Ireland - English - HPRA (Health Products Regulatory Authority)

sanofi-aventis ireland limited t/a sanofi - rosuvastatin; ezetimibe - film-coated tablet - 10/10 mg/mg - rosuvastatin and ezetimibe

Ireland - English - HPRA (Health Products Regulatory Authority)

sanofi-aventis ireland limited t/a sanofi - rosuvastatin; ezetimibe - film-coated tablet - 20/10 mg/mg - rosuvastatin and ezetimibe

Ireland - English - HPRA (Health Products Regulatory Authority)

sanofi-aventis ireland limited t/a sanofi - rosuvastatin; ezetimibe - film-coated tablet - 40/10 milligram(s) - rosuvastatin and ezetimibe

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

remedyrepack inc. - rosuvastatin calcium (unii: 83mvu38m7q) (rosuvastatin - unii:413kh5zj73) - rosuvastatin 20 mg - rosuvastatin calcium tablets are indicated as an adjunct to diet to: ●       reduce ldl-c, total-c, non-hdl-c and apo-b in children and adolescents 7 to 17 years of age with homozygous familial hypercholesterolemia, either alone or with other lipid-lowering treatments (e.g., ldl apheresis). pediatric use information for patients ages 8 to less than 10 years is approved for astrazeneca’s crestor (rosuvastatin calcium) tablets. however, due to astrazeneca’s marketing exclusivity rights, this drug product is not labeled with that pediatric information. rosuvastatin calcium tablets are indicated as adjunctive therapy to diet for the treatment of adult patients with hypertriglyceridemia. rosuvastatin calcium tablets are indicated as an adjunct to diet for the treatment of adult patients with primary dysbetalipoproteinemia (type iii hyperlipoproteinemia). rosuvastatin calcium tablets are indicated as adjunctive therapy to other lipid-lowering treatments (e.g., ldl apheresis) or alone if such treatments are unavaila

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

american health packaging - rosuvastatin calcium (unii: 83mvu38m7q) (rosuvastatin - unii:413kh5zj73) - rosuvastatin 5 mg - rosuvastatin tablets are indicated as adjunctive therapy to diet to reduce elevated total-c, ldl-c, apob, nonhdl-c, and triglycerides and to increase hdl-c in adult patients with primary hyperlipidemia or mixed dyslipidemia. lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and nonpharmacological interventions alone has been inadequate. rosuvastatin tablets are indicated as an adjunct to diet to: - reduce total-c, ldl-c and apob levels in children and adolescents 8 to 17 years of age with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: ldl-c >190 mg/dl, or >160 mg/dl along with a positive family history of premature cardiovascular disease (cvd) or two or more other cvd risk factors. pediatric use information for patients 7 to 17 years of age is approved for astrazeneca’s crestor (rosuvastatin calcium) tablets. however, due to astrazeneca’s marketing exclusivity r

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

glenmark pharmaceutials inc., usa - rosuvastatin calcium (unii: 83mvu38m7q) (rosuvastatin - unii:413kh5zj73) - rosuvastatin 5 mg - rosuvastatin tablets are indicated: rosuvastatin tablets are contraindicated in the following conditions: risk summary discontinue rosuvastatin when pregnancy is recognized. alternatively, consider the ongoing therapeutic needs of the individual patient. rosuvastatin decreases synthesis of cholesterol and possibly other biologically active substances derived from cholesterol; therefore, rosuvastatin may cause fetal harm when administered to pregnant patients based on the mechanism of action [see clinical pharmacology ( 12.1)]. in addition, treatment of hyperlipidemia is not generally necessary during pregnancy. atherosclerosis is a chronic process and the discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hyperlipidemia for most patients. available data from case series and prospective and retrospective observational cohort studies over decades of use with statins in pregnant women have not identified a drug-associated risk of maj

