パキスタン - 英語 - Zafa Pharmaceutical

zafa pharmaceutical - tablets - ranitidine 150mg - h2 receptor blocker

アメリカ合衆国 - 英語 - NLM (National Library of Medicine)

ingenus pharmaceuticals, llc - quinine sulfate (unii: kf7z0e0q2b) (quinine - unii:a7v27phc7a) - quinine sulfate 324 mg - quinine sulfate capsules, usp is an antimalarial drug indicated only for treatment of uncomplicated plasmodium falciparum malaria. quinine sulfate has been shown to be effective in geographical regions where resistance to chloroquine has been documented [see clinical studies (14)].   limitations of use: quinine sulfate is not approved for: - treatment of severe or complicated p. falciparum malaria. - prevention of malaria. - treatment or prevention of nocturnal leg cramps [see warnings and precautions (5.1)]. quinine sulfate is contraindicated in patients with the following: - prolonged qt interval. one case of a fatal ventricular arrhythmia was reported in an elderly patient with a prolonged qt interval at baseline, who received quinine sulfate intravenously for p. falciparum malaria [see warnings and precautions (5.4) ]. - known hypersensitivity reactions to quinine. these include, but are not limited to, the following [see warnings and precautions (5.

アメリカ合衆国 - 英語 - NLM (National Library of Medicine)

aidarex pharmaceuticals llc - glimepiride (unii: 6ky687524k) (glimepiride - unii:6ky687524k) - glimepiride tablets usp are indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus [see clinical studies ( 14.1)]. glimepiride tablets usp should not be used for the treatment of type 1 diabetes mellitus or diabetic ketoacidosis, as it would not be effective in these settings. glimepiride tablet is contraindicated in patients with a history of a hypersensitivity reaction to: - glimepiride or any of the product’s ingredients [see warnings and precautions ( 5.2)]. sulfonamide derivatives: patients who have developed an allergic reaction to sulfonamide derivatives may develop an allergic reaction to glimepiride. do not use glimepiride in patients who have a history of an allergic reaction to sulfonamide derivatives. reported hypersensitivity reactions include cutaneous eruptions with or without pruritus as well as more serious reactions (e.g. anaphylaxis, angioedema, stevens-johnson syndrome, dys

アメリカ合衆国 - 英語 - NLM (National Library of Medicine)

novitium pharma llc - ranitidine hydrochloride (unii: bk76465ihm) (ranitidine - unii:884kt10yb7) - ranitidine is indicated in: - short-term treatment of active duodenal ulcer. most patients heal within 4 weeks. studies available to date have not assessed the safety of ranitidine in uncomplicated duodenal ulcer for periods of more than 8 weeks. - maintenance therapy for duodenal ulcer patients at reduced dosage after healing of acute ulcers. no placebo-controlled comparative studies have been carried out for periods of longer than 1 year. - the treatment of pathological hypersecretory conditions (e.g., zollinger-ellison syndrome and systemic mastocytosis). - short-term treatment of active, benign gastric ulcer. most patients heal within 6 weeks and the usefulness of further treatment has not been demonstrated. studies available to date have not assessed the safety of ranitidine in uncomplicated, benign gastric ulcer for periods of more than 6 weeks. - maintenance therapy for gastric ulcer patients at reduced dosage after healing of acute ulcers. placebo-controlled studies have been carried out for 1 year. -

アメリカ合衆国 - 英語 - NLM (National Library of Medicine)

burel pharmaceuticals, llc - ketoconazole (unii: r9400w927i) (ketoconazole - unii:r9400w927i) - ketoconazole tablets are not indicated for treatment of onychomycosis, cutaneous dermatophyte infections, or candida infections. ketoconazole tablets should be used only when other effective antifungal therapy is not available or tolerated and the potential benefits are considered to outweigh the potential risks. ketoconazole tablets are indicated for the treatment of the following systemic fungal infections in patients who have failed or who are intolerant to other therapies: blastomycosis, coccidioidomycosis, histoplasmosis, chromomycosis, and paracoccidioidomycosis. ketoconazole tablets should not be used for fungal meningitis because it penetrates poorly into the cerebrospinal fluid. coadministration of a number of cyp3a4 substrates such as dofetilide, quinidine cisapride and pimozide is contraindicated with ketoconazole tablets. coadministration with ketoconazole can cause elevated plasma concentrations of these drugs and may increase or prolong both therapeutic and adverse effects to such an extent that

