a 7.2% rise on placebo. High-density lipoprotein cholesterol rose 22.9%. Low-density lipoprotein cholesterol rose 45.0% in this group, and the label notes that treating very high triglycerides often raises low-density lipoprotein cholesterol.
• High cholesterol or mixed blood fats, 3 to 6 months: total cholesterol fell 18.7%, low-density lipoprotein cholesterol 20.6% and triglycerides 28.9%, while high-density lipoprotein cholesterol rose 11.0%. On placebo the changes were −0.4%, −2.2%, +7.7% and +0.7%.

The label also lists the reverse effect as a warning: in some people high-density lipoprotein cholesterol falls sharply instead of rising. Post-marketing reports describe severely depressed levels.

For background on how these numbers are measured, see the lipid panel page. The cholesterol management page compares fibrates with the other drug classes.

The Heart Trials in Diabetes

People with type 2 diabetes often have the blood-fat pattern fibrates change most: high triglycerides and low high-density lipoprotein cholesterol. Two large trials tested whether fenofibrate turned those blood changes into fewer heart attacks and strokes. A third trial, of the related drug pemafibrate, is part of the same story.

The FIELD trial (2005)

The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial gave 9,795 people aged 50 to 75 with type 2 diabetes either 200 mg of micronised fenofibrate a day or placebo for about five years. None were taking a statin at the start.

• Main result, null: coronary events (coronary death or non-fatal heart attack) occurred in 5.2% on fenofibrate and 5.9% on placebo, a hazard ratio of 0.89 (95% confidence interval 0.75 to 1.05; p=0.16), which is not a statistically significant difference.
• In favour: non-fatal heart attacks fell 24% (hazard ratio 0.76), and total cardiovascular events fell from 13.9% to 12.5% (hazard ratio 0.89, 0.80 to 0.99), driven mainly by fewer non-fatal heart attacks and fewer coronary artery procedures.
• Against: coronary heart disease deaths were non-significantly higher (hazard ratio 1.19, 0.90 to 1.57), and total deaths were 7.3% on fenofibrate against 6.6% on placebo (p=0.18). Pancreatitis (0.8% against 0.5%) and pulmonary embolism (1.1% against 0.7%) were both slightly but significantly more common on fenofibrate.
• A complication in the design: 17% of the placebo group started other cholesterol drugs, mostly statins, against 8% of the fenofibrate group. The investigators wrote that this might have hidden a larger benefit.

The ACCORD-Lipid trial (2010) and its follow-on

The Action to Control Cardiovascular Risk in Diabetes (ACCORD) Lipid trial asked a different question: whether fenofibrate added anything to a statin. It gave 5,518 people with type 2 diabetes open-label simvastatin plus either fenofibrate or placebo, for an average of 4.7 years.

• Main result, null: the yearly rate of heart attack, stroke or cardiovascular death was 2.2% with fenofibrate and 2.4% with placebo (hazard ratio 0.92, 0.79 to 1.08; p=0.32). No secondary outcome differed, and yearly death rates were 1.5% against 1.6%.
• Subgroups: the results differed by sex, with a benefit in men and possible harm in women. The label gives hazard ratios of 0.82 for men and 1.38 for women and calls the clinical significance unclear. There was also a possible benefit in people who started with both high triglycerides and low high-density lipoprotein cholesterol (p=0.057 for that interaction, short of the usual threshold).
• Investigators' conclusion: the results did not support routine use of the combination to cut cardiovascular risk in most high-risk people with type 2 diabetes.

The ACCORD follow-on study tracked 4,644 of the participants to a median of 9.7 years in total, although only 4.3% kept taking fenofibrate after the trial ended. The overall result stayed neutral (hazard ratio 0.93, 0.83 to 1.05). In the subgroup with triglycerides above 204 mg/dL and high-density lipoprotein cholesterol below 34 mg/dL, the hazard ratio was 0.73 (0.56 to 0.95). The authors called for a dedicated trial in that group.

PROMINENT, the pemafibrate trial (2022)

PROMINENT was that kind of trial, using pemafibrate, a newer and more selective drug acting on the same receptor. It enrolled 10,497 people with type 2 diabetes, triglycerides of 200 to 499 mg/dL and high-density lipoprotein cholesterol of 40 mg/dL or lower, most already on statins. Pemafibrate cut triglycerides by 26.2% and apolipoprotein C-III by 27.6%, while apolipoprotein B rose 4.8%. After a median 3.4 years, cardiovascular events occurred in 572 people on pemafibrate and 560 on placebo (hazard ratio 1.03, 0.91 to 1.15), with no subgroup showing a different effect. Pemafibrate was linked to more kidney adverse events and more venous blood clots, and to less fatty liver disease. The current fenofibrate label now cites this trial as relevant to fenofibrate.