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

rising pharma holdings, inc. - rosuvastatin calcium (unii: 83mvu38m7q) (rosuvastatin - unii:413kh5zj73) - rosuvastatin 5 mg - rosuvastatin tablets are indicated: - to reduce the risk of stroke, myocardial infarction, and arterial revascularization procedures in adults without established coronary heart disease who are at increased risk of cardiovascular (cv) disease based on age, hscrp ≥2 mg/l, and at least one additional cv risk factor. - as an adjunct to diet to: reduce ldl-c in adults with primary hyperlipidemia. reduce low-density lipoprotein cholesterol (ldl-c) and slow the progression of atherosclerosis in adults. reduce ldl-c in adults and pediatric patients aged 8 years and older with heterozygous familial hypercholesterolemia (hefh). - reduce ldl-c in adults with primary hyperlipidemia. - reduce low-density lipoprotein cholesterol (ldl-c) and slow the progression of atherosclerosis in adults. - reduce ldl-c in adults and pediatric patients aged 8 years and older with heterozygous familial hypercholesterolemia (hefh). -  as an adjunct to other ldl-c-lowering therapies, or alone if such treatments are unavailable, to reduce ldl-c in adults and pediatric patients aged 7 years and older with homozygous familial hypercholesterolemia (hofh). - as an adjunct to diet for the treatment of adults with: primary dysbetalipoproteinemia. hypertriglyceridemia. - primary dysbetalipoproteinemia. - hypertriglyceridemia. rosuvastatin tablets are contraindicated in the following conditions: - acute liver failure or decompensated cirrhosis [see warnings and precautions (5.3)]. - hypersensitivity to rosuvastatin or any excipients in rosuvastatin tablets. hypersensitivity reactions including rash, pruritus, urticaria, and angioedema have been reported with rosuvastatin [see adverse reactions (6.1)] . risk summary discontinue rosuvastatin when pregnancy is recognized. alternatively, consider the ongoing therapeutic needs of the individual patient. rosuvastatin decreases synthesis of cholesterol and possibly other biologically active substances derived from cholesterol; therefore, rosuvastatin may cause fetal harm when administered to pregnant patients based on the mechanism of action [see clinical pharmacology (12.1)]. in addition, treatment of hyperlipidemia is not generally necessary during pregnancy. atherosclerosis is a chronic process and the discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hyperlipidemia for most patients. available data from case series and prospective and retrospective observational cohort studies over decades of use with statins in pregnant women have not identified a drug-associated risk of major congenital malformations. published data from prospective and retrospective observational cohort studies with rosuvastatin use in pregnant women are insufficient to determine if there is a drug-associated risk of miscarriage (see data) . in animal reproduction studies, no adverse developmental effects were observed in pregnant rats or rabbits orally administered rosuvastatin during the period of organogenesis at doses that resulted in systemic exposures equivalent to human exposures at the maximum recommended human dose (mrhd) of 40 mg/day, based on auc and body surface area (mg/m2 ), respectively (see data) . 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   human data a medicaid cohort linkage study of 1152 statin-exposed pregnant women compared to 886,996 controls did not find a significant teratogenic effect from maternal use of statins in the first trimester of pregnancy, after adjusting for potential confounders – including maternal age, diabetes mellitus, hypertension, obesity, and alcohol and tobacco use – using propensity score-based methods. the relative risk of congenital malformations between the group with statin use and the group with no statin use in the first trimester was 1.07 (95% confidence interval 0.85 to 1.37) after controlling for confounders, particularly pre-existing diabetes mellitus. there were also no statistically significant increases in any of the organ-specific malformations assessed after accounting for confounders. in the majority of pregnancies, statin treatment was initiated prior to pregnancy and was discontinued at some point in the first trimester when pregnancy was identified. study limitations include reliance on physician coding to define the presence of a malformation, lack of control for certain confounders such as body mass index, use of prescription dispensing as verification for the use of a statin, and lack of information on non-live births. animal data in female rats given 5, 15 and 50 mg/kg/day before mating and continuing through to gestation day 7 resulted in decreased fetal body weight (female pups) and delayed ossification at 50 mg/kg/day (10 times the human exposure at the mrhd dose of 40 mg/day based on auc). in