United States - English - NLM (National Library of Medicine)

par pharmaceutical, inc. - choline fenofibrate (unii: 4bmh7izt98) (fenofibric acid - unii:bgf9mn2hu1) - fenofibric acid 45 mg - fenofibric acid delayed-release capsules are indicated as adjunctive therapy to diet to reduce triglycerides (tg) in patients with severe hypertriglyceridemia. improving glycemic control in diabetic patients showing fasting chylomicronemia will usually obviate the need for pharmacological intervention. markedly elevated levels of serum triglycerides (e.g., > 2,000 mg/dl) may increase the risk of developing pancreatitis. the effect of fenofibric acid delayed-release capsules therapy on reducing this risk has not been adequately studied. fenofibric acid delayed-release capsules are indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein cholesterol (ldl-c), total cholesterol (total-c), triglycerides (tg), and apolipoprotein b (apo b), and to increase high-density lipoprotein cholesterol (hdl-c) in patients with primary hypercholesterolemia or mixed dyslipidemia. fenofibrate at a dose equivalent to 135 mg of fenofibric acid delayed-release capsules did not reduce coronary heart disease

United States - English - NLM (National Library of Medicine)

lupin pharmaceuticals, inc. - fenofibrate (unii: u202363uos) (fenofibric acid - unii:bgf9mn2hu1) - fenofibrate 54 mg - fenofibrate tablet usp is indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein cholesterol (ldl-c), total cholesterol (total-c), triglycerides and apolipoprotein b (apo b), and to increase high-density lipoprotein cholesterol (hdl-c) in adult patients with primary hypercholesterolemia or mixed dyslipidemia. fenofibrate tablet usp is also indicated as adjunctive therapy to diet for treatment of adult patients with severe hypertriglyceridemia. improving glycemic control in diabetic patients showing fasting chylomicronemia will usually obviate the need for pharmacologic intervention. markedly elevated levels of serum triglycerides (e.g. > 2,000 mg/dl) may increase the risk of developing pancreatitis. the effect of fenofibrate therapy on reducing this risk has not been adequately studied. fenofibrate at a dose equivalent to 160 mg of fenofibrate tablet usp was not shown to reduce coronary heart disease morbidity and mortality in a large, randomized controlled trial of patients with type 2 diabetes mellitus [see warnings and precautions (5.1)] . 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 (5.2)] . - patients with preexisting gallbladder disease [see warnings and precautions (5.5)] . - nursing mothers [see use in specific populations (8.2)] - patients with known hypersensitivity to fenofibrate or fenofibric acid [see warnings and precautions (5.9)]. risk summary limited available data with fenofibrate use in pregnant women are insufficient to determine a drug associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes. in animal reproduction studies, no evidence of embryo-fetal toxicity was observed with oral administration of fenofibrate in rats and rabbits during organogenesis at doses less than or equivalent to the maximum recommended clinical dose of 160 mg daily, based on body surface area (mg/m2 ). adverse reproductive outcomes occurred at higher doses in the presence of maternal toxicity (see data). fenofibrate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2 to 4% and 15 to 20%, respectively. data animal data 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, no adverse developmental findings were observed at 14 mg/kg/day (less than the clinical exposure at the maximum recommended human dose [mrhd] of 300 mg fenofibrate daily, equivalent to 160 mg fenofibrate tablets daily, based on body surface area comparisons). increased fetal skeletal malformations were observed at maternally toxic doses (361 mg/kg/day, corresponding to 12 times the clinical exposure at the mrhd) that significantly suppressed maternal body weight gain. 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, no adverse developmental findings were observed at 15 mg/kg/day (a dose that approximates the clinical exposure at the mrhd, based on body surface area comparisons). aborted litters were observed at maternally toxic doses (≥ 150 mg/kg/day, corresponding to ≥ 10 times the clinical exposure at the mrhd) that suppressed maternal body weight gain. in pregnant rats given oral dietary doses of 15, 75, and 300 mg/kg/day from gestation day 15 through lactation day 21 (weaning), no adverse developmental effects were observed at 15 mg/kg/day (less than the clinical exposure at the mrhd, based on body surface area comparisons), despite maternal toxicity (decreased weight gain). post-implantation loss was observed at ≥ 75 mg/kg/day (≥ 2 times the clinical exposure at the mrhd) in the presence of maternal toxicity (decreased weight gain). decreased pup survival was noted at 300 mg/kg/day (10 times the clinical exposure at the mrhd), which was associated with decreased maternal body weight gain/maternal neglect. risk summary there is no available information on the presence of fenofibrate in human milk, effects of the drug on the breastfed infant, or the effects on milk production. fenofibrate is present in the milk of rats, and is therefore likely to be present in human milk. because of the potential for serious adverse reactions in breastfed infants, such as disruption of infant lipid metabolism, women should not breastfeed during treatment with fenofibrate and for 5 days after the final dose [see  contraindications (4)] . 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. the use of fenofibrate should be avoided in patients who have severe renal impairment [see contraindications (4)] . dose reduction is required in patients with mild to moderate renal impairment [see dosage and administration (2.4) and clinical pharmacology (12.3)]. monitoring renal function in patients with renal impairment is recommended. the use of fenofibrate has not been evaluated in subjects with hepatic impairment [see contraindications (4) and clinical pharmacology (12.3)].