The Eye Signal Inside the Heart Trials

Both large fenofibrate trials also recorded eye outcomes, and both pointed the same way, although neither had been designed mainly to test the eye.

FIELD: laser treatment and the photography substudy (2007)

FIELD recorded every laser treatment for diabetic eye disease, and ophthalmologists who did not know who was taking what judged the reason for each. A first laser treatment for retinopathy was needed by 164 people (3.4%) on fenofibrate against 238 (4.9%) on placebo, a hazard ratio of 0.69 (0.56 to 0.84; p=0.0002), an absolute difference of 1.5 percentage points. (The main 2005 paper, using a broader count, gave 3.6% against 5.2%.) Laser treatment was more common in people with poorer blood sugar or blood pressure control, but plasma lipid levels did not predict it.

A substudy of 1,012 people had standardised retinal photographs graded on the Early Treatment Diabetic Retinopathy Study scale:

• Overall, null: a two-step worsening of retinopathy occurred in 9.6% on fenofibrate and 12.3% on placebo (p=0.19).
• No retinopathy at the start, null: 11.4% against 11.7% (p=0.87).
• Retinopathy already present, in favour: 3 people (3.1%) worsened on fenofibrate against 14 (14.6%) on placebo (p=0.004).
• Exploratory combined outcome (two-step worsening, macular swelling or laser treatment): hazard ratio 0.66 (0.47 to 0.94).

The investigators concluded that fenofibrate reduced the need for laser treatment but that the effect did not seem to be related to blood lipid levels.

ACCORD-Eye (2010)

In 2,856 ACCORD participants who had eye photographs at the start and at four years, retinopathy worsened by three or more steps, or needed laser or eye surgery, in 6.5% of those given fenofibrate (160 mg a day) plus simvastatin against 10.2% given placebo plus simvastatin. The adjusted odds ratio was 0.60 (0.42 to 0.87; p=0.006). In the same study, intensive blood sugar control also slowed retinopathy (7.3% against 10.4%), while intensive blood pressure control did not (10.4% against 8.8%).

The effect did not outlast the drug

The ACCORD follow-on eye study re-examined 1,310 participants four years after the trial closed, when almost nobody was still taking fenofibrate. Retinopathy had progressed in 11.8% of those originally given fenofibrate against 10.2% given placebo (odds ratio 1.13, 0.71 to 1.79; p=0.60). The benefit of earlier intensive blood sugar control persisted, but the fenofibrate benefit did not.

The diabetes complications page summarises these two trials alongside the kidney and nerve complications.

The LENS Trial in Scotland

The LENS trial was the first large trial built specifically to test fenofibrate on the eye. It was run inside Scotland's national diabetic eye screening programme and funded by the United Kingdom's National Institute for Health and Care Research, and the study drug was mailed to people's homes.

• Who took part: 1,151 adults with early retinopathy or macular changes that did not yet need referral to an eye specialist. Their average age was 61, 27% were women, and 26% had type 1 diabetes. 96% had mild background retinopathy in both eyes.
• What the trial gave: a 145-mg fenofibrate tablet or placebo, daily, or on alternate days in people with reduced kidney function. Everyone first took fenofibrate in a run-in period before randomisation; 1,484 entered the run-in.
• Main result: over a median of 4.0 years, progression to referable retinopathy or macular disease, or treatment for it, occurred in 131 of 576 people (22.7%) on fenofibrate against 168 of 575 (29.2%) on placebo, a hazard ratio of 0.73 (0.58 to 0.91; p=0.006).
• Any worsening of retinopathy or macular changes: 32.1% against 40.2% (hazard ratio 0.74).
• Macular swelling (macular edema): 3.8% against 7.5% (hazard ratio 0.50, 0.30 to 0.84).
• Eye treatment (injections, laser or surgery): 3.0% against 4.9% (hazard ratio 0.58, 0.31 to 1.06), a difference that was not statistically significant.
• No difference in sight: the trial found no effect on visual function, quality of life or visual acuity.
• Kidney measure: estimated glomerular filtration rate, a blood-test estimate of kidney filtering, averaged 7.9 units (ml/min/1.73 m²) lower on fenofibrate over the trial.
• Serious adverse events: 36.1% on fenofibrate against 35.5% on placebo.