アメリカ合衆国 - 英語 - NLM (National Library of Medicine)

northwind pharmaceuticals, llc - glipizide (unii: x7wdt95n5c) (glipizide - unii:x7wdt95n5c) - glipizide xl is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. glipizide xl is not recommended for the treatment of type 1 diabetes mellitus or diabetic ketoacidosis. glipizide is contraindicated in patients with: - known hypersensitivity to glipizide or any of the product's ingredients. - hypersensitivity to sulfonamide derivatives. risk summary available data from a small number of published studies and postmarketing experience with glipizide xl use in pregnancy over decades have not identified any drug associated risks for major birth defects, miscarriage, or adverse maternal outcomes. however, sulfonylureas (including glipizide) cross the placenta and have been associated with neonatal adverse reactions such as hypoglycemia. therefore, glipizide xl should be discontinued at least two weeks before expected delivery (see clinical considerations). poorly controlled diabetes in pregnancy is also associated with risks to the mother and fetus (see clinical considerations). in animal studies, there were no effects on embryofetal development following administration of glipizide to pregnant rats and rabbits during organogenesis at doses 833 times and 8 times the human dose based on body surface area, respectively. however, increased pup mortality was observed in rats administered glipizide from gestation day 15 throughout lactation at doses 2 times the maximum human dose based on body surface area (see data) . the estimated background risk of major birth defects is 6–10% in women with pre-gestational diabetes with a hba1c >7 and has been reported to be as high as 20–25% in women with hba1c >10. the estimated background risk of 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. clinical considerations disease-associated maternal and/or embryo/fetal risk poorly-controlled diabetes in pregnancy increases the maternal risk for diabetic ketoacidosis, pre-eclampsia, miscarriage, preterm delivery, stillbirth, and delivery complications. poorly controlled diabetes increases the fetal risk for major birth defects, stillbirth, and macrosomia related morbidity. fetal/neonatal adverse reactions neonates of women with gestational diabetes who are treated with sulfonylureas during pregnancy may be at increased risk for neonatal intensive care admission and may develop respiratory distress, hypoglycemia, birth injury, and be large for gestational age. prolonged severe hypoglycemia, lasting 4–10 days, has been reported in neonates born to mothers receiving a sulfonylurea at the time of delivery and has been reported with the use of agents with a prolonged half-life. observe newborns for symptoms of hypoglycemia and respiratory distress and manage accordingly. dose adjustments during pregnancy and the postpartum period due to reports of prolonged severe hypoglycemia in neonates born to mothers receiving a sulfonylurea at the time of delivery, glipizide xl should be discontinued at least two weeks before expected delivery (see fetal/neonatal adverse reactions) . data animal data in teratology studies in rats and rabbits, pregnant animals received daily oral doses of glipizide during the period of organogenesis at doses up to 2000 mg/kg/day and 10 mg/kg/day (approximately 833 and 8 times the human dose based on body surface area), respectively. there were no adverse effects on embryo-fetal development at any of the doses tested. in a peri- and postnatal study in pregnant rats, there was a reduced number of pups born alive following administration of glipizide from gestation day 15 throughout lactation through weaning at doses ≥5 mg/kg/day (about 2 times the recommended maximum human dose based on body surface area). risk summary breastfed infants of lactating women using glipizide xl should be monitored for symptoms of hypoglycemia (see clinical considerations) . although glipizide was undetectable in human milk in one small clinical lactation study; this result is not conclusive because of the limitations of the assay used in the study. there are no data on the effects of glipizide on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for glipizide xl and any potential adverse effects on the breastfed child from glipizide xl or from the underlying maternal condition. clinical considerations monitoring for adverse reactions monitor breastfed infants for signs of hypoglycemia (e.g., jitters, cyanosis, apnea, hypothermia, excessive sleepiness, poor feeding, seizures). safety and effectiveness in children have not been established. there were no overall differences in effectiveness or safety between younger and older patients, but greater sensitivity of some individuals cannot be ruled out. elderly patients are particularly susceptible to the hypoglycemic action of anti-diabetic agents. hypoglycemia may be difficult to recognize in these patients. therefore, dosing should be conservative to avoid hypoglycemia [see dosage and administration (2.1), warnings and precautions (5.1) and clinical pharmacology (12.3)] . there is no information regarding the effects of hepatic impairment on the disposition of glipizide. however, since glipizide is highly protein bound and hepatic biotransformation is the predominant route of elimination, the pharmacokinetics and/or pharmacodynamics of glipizide may be altered in patients with hepatic impairment. if hypoglycemia occurs in such patients, it may be prolonged and appropriate management should be instituted [see dosage and administration (2.1), warnings and precautions (5.1) and clinical pharmacology (12.3)] .