United States - English - NLM (National Library of Medicine)

apotex corp. - fenofibrate (unii: u202363uos) (fenofibric acid - unii:bgf9mn2hu1) - fenofibrate 43 mg - fenofibrate capsules, usp are indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein  cholesterol  (ldl-c),  total  cholesterol  (total-c), triglycerides (tg), and apolipoprotein b (apo b), and to increase high-density lipoprotein cholesterol (hdl-c) in adult patients with primary hypercholesterolemia or mixed dyslipidemia. fenofibrate capsules, usp are also indicated as adjunctive therapy to diet for treatment of adult patients with severe hypertriglyceridemia. improving glycemic control in diabetic patients showing fasting chylomicronemia will usually reduce fasting triglycerides and eliminate chylomicronemia thereby obviating the need for pharmacologic intervention. markedly elevated levels of serum triglycerides (e.g. > 2,000 mg/dl) may increase the risk of developing pancreatitis. the effect of fenofibrate therapy on reducing this risk has not been adequately studied. fenofibrate was not shown to reduce coronary heart disease morbidity and mortality in patients with type 2 diabetes mellitus [see warnings and precautions (5.1) ]. fenofibrate is contraindicated in: - patients with severe renal impairment, including those receiving dialysis [see clinical pharmacology (12.3) ]. 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 (5.2) ]. patients with active liver disease, including those with primary biliary cirrhosis and  unexplained persistent liver  function abnormalities [see warnings and precautions (5.2) ]. - patients with pre-existing gallbladder disease [see warnings and precautions (5.5) ]. patients with pre-existing gallbladder disease [see warnings and precautions (5.5) ]. - nursing mothers [see use in specific populations (8.3) ]. nursing mothers [see use in specific populations (8.3) ]. - patients  with known hypersensitivity  to  fenofibric  acid or fenofibrate [see warnings and precautions (5.9) ]. patients  with known hypersensitivity  to  fenofibric  acid or fenofibrate [see warnings and precautions (5.9) ]. 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. fenofibrate should be avoided in patients with severe renal impairment [see contraindications (4) ]. dose reduction is required in patients with mild to moderate renal impairment [see dosage and administration (2.4) and clinical pharmacology (12.3) ]. monitoring renal function in patients with renal impairment is recommended. the use of fenofibrate has not been evaluated in subjects with hepatic impairment [see contraindications (4) and clinical pharmacology (12.3) ].