The full trial report, published in 2026, adds that health-service costs were slightly lower in the fenofibrate group (not statistically significant) and, from modelling, an estimated cost of £406 per quality-adjusted life-year gained. It also notes a limit: Scotland's screening grades are based on the Early Treatment Diabetic Retinopathy Study scale but are less detailed, so LENS outcomes are not directly the same as those in FIELD or ACCORD-Eye. Participants are to be followed for 10 years.

What the Pooled Analyses Show

The Cochrane review (2023, before LENS)

A Cochrane review pooled FIELD and ACCORD and their eye substudies, 15,313 people with type 2 diabetes. In the mixed group with and without retinopathy, it judged that fenofibrate likely makes little or no difference to progression (risk ratio 0.86, 0.60 to 1.25; moderate certainty). In people without retinopathy at the start there was no difference (risk ratio 1.00); in people who already had it, progression was slower (risk ratio 0.21, 0.06 to 0.71; 208 people). Serious adverse events were rare but more frequent on fenofibrate (risk ratio 1.55, 1.05 to 2.27; high certainty). The review found no evidence at all in type 1 diabetes, and no data on loss of vision.

The 2026 meta-analysis that includes LENS

A systematic review published in 2026 counted ten randomised trials: six completed and four still running. Three completed trials with 3,756 people contributed to its main result:

• Retinopathy progression: risk ratio 0.77 (0.68 to 0.88), about 45 fewer events per 1,000 people, moderate certainty, with no disagreement between trials. A more conservative statistical method gave 0.60 to 0.99.
• Need for eye treatment: risk ratio 0.68 (0.57 to 0.82) by the standard method, but only low certainty. 90.2% of the weight came from one trial run before modern eye injections were in use, and the conservative interval (0.42 to 1.11) included no effect. The authors wrote that this is not firm evidence about treatment needs today.
• Vision: no trial found a benefit for visual acuity or function (low certainty), and the macular swelling results could not be combined.
• Blood clots: venous thromboembolism was more common on fenofibrate (risk ratio 1.52, 1.12 to 2.06), an estimate that came entirely from FIELD (103 of 4,755 against 68 of 4,767).

The authors' summary: in adults with diabetes, mostly type 2, fenofibrate slows structural retinopathy progression but is not established as preserving vision.

Proposed Explanations for the Eye Effect

The FIELD investigators found the drop in laser treatment did not track blood-fat levels, and reviewers since then describe the eye benefit as largely independent of lipid lowering. The explanations below are proposals, mostly drawn from animal and cell work. None has been shown to be the reason in people.

• A direct action on the eye's own receptor (animal evidence). In 2013, Chen and colleagues reported that fenofibrate given by mouth reduced retinal blood-vessel leakage and the sticking of white blood cells to retinal vessels in diabetic rats and in Akita mice, a type 1 diabetes model. Injecting fenofibrate into the eye worked too. In mice lacking the receptor, fenofibrate no longer lowered retinal vascular endothelial growth factor or leakage, which the authors took as evidence that the drug acts through peroxisome proliferator-activated receptor alpha in eye tissue.
• Less inflammation and less new vessel growth (animal and cell evidence). In the same work, fenofibrate lowered retinal levels of inflammatory signals and of vascular endothelial growth factor, the protein that today's eye injections block, and blocked two inflammation and low-oxygen switches (nuclear factor kappa B and hypoxia-inducible factor 1) in rodent retinas. In cultured endothelial cells it reduced vessel-like tube formation.
• Diabetes may switch the receptor down (mouse evidence). A 2017 study in diabetic db/db mice found the receptor reduced in the retina, partly because of a rise in a small regulatory RNA, microRNA-21. Removing microRNA-21 kept receptor levels up and lessened retinal vessel damage in mice.
• Broader protective actions (reviews). A 2026 review describes anti-inflammatory, antioxidant, nerve-protective and anti-scarring actions in laboratory studies, some through the receptor and some apparently not, and proposes these could act even in people with normal blood fats.

The Label: Uses and Doses

The current United States labelling for fenofibrate 145-mg tablets (a generic label dated January 2026 was read for this page) lists two uses, both alongside diet:

• to reduce triglycerides in adults with severe hypertriglyceridemia, defined as 500 mg/dL or higher;
• to reduce elevated low-density lipoprotein cholesterol in adults with primary hyperlipidemia when use of recommended low-density lipoprotein lowering therapy is not possible.