アメリカ合衆国 - 英語 - NLM (National Library of Medicine)

northwind pharmaceuticals, llc - glipizide (unii: x7wdt95n5c) (glipizide - unii:x7wdt95n5c) - glipizide extended-release tablets are indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. glipizide extended-release tablets are not recommended for the treatment of type 1 diabetes mellitus or diabetic ketoacidosis. glipizide is contraindicated in patients with: - known hypersensitivity to glipizide or any of the product’s ingredients. - hypersensitivity to sulfonamide derivatives. risk summary available data from a small number of published studies and postmarketing experience with glipizide extended-release tablets use in pregnancy over decades have not identified any drug associated risks for major birth defects, miscarriage, or adverse maternal outcomes. however, sulfonylureas (including glipizide) cross the placenta and have been associated with neonatal adverse reactions such as hypoglycemia. therefore, glipizide extended-release tablets should be discontinued at least two weeks before expected delivery ( see clinical considerations ). poorly controlled diabetes in pregnancy is also associated with risks to the mother and fetus ( see clinical considerations ). in animal studies, there were no effects on embryofetal development following administration of glipizide to pregnant rats and rabbits during organogenesis at doses 833 times and 8 times the human dose based on body surface area, respectively. however, increased pup mortality was observed in rats administered glipizide from gestation day 15 throughout lactation at doses 2 times the maximum human dose based on body surface area ( see data ). the estimated background risk of major birth defects is 6-10% in women with pre-gestational diabetes with a hba1c >7 and has been reported to be as high as 20-25% in women with hba1c >10. the estimated background risk of 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.    clinical considerations     disease-associated maternal and/or embryo/fetal risk poorly-controlled diabetes in pregnancy increases the maternal risk for diabetic ketoacidosis, pre-eclampsia, miscarriage, preterm delivery, stillbirth, and delivery complications. poorly controlled diabetes increases the fetal risk for major birth defects, stillbirth, and macrosomia related morbidity. fetal/neonatal adverse reactions     neonates of women with gestational diabetes who are treated with sulfonylureas during pregnancy may be at increased risk for neonatal intensive care admission and may develop respiratory distress, hypoglycemia, birth injury, and be large for gestational age. prolonged severe hypoglycemia, lasting 4-10 days, has been reported in neonates born to mothers receiving a sulfonylurea at the time of delivery and has been reported with the use of agents with a prolonged half-life. observe newborns for symptoms of hypoglycemia and respiratory distress and manage accordingly.   dose adjustments during pregnancy and the postpartum period due to reports of prolonged severe hypoglycemia in neonates born to mothers receiving a sulfonylurea at the time of delivery, glipizide extended-release tablets should be discontinued at least two weeks before expected delivery ( see fetal/neonatal adverse reactions ). data   animal data in teratology studies in rats and rabbits, pregnant animals received daily oral doses of glipizide during the period of organogenesis at doses up to 2000 mg/kg/day and 10 mg/kg/day (approximately 833 and 8 times the human dose based on body surface area), respectively. there were no adverse effects on embryo-fetal development at any of the doses tested. in a peri-and postnatal study in pregnant rats, there was a reduced number of pups born alive following administration of glipizide from gestation day 15 throughout lactation through weaning at doses ≥5 mg/kg/day (about 2 times the recommended maximum human dose based on body surface area).     risk summary   breastfed infants of lactating women using glipizide extended-release tablets should be monitored for symptoms of hypoglycemia ( see clinical considerations ). although glipizide was undetectable in human milk in one small clinical lactation study; this result is not conclusive because of the limitations of the assay used in the study. there are no data on the effects of glipizide on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for glipizide extended-release tablets and any potential adverse effects on the breastfed child from glipizide extended-release tablets or from the underlying maternal condition. clinical considerations      monitoring for adverse reactions monitor breastfed infants for signs of hypoglycemia (e.g., jitters, cyanosis, apnea, hypothermia, excessive sleepiness, poor feeding, seizures). safety and effectiveness in children have not been established. there were no overall differences in effectiveness or safety between younger and older patients, but greater sensitivity of some individuals cannot be ruled out. elderly patients are particularly susceptible to the hypoglycemic action of anti-diabetic agents. hypoglycemia may be difficult to recognize in these patients. therefore, dosing should be conservative to avoid hypoglycemia [ see dosage and administration (2.1),warnings and precautions (5.1) and clinical pharmacology (12.3)]. there is no information regarding the effects of hepatic impairment on the disposition of glipizide. however, since glipizide is highly protein bound and hepatic biotransformation is the predominant route of elimination, the pharmacokinetics and/or pharmacodynamics of glipizide may be altered in patients with hepatic impairment. if hypoglycemia occurs in such patients, it may be prolonged and appropriate management should be instituted [ see dosage and administration (2.1),warnings and precautions (5.1) and clinical pharmacology (12.3)].

