Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

apotex corp. - celecoxib (unii: jcx84q7j1l) (celecoxib - unii:jcx84q7j1l) - celecoxib 50 mg - celecoxib capsules are indicated for the management of the signs and symptoms of oa [see clinical studies (14.1) ]. for the management of the signs and symptoms of ra [see clinical studies (14.2) ]. for the management of the signs and symptoms of jra in patients 2 years and older [see clinical studies (14.3) ]. for the management of the signs and symptoms of as [see clinical studies (14.4) ]. for the management of acute pain in adults [see clinical studies (14.5) ]. for the management of primary dysmenorrhea [see clinical studies (14.5) ]. celecoxib capsules are contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to celecoxib, any components of the drug product [see warnings and precautions (5.7, 5.9) ]. - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids, have been reported in such patients [see warnings and precautions (

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

apotex corp - omeprazole (unii: kg60484qx9) (omeprazole - unii:kg60484qx9) - omeprazole 10 mg - omeprazole delayed-release capsules are indicated for short-term treatment of active duodenal ulcer in adults. most patients heal within four weeks. some patients may require an additional four weeks of therapy. eradication of h. pylori has been shown to reduce the risk of duodenal ulcer recurrence. triple therapy omeprazole delayed-release capsules in combination with clarithromycin and amoxicillin, are indicated for treatment of patients with h. pylori infection and duodenal ulcer disease (active or up to 1-year history) to eradicate h. pylori in adults. dual therapy omeprazole delayed-release capsules in combination with clarithromycin are indicated for treatment of patients with h. pylori infection and duodenal ulcer disease to eradicate h. pylori in adults. among patients who fail therapy, omeprazole delayed-release capsules with clarithromycin are more likely to be associated with the development of clarithromycin resistance as compared with triple therapy. in patients who fail therapy, susceptibil

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

apotex corp - ibandronate sodium (unii: j12u072ql0) (ibandronic acid - unii:umd7g2653w) - ibandronic acid 150 mg - ibandronate sodium tablets are indicated for the treatment and prevention of osteoporosis in postmenopausal women. ibandronate sodium increases bone mineral density (bmd) and reduces the incidence of vertebral fractures. the optimal duration of use has not been determined. the safety and effectiveness of ibandronate sodium tablets for the treatment of osteoporosis are based on clinical data of three years duration. all patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis. patients at low-risk for fracture should be considered for drug discontinuation after 3 to 5 years of use. patients who discontinue therapy should have their risk for fracture re-evaluated periodically. ibandronate sodium tablets are contraindicated in patients with the following conditions: - abnormalities of the esophagus which delay esophageal emptying such as stricture or achalasia (see warnings and precautions [5.1]) - inability to stand or sit upright for at least 60 minutes (

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

apotex corp. - diclofenac sodium (unii: qtg126297q) (diclofenac - unii:144o8ql0l1) - diclofenac sodium topical solution is indicated for the treatment of the pain of osteoarthritis of the knee(s). diclofenac sodium topical solution is contraindicated in the following patients: - known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to diclofenac or any components of the drug product [see warnings and precautions (5.7, 5.9)] - history of asthma, urticaria, or other allergic-type reactions after taking aspirin or other nsaids. severe, sometimes fatal, anaphylactic reactions to nsaids have been reported in such patients [see warnings and precautions (5.7, 5.8)] - in the setting of coronary artery bypass graft (cabg) surgery [see warnings and precautions (5.1)] risk summary use of nsaids, including diclofenac sodium topical solution, can cause premature closure of the fetal ductus arteriosus and fetal renal dysfunction leading to oligohydramnios and, in some cases, neonatal renal impairment. because of these risks, limit dose and duration of diclofenac sodium topical

