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aurobindo pharma limited - teriflunomide (unii: 1c058ikg3b) (teriflunomide - unii:1c058ikg3b) - teriflunomide tablets are indicated for the treatment of relapsing forms of multiple sclerosis (ms), to include clinically isolated syndrome, relapsing-remitting disease, and active secondary progressive disease, in adults. teriflunomide tablets are contraindicated in/with: - patients with severe hepatic impairment [see warnings and precautions (5.1)] . - pregnant women and females of reproductive potential not using effective contraception. teriflunomide tablets may cause fetal harm [see warnings and precautions (5.2, 5.3) and use in specific populations (8.1)] . - patients with a history of a hypersensitivity reaction to teriflunomide, leflunomide, or to any of the inactive ingredients in teriflunomide tablets. reactions have included anaphylaxis, angioedema, and serious skin reactions [see warnings and precautions (5.5)].   - coadministration with leflunomide [see clinical pharmacology (12.3)]. risk summary teriflunomide is contraindicated for use in pregnant women and females of reproductive potential not using effective contraception because of the potential for fetal harm based on animal data [see contraindications (4) and warnings and precautions (5.2)] . in animal reproduction studies in rat and rabbit, oral administration of teriflunomide during organogenesis caused teratogenicity and embryolethality at plasma exposures (auc) lower than that at the maximum recommended human dose (mrhd) of 14 mg/day [see data]. available human data from pregnancy registries, clinical trials, pharmacovigilance cases, and published literature are too limited to draw any conclusions, but they do not clearly indicate increased birth defects or miscarriage associated with inadvertent teriflunomide exposure in the early first trimester when followed by an accelerated elimination procedure [see clinical considerations and data] . there are no human data pertaining to exposures later in the first trimester or beyond. in the us 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. the background risk of major birth defects and miscarriage in the indicated population is unknown. clinical considerations fetal/neonatal adverse reactions lowering the plasma concentration of teriflunomide by instituting an accelerated drug elimination procedure as soon as pregnancy is detected may decrease the risk to the fetus from teriflunomide. the accelerated drug elimination procedure includes verification that the plasma teriflunomide concentration is less than 0.02 mg/l [see warnings and precautions (5.3) and clinical pharmacology (12.3)]. data human data available human data are limited. prospectively reported data (from clinical trials and postmarketing reports) from >150 pregnancies in patients treated with teriflunomide and >300 pregnancies in patients treated with leflunomide have not demonstrated an increased rate of congenital malformations or miscarriage following teriflunomide exposure in the early first trimester when followed by an accelerated elimination procedure. specific patterns of major congenital malformations in humans have not been observed. limitations of these data include an inadequate number of reported pregnancies from which to draw conclusions, the short duration of drug exposure in reported pregnancies, which precludes a full evaluation of the fetal risks, incomplete reporting, and the inability to control for confounders (such as underlying maternal disease and use of concomitant medications). animal data when teriflunomide (oral doses of 1, 3, or 10 mg/kg/day) was administered to pregnant rats throughout the period of organogenesis, high incidences of fetal malformation (primarily craniofacial, and axial and appendicular skeletal defects) and fetal death were observed at doses not associated with maternal toxicity. adverse effects on fetal development were observed following dosing at various stages throughout organogenesis. maternal plasma exposure at the no-effect level (1 mg/kg/day) for fetal developmental toxicity in rats was less than that in humans at the maximum recommended human dose (mrhd, 14 mg/day). administration of teriflunomide (oral doses of 1, 3.5, or 12 mg/kg/day) to pregnant rabbits throughout organogenesis resulted in high incidences of fetal malformation (primarily craniofacial, and axial and appendicular skeletal defects) and fetal death at doses associated with minimal maternal toxicity. maternal plasma exposure at the no-effect dose (1 mg/kg/day) for fetal developmental toxicity in rabbits was less than that in humans at the mrhd. in studies in which teriflunomide (oral doses of 0.05, 0.1, 0.3, 0.6, or 1 