The label's limitations of use say that very high triglycerides (for example above 2,000 mg/dL) may raise the risk of pancreatitis, but the effect of fenofibrate on reducing that risk has not been determined. The label also states that fenofibrate did not reduce coronary heart disease morbidity and mortality in two large, randomized controlled trials of patients with type 2 diabetes mellitus, meaning FIELD and ACCORD-Lipid. Older versions of the label, still found on some repackaged products, worded the uses more broadly, including raising high-density lipoprotein cholesterol.

Doses in the label (145-mg tablet product):

• Severe hypertriglyceridemia: 48 to 145 mg once a day, adjusted to response, with triglycerides rechecked at 4 to 8 weeks.
• Primary hyperlipidemia: 145 mg once a day.
• Mild to moderate kidney impairment: starting dose 48 mg a day.
• Older adults: dose chosen on the basis of kidney function.
• Taken at any time of day, with or without food. The label directs stopping the drug if there is no adequate response after two months.

The trial doses differed by formulation: 200 mg micronised in FIELD, 160 mg in ACCORD, and 145 mg (or alternate days with reduced kidney function) in LENS.

Safety Findings in the Label and the Trials

Contraindications in the label: severe kidney impairment (estimated glomerular filtration rate below 30), including end-stage kidney disease and dialysis; active liver disease, including unexplained persistent liver test abnormalities; existing gallbladder disease; and known hypersensitivity to fenofibrate or fenofibric acid. The label's lactation section directs no breastfeeding during treatment and for 5 days after the last dose, citing possible harm to the infant's fat metabolism.

• Liver. Serious drug-induced liver injury, including cases that led to liver transplantation and death, has been reported. It has appeared within the first few weeks or after months of treatment, sometimes reversing when the drug was stopped. Reported signs include dark urine, jaundice, abdominal pain, itching, nausea and tiredness. In a pooled analysis of 10 trials, the liver enzyme alanine aminotransferase rose above three times the upper limit of normal in 5.3% on fenofibrate against 1.1% on placebo. The label calls for liver tests at baseline and periodically.
• Muscle. Fenofibrate can cause muscle damage (myopathy) and its severe form, rhabdomyolysis, in which broken-down muscle can injure the kidneys. The label lists age 65 or over, untreated low thyroid function, kidney impairment and certain other drugs as risk factors. Unexplained muscle pain, tenderness or weakness, especially with fever or malaise, is the warning sign the label names.
• Kidney function tests. Serum creatinine rises on fenofibrate and tends to return to baseline after stopping. In FIELD, creatinine rose by 10.0 µmol/L during the active run-in and fell back quickly on placebo. Over five years, estimated filtration declined more slowly on fenofibrate (1.19 against 2.03 units a year), and after an 8-week washout it had fallen 1.9 units from baseline on fenofibrate against 6.9 on placebo. Albuminuria fell more on fenofibrate, and end-stage kidney events were similar (21 against 26). In LENS, estimated filtration was 7.9 units lower on fenofibrate during treatment.
• Gallstones. Fenofibrate may increase cholesterol output into the bile, leading to gallstones. The label directs stopping the drug if gallstones are found.
• Pancreatitis. Pancreatitis has been reported. The label says this may reflect failure to control very high triglycerides, a direct drug effect, or gallstones or sludge blocking the bile duct. In FIELD it occurred in 0.8% on fenofibrate against 0.5% on placebo. The pancreatitis page covers the condition.
• Blood counts. Mild to moderate falls in hemoglobin, hematocrit and white blood cells occur after starting and then stabilise. Low platelets (thrombocytopenia) and a dangerous loss of infection-fighting white cells (agranulocytosis) have been reported. The label calls for periodic blood counts during the first 12 months.
• Blood clots. In FIELD, deep vein thrombosis occurred in 1.4% on fenofibrate against 1.0% (p=0.074) and pulmonary embolism in 1.1% against 0.7% (p=0.022).
• Allergic and skin reactions. Anaphylaxis and angioedema, some life-threatening and needing emergency treatment, have been reported, as have severe skin reactions (Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms) days to weeks after starting.
• Common side effects in trials (2% or more and above placebo): abnormal liver tests (8% against 1%), abdominal pain, raised liver enzymes, raised creatine kinase, constipation and a runny nose. Post-marketing reports also include interstitial lung disease and sun sensitivity.
• Pregnancy. The label states that human data are too limited to determine a risk.