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

apotex corp. - tolvaptan (unii: 21g72t1950) (tolvaptan - unii:21g72t1950) - tolvaptan is indicated for the treatment of clinically significant hypervolemic and euvolemic hyponatremia (serum sodium <125 meq/l or less marked hyponatremia that is symptomatic and has resisted correction with fluid restriction), including patients with heart failure and syndrome of inappropriate antidiuretic hormone (siadh). limitations of use patients requiring intervention to raise serum sodium urgently to prevent or to treat serious neurological symptoms should not be treated with tolvaptan. it has not been established that raising serum sodium with tolvaptan provides a symptomatic benefit to patients. tolvaptan is contraindicated in the following conditions: - patients with autosomal dominant polycystic kidney disease (adpkd) outside of fda-approved rems [see warnings and precautions (5.2)] - unable to sense or respond to thirst - hypovolemic hyponatremia - taking strong cyp3a inhibitors [see warnings and precautions (5.5)] - anuria - hypersensitivity (e.g., anaphylactic shock, rash generalized) to tolvaptan or any components of the product [see adverse reactions (6)] risk summary available data with tolvaptan tablet use in pregnant women are insufficient to determine if there is a drug-associated risk of adverse developmental outcomes. tolvaptan did not cause any developmental toxicity in rats or in rabbits at exposures approximately 2.8 and 0.8 times, respectively, the exposure in congestive heart failure (chf) patients at the maximum recommended human dose (mrhd) of 60 mg once daily. however, effects on embryo-fetal development occurred in both species at doses causing significant maternally toxic doses. in rats, reduced fetal weights and delayed fetal ossification occurred at 11 times the exposure in chf patients, based on auc. in rabbits, increased abortions, embryo-fetal death, fetal microphthalmia, open eyelids, cleft palate, brachymelia and skeletal malformations occurred at approximately 1.6 times the exposure in chf patients (see data ). the estimated background risk of major birth defects and miscarriage for the indicated population is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. the estimated background risk of major birth defects and miscarriage in the u.s. general population is 2 to 4% and 15 to 20% of clinically recognized pregnancies, respectively. data animal data oral administration of tolvaptan during the period of organogenesis in sprague-dawley rats produced no evidence of teratogenesis at doses up to 100 mg/kg/day. delayed ossification was seen at 1000 mg/kg, which is approximately 11 times the exposure in chf patients at the mrhd of 60 mg (auc24h  10271 ng*h/ml). the fetal effects are likely secondary to maternal toxicity (decreased food intake and low body weights). in a prenatal and postnatal study in rats, tolvaptan had no effect on physical development, reflex function, learning ability or reproductive performance at doses up to 1,000 mg/kg/day (11 times the exposure in chf patients at the mrhd of 60 mg). in rabbits, teratogenicity (microphthalmia, embryo-fetal mortality, cleft palate, brachymelia and skeletal malformations) was observed in rabbits at 1,000 mg/kg (approximately 1.6 times the exposure in chf patients at the mrhd of 60 mg dose). this dose also caused maternal toxicity (lower body weight gains and food consumption). risk summary there are no data on the presence of tolvaptan or its metabolites in human milk, the effects on the breastfed infant, or the effects on milk production. tolvaptan is present in rat milk (see data). when a drug is present in animal milk, it is possible that the drug will be present in human milk, but relative levels may vary (see data ). because of the potential for serious adverse reactions, including electrolyte abnormalities (e.g., hypernatremia), hypotension, and volume depletion in breastfed infants, advise women not to breastfeed during treatment with tolvaptan tablets. data in lactating rats administered radiolabeled tolvaptan, lacteal radioactivity concentrations reached the highest level at 8 hours after administration and then decreased gradually with time with a half-life of 27.3 hours. the level of activity in milk ranged from 1.5- to 15.8-fold those in maternal blood over a period of 72 hours post-dose. increased perinatal death and decreased body weight of the offspring were observed during the lactation period and after weaning at approximately 11 times the exposure in chf patients at the mrhd of 60 mg. safety and effectiveness of tolvaptan in pediatric patients have not been established. of the total number of hyponatremic subjects treated with tolvaptan in clinical studies, 42% were 65 years old and over, while 19% were 75 years old and over. no overall differences in safety or effectiveness were observed between these subjects and younger subjects, and other reported clinical experience has not identified differences in responses between the elderly and younger patients, but greater sensitivity of some older individuals cannot be ruled out. increasing age has no effect on tolvaptan plasma concentrations. moderate and severe hepatic impairment do not affect exposure to tolvaptan to a clinically relevant extent. avoid use of tolvaptan in patients with underlying liver disease. no dose adjustment is necessary based on renal function. there are no clinical trial data in patients with crcl <10 ml/min, and, because drug effects on serum sodium levels are likely lost at very low levels of renal function, use in patients with a crcl <10 ml/min is not recommended. no benefit can be expected in patients who are anuric [see contraindications (4) and clinical pharmacology (12.3)].

