Bezafibrate Chemical formula
Synonyms: Betsafibraatti; Bezafibrát; Bezafibrat; Bezafibratas; Bézafibrate; Bezafibrato; Bezafibratum; BM-15075; LO-44. 2-[4-(2p-Chlorobenzamidoethyl)phenoxy]2-methylpropionic acid.
Cyrillic synonym: Безафибрат.

💊 Chemical information

Chemical formula: C19H20ClNO4 = 361.8.
CAS — 41859-67-0.
ATC — C10 AB02.
ATC Vet — QC10AB02.


In Eur. and Jpn.

Ph. Eur. 6.2

(Bezafibrate). A white or almost white, crystalline powder. It exhibits polymorphism. Practically insoluble in water; sparingly soluble in alcohol and in acetone; freely soluble in dimethylformamide; it dissolves in dilute solutions of alkali hydroxides.

💊 Adverse Effects and Precautions

The commonest adverse effects of bezafibrate therapy are gastrointestinal disturbances including anorexia, nausea, and gastric discomfort. Other adverse effects reported to occur less frequently include headache, dizziness, vertigo, fatigue, skin rashes, pruritus, photosensitivity, alopecia, impotence, anaemia, leucopenia, and thrombocytopenia. Raised serum-aminotransferase concentrations have occasionally been reported. Elevated creatine phosphokinase concentrations during bezafibrate therapy may be associated with a syndrome of myositis, myopathy, and rarely rhabdomyolysis; patients with hypoalbuminaemia resulting from nephrotic syndrome or with renal impairment may be at increased risk. Bezafibrate should not be given with statins in patients with risk factors for myopathy. Bezafibrate may increase the lithogenic index, and there have been isolated reports of gallstones, although the risk from fibrates as a class is unclear (see Gallstones, below). Bezafibrate should not be given to patients with severe hepatic impairment or significant liver disease, gallstones or gallbladder disorders, or hypoalbuminaemic states such as nephrotic syndrome. It should be used with caution in renal impairment and is contra-indicated if creatinine clearance is below 15 mL/minute unless the patient is on dialysis (see under Uses and Administration, below).
1. Davidson MH, et al. Safety considerations with fibrate therapy. Am J Cardiol 2007; 99 (Issue 6 suppl 1): 3C–18C.

Effects on glucose metabolism.

Use of fibrates in diabetic patients has generally been reported to either improve1-3 or have no effect4-6 on insulin sensitivity and glucose metabolism, and they are considered a suitable treatment for type 2 diabetics with hypertriglyceridaemia.7 There is also some evidence that fibrates may reduce the incidence or delay the onset of diabetes in patients with obesity8 or impaired glucose tolerance.9 However, there has been a report10 of recurrent hypoglycaemia in a type 2 diabetic when gemfibrozil was added to high-dose insulin therapy although eventually a reduced insulin dosage, with fibrate therapy, produced good glucose control. Gemfibrozil is contraindicated in patients receiving repaglinide due to the risk of severe hypoglycaemia. Conversely, a study in 20 diabetic patients11 given gemfibrozil reported a slight increase in requirements for antidiabetic therapy (oral hypoglycaemics or insulin) in 9 and a decrease in 1.
1. Ogawa S, et al. Bezafibrate reduces blood glucose in type 2 diabetes mellitus. Metabolism 2000; 49: 331–4
2. Jones IR, et al. Lowering of plasma glucose concentrations with bezafibrate in patients with moderately controlled NIDDM. Diabetes Care 1990; 13: 855–63
3. Notarbartolo A, et al. Effects of gemfibrozil in hyperlipidemic patients with or without diabetes. Curr Ther Res 1993; 53: 381–93
4. Leaf DA, et al. The hypolipidemic effects of gemfibrozil in type V hyperlipidemia. JAMA 1989; 262: 3154–60
5. Pagani A, et al. Effect of short-term gemfibrozil administration on glucose metabolism and insulin secretion in non-insulin-dependent diabetics. Curr Ther Res 1989; 45: 14–20
6. Hernández-Mijares A, et al. Ciprofibrate effects on carbohydrate and lipid metabolism in type 2 diabetes mellitus subjects. Nutr Metab Cardiovasc Dis 2000; 10: 1–6
7. Buse JB, et al. Primary prevention of cardiovascular diseases in people with diabetes mellitus: a scientific statement from the American Heart Association and the American Diabetes Association. Circulation 2007; 115: 114–26. Also published in Diabetes Care 2007; 30: 162–72
8. Tenenbaum A, et al. Effect of bezafibrate on incidence of type 2 diabetes mellitus in obese patients. Eur Heart J 2005; 26: 2032–8
9. Tenenbaum A, et al. Peroxisome proliferator-activated receptor ligand bezafibrate for prevention of type 2 diabetes mellitus in patients with coronary artery disease. Circulation 2004; 109: 2197–2202
10. Klein J, et al. Recurrent hypoglycaemic episodes in a patient with type 2 diabetes under fibrate therapy. J Diabetes Complications 2002; 16: 246–8
11. Konttinen A, et al. The effect of gemfibrozil on serum lipids in diabetic patients. Ann Clin Res 1979; 11: 240–5.