mg/kg/day) was administered to rats during gestation and lactation, decreased growth, eye and skin abnormalities, and high incidences of malformation (limb defects) and postnatal death were observed in the offspring at doses not associated with maternal toxicity. maternal plasma exposure at the no-effect dose for prenatal and postnatal developmental toxicity in rats (0.10 mg/kg/day) was less than that in humans at the mrhd. in animal reproduction studies of leflunomide, embryolethality and teratogenic effects were observed in pregnant rat and rabbit at or below clinically relevant plasma teriflunomide exposures (auc). in published reproduction studies in pregnant mice, leflunomide was embryolethal and increased the incidence of malformations (craniofacial, axial skeletal, heart and great vessel). supplementation with exogenous uridine reduced the teratogenic effects in pregnant mice, suggesting that the mode of action (inhibition of mitochondrial enzyme dihydroorotate dehydrogenase) is the same for therapeutic efficacy and developmental toxicity. at recommended doses in humans, teriflunomide and leflunomide result in a similar range of plasma concentrations of teriflunomide. risk summary there are no data on the presence of teriflunomide in human milk, the effects on the breastfed infant, or the effects on milk production. teriflunomide was detected in rat milk following a single oral dose. because of the potential for adverse reactions in a breastfed infant from teriflunomide, women should not breastfeed during treatment with teriflunomide. pregnancy testing exclude pregnancy prior to initiation of treatment with teriflunomide in females of reproductive potential. advise females to notify their healthcare provider immediately if pregnancy occurs or is suspected during treatment [see warnings and precautions (5.2, 5.3) and use in specific populations (8.1)]. contraception females females of reproductive potential should use effective contraception while taking teriflunomide. if teriflunomide is discontinued, use of contraception should be continued until it is verified that plasma concentrations of teriflunomide are less than 0.02 mg/l (0.02 mcg/ml, the level expected to have minimal fetal risk, based on animal data). females of reproductive potential who wish to become pregnant should discontinue teriflunomide and undergo an accelerated elimination procedure. effective contraception should be used until it is verified that plasma concentrations of teriflunomide are less than 0.02 mg/l (0.02 mcg/ml) [see warnings and precautions (5.2, 5.3) and use in specific populations (8.1)] . males teriflunomide is detected in human semen. animal studies to specifically evaluate the risk of male mediated fetal toxicity have not been conducted. to minimize any possible risk, men not wishing to father a child and their female partners should use effective contraception. men wishing to father a child should discontinue use of teriflunomide and either undergo an accelerated elimination procedure or wait until verification that the plasma teriflunomide concentration is less than 0.02 mg/l (0.02 mcg/ml) [see warnings and precautions (5.3)]. safety and effectiveness in pediatric patients have not been established. pancreatitis has been reported in adults in the postmarketing setting, but appears to occur at higher frequency in the pediatric population [see warnings and precautions (5.11)] . additionally, elevated or abnormal blood creatine phosphokinase was reported. juvenile animal toxicity data oral administration of teriflunomide (0, 0.3, 3, or 6 mg/kg/day) to young rats on postnatal days 21 to 70 resulted in suppression of immune function (t-cell dependent antibody response) at the mid and high doses, and adverse effects on male reproductive organs (reduced sperm count) and altered neurobehavioral function (increased locomotor activity) at the high dose. pediatric information describing a clinical study in which efficacy was not demonstrated is approved for sanofi-aventis u.s. llc’s aubagio® (teriflunomide) tablets. however, due to sanofi-aventis u.s. llc’s marketing exclusivity rights, this drug product is not labeled with that information. clinical studies of teriflunomide did not include patients over 65 years old. no dosage adjustment is necessary for patients with mild and moderate hepatic impairment. the pharmacokinetics of teriflunomide in severe hepatic impairment has not been evaluated. teriflunomide is contraindicated in patients with severe hepatic impairment [see contraindications (4), warnings and precautions (5.1), and clinical pharmacology (12.3)] . no dosage adjustment is necessary for patients with mild, moderate, and severe renal impairment [see clinical pharmacology (12.3)] .