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

apotex corp. - fingolimod hydrochloride (unii: g926ec510t) (fingolimod - unii:3qn8byn5qf) - fingolimod capsules 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 patients 10 years of age and older. fingolimod capsules are contraindicated in patients who have: - in the last 6 months experienced myocardial infarction, unstable angina, stroke, transient ischemic attack (tia), decompensated heart failure requiring hospitalization or class iii/iv heart failure - a history or presence of mobitz type ii second-degree or third-degree av block or sick sinus syndrome, unless patient has a functioning pacemaker [see warnings and precautions (5.1)] - a baseline qtc interval ≥ 500 msec - cardiac arrhythmias requiring anti-arrhythmic treatment with class ia or class iii anti-arrhythmic drugs - had a hypersensitivity reaction to fingolimod or any of the excipients in fingolimod capsules. observed reactions include rash, urticaria and angioedema upon treatment initiation

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

apotex corp. - lacosamide (unii: 563ks2pqy5) (lacosamide - unii:563ks2pqy5) - lacosamide oral solution is indicated for the treatment of partial-onset seizures in patients 4 years of age and older. additional pediatric use information is approved for ucb, inc.’s vimpat® (lacosamide) oral solution. however, due to ucb, inc.’s marketing exclusivity rights, this drug product is not labeled with that information. lacosamide oral solution is indicated as adjunctive therapy in the treatment of primary generalized tonic-clonic seizures in patients 4 years of age and older. none. there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as lacosamide oral solution, during pregnancy. encourage women who are taking lacosamide oral solution  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/. available data from the north american antiepileptic drug (naaed) pregnancy registry, a prospective cohort study, case reports, and a case series with lacosamide oral solution use in pregnant women are insufficient to identify a drug associated risk of major birth defects, miscarriage or other adverse maternal or fetal outcomes. lacosamide produced developmental toxicity (increased embryofetal and perinatal mortality, growth deficit) in rats following administration during pregnancy. developmental neurotoxicity was observed in rats following administration during a period of postnatal development corresponding to the third trimester of human pregnancy. these effects were observed at doses associated with clinically relevant plasma exposures (see data) .   the background risk of major birth defects and miscarriage for the indicated population is unknown. all pregnancies have a background risk of birth defect, loss, or other adverse outcomes. 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. animal data oral administration of lacosamide to pregnant rats (20, 75, or 200 mg/kg/day) and rabbits (6.25, 12.5, or 25 mg/kg/day) during the period of organogenesis did not produce any effects on the incidences of fetal structural abnormalities. however, the maximum doses evaluated were limited by maternal toxicity in both species and embryofetal death in rats. these doses were associated with maternal plasma lacosamide exposures (auc) approximately 2 and 1 times (rat and rabbit, respectively) that in humans at the maximum recommended human dose (mrhd) of 400 mg/day.   in two studies in which lacosamide (25, 70, or 200 mg/kg/day and 50, 100, or 200 mg/kg/day) was orally administered to rats throughout pregnancy and lactation, increased perinatal mortality and decreased body weights in the offspring were observed at the highest dose tested. the no-effect dose for pre-and postnatal developmental toxicity in rats (70 mg/kg/day) was associated with a maternal plasma lacosamide auc similar to that in humans at the mrhd.   oral administration of lacosamide (30, 90, or 180 mg/kg/day) to rats during the neonatal and juvenile periods of development resulted in decreased brain weights and long-term neurobehavioral changes (altered open field performance, deficits in learning and memory). the early postnatal period in rats is generally thought to correspond to late pregnancy in humans in terms of brain development. the no-effect dose for developmental neurotoxicity in rats was associated with a plasma lacosamide auc less than that in humans at the mrhd.  in vitro data lacosamide has been shown in vitro to interfere with the activity of collapsin response mediator protein-2 (crmp-2), a protein involved in neuronal differentiation and control of axonal outgrowth. potential adverse effects on cns development related to this activity cannot be ruled out. risk summary data from published literature indicate that lacosamide is present in human milk. there are reports of increased sleepiness in breastfed infants exposed to lacosamide (see clinical considerations). there is no information on the effects of lacosamide on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for lacosamide and any potential adverse effects on the breastfed infant from lacosamide or from the underlying maternal condition.  