Fenofibrate capsule is a peroxisome proliferator receptor alpha (PPAR ) activator indicated as an adjunct to diet: to reduce elevated LDL-C, Total-C, triglycerides, and Apo B, and to increase HDL-C in adult patients with primary hypercholesterolemia or mixed dyslipidemia (1.1). to reduce triglyceride (TG) levels in adult patients with severe hypertriglyceridemia (1.2).
💊How to take it
Fenofibrate capsules can be taken without regard to meals (2.1). Primary hypercholesterolemia and mixed dyslipidemia: 130 mg per day (2.2). Severe Hypertriglyceridemia: 43 to 130 mg per day; the dose should be adjusted according to patient response (2.3). Renally impaired patients: Initial dose of 43 mg per day (2.4). Geriatric patients: Select the dose on the basis of renal function (2.5).
ℹ️Common side effects
Most common adverse reactions (> 2% and greater than 1% in placebo) are abnormal liver tests, increased AST, increased ALT, increased CPK, and rhinitis (6.1). To report SUSPECTED ADVERSE REACTIONS, contact Dr. Reddy s Laboratories Inc., at 1-888-375-3784 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
⚠️Serious risks
Myopathy and rhabdomyolysis have been reported in patients taking fenofibrate. The risk for serious muscle toxicity appears to be increased when fenofibrate is co-administered with a statin (with a significantly higher rate observed with gemfibrozil), particularly in elderly patients and in patients with diabetes, renal failure, or hypothyroidism (5.2). Fenofibrate can increase serum transaminases. Monitor liver tests, including ALT. periodically during therapy (5.3).
Fenofibrate Capsules, are available in two strengths: Fenofibrate Capsules USP 43 mg are size 4 capsules with light green cap and off white body imprinted in black ink with LU on cap and C21 on body containing white to off white pellets .They are supplied as follows: Bottles of 30 NDC 55111-349-30 Bottles of 100 NDC 55111-349-01 Fenofibrate Capsules USP 130 mg are size 1 capsules with dark green cap and white body imprinted in black ink with LU on cap and C22 on body containing white to off…
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Fenofibrate capsule is a peroxisome proliferator receptor alpha (PPAR ) activator indicated as an adjunct to diet: to reduce elevated LDL-C, Total-C, triglycerides, and Apo B, and to increase HDL-C in adult patients with primary hypercholesterolemia or mixed dyslipidemia (1.1). to reduce triglyceride (TG) levels in adult patients with severe hypertriglyceridemia (1.2). Important Limitations of Use: Fenofibrate was not shown to reduce coronary heart disease morbidity and mortality in patients with type 2 diabetes mellitus (5.1).