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

aurobindo pharma limited - roflumilast (unii: 0p6c6zop5u) (roflumilast - unii:0p6c6zop5u) - roflumilast tablets are indicated as a treatment to reduce the risk of copd exacerbations in patients with severe copd associated with chronic bronchitis and a history of exacerbations. limitations of use roflumilast tablets are not a bronchodilator and is not indicated for the relief of acute bronchospasm. roflumilast tablets 250 mcg is a starting dose, for the first 4 weeks of treatment only and is not the effective (therapeutic) dose. the use of roflumilast tablets are contraindicated in the following condition: moderate to severe liver impairment (child-pugh b or c) [see clinical pharmacology (12.3) and use in specific populations (8.6)] . risk summary there are no randomized clinical studies of roflumilast in pregnant women. in animal reproductive toxicity studies, roflumilast administered to pregnant rats and rabbits during the period of organogenesis produced no fetal structural abnormalities. the highest roflumilast dose in these studies was approximately 30 and 26 times, respectively, the maximu

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aurobindo pharma limited - saxagliptin hydrochloride (unii: z8j84yix6l) (saxagliptin anhydrous - unii:8i7io46ivq) - saxagliptin tablets are indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus [see clinical studies (14) ]. saxagliptin tablets are not indicated for the treatment of type 1 diabetes mellitus or diabetic ketoacidosis, as it would not be effective in these settings. saxagliptin is contraindicated in patients with a history of a serious hypersensitivity reaction to saxagliptin tablets, such as anaphylaxis, angioedema, or exfoliative skin conditions [see  warnings and precautions (5.4) and adverse reactions (6.2) ]. risk summary limited data with saxagliptin in pregnant women are not sufficient to determine a drug-associated risk for major birth defects or miscarriages. there are risks to the mother and fetus associated with poorly controlled diabetes in pregnancy [see clinical considerations] . no adverse developmental effects independent of maternal toxicity were observed when saxagliptin was administered to pregnant rats and rabbits during the period of organogenesis and in pregnant and lactating rats during the pre- and postnatal period [see data] . the estimated background risk of major birth defects is 6 to 10% in women with pre-gestational diabetes with an hba1c greater than 7 and has been reported to be as high as 20 to 25% in women with an hba1c greater than 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, preeclampsia, spontaneous abortions, preterm delivery, still birth and delivery complications. poorly controlled diabetes increases the fetal risk for major birth defects, stillbirth, and macrosomia related morbidity. data animal data in embryo-fetal development studies, saxagliptin was administered to pregnant rats and rabbits during the period of organogenesis, corresponding to the first trimester of human pregnancy. no adverse developmental effects were observed in either species at exposures 1503- and 152-times the 5 mg clinical dose in rats and rabbits, respectively, based on auc. saxagliptin crosses the placenta into the fetus following dosing in pregnant rats. in a prenatal and postnatal development study, no adverse developmental effects were observed in maternal rats administered saxagliptin from gestation day 6 through lactation day 21 at exposures up to 470-times the 5 mg clinical dose, based on auc. risk summary there is no information regarding the presence of saxagliptin in human milk, the effects on the breastfed infant, or the effects on milk production. saxagliptin is present in the milk of lactating rats [see data] . the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for saxagliptin and any potential adverse effects on the breastfed infant from saxagliptin or from the underlying maternal condition. data saxagliptin is secreted in the milk of lactating rats at approximately a 1:1 ratio with plasma drug concentrations. safety and effectiveness of saxagliptin in pediatric patients under 18 years of age have not been established. additionally, studies characterizing the pharmacokinetics of saxagliptin in pediatric patients have not been performed. in the seven, double-blind, controlled clinical safety and efficacy trials of saxagliptin, a total of 4751 (42.0%) of the 11301 patients randomized to saxagliptin were 65 years and over, and 1210 (10.7%) were 75 years and over. no overall differences in safety or effectiveness were observed between subjects ≥65 years old and younger subjects. while this clinical experience has not identified differences in responses between the elderly and younger patients, greater sensitivity of some older individuals cannot be ruled out. saxagliptin and its active metabolite are eliminated in part by the kidney. because elderly patients are more likely to have decreased renal function, care should be taken in dose selection in the elderly based on renal function [see dosage and administration (2.2)   and  clinical pharmacology (12.3) ]. in a 12-week randomized placebo-controlled trial, saxagliptin 2.5 mg was administered to 85 subjects with moderate (n=48) or severe (n=18) renal impairment or end-stage renal disease (esrd) (n=19) [see clinical studies (14) ]. the incidence of adverse events, including serious adverse events and discontinuations due to adverse events, was similar between saxagliptin and placebo. the overall incidence of reported hypoglycemia was 20% among subjects treated with saxagliptin 2.5 mg and 22% among subjects treated with placebo. four saxagliptin-treated subjects (4.7%) and three placebo-treated subjects (3.5%) reported at least one episode of confirmed symptomatic hypoglycemia (accompanying fingerstick glucose ≤50 mg/dl).