マレーシア - 英語 - NPRA (National Pharmaceutical Regulatory Agency, Bahagian Regulatori Farmasi Negara)

idaman pharma manufacturing sdn bhd - gliclazide -

アメリカ合衆国 - 英語 - NLM (National Library of Medicine)

northwind pharmaceuticals, llc - glipizide (unii: x7wdt95n5c) (glipizide - unii:x7wdt95n5c) - glipizide extended-release tablets are indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. glipizide extended-release tablets are not recommended for the treatment of type 1 diabetes mellitus or diabetic ketoacidosis. glipizide is contraindicated in patients with: - known hypersensitivity to glipizide or any of the product’s ingredients. - hypersensitivity to sulfonamide derivatives. risk summary available data from a small number of published studies and postmarketing experience with glipizide extended-release tablets use in pregnancy over decades have not identified any drug associated risks for major birth defects, miscarriage, or adverse maternal outcomes. however, sulfonylureas (including glipizide) cross the placenta and have been associated with neonatal adverse reactions such as hypoglycemia. therefore, glipizide extended-release tablets should be discontinued at least two weeks before expected delivery ( see clinical considerations ). poorly controlled diabetes in pregnancy is also associated with risks to the mother and fetus ( see clinical considerations ). in animal studies, there were no effects on embryofetal development following administration of glipizide to pregnant rats and rabbits during organogenesis at doses 833 times and 8 times the human dose based on body surface area, respectively. however, increased pup mortality was observed in rats administered glipizide from gestation day 15 throughout lactation at doses 2 times the maximum human dose based on body surface area ( see data ). the estimated background risk of major birth defects is 6-10% in women with pre-gestational diabetes with a hba1c >7 and has been reported to be as high as 20-25% in women with hba1c >10. the estimated background risk of 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.   clinical considerations    disease-associated maternal and/or embryo/fetal risk poorly-controlled diabetes in pregnancy increases the maternal risk for diabetic ketoacidosis, pre-eclampsia, miscarriage, preterm delivery, stillbirth, and delivery complications. poorly controlled diabetes increases the fetal risk for major birth defects, stillbirth, and macrosomia related morbidity. fetal/neonatal adverse reactions    neonates of women with gestational diabetes who are treated with sulfonylureas during pregnancy may be at increased risk for neonatal intensive care admission and may develop respiratory distress, hypoglycemia, birth injury, and be large for gestational age. prolonged severe hypoglycemia, lasting 4-10 days, has been reported in neonates born to mothers receiving a sulfonylurea at the time of delivery and has been reported with the use of agents with a prolonged half-life. observe newborns for symptoms of hypoglycemia and respiratory distress and manage accordingly.   