pregnant rats given 2, 10 and 50 mg/kg/day of rosuvastatin from gestation day 7 through lactation day 21 (weaning), decreased pup survival occurred at 50 mg/kg/day (dose equivalent to 12 times the mrhd of 40 mg/day based body surface area). in pregnant rabbits given 0.3, 1, and 3 mg/kg/day of rosuvastatin from gestation day 6 to day 18, decreased fetal viability and maternal mortality was observed at 3 mg/kg/day (dose equivalent to the mrhd of 40 mg/day based on body surface area). rosuvastatin crosses the placenta in rats and rabbits and is found in fetal tissue and amniotic fluid at 3% and 20%, respectively, of the maternal plasma concentration following a single 25 mg/kg oral gavage dose on gestation day 16 in rats. in rabbits, fetal tissue distribution was 25% of maternal plasma concentration after a single oral gavage dose of 1 mg/kg on gestation day 18.   risk summary limited data from case reports in published literature indicate that rosuvastatin is present in human milk. there is no available information on the effects of the drug on the breastfed infant or the effects of the drug on milk production. statins, including rosuvastatin, decrease cholesterol synthesis and possibly the synthesis of other biologically active substances derived from cholesterol and may cause harm to the breastfed infant. because of the potential for serious adverse reactions in a breastfed infant, based on the mechanism of action, advise patients that breastfeeding is not recommended during treatment with rosuvastatin [ see use in specific populations (8.1) and clinical pharmacology (12.1)] . the safety and effectiveness of rosuvastatin as an adjunct to diet to reduce ldl-c have been established in pediatric patients 8 years of age and older with hefh. use of rosuvastatin for this indication is based on one 12-week controlled trial with a 40-week open-label extension period in 176 pediatric patients 10 years of age and older with hefh and one 2-year open-label, uncontrolled trial in 175 pediatric patients 8 years of age and older with hefh [ see clinical studies (14)] . in the 1-year trial with a 12-week controlled phase, there was no detectable effect of rosuvastatin on growth, weight, bmi (body mass index), or sexual maturation in patients aged 10 to 17 years. the safety and effectiveness of rosuvastatin as an adjunct to other ldl-c-lowering therapies to reduce ldl-c have been established pediatric patients 7 years of age and older with hofh. use of rosuvastatin for this indication is based on a randomized, placebo-controlled, cross-over study in 14 pediatric patients 7 years of age and older with hofh [ see clinical studies (14)] . the safety and effectiveness of rosuvastatin have not been established in pediatric patients younger than 8 years of age with hefh, younger than 7 years of age with hofh, or in pediatric patients with other types of hyperlipidemia (other than hefh or hofh). of the total number of rosuvastatin-treated patients in clinical studies, 3159 (31%) were 65 years and older, and 698 (6.8%) were 75 years and older. no overall differences in safety or effectiveness were observed between these subjects and younger subjects. advanced age (≥65 years) is a risk factor for rosuvastatin-associated myopathy and rhabdomyolysis. dose selection for an elderly patient should be cautious, recognizing the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy and the higher risk of myopathy. monitor geriatric patients receiving rosuvastatin for the increased risk of myopathy [see warnings and precautions (5.1)]. rosuvastatin exposure is not influenced by mild to moderate renal impairment (clcr ≥30 ml/min/1.73 m2 ). exposure to rosuvastatin is increased to a clinically significant extent in patients with severe renal impairment (clcr <30 ml/min/1.73 m2 ) who are not receiving hemodialysis [see clinical pharmacology (12.3)] . renal impairment is a risk factor for myopathy and rhabdomyolysis. monitor all patients with renal impairment for development of myopathy. in patients with severe renal impairment not on hemodialysis, the recommended starting dosage is 5 mg daily and should not exceed 10 mg daily [see  dosage and administration (2.5) and warnings and precautions (5.1)]. rosuvastatin is contraindicated in patients with acute liver failure or decompensated cirrhosis. chronic alcohol liver disease is known to increase rosuvastatin exposure. patients who consume substantial quantities of alcohol and/or have a history of liver disease may be at increased risk for hepatic injury [see contraindications (4), warning and precautions (5.3) and clinical pharmacology (12.3)]. pharmacokinetic studies have demonstrated an approximate 2-fold increase in median exposure to rosuvastatin in asian subjects when compared with white controls. adjust the rosuvastatin dosage in asian patients [see dosage and administration (2.4) and clinical pharmacology (12.3)] .