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dr.reddy's laboratories limited - famotidine (unii: 5qzo15j2z8) (famotidine - unii:5qzo15j2z8) - famotidine 20 mg - famotidine tablets are indicated in adult and pediatric patients 40 kg and greater for the treatment of: • active duodenal ulcer (du). • active gastric ulcer (gu). • symptomatic nonerosive gastroesophageal reflux disease (gerd). • erosive esophagitis due to gerd, diagnosed by biopsy. famotidine tablets are indicated in adults for the: • treatment of pathological hypersecretory conditions (e.g., zollinger-ellison syndrome, multiple endocrine neoplasias). • reduction of the risk of duodenal ulcer recurrence. famotidine tablets are contraindicated in patients with a history of serious hypersensitivity reactions (e.g., anaphylaxis) to famotidine or other histamine-2 (h2 ) receptor antagonists. risk summary available data with h2 -receptor antagonists, including famotidine, in pregnant women are insufficient to establish a drug-associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes. in animal reproduction studies, no adverse development effects were observed with oral administrat

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dr.reddy's laboratories limited - amlodipine besylate (unii: 864v2q084h) (amlodipine - unii:1j444qc288), benazepril hydrochloride (unii: n1sn99t69t) (benazeprilat - unii:jrm708l703) - amlodipine 5 mg - amlodipine and benazepril hydrochloride capsules are indicated for the treatment of hypertension in patients not adequately controlled on monotherapy with either agent. - do not coadminister aliskiren with angiotensin receptor blockers (arbs), ace inhibitors, including amlodipine and benazepril hydrochloride in patients with diabetes. - amlodipine and benazepril hydrochloride is contraindicated in patients with a history of angioedema, with or without previous ace inhibitor treatment, or patients who are hypersensitive to benazepril, to any other ace inhibitor, to amlodipine, or to any of the excipients of amlodipine and benazepril hydrochloride. - amlodipine and benazepril hydrochloride is contraindicated in combination with a neprilysin inhibitor (e.g., sacubitril). do not administer amlodipine and benazepril hydrochloride within 36 hours of switching to or from a neprilysin inhibitor, e.g., sacubitril/valsartan. [see warnings and precautions (5.1)]. risk summary amlodipine and benazepril hydrochloride

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micro labs limited - rasagiline mesylate (unii: lh8c2ji290) (rasagiline - unii:003n66ts6t) -   rasagiline tablets are indicated for the treatment of parkinson's disease (pd). rasagiline tablet is contraindicated for use with meperidine, tramadol, methadone, propoxyphene, and mao inhibitors (maois), including other selective mao-b inhibitors, because of risk of serotonin syndrome [see warnings and precautions (5.2)] . at least 14 days should elapse between discontinuation of rasagiline tablet and initiation of treatment with these medications. rasagiline tablet is contraindicated for use with st. john’s wort and with cyclobenzaprine. rasagiline tablet is contraindicated for use with dextromethorphan because of risk of episode of psychosis or bizarre behavior. risk summary there are no adequate data on the developmental risks associated with the use of rasagiline in pregnant women. in animal studies, oral administration of rasagiline to rats during gestation and lactation resulted in decreased survival and reduced body weight in the offspring at doses si

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indoco remedies limited - febuxostat (unii: 101v0r1n2e) (febuxostat - unii:101v0r1n2e) - febuxostat tablets are xanthine oxidase (xo) inhibitor indicated for the chronic management of hyperuricemia in adult patients with gout who have an inadequate response to a maximally titrated dose of allopurinol, who are intolerant to allopurinol, or for whom treatment with allopurinol is not advisable. for the safe and effective use of allopurinol, see allopurinol prescribing information. limitations of use :  febuxostat tablets are not recommended for the treatment of asymptomatic hyperuricemia. febuxostat tablets are contraindicated in patients being treated with azathioprine or mercaptopurine [see drug interactions (7)] . risk summary limited available data with febuxostat tablets use in pregnant women are insufficient to inform a drug associated risk of adverse developmental outcomes. no adverse developmental effects were observed in embryo-fetal development studies with oral administration of febuxostat to pregnant rats and rabbits during organogenesis at doses that produced maternal exposures up to 40