Effects on the kidneys.

Small increases in creatinine concentration are common during treatment with bezafibrate and have also been reported with other fibrates,1 although possibly not with gemfibrozil. There have also been reports of acute renal failure associated with treatment with bezafibrate,2 and with clofibrate,3,4 and an accelerated decline in renal function has been reported with bezafibrate in patients with chronic renal failure.5Renal failure may also occur due to rhabdomyolysis in patients receiving fibrates, including gemfibrozil (see Effects on Skeletal Muscle, below).
1. Broeders N, et al. Fibrate-induced increase in blood urea and creatinine: is gemfibrozil the only innocuous agent? Nephrol Dial Transplant 2000; 15: 1993–9
2. Lipkin GW, Tomson CRV. Severe reversible renal failure with bezafibrate. Lancet 1993; 341: 371
3. Dosa S, et al. Acute-on-chronic renal failure precipitated by clofibrate. Lancet 1976; i: 250
4. Cumming A. Acute renal failure and interstitial nephritis after clofibrate treatment. BMJ 1980; 281: 1529–30
5. Williams AJ, et al. The short term effects of bezafibrate on the hypertriglyceridaemia of moderate to severe uraemia. Br J Clin Pharmacol 1984; 18: 361–7.

Effects on the nervous system.

Adverse effects on the peripheral nervous system have been reported with fibrates. Peripheral neuropathy has been reported1 with bezafibrate, and was substantiated by nerve conduction studies. There have also been reports of peripheral neuropathy with clofibrate,2 and with fenofibrate,3 which resolved when therapy was withdrawn. In addition, by 1993, the Adverse Drug Reactions Advisory Committee in Australia had received reports of paraesthesia occurring in 6 patients in association with gemfibrozil treatment.4
1. Ellis CJ, et al. Peripheral neuropathy with bezafibrate. BMJ 1994; 309: 929
2. Gabriel R, Pearce JMS. Clofibrate-induced myopathy and neuropathy. Lancet 1976; ii: 906
3. Corcia P, et al. Severe toxic neuropathy due to fibrates. J Neurol Neurosurg Psychiatry 1999; 66: 410
4. Anonymous. Paraesthesia and neuropathy with hypolipidaemic agents. Aust Adverse Drug React Bull 1993; 12: 6.

Effects on the pancreas.

Acute pancreatitis has been reported1 in a patient receiving bezafibrate, and recurred on 2 occasions when bezafibrate was restarted. There has also been a report2 of acute pancreatitis in a patient receiving both fenofibrate and simvastatin, although simvastatin was considered more likely to be responsible. An increased incidence of pancreatitis was also reported with fenofibrate in the FIELD study,3 although the number of cases was small.
1. Gang N, et al. Relapsing acute pancreatitis induced by re-exposure to the cholesterol lowering agent bezafibrate. Am J Gastroenterol 1999; 94: 3626–8
2. McDonald KB, et al. Pancreatitis associated with simvastatin plus fenofibrate. Ann Pharmacother 2002; 36: 275–9
3. 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: 1849–61. Corrections. ibid. 2006; 368: 1415 and 1420.

Effects on sexual function.