clinical considerations monitor infants exposed to lacosamide through breastmilk for excess sedation. partial-onset seizures safety and effectiveness of lacosamide oral solution for the treatment of partial-onset seizures have been established in pediatric patients 4 years to less than 17 years of age. use of lacosamide oral solution in this age group is supported by evidence from adequate and well-controlled studies of lacosamide oral solution in adults with partial-onset seizures, pharmacokinetic data from adult and pediatric patients, and safety data in 328 pediatric patients 4 years to less than 17 years of age [see adverse reactions (6.1),  clinical pharmacology (12.3), and clinical studies (14.1, 14.2)] . safety and effectiveness in pediatric patients below 1 month of age have not been established. primary generalized tonic-clonic seizures safety and effectiveness of lacosamide oral solution as adjunctive therapy in the treatment of primary generalized tonic-clonic seizures in pediatric patients with idiopathic generalized epilepsy 4 years of age and older was established in a 24-week double-blind, randomized, placebo-controlled, parallel-group, multi-center study (study 5), which included 37 pediatric patients 4 years to less than 17 years of age [see adverse reactions (6.1) and clinical studies (14.3)] . safety and effectiveness in pediatric patients below the age of 4 years have not been established. animal data lacosamide has been shown in vitro to interfere with the activity of collapsin response mediator protein-2 (crmp-2), a protein involved in neuronal differentiation and control of axonal outgrowth. potential related adverse effects on cns development cannot be ruled out. administration of lacosamide to rats during the neonatal and juvenile periods of postnatal development (approximately equivalent to neonatal through adolescent development in humans) resulted in decreased brain weights and long-term neurobehavioral changes (altered open field performance, deficits in learning and memory). the no-effect dose for developmental neurotoxicity in rats was associated with a plasma lacosamide exposure (auc) less than that in humans at the maximum recommended human dose of 400 mg/day. additional pediatric use information is approved for ucb, inc.’s vimpat® (lacosamide) oral solution. however, due to ucb, inc.’s marketing exclusivity rights, this drug product is not labeled with that information . there were insufficient numbers of elderly patients enrolled in partial-onset seizure trials (n=18) to adequately determine whether they respond differently from younger patients. no lacosamide oral solution dose adjustment based on age is necessary. in elderly patients, dose titration should be performed with caution, usually starting at the lower end of the dosing range, reflecting the greater frequency of decreased hepatic function, decreased renal function, increased cardiac conduction abnormalities, and polypharmacy [see dosage and administration ( 2.1, 2.4, 2.5) and clinical pharmacology ( 12.3)]. no dose adjustment is necessary in patients with mild to moderate renal impairment (clcr ≥30 ml/min). in patients with severe renal impairment (clcr <30 ml/min as estimated by the cockcroft-gault equation for adults; clcr less than 30 ml/min/ 1.73m2 as estimated by the schwartz equation for pediatric patients) and in those with end-stage renal disease, a reduction of 25% of the maximum dosage is recommended [see dosage and administration (2.4) and clinical pharmacology (12.3)]. in all patients with renal impairment, dose initiation and titration should be based on clinical response and tolerability. lacosamide is effectively removed from plasma by hemodialysis. dosage supplementation of up to 50% following hemodialysis should be considered. for adult and pediatric patients with mild to moderate hepatic impairment, a reduction of 25% of the maximum dosage is recommended. patients with mild to moderate hepatic impairment should be observed closely for adverse reactions, and dose initiation and titration should be based on clinical response and tolerability [see dosage and administration (2.5), clinical pharmacology (12.3)]. the pharmacokinetics of lacosamide has not been evaluated in severe hepatic impairment. lacosamide oral solution  use is not recommended in patients with severe hepatic impairment. lacosamide oral solution contains lacosamide, a schedule v controlled substance. abuse is the intentional, non-therapeutic use of a drug, even once, for its desirable psychological or physiological effects. in a human abuse potential study, single doses of 200 mg (equal to the maximum single dosage) and 800 mg lacosamide (equal to twice the recommended daily maintenance dosage)  produced euphoria-type subjective responses that differentiated statistically from placebo; at 800 mg, these euphoria-type responses were statistically indistinguishable from those produced by alprazolam, a schedule iv drug. the duration of the euphoria-type responses following lacosamide was less than that following alprazolam. a high rate of euphoria was also reported as an adverse event in the human abuse potential study following single doses of 800 mg lacosamide (15% [5/34]) compared to placebo (0%) and in two pharmacokinetic studies following single and multiple doses of 300 to 800 mg lacosamide (ranging from 6% [2/33] to 25% [3/12]) compared to placebo (0%). however, the rate of euphoria reported as an adverse event in the lacosamide development program at therapeutic doses was less than 1%. physical dependence is a state that develops as a result of physiological adaptation in response to repeated drug use, manifested by withdrawal signs and symptoms after abrupt discontinuation or a significant dose reduction of a drug. abrupt termination of lacosamide in clinical trials with diabetic neuropathic pain patients produced no signs or symptoms that are associated with a withdrawal syndrome indicative of physical dependence. however, psychological dependence cannot be excluded due to the ability of lacosamide to produce euphoria-type adverse events in humans.