The effects of fenofibrate on serum triglycerides were studied in two randomized, double-blind, placebo-controlled clinical trials of 147 hypertriglyceridemic patients. Patients were treated for eight weeks under protocols that differed only in that one entered patients with baseline TG levels of 500 to 1500 mg/dL, and the other TG levels of 350 to 499 mg/dL. In patients with hypertriglyceridemia and normal cholesterolemia with or without hyperchylomicronemia, treatment with fenofibrate at dosages equivalent to 130 mg fenofibrate per day decreased primarily very low density lipoprotein (VLDL) triglycerides and VLDL cholesterol Treatment of patients with elevated triglycerides often results in an increase of LDL-C (See Table 5). Table 5 Effects of Fenofibrate in Patients with Hypertriglyceridemia Study 1 Placebo Fenofibrate Baseline TG levels 350 to 499 mg/dL N Baseline (mean) Endpoint (mean) % Change (mean) N Baseline (mean) Endpoint (mean) % Change (mean) Triglycerides 28 449 450 -0.5 27 432 223 -46.2 * VLDL Triglycerides 19 367 350 2.7 19 350 178 -44.1 * Total Cholesterol 28 255 261 2.8 27 252 227 -9.1 * HDL Cholesterol 28 35 36 4 27 34 40 19.6 * LDL Cholesterol 28 120 129 1.2 27 128 137 14.5 VLDL Cholesterol 27 99 99 5.8 27 92 46 -44.7 * Study 2 Placebo Fenofibrate Baseline TG levels 500 to 1500 mg/dL N Baseline (mean) Endpoint (mean) % Change (mean) N Baseline (mean) Endpoint (mean) % Change (mean) Triglycerides 44 710 750 7.2 48 726 308 -54.5 * VLDL Triglycerides 29 537 571 18.7 33 543 205 -50.6 * Total Cholesterol 44 272 271 0.4 48 261 223 -13.8 * HDL Cholesterol 44 27 28 5 48 30 36 22.9 * LDL Cholesterol 42 100 90 -4.2 45 103 131 45* VLDL Cholesterol 42 137 142 11 45 126 54 -49.4 * * p < 0.05 vs. placebo The effect of fenofibrate on serum triglycerides was studied in a double-blind, randomized, 3 arm parallel-group trial of 146. The study population was comprised of 61 % male and 39% female patients. Approximately 70% of patients had hypertension and 32% had diabetes. Patients were treated for eight weeks with either fenofibrate 130 mg taken once daily with meals, fenofibrate 130 mg taken once daily between meals, or placebo. Fenofibrate 130 mg, whether taken with meals or between meals, had comparable effects on TG and all lipid parameters (See Table 6). Table 6 Fenofibrate Treatment in Patients with Hypertriglyceridemia Placebo (n=50) Fenofibrate capsules with meals (n=54) Fenofibrate capsules between meals (n=42 Baseline mg/dL (mean) % Change at endpoint (mean) Baseline mg/dL (mean) % Change at endpoint (mean) Baseline mg/dL (mean) % Change at endpoint (mean) Triglycerides 479 +0.7 475 -36.7* 487 -36.6* Total Cholesterol 237 -0.8 248 -5.1 241 -3.4 HDL Cholesterol 35 +0.8 36 +13.7* 36 +14.3* Non-HDL Cholesterol 202 -1.1 212 -8.2** 205 -6.6** LDL Cholesterol 115 +3.2 120 +15.4* 122 +14.5 VLDL Cholesterol 87 -1.6 92 -34.4* 83 -30.4* * p 0.05 vs placebo ** p 0.05 vs placebo (log transformed data) The effect of fenofibrate on cardiovascular morbidity and mortality has not been determined.
Fenofibrate capsules can be taken without regard to meals (2.1). Primary hypercholesterolemia and mixed dyslipidemia: 130 mg per day (2.2). Severe Hypertriglyceridemia: 43 to 130 mg per day; the dose should be adjusted according to patient response (2.3). Renally impaired patients: Initial dose of 43 mg per day (2.4). Geriatric patients: Select the dose on the basis of renal function (2.5).