United States - English - NLM (National Library of Medicine)

amneal pharmaceuticals of new york llc - fenofibrate (unii: u202363uos) (fenofibric acid - unii:bgf9mn2hu1) - fenofibrate 54 mg - fenofibrate tablets are indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein cholesterol (ldl-c), total cholesterol (total-c), triglycerides and apolipoprotein b (apo b), and to increase high-density lipoprotein cholesterol (hdl-c) in adult patients with primary hypercholesterolemia or mixed dyslipidemia. fenofibrate tablets are also indicated as adjunctive therapy to diet for treatment of adult patients with severe hypertriglyceridemia. improving glycemic control in diabetic patients showing fasting chylomicronemia will usually obviate the need for pharmacologic intervention. markedly elevated levels of serum triglycerides (e.g. > 2,000 mg/dl) may increase the risk of developing pancreatitis. the effect of fenofibrate therapy on reducing this risk has not been adequately studied. fenofibrate at a dose equivalent to 160 mg of fenofibrate tablet was not shown to reduce coronary heart disease morbidity and mortality in a large, randomized controlled trial of patients with type 2 diabetes mellitus [see warnings and precautions (5.1)] . fenofibrate tablets are 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 (5.2)]. - patients with preexisting gallbladder disease [see warnings and precautions (5.5)]. - nursing mothers [see use in specific populations (8.2)]. - patients with known hypersensitivity to fenofibrate or fenofibric acid [see warnings and precautions (5.9)]. risk summary limited available data with fenofibrate use in pregnant women are insufficient to determine a drug associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes. in animal reproduction studies, no evidence of embryo-fetal toxicity was observed with oral administration of fenofibrate in rats and rabbits during organogenesis at doses less than or equivalent to the maximum recommended clinical dose of 160 mg daily, based on body surface area (mg/m2 ). adverse reproductive outcomes occurred at higher doses in the presence of maternal toxicity (see data). fenofibrate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. data animal data 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, no adverse developmental findings were observed at 14 mg/kg/day (less than the clinical exposure at the maximum recommended human dose [mrhd] of 300 mg fenofibrate daily, equivalent to 160 mg fenofibrate daily, based on body surface area comparisons). increased fetal skeletal malformations were observed at maternally toxic doses (361 mg/kg/day, corresponding to 12 times the clinical exposure at the mrhd) that significantly suppressed maternal body weight gain. 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, no adverse developmental findings were observed at 15 mg/kg/day (a dose that approximates the clinical exposure at the mrhd, based on body surface area comparisons). aborted litters were observed at maternally toxic doses (≥ 150 mg/kg/day, corresponding to ≥ 10 times the clinical exposure at the mrhd) that suppressed maternal body weight gain. in pregnant rats given oral dietary doses of 15, 75, and 300 mg/kg/day from gestation day 15 through lactation day 21 (weaning), no adverse developmental effects were observed at 15 mg/kg/day (less than the clinical exposure at the mrhd, based on body surface area comparisons), despite maternal toxicity (decreased weight gain). post-implantation loss was observed at ≥ 75 mg/kg/day (≥ 2 times the clinical exposure at the mrhd) in the presence of maternal toxicity (decreased weight gain). decreased pup survival was noted at 300 mg/kg/day (10 times the clinical exposure at the mrhd), which was associated with decreased maternal body weight gain/maternal neglect. risk summary there is no available information on the presence of fenofibrate in human milk, effects of the drug on the breastfed infant, or the effects on milk production. fenofibrate is present in the milk of rats, and is therefore likely to be present in human milk. because of the potential for serious adverse reactions in breastfed infants, such as disruption of infant lipid metabolism, women should not breastfeed during treatment with fenofibrate and for 5 days after the final dose [see contraindications (4)] . 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. the use of fenofibrate tablets should be avoided in patients who have severe renal impairment [see contraindications (4)]. dose reduction is required in patients with mild to moderate renal impairment [see dosage and administration (2.4) and clinical pharmacology (12.3)]. monitoring renal function in patients with renal impairment is recommended. the use of fenofibrate tablets has not been evaluated in subjects with hepatic impairment [see c ontraindications (4) and clinical pharmacology (12.3)].