Drug Interactions in the Label

• Statins. Observational data show a higher risk of rhabdomyolysis when fibrates are combined with a statin. The label presents the combination as a weighing of benefit against that added muscle risk, with monitoring for muscle symptoms, especially at the start and when the statin dose is raised. Within the class, a 2005 analysis of reports to the Food and Drug Administration found fewer rhabdomyolysis reports per million prescriptions for fenofibrate with a statin than for gemfibrozil with a statin. In ACCORD, 2,765 people took fenofibrate with simvastatin for an average of 4.7 years.
• Colchicine. Myopathy and rhabdomyolysis have been reported with the combination.
• Warfarin and other coumarin anticoagulants. Fenofibrate strengthens their effect and prolongs the international normalized ratio (INR), a measure of how long blood takes to clot. The label calls for a lower anticoagulant dose and frequent clotting tests until the international normalized ratio is stable, to prevent bleeding.
• Cyclosporine, tacrolimus and other drugs that can harm the kidneys. These immune-suppressing drugs can reduce kidney function. Fenofibric acid leaves the body mainly through the kidneys, so the label warns that the combination may worsen kidney function, and it calls for the lowest effective dose and kidney monitoring.
• Bile-acid binding resins. These cholesterol drugs can bind fenofibrate in the gut. The label's timing is fenofibrate at least 1 hour before or 4 to 6 hours after the resin.

What Is Not Known

• Whether it saves sight. Every trial so far measured how the retina looks or whether treatment was needed. None found a difference in visual acuity, visual function or quality of life.
• How long the effect lasts. In ACCORD the eye benefit was gone four years after people stopped the drug. LENS plans a 10-year follow-up, and its results are not yet known.
• Type 1 diabetes. The 2023 Cochrane review found no evidence in type 1 diabetes. LENS included 26% with type 1, but the 2026 meta-analysis reports no separate estimate for them.
• The mechanism in people. The receptor-in-the-eye explanation rests mainly on rodent and cell studies.
• The kidney question. Fenofibrate lowers estimated filtration while on treatment, and part of that reverses after stopping. Whether this matters for people whose kidneys are already damaged, many of whom have retinopathy too, has not been settled. The label calls the clinical significance of the creatinine rise unknown.
• Need for eye treatment today. The strongest data on fewer laser treatments come from before eye injections were common, and LENS was too small to show a clear difference in eye treatment.
• Heart benefit in the high-triglyceride, low high-density lipoprotein group. The subgroup signal from FIELD and ACCORD was not confirmed when PROMINENT tested pemafibrate in exactly that group.
• Trials still running. The 2026 meta-analysis counted four ongoing trials of fenofibrate with eye outcomes.

The diabetic retinopathy page covers screening, stages and eye treatments, and the retinal imaging page explains how retinopathy is photographed and graded.