Sexual dysfunction has occurred with some fibrates. Erectile dysfunction and loss of libido has been reported in 3 patients1-3 during gemfibrozil treatment. In 2 of the men1,2 bezafibrate did not produce this adverse effect. The UK CSM was reported to be aware of a further 6 cases.2 Of a further 3 cases of erectile dysfunction associated with gemfibrozil reported from Spain, 1 patient had previously reacted similarly to clofibrate.4 A systematic review,5 including these and other reports, supported the conclusion that fibrates could cause erectile dysfunction. Gynaecomastia was reported6 in a 56-year-old man receiving fenofibrate and recurred on rechallenge; there were no other effects on sexual function.
1. Pizarro S, et al. Gemfibrozil-induced impotence. Lancet 1990; 336: 1135
2. Bain SC, et al. Gemfibrozil-induced impotence. Lancet 1990; 336: 1389
3. Bharani A. Sexual dysfunction after gemfibrozil BMJ 1992; 305: 693
4. Figueras A, et al. Gemfibrozil-induced impotence. Ann Pharmacother 1993; 27: 982
5. Rizvi K, et al. Do lipid-lowering drugs cause erectile dysfunction? A systematic review. Fam Pract 2002; 19: 95–8
6. Gardette V, et al. Gynecomastia associated with fenofibrate. Ann Pharmacother 2007; 41: 508–11.

Effects on skeletal muscle.

Muscle disorders including myositis and myopathy are well known to occur with lipid regulating drugs such as fibrates.1 Rhabdomyolysis, presenting as muscle pain with elevated creatine phosphokinase and myoglobinuria leading to renal failure, has also been reported but appears to be rare. Patients with renal impairment, and possibly with hypothyroidism, may be at increased risk of muscle toxicity. The UK CSM has advised1 that patients treated with fibrates should consult their doctor if they develop muscle pain, tenderness, or weakness, and treatment should be stopped if muscle toxicity is suspected clinically or if creatine phosphokinase is markedly raised or progressively rising. Other lipid regulating drugs, particularly the statins, have also been associated with myopathy and the risk of muscle toxicity is increased if fibrates and statins are taken together; combination therapy may be appropriate in some patients but careful monitoring is required.2
1. Committee on Safety of Medicines/Medicines Control Agency. Rhabdomyolysis associated with lipid-lowering drugs. Current Problems 1995; 21: 3. Available at: FILE&dDocName=CON2015618&RevisionSelectionMethod= LatestReleased (accessed 30/05/08
2. Shek A, Ferrill MJ. Statin-fibrate combination therapy. Ann Pharmacother 2001; 35: 908–917.


Fibrates, including fenofibrate1-3 and gemfibrozil4have been reported to increase indices of bile lithogenicity, and some studies5,6 have suggested an increased risk of gallstones in patients receiving fibrates. However, in the Helsinki Heart Study7 no significant increase in gallstone operations was reported among 2051 patients taking gemfibrozil compared with 2030 taking placebo, although a follow-up study8 reported that cholecystectomies were consistently more common in those receiving gemfibrozil during the entire 8.5-year observation period.
1. Brown WV. Treatment of hypercholesterolaemia with fenofibrate: a review. Curr Med Res Opin 1989; 11: 321–30
2. Blane GF. Comparative toxicity and safety profile of fenofibrate and other fibric acid derivatives. Am J Med 1987; 83 (suppl 5B): 26–36
3. Palmer RH. Effects of fibric acid derivatives on biliary lipid composition. Am J Med 1987; 83 (suppl 5B): 37–43
4. Leiss O, et al. Effect of gemfibrozil on biliary lipid metabolism in normolipemic subjects. Metabolism 1985; 34: 74–82
5. Mamdani MM, et al. Is there an association between lipid-lowering drugs and cholecystectomy? Am J Med 2000; 108: 418–21
6. Caroli-Bosc F-X, et al. Role of fibrates and HMG-CoA reductase inhibitors in gallstone formation: epidemiological study in an unselected population. Dig Dis Sci 2001; 46: 540–4
7. Frick MH, et al. Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia: safety of treatment, changes in risk factors, and incidence of coronary heart disease. N Engl J Med 1987; 317: 1237–45
8. Huttunen JK, et al. The Helsinki Heart Study: an 8.5-year safety and mortality follow-up. J Intern Med 1994; 235: 31–9.