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

ascend laboratories, llc - rosuvastatin calcium (unii: 83mvu38m7q) (rosuvastatin - unii:413kh5zj73) - rosuvastatin 5 mg - rosuvastatin tablets is indicated:  • to reduce the risk of stroke, myocardial infarction, and arterial revascularization procedures in adults without established coronary heart disease who are at increased risk of cardiovascular (cv) disease based on age, hscrp ≥2 mg/l, and at least one additional cv risk factor.  • as an adjunct to diet to:  o reduce ldl-c in adults with primary hyperlipidemia.  o reduce low-density lipoprotein cholesterol (ldl-c) and slow the progression of atherosclerosis in adults.  o reduce ldl-c in adults and pediatric patients aged 8 years and older with heterozygous familial hypercholesterolemia (hefh).  •      as an adjunct to other ldl-c-lowering therapies, or alone if such treatments are unavailable, to reduce ldl-c in adults and pediatric patients aged 7 years and older with homozygous familial hypercholesterolemia (hofh). • as an adjunct to diet for the treatment of adults with:  o primary dysbetalipoproteinemia.  o hypertriglyceridemia. rosuvastatin tablets is contraindicated in the following conditions: - acute liver failure or decompensated cirrhosis [see warnings and precautions (5.3)]. - hypersensitivity to rosuvastatin or any excipients in rosuvastatin tablets. hypersensitivity reactions including rash, pruritus, urticaria, and angioedema have been reported with rosuvastatin tablets [see adverse reactions (6.1)].   risk summary discontinue rosuvastatin tablets when pregnancy is  recognized. alternatively, consider the ongoing therapeutic needs of the individual patient. rosuvastatin tablets decreases synthesis of cholesterol and possibly other biologically active substances derived from cholesterol; therefore, rosuvastatin tablets may cause fetal harm when administered to pregnant patients based on the mechanism of action [ see clinical pharmacology (12.1)]. in addition, treatment of hyperlipidemia is not generally necessary during pregnancy. atherosclerosis is a chronic process and the discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hyperlipidemia for most patients. available data from case series and prospective and retrospective observational cohort studies over decades of use with statins in pregnant women have not identified a drug-associated risk of major congenital malformations. published data from prospective and retrospective observational cohort studies with rosuvastatin tablets use in pregnant women are insufficient to determine if there is a drug-associated risk of miscarriage (see data) . in animal reproduction studies, no adverse developmental effects were observed in pregnant rats or rabbits orally administered rosuvastatin during the period of organogenesis at doses that resulted in systemic exposures equivalent to human exposures at the maximum recommended human dose (mrhd) of 40 mg/day, based on auc and body surface area (mg/m2 ), respectively (see data) . 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 human data a medicaid cohort linkage study of 1152 statin-exposed pregnant women compared to 886,996 controls did not find a significant teratogenic effect from maternal use of statins in the first trimester of pregnancy, after adjusting for potential confounders – including maternal age, diabetes mellitus, hypertension, obesity, and alcohol and tobacco use – using propensity score-based methods. the relative risk of congenital malformations between the group with statin use and the group with no statin use in the first trimester was 1.07 (95% confidence interval 0.85 to 1.37) after controlling for confounders, particularly pre-existing diabetes mellitus. there were also no statistically significant increases in any of the organ-specific malformations assessed after accounting for confounders. in the majority of pregnancies, statin treatment was initiated prior to pregnancy and was discontinued at some point in the first trimester when pregnancy was identified. study limitations include reliance on physician coding to define the presence of a malformation, lack of control for certain confounders such as body mass index, use of prescription dispensing as verification for the use of a statin, and lack of information on non-live births.   