Fenofibrate Capsules USP 43 mg are size 4 capsules with light green cap and off white body imprinted in black ink with LU on cap and C21 on body containing white to off white pellets. Fenofibrate Capsules USP 130 mg are size 1 capsules with dark green cap and white body imprinted in black ink with LU on cap and C22 on body containing white to off white pellets. Oral capsules: 43 mg and 130 mg (3)
Fenofibrate is contraindicated in: patients with severe renal impairment, including those receiving dialysis [see Clinical Pharmacology (12.3)]. patients with active liver disease, including those with primary biliary cirrhosis and unexplained persistent liver function abnormalities [see Warnings and Precautions (5.3)]. patients with pre-existing gallbladder disease [see Warnings and Precautions (5.5)]. nursing mothers [see Use in Specific Populations (8.3)]. patients with known hypersensitivity to fenofibric acid or fenofibrate [see Warnings and Precautions (5.9) ]. Severe renal dysfunction, including patients receiving dialysis (4, 12.3) Active liver disease (4, 5.3) Gallbladder disease (4, 5.5) Nursing mothers (4, 8.3) Known hypersensitivity to fenofibrate (4, 5.9)
Myopathy and rhabdomyolysis have been reported in patients taking fenofibrate. The risk for serious muscle toxicity appears to be increased when fenofibrate is co-administered with a statin (with a significantly higher rate observed with gemfibrozil), particularly in elderly patients and in patients with diabetes, renal failure, or hypothyroidism (5.2). Fenofibrate can increase serum transaminases. Monitor liver tests, including ALT. periodically during therapy (5.3). Fenofibrate can reversibly increase serum creatinine levels. Monitor renal function periodically in patients with renal impairment (5.4). Fenofibrate increases cholesterol excretion into the bile, leading to risk of cholelithiasis. If cholelithiasis is suspected, gallbladder studies are indicated (5.5). Exercise caution in concomitant treatment with coumarin anticoagulants. Reduce the dosage of coumarin to maintain the PT/INR at the desired level to prevent bleeding complications (5.6). Acute hypersensitivity reactions, including anaphylaxis and angioedema, and delayed hypersensitivity reactions, including severe cutaneous adverse drug reactions have been reported postmarketing. Some cases were life-threatening and required emergency treatment. Discontinue fibrate and treat patients appropriately if reactions occur (5.9).
Most common adverse reactions (> 2% and greater than 1% in placebo) are abnormal liver tests, increased AST, increased ALT, increased CPK, and rhinitis (6.1). To report SUSPECTED ADVERSE REACTIONS, contact Dr. Reddy s Laboratories Inc., at 1-888-375-3784 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
Geriatric use: Determine dose selection based on renal function (8.5). Renal impairment: Avoid in patients with severe renal impairment; dose reduction required in patients with mild to moderate renal impairment (8.6).
Pregnancy Category: C Safety in pregnant women has not been established. There are no adequate and well controlled studies of fenofibrate in pregnant women. Fenofibrate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. In female rats given oral dietary doses of 15, 75, and 300 mg/kg/day of fenofibrate from 15 days prior to mating through weaning, maternal toxicity was observed at 0.3 times the maximum recommended human dose (MRHD), based on body surface area comparisons; mg/m2. In pregnant rats given oral dietary doses of 14, 127, and 361 mg/kg/day from gestation day 6 to 15 during the period of organogenesis, adverse developmental findings were not observed at 14 mg/kg/day (less than 1 times the MRHD, based on body surface area comparisons; mg/ m2). At higher multiples of human doses, evidence of maternal toxicity was observed. In pregnant rabbits given oral gavage doses of 15, 150, and 300 mg/kg/day from gestation day 6 to 18 during the period of organogenesis and allowed to deliver, aborted litters were observed at 150 mg/kg/day (10 times the MRHD, based on body surface area comparisons; mg/ m2). No developmental findings were observed at 15 mg/kg/day (at less than 1 times the MRHD, based on body surface area comparisons; mg/ m2). In pregnant rats given oral dietary doses of 15, 75, and 300 mg/kg/day from gestation day 15 through lactation day 21 (weaning), maternal toxicity was observed at less than 1 times the MRHD, based on body surface area comparisons; mg/ m2.
Fenofibrate should not be used in nursing mothers. A decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
Safety and effectiveness have not been established in pediatric patients.
Fenofibric acid is known to be substantially excreted by the kidney, and the risk of adverse reactions to this drug may be greater in patients with impaired renal function. Fenofibric acid exposure is not influenced by age. Since elderly patients have a higher incidence of renal impairment, dose selection for the elderly should be made on the basis of renal function [see Dosage and Administration (2.5) and Clinical Pharmacology (12.3)]. Elderly patients with normal renal function should require no dose modifications. Consider monitoring renal function in elderly patients taking fenofibrate.