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avkare - lamotrigine (unii: u3h27498ks) (lamotrigine - unii:u3h27498ks) - lamotrigine extended-release tablets are indicated as adjunctive therapy for primary generalized tonic-clonic (pgtc) seizures and partial-onset seizures with or without secondary generalization in patients aged 13 years and older. lamotrigine extended-release tablets are indicated for conversion to monotherapy in patients aged 13 years  and older with partial-onset seizures who are receiving treatment with a single antiepileptic drug (aed). safety and effectiveness of lamotrigine extended-release tablets have not been established (1) as initial monotherapy or (2) for simultaneous conversion to monotherapy from 2 or more concomitant aeds. safety and effectiveness of lamotrigine extended-release tablets for use in patients younger than 13 years have not been established. lamotrigine extended-release tablets are contraindicated in patients who have demonstrated hypersensitivity (e.g., rash, angioedema, acute urticaria, extensive pruritus, mucosal ulceration) to the drug or its ingredients [see  boxed warning,  warnings and precautions (5.1,  5.3)] . pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to aeds, including lamotrigine extended-release, during pregnancy. encourage women who are taking lamotrigine extended-release during pregnancy to enroll in the north american antiepileptic drug (naaed) pregnancy registry by calling 1-888-233-2334 or visiting http://www.aedpregnancyregistry.org/. risk summary data from several prospective pregnancy exposure registries and epidemiological studies of pregnant women have not detected an increased frequency of major congenital malformations or a consistent pattern of malformations among women exposed to lamotrigine compared with the general population (see data) . in animal studies, administration of lamotrigine during pregnancy resulted in developmental toxicity (increased mortality, decreased body weight, increased structural variation, neurobehavioral abnormalities) at doses lower than those administered clinically. lamotrigine decreased fetal folate concentrations in rats, an effect known to be associated with adverse pregnancy outcomes in animals and humans (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. clinical considerations as with other aeds, physiological changes during pregnancy may affect lamotrigine concentrations and/or therapeutic effect. there have been reports of decreased lamotrigine concentrations during pregnancy and restoration of pre-pregnancy concentrations after delivery. dose adjustments may be necessary to maintain clinical response. data human data: data from several international pregnancy registries have not shown an increased risk for malformations overall. the international lamotrigine pregnancy registry reported major congenital malformations in 2.2% (95% ci: 1.6%, 3.1%) of 1,558 infants exposed to lamotrigine monotherapy in the first trimester of pregnancy. the naaed pregnancy registry reported major congenital malformations among 2.0% of 1,562 infants exposed to lamotrigine monotherapy in the first trimester. eurap, a large international pregnancy registry focused outside of north america, reported major birth defects in 2.9% (95% ci: 2.3%, 3.7%) of 2,514 exposures to lamotrigine monotherapy in the first trimester. the frequency of major congenital malformations was similar to estimates from the general population. the naaed pregnancy registry observed an increased risk of isolated oral clefts: among 2,200 infants exposed to lamotrigine early in pregnancy, the risk of oral clefts was 3.2 per 1,000 (95% ci: 1.4, 6.3), a 3-fold increased risk versus unexposed healthy controls. this finding has not been observed in other large international pregnancy registries. furthermore, a case-control study based on 21 congenital anomaly registries covering over 10 million births in europe reported an adjusted odds ratio for isolated oral clefts with lamotrigine exposure of 1.45 (95% ci: 0.8, 2.63). several meta-analyses have not reported an increased risk of major congenital malformations following lamotrigine exposure in pregnancy compared with healthy and disease-matched controls. no patterns of specific malformation types were observed. the same meta-analyses evaluated the risk of additional maternal and infant outcomes including fetal death, stillbirth, preterm