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

apotex corp. - ibandronate sodium (unii: j12u072ql0) (ibandronic acid - unii:umd7g2653w) - ibandronic acid 3 mg in 3 ml - ibandronate sodium injection is indicated for the treatment of osteoporosis in postmenopausal women. in postmenopausal women with osteoporosis, ibandronate sodium injection increases bone mineral density (bmd) and reduces the incidence of vertebral fractures [see clinical studies (14)] . the safety and effectiveness of ibandronate sodium injection for the treatment of osteoporosis are based on clinical data of one year duration. the optimal duration of use has not been determined. all patients on bisphosphonate therapy should have the need for continued therapy re-evaluated on a periodic basis. patients at low-risk for fracture should be considered for drug discontinuation after 3 to 5 years of use. patients who discontinue therapy should have their risk for fracture re-evaluated periodically. ibandronate sodium is contraindicated in patients with the following conditions: - hypocalcemia [see warnings and precautions (5.1)] - known hypersensitivity to ibandronate sodium injection or to any of its excipients. cases of anaphylaxis, including fatal events, have been reported. [ see warnings and precautions (5.2) , adverse reactions (6.2) ] risk summary ibandronate sodium is not indicated for use in women of reproductive potential. there are no data with ibandronate sodium use in pregnant women to inform any drug-associated risks. in reproductive toxicity studies in the rat, ibandronate sodium caused obstruction of labor, with maternal periparturient mortality, pup loss and reduced pup weight at greater than or equal to 2 times human exposure at the recommended human intravenous dose of 3 mg. abnormal pup odontogeny was observed at greater than or equal to 18 times human exposure. in rats dosed during pregnancy, kidney developmental toxicity occurred in offspring at greater than or equal to 47 times human exposure. also, fetal weight and pup growth were reduced at greater than or equal to 5 times human exposure. in reproductive studies in the rabbit, ibandronate sodium caused maternal mortality, reduced maternal body weight gain, decreased litter size due to increased resorption rate, and decreased fetal weight at 19 times the recommended human dose (see data ). data animal data in pregnant rats given intravenous doses producing greater than or equal to 2 times human exposure from day 17 post­-coitum until day 20 post-partum, ibandronate treatment resulted in dystocia, maternal mortality, and early postnatal pup loss in all dose groups. reduced body weight at birth was observed at greater than or equal to 4 times the human exposure. pups exhibited abnormal odontogeny that decreased food consumption and body weight gain at greater than or equal to 18 times human exposure. periparturient mortality has also been observed with other bisphosphonates and appears to be a class effect related to inhibition of skeletal calcium mobilization resulting in hypocalcemia and dystocia. exposure of pregnant rats during the period of organogenesis resulted in an increased fetal incidence of rpu (renal pelvis ureter) syndrome at an intravenous dose producing greater than or equal to 47 times human exposure. in this spontaneous delivery study, dystocia was counteracted by perinatal calcium supplementation. in rat studies with intravenous dosing during gestation, fetal weight and pup growth were reduced at doses producing greater than or equal to 5 times human exposure.  in pregnant rabbits given intravenous doses during the period of organogenesis, maternal mortality, reduced maternal body weight gain, decreased litter size due to increased resorption rate, and decreased fetal weight were observed at 19 times the recommended human intravenous dose. exposure multiples for the rat studies were calculated using human exposure at the recommended intravenous dose of 3 mg every 3 months and were based on cumulative area under the curve (auc) comparison. exposure multiples for the rabbit study were calculated for the recommended human intravenous dose of 3 mg every 3 months and were based on cumulative dose/[body surface area] comparison. doses in pregnant animals were 0.05, 0.1, 0.15, 0.3, 0.5 or 1 mg/kg/day in rats, and 0.03, 0.07, or 0.2 mg/kg/day in rabbits. risk summary ibandronate sodium is not indicated for use in women of reproductive potential. there is no information on the presence of ibandronate in human milk, the effects of ibandronate on the breastfed infant, or the effects of ibandronate on milk production. ibandronate is present in rat milk (see data). the clinical relevance of this data is unclear. data animal data in lactating rats treated with intravenous doses of 0.08 mg/kg, ibandronate was present in breast milk at concentrations of 8.1 to 0.4 ng/ml from 2 to 24 hours after dose administration. concentrations in milk averaged 1.5 times plasma concentrations. safety and effectiveness of ibandronate sodium injection in pediatric patients have not been established. of the patients receiving ibandronate sodium injection 3 mg every 3 months for 1 year, 51% were over 65 years of age. no overall differences in effectiveness or safety were observed between these patients and younger patients, but greater sensitivity in some older individuals cannot be ruled out. ibandronate sodium injection should not be administered to patients with severe renal impairment (creatinine clearance less than 30 ml/min) [see warnings and precautions (5.3)] .