Severe recurrent headaches have been reported1 in a patient receiving bezafibrate. The headaches started about 24 hours after therapy with bezafibrate began, and recurred about 1 hour after each dose. Headaches occurred 30 to 90 minutes after each dose of gemfibrozil in 2 patients.2,3 In both patients, the headaches were accompanied by dry mouth, and in 1 also by blurred vision. The headaches stopped when gemfibrozil was withdrawn and recurred one week after re-exposure.
1. Hodgetts TJ, Tunnicliffe C. Bezafibrate-induced headache. Lancet 1989; i: 163
2. Arellano F, et al. Gemfibrozil-induced headache. Lancet 1988; i: 705
3. Alvarez-Sabin J, et al. Gemfibrozil-induced headache. Lancet 1988; ii: 1246.


Hyperhomocysteinaemia has been associated with an increased risk for cardiovascular disease. Small studies have found that both bezafibrate1,2 and fenofibrate1,3 increase plasma-homocysteine concentrations, although the clinical significance of this is not clear.4 Folic acid and vitamin B12 have been given4,5 with fenofibrate to reduce homocysteine concentrations, but the role of such treatment is not established.
1. Dierkes J, et al. Serum homocysteine increases after therapy with fenofibrate or bezafibrate. Lancet 1999; 354: 219–20
2. Jonkers IJAM, et al. Implication of fibrate therapy for homocysteine. Lancet 1999; 354: 1208
3. de Lorgeril M, et al. Lipid-lowering drugs and homocysteine. Lancet 1999; 353: 209–10
4. Dierkes J, et al. Fenofibrate-induced hyperhomocysteinaemia: clinical implications and management. Drug Safety 2003; 26: 81–91
5. Melenovsky V, et al. Effect of folic acid on fenofibrate-induced elevation of homocysteine and cysteine. Am Heart J 2003; 146: 110. Full version available at: 0002-8703/PIIS0002870303001224.pdf (accessed 30/05/08)


Fibrates have been associated with photosensitivity reactions1 and there may be cross-sensitivity with ketoprofen.
1. Serrano G, et al. Photosensitivity induced by fibric acid derivatives and its relation to photocontact dermatitis to ketoprofen J Am Acad Dermatol 1992; 27: 204–8.

💊 Interactions

Bezafibrate and other fibrates are highly protein-bound and may displace other drugs from protein binding sites. Interactions may also occur through changes in the activity of cytochrome P450 isoenzymes, particularly CYP3A4. Fibrates may enhance the effects of oral anticoagulants; the dose of anticoagulant should be reduced when treatment with a fibrate is started, and then adjusted gradually if necessary. Recommendations vary; licensed product information for bezafibrate suggests a reduction of up to 50% in the dosage of anticoagulant. The mechanism of the interaction is unclear; fibrates have been reported to displace warfarin from protein binding sites but other mechanisms are probably also involved. Other drugs that may be displaced from plasma proteins by fibrates include tolbutamide and other sulfonylurea antidiabetics, phenytoin, and, in patients with hypoalbuminaemia, furosemide. The interaction with antidiabetics is complex since fibrates may alter glucose tolerance in diabetic patients (see Effects on Glucose Metabolism, above). The dosage of antidiabetics may need adjusting during bezafibrate therapy. There is an increased risk of myopathy if fibrates are used with statins. Fibrates may interact with ciclosporin, although reports have been conflicting. However, nephrotoxicity associated with increased ciclosporin concentrations has been reported with bezafibrate and renal function should be monitored. Cholestasis has been reported in a patient given fenofibrate with raloxifene.
1. Lozada A, Dujovne CA. Drug interactions with fibric acids. Pharmacol Ther 1994; 63: 163–76.

Lipid regulating drugs.

The bioavailability of gemfibrozil was reduced by colestipol, but was unaffected when gemfibrozil was taken either 2 hours before or 2 hours after colestipol.1 For discussion of the interaction between fibrates and statins.
1. Forland SC, et al. Apparent reduced absorption of gemfibrozil when given with colestipol. J Clin Pharmacol 1990; 30: 29–32.


Acute renal failure due to rhabdomyolysis in a patient has been attributed to an interaction between ciprofibrate and ibuprofen.1 Ibuprofen was believed to have displaced ciprofibrate from protein binding sites. The use of radiological contrast media may also have been a contributory factor.
1. Ramachandran S, et al. Acute renal failure due to rhabdomyolysis in presence of concurrent ciprofibrate and ibuprofen treatment. BMJ 1997; 314: 1593.