birth, small for gestational age, and neurodevelopmental delay. although there are no data suggesting an increased risk of these outcomes with lamotrigine monotherapy exposure, differences in outcome definition, ascertainment methods, and comparator groups limit the conclusions that can be drawn. animal data: when lamotrigine was administered to pregnant mice, rats, or rabbits during the period of organogenesis (oral doses of up to 125, 25, and 30 mg/kg, respectively), reduced fetal body weight and increased incidences of fetal skeletal variations were seen in mice and rats at doses that were also maternally toxic. the no-effect doses for embryofetal developmental toxicity in mice, rats, and rabbits (75, 6.25, and 30 mg/kg, respectively) are similar to (mice and rabbits) or less than (rats) the human dose of 400 mg/day on a body surface area (mg/m 2 ) basis. in a study in which pregnant rats were administered lamotrigine (oral doses of 0, 5 or 25 mg/kg) during the period of organogenesis and offspring were evaluated postnatally, neurobehavioral abnormalities were observed in exposed offspring at both doses. the lowest effect dose for developmental neurotoxicity in rats is less than the human dose of 400 mg/day on a mg/m 2 basis. maternal toxicity was observed at the higher dose tested. when pregnant rats were administered lamotrigine (oral doses of 0, 5, 10, or 20 mg/kg) during the latter part of gestation and throughout lactation, increased offspring mortality (including stillbirths) was seen at all doses. the lowest effect dose for pre- and post-natal developmental toxicity in rats is less than the human dose of 400 mg/day on a mg/m 2 basis. maternal toxicity was observed at the 2 highest doses tested. when administered to pregnant rats, lamotrigine decreased fetal folate concentrations at doses greater than or equal to 5 mg/kg/day, which is less than the human dose of 400 mg/day on a mg/m 2 basis. risk summary lamotrigine is present in milk from lactating women taking lamotrigine extended-release (see data) . neonates and young infants are at risk for high serum levels because maternal serum and milk levels can rise to high levels postpartum if lamotrigine dosage has been increased during pregnancy but is not reduced after delivery to the pre-pregnancy dosage. glucuronidation is required for drug clearance. glucuronidation capacity is immature in the infant and this may also contribute to the level of lamotrigine exposure. events including rash, apnea, drowsiness, poor sucking, and poor weight gain (requiring hospitalization in some cases) have been reported in infants who have been human milk-fed by mothers using lamotrigine; whether or not these events were caused by lamotrigine is unknown. no data are available on the effects of the drug on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for lamotrigine extended-release and any potential adverse effects on the breastfed infant from lamotrigine extended-release or from the underlying maternal condition. clinical considerations human milk-fed infants should be closely monitored for adverse events resulting from lamotrigine. measurement of infant serum levels should be performed to rule out toxicity if concerns arise. human milk-feeding should be discontinued in infants with lamotrigine toxicity. data data from multiple small studies indicate that lamotrigine plasma levels in nursing infants have been reported to be as high as 50% of maternal plasma concentrations. lamotrigine extended-release is indicated as adjunctive therapy for pgtc and partial-onset seizures with or without secondary generalization in patients aged 13 years and older. safety and effectiveness of lamotrigine extended-release for any use in patients younger than 13 years have not been established. immediate-release lamotrigine is indicated as adjunctive therapy in patients aged 2 years and older for partial-onset seizures, the generalized seizures of lennox-gastaut syndrome and pgtc seizures. safety and efficacy of immediate-release lamotrigine used as adjunctive treatment for partial-onset seizures were not demonstrated in a small, randomized, double-blind, placebo-controlled withdrawal trial in very young pediatric patients (aged 1 to 24 months). immediate-release lamotrigine was associated with an increased risk for infectious adverse reactions (lamotrigine 37%, placebo 5%), and respiratory adverse reactions (lamotrigine 26%, placebo 5%). infectious adverse reactions included bronchiolitis, bronchitis, ear infection, eye infection, otitis externa, pharyngitis, urinary