There is no specific treatment for overdose with fenofibrate. General supportive care of the patient is indicated, including monitoring of vital signs and observation of clinical status, should an overdose occur. If indicated, elimination of unabsorbed drug should be achieved by emesis or gastric lavage; usual precautions should be observed to maintain the airway. Because fenofibrate is highly bound to plasma proteins, hemodialysis should not be considered.
Fenofibrate capsules USP, is a lipid regulating agent available as capsules for oral administration. Each capsule contains 43 mg or 130 mg of micronized fenofibrate USP. The chemical name for fenofibrate USP is 2-[4-(4-chlorobenzoyl) phenoxy]-2-methyl-propanoic acid, 1-methylethyl ester with the following structural formula: The molecular formula is C20H21O4CI and the molecular weight is 360.83; fenofibrate is insoluble in water. The melting point is 79 to 82 C. Fenofibrate USP is a white or almost white crystalline powder which is sparingly soluble in methanol, ethanol and dimethylformamide. Each capsule contains the labeled amount of fenofibrate USP and the inactive ingredients: ammonio metha copolymer dispersion, D & C yellow No.10, FD & C Blue No. 2, gelatin, hypromellose, iron oxide yellow, iron oxide black, potasium hydroxide, shellac, simethicone emulsion, sodium lauryl sulphate, sugar spheres, talc, titanium dioxide and triethyl citrate. Fenofibrate capsules meets USP Dissolution Test 3.
The active moiety of fenofibrate is fenofibric acid. The pharmacological effects of fenofibric acid in both animals and humans have been extensively studied through oral administration of fenofibrate. The lipid-lowering effects of fenofibric acid seen in clinical practice have been explained in vivo in transgenic mice and in vitro in human hepatocyte cultures by the activation of peroxisome proliferator activated receptor (PPAR ). Through this mechanism, fenofibrate increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoprotein C-III (an inhibitor of lipoprotein lipase activity). The resulting decrease in triglycerides produces an alteration in the size and composition of LDL from small, dense particles (which are thought to be atherogenic due to their susceptibility to oxidation) to large buoyant particles. These larger particles have a greater affinity for cholesterol receptors and are catabolized rapidly. Activation of PPAR also induces an increase in the synthesis of apoproteins A-I, A-II and HDL-cholesterol. Fenofibrate also reduces serum uric acid levels in hyperuricemic and normal individuals by increasing the urinary excretion of uric acid.
A variety of clinical studies have demonstrated that elevated levels of total-C, DL-C, and Apo B, an LDL membrane complex, are associated with human atherosclerosis. Similarly, decreased levels of HDL-C and its transport complex, apolipoprotein A (Apo AI and Apo All) are associated with the development of atherosclerosis. Epidemiologic investigations have established that cardiovascular morbidity and mortality vary directly with the level of total-C, LDL-C, and triglycerides, and inversely with the level of HDL-C. The independent effect of raising HDL-C or lowering TG on the risk of cardiovascular morbidity and mortality has not been determined. Fenofibric acid, the active metabolite of fenofibrate, produces reductions in total cholesterol, LDL cholesterol, apolipoprotein B, total triglycerides, and triglyceride-rich lipoprotein in treated patients. In addition, treatment with fenofibrate results in increases in high density lipoprotein (HDL) and apoproteins Apo AI and Apo AII.