Key Research Papers

1. Preiss D, Logue J, Sammons E, Zayed M, Emberson J, Wade R, et al. Effect of Fenofibrate on Progression of Diabetic Retinopathy. NEJM Evid. 2024;3(8):EVIDoa2400179. PubMed PMID: 38905569
2. Preiss D, Logue J, Sammons E, Zayed M, Scotland G, Tsehaye M, et al. Fenofibrate and progression of retinopathy in adults with diabetes: the randomised placebo-controlled LENS trial. Health Technol Assess. 2026;30(41):1-70. PubMed PMID: 42117585
3. LENS Collaborative Group. Design, recruitment and baseline characteristics of the LENS trial. Diabet Med. 2024;41(9):e15310. PubMed PMID: 38385587
4. Bhandari M, Devkota S, Dhital R, Subedi S, Adhikari S. Effect of fenofibrate on diabetic retinopathy progression: an RCT-Only systematic review and meta-analysis incorporating the LENS trial. Diabetes Res Clin Pract. 2026;241:113543. PubMed PMID: 42697514
5. Keech A, Simes RJ, Barter P, Best J, Scott R, Taskinen MR, et al; 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):1849-61. PubMed PMID: 16310551
6. Keech AC, Mitchell P, Summanen PA, O'Day J, Davis TM, Moffitt MS, et al. Effect of fenofibrate on the need for laser treatment for diabetic retinopathy (FIELD study): a randomised controlled trial. Lancet. 2007;370(9600):1687-97. PubMed PMID: 17988728
7. ACCORD Study Group, Ginsberg HN, Elam MB, Lovato LC, Crouse JR, Leiter LA, et al. Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med. 2010;362(17):1563-74. PubMed PMID: 20228404
8. ACCORD Study Group, ACCORD Eye Study Group, Chew EY, Ambrosius WT, Davis MD, Danis RP, et al. Effects of medical therapies on retinopathy progression in type 2 diabetes. N Engl J Med. 2010;363(3):233-44. PubMed PMID: 20587587
9. Action to Control Cardiovascular Risk in Diabetes Follow-On (ACCORDION) Eye Study Group and the Action to Control Cardiovascular Risk in Diabetes Follow-On (ACCORDION) Study Group. Persistent Effects of Intensive Glycemic Control on Retinopathy in Type 2 Diabetes in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) Follow-On Study. Diabetes Care. 2016;39(7):1089-100. PubMed PMID: 27289122
10. Elam MB, Ginsberg HN, Lovato LC, Corson M, Largay J, Leiter LA, et al. Association of Fenofibrate Therapy With Long-term Cardiovascular Risk in Statin-Treated Patients With Type 2 Diabetes. JAMA Cardiol. 2017;2(4):370-380. PubMed PMID: 28030716
11. Das Pradhan A, Glynn RJ, Fruchart JC, MacFadyen JG, Zaharris ES, Everett BM, et al. Triglyceride Lowering with Pemafibrate to Reduce Cardiovascular Risk. N Engl J Med. 2022;387(21):1923-1934. PubMed PMID: 36342113
12. Kataoka SY, Lois N, Kawano S, Kataoka Y, Inoue K, Watanabe N. Fenofibrate for diabetic retinopathy. Cochrane Database Syst Rev. 2023;6(6):CD013318. PubMed PMID: 37310870
13. Davis TM, Ting R, Best JD, Donoghoe MW, Drury PL, Sullivan DR, et al. Effects of fenofibrate on renal function in patients with type 2 diabetes mellitus: the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) Study. Diabetologia. 2011;54(2):280-90. PubMed PMID: 21052978
14. 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):2088-93. PubMed PMID: 9808609
15. Chen Y, Hu Y, Lin M, Jenkins AJ, Keech AC, Mott R, et al. Therapeutic effects of PPARα agonists on diabetic retinopathy in type 1 diabetes models. Diabetes. 2013;62(1):261-72. PubMed PMID: 23043158
16. Chen Q, Qiu F, Zhou K, Matlock HG, Takahashi Y, Rajala RVS, et al. Pathogenic Role of microRNA-21 in Diabetic Retinopathy Through Downregulation of PPARα. Diabetes. 2017;66(6):1671-1682. PubMed PMID: 28270521
17. Liu M, Lim ST, Song W, Coffman TM, Wang X. Beyond lipids: fenofibrate in diabetic retinopathy and nephropathy. Trends Pharmacol Sci. 2026;47(3):325-341. PubMed PMID: 40835560
18. Dissanayake HA, Kiire CA, Preiss D, Tan GD. The use of fenofibrate in diabetic retinopathy: Narrative review. J Diabetes Complications. 2025;39(10):109135. PubMed PMID: 40674809
19. Jones PH, Davidson MH. Reporting rate of rhabdomyolysis with fenofibrate + statin versus gemfibrozil + any statin. Am J Cardiol. 2005;95(1):120-2. PubMed PMID: 15619408

Label and approval sources: United States prescribing information for fenofibrate tablets 48 mg and 145 mg, generic label revised January 2026, via DailyMed and openFDA; approval dates from Drugs@FDA.

PubMed Topic Searches

1. PubMed: fenofibrate and diabetic retinopathy, randomized trials
2. PubMed: fenofibrate and cardiovascular outcomes in type 2 diabetes
3. PubMed: peroxisome proliferator-activated receptor alpha, the retina and fenofibrate
4. PubMed: fenofibrate and kidney function
5. PubMed: fenofibrate and liver injury

Back to Table of Contents

Connections

• Drugs — every drug page on the site
• Diabetic Retinopathy — stages, screening and eye treatments
• Diabetes Complications — eye, kidney and nerve damage together
• Cholesterol Management — fibrates beside the other drug classes
• Lipid Panel — how triglycerides and cholesterol are measured
• Pancreatitis — the condition very high triglycerides can trigger
• Rhabdomyolysis — the severe muscle injury in the label's warnings
• Retinal Imaging — how retinopathy is photographed and graded
• Metabolic Syndrome — the cluster that includes high triglycerides

Back to Table of Contents

Featured Videos