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

apotex corp. - tolvaptan (unii: 21g72t1950) (tolvaptan - unii:21g72t1950) - tolvaptan tablets are indicated for the treatment of clinically significant hypervolemic and euvolemic hyponatremia (serum sodium <125 meq/l or less marked hyponatremia that is symptomatic and has resisted correction with fluid restriction), including patients with heart failure and syndrome of inappropriate antidiuretic hormone (siadh). patients requiring intervention to raise serum sodium urgently to prevent or to treat serious neurological symptoms should not be treated with tolvaptan tablets. it has not been established that raising serum sodium with tolvaptan tablets provides a symptomatic benefit to patients. tolvaptan tablets are contraindicated in the following conditions: - patients with autosomal dominant polycystic kidney disease (adpkd) outside of fda-approved rems [see warnings and precautions (5.2)] - unable to sense or respond to thirst - hypovolemic hyponatremia - taking strong cyp3a inhibitors [see warnings and precautions (5.5)] - anuria - hypersensitivity (e.g., anaphylactic shock, rash gen

Vereinigte Staaten - Englisch - NLM (National Library of Medicine)

apotex corp - amiodarone hydrochloride (unii: 976728sy6z) (amiodarone - unii:n3rq532iut) - amiodarone hydrochloride 200 mg - amiodarone hydrochloride tablets are indicated for the treatment of documented, life-threatening recurrent ventricular fibrillation and life-threatening recurrent hemodynamically unstable tachycardia in adults who have not responded to adequate doses of other available antiarrhythmics or when alternative agents cannot be tolerated. - cardiogenic shock. - sick sinus syndrome, second- or third-degree atrioventricular block, bradycardia leading to syncope without a functioning pacemaker. - known hypersensitivity to the drug or to any of its components, including iodine. risk summary available data from postmarketing reports and published case series indicate that amiodarone use in pregnant women may increase the risk for fetal adverse effects including neonatal hypo- and hyperthyroidism, neonatal bradycardia, neurodevelopmental abnormalities, preterm birth and fetal growth restriction. amiodarone and its metabolite, desethylamiodarone (dea), cross the placenta. untreated underlying arrhythmias, including ventric