United States - English - NLM (National Library of Medicine)

amneal pharmaceuticals ny llc - fenofibrate (unii: u202363uos) (fenofibric acid - unii:bgf9mn2hu1) - fenofibrate 48 mg - fenofibrate tablets are indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein cholesterol (ldl-c), total cholesterol (total-c), triglycerides and apolipoprotein b (apo b), and to increase high-density lipoprotein cholesterol (hdl-c) in adult patients with primary hypercholesterolemia or mixed dyslipidemia. fenofibrate tablets are also indicated as adjunctive therapy to diet for treatment of adult patients with severe hypertriglyceridemia. improving glycemic control in diabetic patients showing fasting chylomicronemia will usually obviate the need for pharmacologic intervention. markedly elevated levels of serum triglycerides (e.g., > 2,000 mg/dl) may increase the risk of developing pancreatitis. the effect of fenofibrate therapy on reducing this risk has not been adequately studied. fenofibrate at a dose equivalent to 145 mg of fenofibrate tablets was not shown to reduce coronary heart disease morbidity and mortality in a large, randomized controlled trial of patients with type 2 diabetes mellitus [see warnings and precautions (5.1)] . 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 (5.2)] . - patients with preexisting gallbladder disease [see warnings and precautions (5.5)] . - nursing mothers [see use in specific populations (8.2)]. - patients with known hypersensitivity to fenofibrate or fenofibric acid [see warnings and precautions (5.9)] . risk summary limited available data with fenofibrate use in pregnant women are insufficient to determine a drug associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes. in animal reproduction studies, no evidence of embryo-fetal toxicity was observed with oral administration of fenofibrate in rats and rabbits during organogenesis at doses less than or equivalent to the maximum recommended clinical dose of 145 mg daily, based on body surface area (mg/m2 ). adverse reproductive outcomes occurred at higher doses in the presence of maternal toxicity (see data). fenofibrate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. data animal data 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, no adverse developmental findings were observed at 14 mg/kg/day (less than the clinical exposure at the maximum recommended human dose [mrhd] of 300 mg fenofibrate daily, equivalent to 145 mg fenofibrate daily, based on body surface area comparisons). increased fetal skeletal malformations were observed at maternally toxic doses (361 mg/kg/day, corresponding to 12 times the clinical exposure at the mrhd) that significantly suppressed maternal body weight gain. 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, no adverse developmental findings were observed at 15 mg/kg/day (a dose that approximates the clinical exposure at the mrhd, based on body surface area comparisons). aborted litters were observed at maternally toxic doses (≥ 150 mg/kg/day, corresponding to ≥ 10 times the clinical exposure at the mrhd) that suppressed maternal body weight gain. in pregnant rats given oral dietary doses of 15, 75, and 300 mg/kg/day from gestation day 15 through lactation day 21 (weaning), no adverse developmental effects were observed at 15 mg/kg/day (less than the clinical exposure at the mrhd, based on body surface area comparisons), despite maternal toxicity (decreased weight gain). post-implantation loss was observed at ≥ 75 mg/kg/day (≥ 2 times the clinical exposure at the mrhd) in the presence of maternal toxicity (decreased weight gain). decreased pup survival was noted at 300 mg/kg/day (10 times the clinical exposure at the mrhd), which was associated with decreased maternal body weight gain/maternal neglect. risk summary there is no available information on the presence of fenofibrate in human milk, effects of the drug on the breastfed infant, or the effects on milk production. fenofibrate is present in the milk of rats, and is therefore likely to be present in human milk. because of the potential for serious adverse reactions in breastfed infants, such as disruption of infant lipid metabolism, women should not breastfeed during treatment with fenofibrate and for 5 days after the final dose [see contraindications (4) ] . 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. the use of fenofibrate should be avoided in patients who have severe renal impairment [see contraindications (4)] . dose reduction is required in patients with mild to moderate renal impairment [see dosage and administration (2.4)  and clinical pharmacology (12.3)] . monitoring renal function in patients with renal impairment is recommended. the use of fenofibrate has not been evaluated in subjects with hepatic impairment [see contraindications (4)  and clinical pharmacology (12.3)] .