animal data in female rats given 5, 15 and 50 mg/kg/day before mating and continuing through to gestation day 7 resulted in decreased fetal body weight (female pups) and delayed ossification at 50 mg/kg/day (10 times the human exposure at the mrhd dose of 40 mg/day based on auc). in pregnant rats given 2, 10 and 50 mg/kg/day of rosuvastatin from gestation day 7 through lactation day 21 (weaning), decreased pup survival occurred at 50 mg/kg/day (dose equivalent to 12 times the mrhd of 40 mg/day based body surface area). in pregnant rabbits given 0.3, 1, and 3 mg/kg/day of rosuvastatin from gestation day 6 to day 18, decreased fetal viability and maternal mortality was observed at 3 mg/kg/day (dose equivalent to the mrhd of 40 mg/day based on body surface area). rosuvastatin crosses the placenta in rats and rabbits and is found in fetal tissue and amniotic fluid at 3% and 20%, respectively, of the maternal plasma concentration following a single 25 mg/kg oral gavage dose on gestation day 16 in rats. in rabbits, fetal tissue distribution was 25% of maternal plasma concentration after a single oral gavage dose of 1 mg/kg on gestation day 18. risk summary limited data from case reports in published literature indicate that rosuvastatin tablets is present in human milk. there is no available information on the effects of the drug on the breastfed infant or the effects of the drug on milk production. statins, including rosuvastatin tablets, decrease cholesterol synthesis and possibly the synthesis of other biologically active substances derived from cholesterol and may cause harm to the breastfed infant. because of the potential for serious adverse reactions in a breastfed infant, based on the mechanism of action, advise patients that breastfeeding is not recommended during treatment with rosuvastatin tablets [see use in specific populations (8.1) and clinical pharmacology (12.1)]. the safety and effectiveness of rosuvastatin tablets as an adjunct to diet to reduce ldl-c have been established in pediatric patients 8 years of age and older with hefh. use of rosuvastatin tablets for this indication is based on one 12-week controlled trial with a 40-week open-label extension period in 176 pediatric patients 10 years of age and older with hefh and one 2-year open-label, uncontrolled trial in 175 pediatric patients 8 years of age and older with hefh [see clinical studies (14)]. in the 1-year trial with a 12-week controlled phase, there was no detectable effect of rosuvastatin tablets on growth, weight, bmi (body mass index), or sexual maturation in patients aged 10 to 17 years. the safety and effectiveness of rosuvastatin tablets as an adjunct to other ldl-c-lowering therapies to reduce ldl-c have been established pediatric patients 7 years of age and older with hofh. use of rosuvastatin tablets for this indication is based on a randomized, placebo-controlled, cross-over study in 14 pediatric patients 7 years of age and older with hofh [see clinical studies (14)]. the safety and effectiveness of rosuvastatin tablets have not been established in pediatric patients younger than 8 years of age with hefh, younger than 7 years of age with hofh, or in pediatric patients with other types of hyperlipidemia (other than hefh or hofh). of the total number of rosuvastatin tablets-treated patients in clinical studies, 3159 (31%) were 65 years and older, and 698 (6.8%) were 75 years and older. no overall differences in safety or effectiveness were observed between these subjects and younger subjects. advanced age (≥65 years) is a risk factor for rosuvastatin tablets-associated myopathy and rhabdomyolysis. dose selection for an elderly patient should be cautious, recognizing the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy and the higher risk of myopathy. monitor geriatric patients receiving rosuvastatin tablets for the increased risk of myopathy [see warnings and precautions (5.1)]. rosuvastatin exposure is not influenced by mild to moderate renal impairment (clcr ≥30 ml/min/1.73 m2 ). exposure to rosuvastatin is increased to a clinically significant extent in patients with severe renal impairment (clcr <30 ml/min/1.73 m2 ) who are not receiving hemodialysis [see clinical pharmacology (12.3)]. renal impairment is a risk factor for myopathy and rhabdomyolysis. monitor all patients with renal impairment for development of myopathy. in patients with severe renal impairment not on hemodialysis, the recommended starting dosage is 5 mg daily and should not exceed 10 mg daily [see dosage and administration (2.5) and warnings and precautions (5.1)]. rosuvastatin tablets is contraindicated in patients with acute liver failure or decompensated cirrhosis. chronic alcohol liver disease is known to increase rosuvastatin exposure. patients who consume substantial quantities of alcohol and/or have a history of liver disease may be at increased risk for hepatic injury [see contraindications (4), warning and precautions (5.3) and clinical pharmacology (12.3)]. pharmacokinetic studies have demonstrated an approximate 2-fold increase in median exposure to rosuvastatin in asian subjects when compared with white controls. adjust the rosuvastatin tablets dosage in asian patients [see dosage and administration (2.4) and clinical pharmacology (12.3)].