💊 Pharmacokinetics

Bezafibrate is readily absorbed from the gastrointestinal tract. Plasma protein binding is about 95%. The plasma elimination half-life is about 1 to 2 hours. Most of a dose is excreted in the urine, about half as unchanged drug, the remainder as metabolites including 20% as glucuronides. A small proportion (about 3%) of the dose appears in the faeces. Elimination may be increased by forced diuresis. The drug is not dialysable.
1. Abshagen U, et al. Disposition pharmacokinetics of bezafibrate in man. Eur J Clin Pharmacol 1979; 16: 31–8
2. Abshagen U, et al. Steady-state kinetics of bezafibrate and clofibrate in healthy female volunteers. Eur J Clin Pharmacol 1980; 17: 305–8.

The elderly.

In a study comparing the pharmacokinetics of bezafibrate in 19 elderly patients with younger healthy subjects,1maximum plasma concentrations were 1.6 times higher in the elderly group (median 12.1 mg/litre against 7.7 mg/litre) and half-life was increased by 3.8 times (median 6.6 hours against 1.7 hours). The differences could not be attributed solely to diminished renal function in elderly patients. Dosage adjustments in elderly patients should not therefore be based on renal function alone.
1. Neugebauer G, et al. Steady-state kinetics of bezafibrate retard in hyperlipidemic geriatric patients. Klin Wochenschr 1988; 66: 250–6.

Renal impairment.

The half-life of bezafibrate may be prolonged in patients with renal impairment (see under Uses and Administration, below).

💊 Uses and Administration

Bezafibrate, a fibric acid derivative, is a lipid regulating drug. It is used to reduce total cholesterol and triglycerides in the management of hyperlipidaemias, including type IIa, type IIb, type III, type IV, and type V hyperlipoproteinaemias. Bezafibrate and other fibrates reduce triglycerides by reducing the concentration of very-low-density lipoprotein (VLDL). They reduce low-density lipoprotein (LDL)-cholesterol to a lesser extent, although the effect is variable, and may also increase high-density lipoprotein (HDL)cholesterol. Although evidence that this leads to a reduction in cardiovascular events is less good than for statins, some fibrates may have a role in cardiovascular risk reduction (see below). Bezafibrate is given in a usual oral dose of 200 mg three times daily taken with or after food; gastrointestinal disturbances may be reduced in susceptible patients by increasing the dose gradually over 5 to 7 days; 200 mg twice daily may occasionally be adequate for maintenance particularly in the treatment of hypertriglyceridaemia. A modified-release tablet is also available and is given as a single daily dose of 400 mg. The dose of bezafibrate should be reduced in patients with renal impairment (see below).
1. Goa KL, et al. Bezafibrate: an update of its pharmacology and use in the management of dyslipidaemia. Drugs 1996; 52: 725–53
2. Goldenberg I, et al. Update on the use of fibrates: focus on bezafibrate. Vasc Health Risk Manag 2008; 4: 131–41.


Bezafibrate is a typical member of the fibric acid derivative group of drugs (the fibrates) used in the treatment of hyperlipidaemias. One of the primary actions of the fibrates is to promote the catabolism of triglyceride-rich lipoproteins, in particular very-low-density lipoproteins (VLDL), apparently mediated by an enhanced activity of lipoprotein lipase.1 They may also interfere with the synthesis of VLDL, possibly by inhibiting hepatic acetyl coenzyme A carboxylase. The effect of fibrates on low-density lipoprotein (LDL)-cholesterol depends on the overall lipoprotein status of the patient but concentrations tend to decrease if high at baseline and increase if low at baseline. High-density lipoprotein (HDL)-cholesterol concentrations are increased, although there have been a few reports of unexpected falls in HDL-cholesterol with bezafibrate2,3 and ciprofibrate.4,5 Fibrates have three actions on sterol metabolism:1 they inhibit the synthesis of cholesterol, they inhibit the synthesis of bile acids, and they enhance the secretion of cholesterol in bile. It is these latter two effects which are responsible for the raised cholesterol saturation of bile, which may lead to the formation of gallstones in some patients (see Gallstones, under Adverse Effects, above). The effects of fibrates are mediated by their agonist action at peroxisome proliferator-activated receptors (PPARs).6,7 Fibrates are agonists of PPARα, which plays an important role in fatty acid metabolism; some, such as bezafibrate, may also activate other receptors including PPARγ (which plays a role in glucose homoeostasis).7
1. Grundy SM, Vega GL. Fibric acids: effects on lipids and lipoprotein metabolism. Am J Med 1987; 83 (suppl 5B): 9–20
2. Capps NE. Lipid profiles on fibric-acid derivatives. Lancet 1994; 344: 684–5
3. McLeod AJ, et al. Abnormal lipid profiles on fibrate derivatives. Lancet 1996; 347: 261
4. Chandler HA, Batchelor AJ. Ciprofibrate and lipid profile. Lancet 1994; 344: 128–9
5. McLeod AJ, et al. Ciprofibrate and lipid profile. Lancet 1994; 344: 955
6. Fruchart J-C, Duriez P. Mode of action of fibrates in the regulation of triglyceride and HDL-cholesterol metabolism. Drugs Today 2006; 42: 39–64
7. Robinson JG. Should we use PPAR agonists to reduce cardiovascular risk? PPAR Res 2008; 2008: 891425.