United States - English - NLM (National Library of Medicine)

amneal pharmaceuticals ny llc - fenofibrate (unii: u202363uos) (fenofibric acid - unii:bgf9mn2hu1) - fenofibrate 54 mg - fenofibrate tablets are indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein cholesterol (ldl-c), total cholesterol (total-c), triglycerides and apolipoprotein b (apo b), and to increase high-density lipoprotein cholesterol (hdl-c) in adult patients with primary hypercholesterolemia or mixed dyslipidemia. fenofibrate tablets are also indicated as adjunctive therapy to diet for treatment of adult patients with severe hypertriglyceridemia. improving glycemic control in diabetic patients showing fasting chylomicronemia will usually obviate the need for pharmacologic intervention. markedly elevated levels of serum triglycerides (e.g., > 2,000 mg/dl) may increase the risk of developing pancreatitis. the effect of fenofibrate therapy on reducing this risk has not been adequately studied. fenofibrate at a dose equivalent to 160 mg of fenofibrate was not shown to reduce coronary heart disease morbidity and mortality in a large, randomized controlled trial of patients with type 2 diabetes mellitus [see warnings and precautions (5.1)] . fenofibrate tablets are 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 (5.2)] . - patients with preexisting gallbladder disease [see warnings and precautions (5.5)] . - nursing mothers [see use in specific populations (8.2)]. - patients with known hypersensitivity to fenofibrate or fenofibric acid [see warnings and precautions (5.9)] . risk summary limited available data with fenofibrate use in pregnant women are insufficient to determine a drug associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes. in animal reproduction studies, no evidence of embryo-fetal toxicity was observed with oral administration of fenofibrate in rats and rabbits during organogenesis at doses less than or equivalent to the maximum recommended clinical dose of 160 mg daily, based on body surface area (mg/m2 ). adverse reproductive outcomes occurred at higher doses in the presence of maternal toxicity (see data). fenofibrate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2% to 4% and 15% to 20%, respectively. data animal data 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, no adverse developmental findings were observed at 14  mg/kg/day (less than the clinical exposure at the maximum recommended human dose [mrhd] of 300 mg fenofibrate daily, equivalent to 160 mg fenofibrate daily, based on body surface area comparisons). increased fetal skeletal malformations were observed at maternally toxic doses (361 mg/kg/day, corresponding to 12 times the clinical exposure at the mrhd) that significantly suppressed maternal body weight gain. 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, no adverse developmental findings were observed at 15 mg/kg/day (a dose that approximates the clinical exposure at the mrhd, based on body surface area comparisons). aborted litters were observed at maternally toxic doses (≥ 150 mg/kg/day, corresponding to ≥ 10 times the clinical exposure at the mrhd) that suppressed maternal body weight gain. in pregnant rats given oral dietary doses of 15, 75, and 300 mg/kg/day from gestation day 15 through lactation day 21 (weaning), no adverse developmental effects were observed at 15 mg/kg/day (less than the clinical exposure at the mrhd, based on body surface area comparisons), despite maternal toxicity (decreased weight gain). post-implantation loss was observed at ≥ 75 mg/kg/day (≥ 2 times the clinical exposure at the mrhd) in the presence of maternal toxicity (decreased weight gain). decreased pup survival was noted at 300 mg/kg/day (10 times the clinical exposure at the mrhd), which was associated with decreased maternal body weight gain/maternal neglect. risk summary there is no available information on the presence of fenofibrate in human milk, effects of the drug on the breastfed infant, or the effects on milk production. fenofibrate is present in the milk of rats, and is therefore likely to be present in human milk. because of the potential for serious adverse reactions in breastfed infants, such as disruption of infant lipid metabolism, women should not breastfeed during treatment with fenofibrate and for 5 days after the final dose [see contraindications (4)] . 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. the use of fenofibrate should be avoided in patients who have severe renal impairment [see contraindications (4)] . dose reduction is required in patients with mild to moderate renal impairment [see dosage and administration (2.4) and clinical pharmacology (12.3)] . monitoring renal function in patients with renal impairment is recommended. the use of fenofibrate has not been evaluated in subjects with hepatic impairment [see contraindications (4) and clinical pharmacology (12.3)] .