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

major pharmaceuticals - rosuvastatin calcium (unii: 83mvu38m7q) (rosuvastatin - unii:413kh5zj73) - rosuvastatin 5 mg - rosuvastatin calcium tablets are indicated as an adjunct to diet to: pediatric use information for patients ages 8 to less than 10 years is approved for astrazeneca’s crestor (rosuvastatin calcium) tablets. however, due to astrazeneca’s marketing exclusivity rights, this drug product is not labeled with that pediatric information. rosuvastatin calcium tablets are indicated as adjunctive therapy to diet for the treatment of adult patients with hypertriglyceridemia. rosuvastatin calcium tablets are indicated as an adjunct to diet for the treatment of adult patients with primary dysbetalipoproteinemia (type iii hyperlipoproteinemia). rosuvastatin calcium tablets are indicated as adjunctive therapy to other lipid-lowering treatments (e.g., ldl apheresis) or alone if such treatments are unavailable to reduce ldl-c, total-c, and apob in adult patients with homozygous familial hypercholesterolemia. rosuvastatin calcium tablets have not been studied in fredrickson type i and v dyslipidemias. rosuvastatin calcium tabl

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

sun pharmaceutical industries, inc. - rosuvastatin calcium (unii: 83mvu38m7q) (rosuvastatin - unii:413kh5zj73) - rosuvastatin 5 mg - rosuvastatin tablets are indicated: •           to reduce the risk of stroke, myocardial infarction, and arterial revascularization procedures in adults without established coronary heart disease who are at increased risk of cardiovascular (cv) disease based on age, hscrp ≥2 mg/l, and at least one additional cv risk factor. •           as an adjunct to diet to: o   reduce ldl-c in adults with primary hyperlipidemia. o   reduce low-density lipoprotein cholesterol (ldl-c) and slow the progression of atherosclerosis in adults. o   reduce ldl-c in adults and pediatric patients aged 8 years and older with heterozygous familial hypercholesterolemia (hefh). •    as an adjunct to other ldl-c-lowering therapies, or alone if such treatments are unavailable, to reduce ldl-c in adults and pediatric patients aged 7 years and older with homozygous familial hypercholesterolemia (hofh). - as an adjunct to diet for the treatment of adults with: o      primary dysbetalipoproteinemia. o      hypertriglyceridemia. rosuvastatin i