Fenofibrate is a pro-drug of the active chemical moiety fenofibric acid. Fenofibrate is converted by ester hydrolysis in the body to fenofibric acid which is the active constituent measurable in the circulation. Absorption: The absolute bioavailability of fenofibrate cannot be determined as the compound is virtually insoluble in aqueous media suitable for injection. However, fenofibrate is well absorbed from the gastrointestinal tract. Following oral administration in healthy volunteers, approximately 60% of a single dose of radio-labeled fenofibrate appeared in urine, primarily as fenofibric acid and its glucuronate conjugate, and 25% was excreted in the feces. Peak plasma levels of fenofibric acid from fenofibrate occur within 4 to 8 hours after administration. There was less than dose-proportional increase in the systemic exposure of fenofibric acid from 43 mg and 130 mg of fenofibrate under fasting conditions. Doses of three-capsules of 43 mg fenofibrate given concurrently were dose equivalent to single-capsule doses of 130 mg. The extent of absorption of fenofibric acid was unaffected when fenofibrate was taken either in fasted state or with a low-fat meal. However, the Cmax of fenofibrate increased in the presence of a low-fat meal. Tmax was unaffected in the presence of a low-fat meal. In the presence of a high-fat meal, there was a 26% increase in AUC and 108% increase in Cmax of fenofibric acid from fenofibrate relative to fasting state. Distribution: In healthy volunteers, steady-state plasma levels of fenofibric acid were shown to be achieved within a week of dosing and did not demonstrate accumulation across time following multiple dose administration. Serum protein binding was approximately 99% in normal and hyperlipidemic subjects. Metabolism: Following oral administration, fenofibrate is rapidly hydrolyzed by esterases to the active metabolite, fenofibric acid; no unchanged fenofibrate is detected in plasma. Fenofibric acid is primarily conjugated with glucuronic acid and then excreted in urine. A small amount of fenofibric acid is reduced at the carbonyl moiety to a benzhydrol metabolite which is, in turn, conjugated with glucuronic acid and excreted in urine. In vivo metabolism data indicate that neither fenofibrate nor fenofibric acid undergo oxidative metabolism (e.g, cytochrome P450) to a significant extent. Elimination: After absorption, fenofibrate is mainly excreted in the urine in the form of metabolites, primarily fenofibric acid and fenofibric acid glucuronide. After administration of radiolabeled fenofibrate, approximately 60% of the dose appeared in the urine and 25% was excreted in the feces. Fenofibrate acid from fenofibrate is eliminated with a half-life of 23 hours, allowing once daily dosing. Geriatrics: In elderly volunteers 77 to 87 years of age, the oral clearance of fenofibric acid following a single oral dose of fenofibrate was 1.2 L/h, which compares to 1.1 L/h in young adults. This indicates that a similar dosage regimen can be used in the elderly with normal renal function, without increasing accumulation of the drug or metabolites [see Dosage and Administration (2.4) and Use in Specific Populations (8.5)]. Pediatrics: The pharmacokinetics of fenofibrate has not been studied in pediatric populations. Gender: No pharmacokinetic difference between males and females has been observed for fenofibrate. Race: The influence of race on the pharmacokinetics of fenofibrate has not been studied; however, fenofibrate is not metabolized by enzymes known for exhibiting inter-ethnic variability. Renal Impairment: The pharmacokinetics of fenofibric acid was examined in patients with mild, moderate, and severe renal impairment. Patients with severe renal impairment (creatinine clearance [CrCl] 30 mL/min or estimated glomerular filtration rate [eGFR] < 30 mL/min/1.73m2) showed 2.7-fold increase in exposure for fenofibric acid and increased accumulation of fenofibric acid during chronic dosing compared to that of healthy subjects. Patients with mild to moderate (CrCl 30 to 80 mL/min