tract infection and viral infection. respiratory adverse reactions included nasal congestion, cough and apnea. juvenile animal data in a juvenile animal study in which lamotrigine (oral doses of 0, 5, 15, or 30 mg/kg) was administered to young rats from postnatal day 7 to 62, decreased viability and growth were seen at the highest dose tested and long-term neurobehavioral abnormalities (decreased locomotor activity, increased reactivity and learning deficits in animals tested as adults) were observed at the 2 highest doses. the no-effect dose for adverse developmental effects in juvenile animals is less than the human dose of 400 mg/day on a mg/m 2 basis. clinical trials of lamotrigine extended-release for epilepsy did not include sufficient numbers of patients aged 65 years and older to determine whether they respond differently from younger patients or exhibit a different safety profile than that of younger patients. in general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function and of concomitant disease or other drug therapy. experience in patients with hepatic impairment is limited. based on a clinical pharmacology study with immediate-release lamotrigine in 24 subjects with mild, moderate and severe liver impairment [see clinical pharmacology (12.3)] , the following general recommendations can be made. no dosage adjustment is needed in patients with mild liver impairment. initial, escalation and maintenance doses should generally be reduced by approximately 25% in patients with moderate and severe liver impairment without ascites and 50% in patients with severe liver impairment with ascites. escalation and maintenance doses may be adjusted according to clinical response [see dosage and administration (2.1)] . lamotrigine is metabolized mainly by glucuronic acid conjugation, with the majority of the metabolites being recovered in the urine. in a small study comparing a single dose of immediate-release lamotrigine in subjects with varying degrees of renal impairment with healthy volunteers, the plasma half-life of lamotrigine was approximately twice as long in the subjects with chronic renal failure [see clinical pharmacology (12.3)] . initial doses of lamotrigine extended-release should be based on patients’ aed regimens; reduced maintenance doses may be effective for patients with significant renal impairment. few patients with severe renal impairment have been evaluated during chronic treatment with lamotrigine. because there is inadequate experience in this population, lamotrigine extended-release should be used with caution in these patients [see dosage and administration (2.1)] .

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torrent pharmaceuticals limited - erythromycin (unii: 63937kv33d) (erythromycin - unii:63937kv33d) - to reduce the development of drug-resistant bacteria and maintain the effectiveness of erythromycin tablets, usp and other antibacterial drugs, erythromycin tablets, usp should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. when culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. in the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy. erythromycin tablet, usp are indicated in the treatment of infections caused by susceptible strains of the designated microorganisms in the diseases listed below: upper respiratory tract infections of mild to moderate degree caused by streptococcus pyogenes ; streptococcus pneumoniae ; haemophilus influenzae (when used concomitantly with adequat

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torrent pharmaceuticals limited - erythromycin (unii: 63937kv33d) (erythromycin - unii:63937kv33d) - to reduce the development of drug-resistant bacteria and maintain the effectiveness of erythromycin delayed-release tablets and other antibacterial drugs, erythromycin delayed-release tablets should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. when culture and susceptibility information are available, they should be considered in selecting or modifying antibacterial therapy. in the absence of such data, local epidemiology and susceptibility patterns may contribute to the empiric selection of therapy.    erythromycin delayed-release tablets are indicated in the treatment of infections caused by susceptible strains of the designated microorganisms in the diseases listed below:    upper respiratory tract infections of mild to moderate degree caused by streptococcus pyogenes; streptococcus pneumoniae; haemophilus influenzae (when used concomitantly with adequate doses of sulfonamides, since many strains of