Administration in renal impairment.

Bezafibrate is mainly excreted in the urine and dosage alterations may be necessary in patients with renal impairment; fibrates may also impair renal function (see Effects on the Kidneys under Adverse Effects, above). Modified-release preparations are contra-indicated in patients with creatinine clearance (CC) below 60 mL/minute and the dosage of conventional-release formulations should be reduced depending on CC, as follows:
CC 40 to 60 mL/minute: 400 mg daily
CC 15 to 40 mL/minute: 200 mg daily or on alternate days
CC less than 15 mL/minute unless on dialysis: contra-indicated
dialysis patients: 200 mg every 3 days, with careful monitoring In a study in patients with renal impairment1 the half-life of bezafibrate was reported to be prolonged to 4.6 hours in 3 patients with CC greater than 40 mL/minute, 7.8 hours in 8 patients with CC of 20 to 40 mL/minute, and 20.1 hours in a patient with CC of 13 mL/minute.
1. Anderson P, Norbeck H-E. Clinical pharmacokinetics of bezafibrate in patients with impaired renal function. Eur J Clin Pharmacol 1981; 21: 209–14.

Cardiovascular risk reduction.

Lipid lowering therapy has an important role in patients at risk of cardiovascular disease. Although the evidence is less good than for statins, several studies have shown that fibrates may reduce both the progression of atherosclerosis and the incidence of cardiovascular events.1 In the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT)2,3 treatment with bezafibrate for 5 years in young men (less than 45 years of age) after myocardial infarction resulted in fewer coronary events and slowed the progression of focal coronary atherosclerosis when compared with placebo. However, in older men with peripheral vascular disease,4 bezafibrate had no effect on the incidence of coronary events and stroke together, although the severity of intermittent claudication was reduced and, in men under 65 years, there were fewer non-fatal coronary events. In the Diabetes Atherosclerosis Intervention Study (DAIS),5 fenofibrate reduced the angiographic progression of coronary atherosclerosis in type 2 diabetics, and there were also fewer clinical events in those receiving fenofibrate; further analysis showed6 reduced progression to microalbuminuria in the fenofibrate group. However, another study in type 2 diabetics, the FIELD study,7 found no reduction in the risk of major coronary events with fenofibrate, although there were fewer non-fatal myocardial infarctions and revascularisations. A meta-analysis8 of studies including type 2 diabetics concluded that fibrates reduce the incidence of cardiovascular events, but the effect on mortality was not significant. The best evidence for a reduction in cardiovascular events is for gemfibrozil. The Helsinki Heart Study9 assessed gemfibrozil for the primary prevention of ischaemic heart disease in 4081 middle-aged men with hyperlipidaemia. There was an overall reduction of 34% in the incidence of fatal and non-fatal myocardial infarctions and cardiac deaths in the gemfibrozil group compared with the placebo group, with the greatest reduction seen during years 3 to 5. Follow-up for a further 3.5 years10 suggested that long-term treatment with gemfibrozil seemed to postpone coronary events for about 5 years. The Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial (VA-HIT)11 assessed gemfibrozil for the secondary prevention of ischaemic heart disease in 2531 older men (mean age 64 years) whose primary lipid abnormality was a low HDL-cholesterol level. There was an overall reduction of 22% in the incidence of fatal and non-fatal myocardial infarctions and cardiac deaths in the gemfibrozil group compared with the placebo group, with the beneficial effects of gemfibrozil becoming apparent about 2 years after randomisation. There was also a reduction in the incidence of stroke.12