or eGFR 30 to 59 mL/min/1.73m2) renal impairment had similar exposure but an increase in the half-life for fenofibric acid compared to that of healthy subjects. Based on these findings, the use of fenofibrate should be avoided in patients who have severe renal impairment and dose reduction is required in patients having mild to moderate renal impairment [see Dosage and Administration (2.4)]. Hepatic Impairment: No pharmacokinetic studies have been conducted in patients having hepatic impairment. Drug-Drug Interactions: In vitro studies using human liver microsomes indicate that fenofibrate and fenofibric acid are not inhibitors of cytochrome (CYP) P450 isoforms CYP3A4, CYP2D6, CYP2E1, or CYP1A2. They are weak inhibitor of CYP2C8, CYP2C19 and CYP2A6, and mild-to-moderate inhibitors of CYP2C9 at therapeutic concentrations. Table 2 describes the effects of co-administered drugs on fenofibric acid systemic exposure. Table 3 describes the effects of co-administered fenofibric acid on exposure to other drugs. Table 2 Effects of Co-Administered Drugs on Fenofibric Acid Systemic Exposure from Fenofibrate Administration Co-Administered Drug Dosage Regimen of Co-Administered Drug Dosage Regimen of Fenofibrate Changes in Fenofibric Acid Exposure AUC Cmax No dosing adjustments required for fenofibrate with the following co-administered drugs Lipid-lowering agents Atorvastatin 20 mg once daily for 10 days Fenofibrate 160 mg1 once daily for 10 days 2% 4% Pravastatin 40 mg as a single dose Fenofibrate 3 x 67 mg2 as a single dose 1% 2% Fluvastatin 40 mg as a single dose Fenofibrate 160 mg1 as a single dose 2% 10% Anti-diabetic agents Glimepiride 1 mg once daily as a single dose Fenofibrate 145 mg1 once daily for 10 days 1% 1% Metformin 850 mg three times daily for 10 days Fenofibrate 54 mg1 three times daily for 10 days 9% 6% Rosiglitazone 8 mg once daily for 5 days Fenofibrate 145 mg1 once daily for 14 days 10% 3% 1 TriCor (fenofibrate) oral tablet 2 TriCor (fenofibrate) oral micronized capsule Table 3 Effects of Fenofibrate Co-Administration on Systemic Exposure of Other Drugs Dosage Regimen of Fenofibrate Dosage Regimen of Co-Administered Drug Changes in Co-Administered Drug Exposure Analyte AUC Cmax No dosing adjustments required for these co-administered drugs with Fenofibrate Lipid-lowering agents Fenofibrate 160 mg1 once daily for 10 days Atorvastatin, 20 mg once daily for 10 days Atorvastatin 17% 0% Fenofibrate 3 x 67 mg2 as a single dose Pravastatin, 40 mg as a single dose Pravastatin 13% 13% 3 -Hydroxyl-iso-pravastatin 26% 29% Fenofibrate 160 mg1 once daily for 10 days Pravastatin, 40 mg once daily for 10 days Pravastatin 28% 36% 3 -Hydroxyl-iso-pravastatin 39% 55% Fenofibrate 160 mg1 as a single dose Fluvastatin, 40 mg as a single dose (+)-3R, 5S-Fluvastatin 15% 16% Anti-diabetic agents Fenofibrate 145 mg1 once daily for 10 days Glimepiride, 1 mg once daily as a single dose Glimepiride 35% 18% Fenofibrate 54 mg1 three times daily for 10 days Metformin, 850 mg three times daily for 10 days Metformin 3% 6% Fenofibrate 145 mg1 once daily for 14 days Rosiglitazone, 8 mg once daily for 5 days Rosiglitazone 6% 1% 1 TriCor (fenofibrate) oral tablet 2 TriCor (fenofibrate) oral micronized capsule
Two dietary carcinogenicity studies have been conducted in rats with fenofibrate. In the first 24-month study, Wistar rats were dosed with fenofibrate at 10, 45, and 200 mg/kg/day, approximately 0.3, 1, and 6 times the maximum recommended human dose (MRHD), based on body surface area comparisons (mg/m2). At a dose of 200 mg/kg/day (at 6 times the MRHD), the incidence of liver carcinomas was significantly increased in both sexes. A statistically significant increase in pancreatic carcinomas was observed in males at 1 and 6 times the MRHD; an increase in pancreatic adenomas and benign testicular interstitial cell tumors was observed at 6 times the MRHD in males. In a second 24 month rat carcinogenicity study in a different strain of rats (Sprague-Dawley), doses of 10 and 60 mg/kg/day (0.3 and 2 times the MRHD) produced significant