dose adjustments during pregnancy and the postpartum period due to reports of prolonged severe hypoglycemia in neonates born to mothers receiving a sulfonylurea at the time of delivery, glipizide extended-release tablets should be discontinued at least two weeks before expected delivery ( see fetal/neonatal adverse reactions ). data   animal data in teratology studies in rats and rabbits, pregnant animals received daily oral doses of glipizide during the period of organogenesis at doses up to 2000 mg/kg/day and 10 mg/kg/day (approximately 833 and 8 times the human dose based on body surface area), respectively. there were no adverse effects on embryo-fetal development at any of the doses tested. in a peri-and postnatal study in pregnant rats, there was a reduced number of pups born alive following administration of glipizide from gestation day 15 throughout lactation through weaning at doses ≥5 mg/kg/day (about 2 times the recommended maximum human dose based on body surface area).    risk summary   breastfed infants of lactating women using glipizide extended-release tablets should be monitored for symptoms of hypoglycemia ( see clinical considerations ). although glipizide was undetectable in human milk in one small clinical lactation study; this result is not conclusive because of the limitations of the assay used in the study. there are no data on the effects of glipizide on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for glipizide extended-release tablets and any potential adverse effects on the breastfed child from glipizide extended-release tablets or from the underlying maternal condition. clinical considerations     monitoring for adverse reactions monitor breastfed infants for signs of hypoglycemia (e.g., jitters, cyanosis, apnea, hypothermia, excessive sleepiness, poor feeding, seizures). safety and effectiveness in children have not been established. there were no overall differences in effectiveness or safety between younger and older patients, but greater sensitivity of some individuals cannot be ruled out. elderly patients are particularly susceptible to the hypoglycemic action of anti-diabetic agents. hypoglycemia may be difficult to recognize in these patients. therefore, dosing should be conservative to avoid hypoglycemia [ see dosage and administration (2.1),warnings and precautions (5.1)and clinical pharmacology (12.3)]. there is no information regarding the effects of hepatic impairment on the disposition of glipizide. however, since glipizide is highly protein bound and hepatic biotransformation is the predominant route of elimination, the pharmacokinetics and/or pharmacodynamics of glipizide may be altered in patients with hepatic impairment. if hypoglycemia occurs in such patients, it may be prolonged and appropriate management should be instituted [ see dosage and administration (2.1),warnings and precautions (5.1)and clinical pharmacology (12.3)].

アメリカ合衆国 - 英語 - NLM (National Library of Medicine)