1. Després J-P, et al. Role of fibric acid derivatives in the management of risk factors for coronary heart disease. Drugs 2004; 64: 2177–98
2. Ericsson C-G, et al. Angiographic assessment of effects of bezafibrate on progression of coronary artery disease in young male postinfarction patients. Lancet 1996; 347: 849–53
3. Ericsson C-G, et al. Effect of bezafibrate treatment over five years on coronary plaques causing 20% to 50% diameter narrowing (The Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT)). Am J Cardiol 1997; 80: 1125–9
4. Meade T, et al. Bezafibrate in men with lower extremity arterial disease: randomised controlled trial. BMJ 2002; 325: 1139–43
5. Diabetes Atherosclerosis Intervention Study Investigators. Effect of fenofibrate on progression of coronary-artery disease in type 2 diabetes: the Diabetes Atherosclerosis Intervention Study, a randomised study. Lancet 2001; 357: 905–910. Correction. ibid.; 1890
6. Ansquer J-C, et al. Fenofibrate reduces progression to microalbuminuria over 3 years in a placebo-controlled study in type 2 diabetes: results from the Diabetes Atherosclerosis Intervention Study (DAIS). Am J Kidney Dis 2005; 45: 485–93
7. 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: 1849–61. Corrections. ibid. 2006; 368: 1415 and 1420
8. Allemann S, et al. Fibrates in the prevention of cardiovascular disease in patients with type 2 diabetes mellitus: meta-analysis of randomised controlled trials. Curr Med Res Opin 2006; 22: 617–23
9. Frick MH, et al. Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia: safety of treatment, changes in risk factors, and incidence of coronary heart disease. N Engl J Med 1987; 317: 1237–45
10. Heinonen OP, et al. The Helsinki Heart Study: coronary heart disease incidence during an extended follow-up. J Intern Med 1994; 235: 41–9
11. Bloomfield Rubins H, et al. Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. N Engl J Med 1999; 341: 410–18
12. Bloomfield Rubins H, et al. Reduction in stroke with gemfibrozil in men with coronary heart disease and low HDL cholesterol: The Veterans Affairs HDL Intervention Trial (VA-HIT). Circulation 2001; 103: 2828–33.


For reference to a possible reduction in the incidence of dementia associated with lipid regulating drugs, including fibrates, see under Uses of Simvastatin.

💊 Preparations

BP 2008: Bezafibrate Tablets.

Proprietary Preparations

Arg.: Bezacur; Bezalip; Elpi Lip; Nebufur; Austria: Bezacur; Bezalip; Bezaretard; Bezastad; Belg.: Cedur; Eulitop; Braz.: Cedur; Canad.: Bezalip; Chile: Nimus; Oralipin; Cz.: Regadrin B; Fin.: Bezalip; Fr.: Befizal; Ger.: Azufibrat†; Befibrat; Beza; Beza-Puren†; Bezabeta; Bezacur†; Bezadoc; Bezagamma; Bezamerck†; Bezapham†; Cedur; Lipox; Regadrin B†; Sklerofibrat†; Gr.: Bezalip; Getup†; Verbital; Hong Kong: Bezalip; Zafibral†; Hung.: Bezalip; India: Beza†; Bezalip; Israel: Bezalip; Norlip; Ital.: Bezalip; Hadiel; Jpn: Bezalip; Malaysia: Bezalip; Mex.: Befitec; Bexalcor; Bezafisal; Bezalex; Bezalip; Bifaren; Bionolip; Colser; Fazebit; Klestran†; Lesbest; Lipocin; Neptalip; Nivetril; Redalip; Solibay†; Zaf; Neth.: Bezalip; NZ: Bezalip; Fibalip; Philipp.: Bezastad; Pol.: Bezamidin; Port.: Bezalip; S.Afr.: Bezalip; Singapore: Bezalip; Zafibral; Spain: Difaterol; Eulitop; Reducterol†; Swed.: Bezalip; Switz.: Cedur; Thai.: Bezalip; Bezamil; Polyzalip; Raset†; UAE: Lipitrol; UK: Bezagen; Bezalip; Bezalip Mono; Fibrazate; Zimbacol; Venez.: Bezalip; Detrex†.
Published December 23, 2018.