increases in the incidence of pancreatic acinar adenomas in both sexes and increases in testicular interstitial cell tumors in males at 2 times the MRHD. A 117-week carcinogenicity study was conducted in rats comparing three drugs: fenofibrate 10 and 60 mg/kg/day (0.3 and 2 times the MRHD), clofibrate (400 mg/kg/day; 2 times the human dose), and gemfibrozil (250 mg/kg/day; 2 times the human dose, based on mg/m2 surface area). Fenofibrate increased pancreatic acinar adenomas in both sexes. Clofibrate increased hepatocellular carcinoma and pancreatic acinar adenomas in males and hepatic neoplastic nodules in females. Gemfibrozil increased hepatic neoplastic nodules in males and females, while all three drugs increased testicular interstitial cell tumors in males. In a 21-month study in CF-1 mice, fenofibrate 10, 45, and 200 mg/kg/day (approximately 0.2, 1, and 3 times the MRHD on the basis of mg/m2 surface area) significantly increased the liver carcinomas in both sexes at 3 times the MRHD. In a second 18-month study at 10, 60, and 200 mg/kg/day, fenofibrate significantly increased the liver carcinomas in male mice and liver adenomas in female mice at 3 times the MRHD. Electron microscopy studies have demonstrated peroxisomal proliferation following fenofibrate administration to the rat. An adequate study to test for peroxisome proliferation in humans has not been done, but changes in peroxisome morphology and numbers have been observed in humans after treatment with other members of the fibrate class when liver biopsies were compared before and after treatment in the same individual. Mutagenesis: Fenofibrate has been demonstrated to be devoid of mutagenic potential in the following tests: Ames, mouse lymphoma, chromosomal aberration and unscheduled DNA synthesis in primary rat hepatocytes. Impairment of Fertility: In fertility studies rats were given oral dietary doses of fenofibrate, males received 61 days prior to mating and females 15 days prior to mating through weaning which resulted in no adverse effect on fertility at doses up to 300 mg/kg/day (~10 times the MRHD, based on mg/m2 surface area comparisons).
Fenofibrate Capsules, are available in two strengths: Fenofibrate Capsules USP 43 mg are size 4 capsules with light green cap and off white body imprinted in black ink with LU on cap and C21 on body containing white to off white pellets .They are supplied as follows: Bottles of 30 NDC 55111-349-30 Bottles of 100 NDC 55111-349-01 Fenofibrate Capsules USP 130 mg are size 1 capsules with dark green cap and white body imprinted in black ink with LU on cap and C22 on body containing white to off white pellets. They are supplied as follows: Bottles of 30 NDC 55111-395-30 Bottles of 90 NDC 55111-395-90 Bottles of 100 NDC 55111-395-01 Store at 25 C (77 F); excursions permitted to 15 -30 C (59 -86 F) [see USP Controlled Room Temperature].
Patients should be advised: of the potential benefits and risks of fenofibrate. not to use fenofibrate if there is a known hypersensitivity to fenofibrate capsules or fenofibric acid. that if they are taking coumarin anticoagulants, fenofibrate may increase their anticoagulant effect, and increased monitoring may be necessary. of medications that should not be taken in combination with fenofibrate. to continue to follow an appropriate lipid-modifying diet while taking fenofibrate. to take fenofibrate once daily, without regard to food, at the prescribed dose, swallowing each capsule whole. to inform their physician of all medications, supplements, and herbal preparations they are taking and any change to their medical condition. Patients should also be advised to inform their physicians prescribing a new medication that they are taking fenofibrate. to inform their physician of any muscle pain, tenderness or weakness; onset of abdominal pain; or any other new symptoms. to return to their physician s office for routine monitoring. RX Only Manufactured for: Dr. Reddy s Laboratories Limited Bachupally 500 090 INDIA Manufactured by: Lupin Limited Goa 403 722 INDIA Revised: 1218