northwind pharmaceuticals, llc - glipizide (unii: x7wdt95n5c) (glipizide - unii:x7wdt95n5c) - glipizide extended-release tablets are indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. glipizide extended-release tablets are not recommended for the treatment of type 1 diabetes mellitus or diabetic ketoacidosis. glipizide is contraindicated in patients with: • known hypersensitivity to glipizide or any of the product’s ingredients. • hypersensitivity to sulfonamide derivatives. risk summary available data from a small number of published studies and postmarketing experience with glipizide extended-release tablets use in pregnancy over decades have not identified any drug associated risks for major birth defects, miscarriage, or adverse maternal outcomes. however, sulfonylureas (including glipizide) cross the placenta and have been associated with neonatal adverse reactions such as hypoglycemia. therefore, glipizide extended-release tablets should be discontinued at least two weeks before expected delivery (see clinical considerations). poorly controlled diabetes in pregnancy is also associated with risks to the mother and fetus (see clinical considerations). in animal studies, there were no effects on embryofetal development following administration of glipizide to pregnant rats and rabbits during organogenesis at doses 833 times and 8 times the human dose based on body surface area, respectively. however, increased pup mortality was observed in rats administered glipizide from gestation day 15 throughout lactation at doses 2 times the maximum human dose based on body surface area (see data). the estimated background risk of major birth defects is 6 to 10% in women with pre-gestational diabetes with a hba1c >7 and has been reported to be as high as 20 to 25% in women with hba1c >10. the estimated background risk of 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. clinical considerations disease-associated maternal and/or embryo/fetal risk poorly-controlled diabetes in pregnancy increases the maternal risk for diabetic ketoacidosis, pre-eclampsia, miscarriage, preterm delivery, stillbirth, and delivery complications. poorly controlled diabetes increases the fetal risk for major birth defects, stillbirth, and macrosomia related morbidity. fetal/neonatal adverse reactions neonates of women with gestational diabetes who are treated with sulfonylureas during pregnancy may be at increased risk for neonatal intensive care admission and may develop respiratory distress, hypoglycemia, birth injury, and be large for gestational age. prolonged severe hypoglycemia, lasting 4 to 10 days, has been reported in neonates born to mothers receiving a sulfonylurea at the time of delivery and has been reported with the use of agents with a prolonged half-life. observe newborns for symptoms of hypoglycemia and respiratory distress and manage accordingly. dose adjustments during pregnancy and the postpartum period due to reports of prolonged severe hypoglycemia in neonates born to mothers receiving a sulfonylurea at the time of delivery, glipizide extended-release tablets should be discontinued at least two weeks before expected delivery (see fetal/neonatal adverse reactions). data animal data in teratology studies in rats and rabbits, pregnant animals received daily oral doses of glipizide during the period of organogenesis at doses up to 2000 mg/kg/day and 10 mg/kg/day (approximately 833 and 8 times the human dose based on body surface area), respectively. there were no adverse effects on embryo-fetal development at any of the doses tested. in a peri- and postnatal study in pregnant rats, there was a reduced number of pups born alive following administration of glipizide from gestation day 15 throughout lactation through weaning at doses ≥5 mg/kg/day (about 2 times the recommended maximum human dose based on body surface area). risk summary breastfed infants of lactating women using glipizide extended-release tablets should be monitored for symptoms of hypoglycemia (see clinical considerations). although glipizide was undetectable in human milk in one small clinical lactation study; this result is not conclusive because of the limitations of the assay used in the study. there are no data on the effects of glipizide on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for glipizide extended-release tablets and any potential adverse effects on the breastfed child from glipizide extended-release tablets or from the underlying maternal condition. clinical considerations monitoring for adverse reactions monitor breastfed infants for signs of hypoglycemia (e.g., jitters, cyanosis, apnea, hypothermia, excessive sleepiness, poor feeding, seizures). safety and effectiveness in children have not been established. there were no overall differences in effectiveness or safety between younger and older patients, but greater sensitivity of some individuals cannot be ruled out. elderly patients are particularly susceptible to the hypoglycemic action of anti-diabetic agents. hypoglycemia may be difficult to recognize in these patients. therefore, dosing should be conservative to avoid hypoglycemia [see dosage and administration (2.1),  warnings and precautions (5.1)and clinical pharmacology (12.3)]. there is no information regarding the effects of hepatic impairment on the disposition of glipizide. however, since glipizide is highly protein bound and hepatic biotransformation is the predominant route of elimination, the pharmacokinetics and/or pharmacodynamics of glipizide may be altered in patients with hepatic impairment. if hypoglycemia occurs in such patients, it may be prolonged and appropriate management should be instituted [see dosage and administration (2.1),  warnings and precautions (5.1)and clinical pharmacology (12.3)].