United States - English - NLM (National Library of Medicine)

dr. reddy's laboratories limited - fenofibrate (unii: u202363uos) (fenofibric acid - unii:bgf9mn2hu1) - fenofibrate 43 mg - fenofibrate capsules are indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein cholesterol (ldl-c), total cholesterol (total-c), triglycerides (tg), and apolipoprotein b (apo b), and to increase high-density lipoprotein cholesterol (hdl-c) in adult patients with primary hypercholesterolemia or mixed dyslipidemia. fenofibrate capsules are also indicated as adjunctive therapy to diet for treatment of adult patients with severe hypertriglyceridemia. improving glycemic control in diabetic patients showing fasting chylomicronemia will usually reduce fasting triglycerides and eliminate chylomicronemia thereby obviating the need for pharmacologic intervention.   markedly elevated levels of serum triglycerides (e.g > 2,000 mg/dl) may increase the risk of developing pancreatitis. the effect of fenofibrate capsules therapy on reducing this risk has not been adequately studied. fenofibrate capsules were not shown to reduce coronary heart disease morbidity and mortality in patients with type

United States - English - NLM (National Library of Medicine)

mylan pharmaceuticals inc. - fenofibrate (unii: u202363uos) (fenofibric acid - unii:bgf9mn2hu1) - fenofibrate 40 mg - fenofibrate tablets are indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein cholesterol (ldl-c), total cholesterol (total-c), triglycerides (tg), and apolipoprotein b (apo b), and to increase high-density lipoprotein (hdl-c) in adult patients with primary hypercholesterolemia or mixed dyslipidemia. fenofibrate tablets are also indicated as adjunctive therapy to diet for treatment of adult patients with severe hypertriglyceridemia. improving glycemic control in diabetic patients showing fasting chylomicronemia will usually reduce fasting triglycerides and eliminate chylomicronemia thereby obviating the need for pharmacologic intervention. markedly elevated levels of serum triglycerides (e.g., > 2,000 mg/dl) may increase the risk of developing pancreatitis. the effect of fenofibrate tablets therapy on reducing this risk has not been adequately studied. fenofibrate was not shown to reduce coronary heart disease morbidity and mortality in patients with type 2 diabetes mellitus [see warnings and precautions (5.1)] . fenofibrate tablets are contraindicated in: limited available data with fenofibrate use in pregnant women are insufficient to determine a drug-associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes. in animal reproduction studies, no evidence of embryo-fetal toxicity was observed with oral administration of fenofibrate in rats and rabbits during organogenesis at doses less than or equivalent to the maximum recommended clinical dose of 120 mg daily, based on body surface area (mg/m2 ). adverse reproductive outcomes occurred at higher doses in the presence of maternal toxicity [see data] . fenofibrate tablets should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. in the u.s. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2-4% and 15-20%, respectively. in pregnant rats given oral dietary doses of 14, 127, and 361 mg/kg/day from gestation day 6-15 during the period of organogenesis, no adverse developmental findings were observed at 14 mg/kg/day (less than the clinical exposure at the maximum recommended human dose [mrhd] of 300 mg fenofibrate daily, equivalent to 120 mg fenofibrates tablets daily, based on body surface area comparisons). increased fetal skeletal malformations were observed at maternally toxic doses (361 mg/kg/day, corresponding to 12 times the clinical exposure at the mrhd) that significantly suppressed maternal body weight gain. in pregnant rabbits given oral gavage doses of 15, 150, and 300 mg/kg/day from gestation day 6-18 during the period of organogenesis and allowed to deliver, no adverse developmental findings were observed at 15 mg/kg/day (a dose that approximates the clinical exposure at the mrhd, based on body surface area comparisons). aborted litters were observed at maternally toxic doses (≥ 150 mg/kg/day, corresponding to ≥ 10 times the clinical exposure at the mrhd) that suppressed maternal body weight gain. in pregnant rats given oral dietary doses of 15, 75, and 300 mg/kg/day from gestation day 15 through lactation day 21 (weaning), no adverse developmental effects were observed at 15 mg/kg/day (less than the clinical exposure at the mrhd, based on body surface area comparisons), despite maternal toxicity (decreased weight gain). post-implantation loss was observed at ≥ 75 mg/kg/day (≥ 2 times the clinical exposure at the mrhd) in the presence of maternal toxicity (decreased weight gain). decreased pup survival was noted at 300 mg/kg/day (10 times the clinical exposure at the mrhd), which was associated with decreased maternal body weight gain/maternal neglect. there is no available information on the presence of fenofibrate in human milk, effects of the drug on the breastfed infant, or the effects on milk production. fenofibrate is present in the milk of rats, and is therefore likely to be present in human milk. because of the potential for serious adverse reactions in breastfed infants, such as disruption of infant lipid metabolism, women should not breastfeed during treatment with fenofibrate tablets and for 5 days after the final dose [see contraindications (4)] . safety and efficacy 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 tablets. the use of fenofibrate tablets should be avoided in patients with severe renal impairment [see contraindications (4)] . dose reduction is required in patients with mild to moderate renal impairment [see dosage and administration (2.4) and clinical pharmacology (12.3)] . monitoring renal function in patients with renal impairment is recommended. the use of fenofibrate tablets has not been evaluated in subjects with hepatic impairment [see contraindications (4) and clinical pharmacology (12.3)] .

United States - English - NLM (National Library of Medicine)

mylan pharmaceuticals inc. - fenofibrate (unii: u202363uos) (fenofibric acid - unii:bgf9mn2hu1) - fenofibrate 54 mg - fenofibrate tablets are indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein cholesterol (ldl-c), total cholesterol (total-c), triglycerides and apolipoprotein b (apo b), and to increase high-density lipoprotein cholesterol (hdl-c) in adult patients with primary hypercholesterolemia or mixed dyslipidemia. fenofibrate tablets are also indicated as adjunctive therapy to diet for treatment of adult patients with severe hypertriglyceridemia. improving glycemic control in diabetic patients showing fasting chylomicronemia will usually obviate the need for pharmacologic intervention. markedly elevated levels of serum triglycerides (e.g., > 2,000 mg/dl) may increase the risk of developing pancreatitis. the effect of fenofibrate therapy on reducing this risk has not been adequately studied. fenofibrate at a dose equivalent to 160 mg of fenofibrate tablets was not shown to reduce coronary heart disease morbidity and mortality in a large, randomized controlled trial of patients with type 2

United States - English - NLM (National Library of Medicine)

sun pharmaceutical industries, inc. - fenofibrate (unii: u202363uos) (fenofibric acid - unii:bgf9mn2hu1) - fenofibrate 43 mg - fenofibrate capsules, usp are indicated as adjunctive therapy to diet to reduce elevated low-density lipoprotein cholesterol (ldl-c), total cholesterol (total-c), triglycerides (tg), and apolipoprotein b (apo b), and to increase high-density lipoprotein cholesterol (hdl-c) in adult patients with primary hypercholesterolemia or mixed dyslipidemia. fenofibrate capsules, usp are also indicated as adjunctive therapy to diet for treatment of adult patients with severe hypertriglyceridemia. improving glycemic control in diabetic patients showing fasting chylomicronemia will usually reduce fasting triglycerides and eliminate chylomicronemia thereby obviating the need for pharmacologic intervention. markedly elevated levels of serum triglycerides (e.g > 2,000 mg/dl) may increase the risk of developing pancreatitis. the effect of fenofibrate therapy on reducing this risk has not been adequately studied. fenofibrate was not shown to reduce coronary heart disease morbidity and mortality in patients with type 2 diabetes