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

ascend laboratories, llc - lacosamide (unii: 563ks2pqy5) (lacosamide - unii:563ks2pqy5) - lacosamide tablets are 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) tablets. however, due to ucb, inc.'s marketing exclusivity rights, this drug product is not labeled with that pediatric information. none. pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as lacosamide, during pregnancy. encourage women who are taking lacosamide 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 available data from the north american antiepileptic drug (naaed) pregnancy registry, a prospective cohort study, case reports, and a case series with lacosamide 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.  data 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 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 in this age group is supported by evidence from adequate and well- controlled studies of lacosamide 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.    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) tablets. however, due to ucb, inc.’s marketing exclusivity rights, this drug product is not labeled with that pediatric 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 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 <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 use is not recommended in patients with severe hepatic impairment. lacosamide tablets 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.

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

zydus pharmaceuticals usa inc. - lacosamide (unii: 563ks2pqy5) (lacosamide - unii:563ks2pqy5) - lacosamide is indicated for the treatment of partial-onset seizures in patients 4 years of age and older. pediatric use information is approved for ucb, inc.'s vimpat® (lacosamide) injection. however, due to ucb, inc.'s marketing exclusivity rights, this drug product is not labeled with that information. lacosamide is indicated as adjunctive therapy in the treatment of primary generalized tonic-clonic seizures in patients 4 years of age and older. none. pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as lacosamide, during pregnancy. encourage women who are taking lacosamide 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 available data from the north american antiepileptic drug (naaed) pregnancy registry, a prospective cohort study, case reports, and a case series with lacosamide 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. data 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 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 in this age group is supported by evidence from adequate and well-controlled studies of lacosamide 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) and clinical pharmacology (12.3)] . 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 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. pediatric use information is approved for ucb, inc.'s vimpat® (lacosamide) injection. 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 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 <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 use is not recommended in patients with severe hepatic impairment. lacosamide is 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 300-800 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.

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

aurobindo pharma limited - lacosamide (unii: 563ks2pqy5) (lacosamide - unii:563ks2pqy5) - lacosamide tablets are 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) tablets. however, due to ucb, inc.’s marketing exclusivity rights, this drug product is not labeled with that information. lacosamide tablets are indicated as adjunctive therapy in the treatment of primary generalized tonic-clonic seizures in patients 4 years of age and older. none. pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as lacosamide, during pregnancy. encourage women who are taking lacosamide 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 available data from the north american antiepileptic drug (naaed) pregnancy registry, a prospective cohort study, case reports, and a case series with lacosamide 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. data 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 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 in this age group is supported by evidence from adequate and well-controlled studies of lacosamide 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 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) tablets. 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 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 <30 ml/min/1.73 m2 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 use is not recommended in patients with severe hepatic impairment. lacosamide tablets contain 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.

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

northstar rx llc. - lacosamide (unii: 563ks2pqy5) (lacosamide - unii:563ks2pqy5) - lacosamide is indicated for the treatment of partial-onset seizures in patients 4 years of age and older. pediatric use information is approved for ucb, inc.'s vimpat® (lacosamide) injection. however, due to ucb, inc.'s marketing exclusivity rights, this drug product is not labeled with that information. lacosamide is indicated as adjunctive therapy in the treatment of primary generalized tonic-clonic seizures in patients 4 years of age and older. none. pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as lacosamide, during pregnancy. encourage women who are taking lacosamide 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 available data from the north american antiepileptic drug (naaed) pregnancy registry, a prospective cohort study, case reports, and a case series with lacosamide 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. data 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 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 in this age group is supported by evidence from adequate and well-controlled studies of lacosamide 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) and clinical pharmacology (12.3)] . 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 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. pediatric use information is approved for ucb, inc.'s vimpat® (lacosamide) injection. 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 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; cl cr <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 use is not recommended in patients with severe hepatic impairment. lacosamide is 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.

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

ucb, inc. - levetiracetam (unii: 44yrr34555) (levetiracetam - unii:44yrr34555) - levetiracetam 250 mg - keppra is indicated for the treatment of partial-onset seizures in patients 1 month of age and older. keppra is indicated as adjunctive therapy for the treatment of myoclonic seizures in patients 12 years of age and older with juvenile myoclonic epilepsy. keppra is indicated as adjunctive therapy for the treatment of primary generalized tonic-clonic seizures in patients 6 years of age and older with idiopathic generalized epilepsy. keppra is contraindicated in patients with a hypersensitivity to levetiracetam. reactions have included anaphylaxis and angioedema [see warnings and precautions (5.4)] . pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), including keppra, during pregnancy. encourage women who are taking keppra 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 prolonged experience with keppra in pregnant women has not identified a drug-associated risk of major birth defects or miscarriage, based on published literature, which includes data from pregnancy registries and reflects experience over two decades [see human data] . in animal studies, levetiracetam produced developmental toxicity (increased embryofetal and offspring mortality, increased incidences of fetal structural abnormalities, decreased embryofetal and offspring growth, neurobehavioral alterations in offspring) at doses similar to human therapeutic doses [see animal data] . 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. the background risk of major birth defects and miscarriage for the indicated population is unknown. clinical considerations levetiracetam blood levels may decrease during pregnancy [see warnings and precautions (5.11)] . physiological changes during pregnancy may affect levetiracetam concentration. decrease in levetiracetam plasma concentrations has been observed during pregnancy. this decrease is more pronounced during the third trimester. dose adjustments may be necessary to maintain clinical response. data human data while available studies cannot definitively establish the absence of risk, data from the published literature and pregnancy registries have not established an association with levetiracetam use during pregnancy and major birth defects or miscarriage. animal data when levetiracetam (0, 400, 1200, or 3600 mg/kg/day) was administered orally to pregnant rats during the period of organogenesis, reduced fetal weights and increased incidence of fetal skeletal variations were observed at the highest dose tested. there was no evidence of maternal toxicity. the no-effect dose for adverse effects on embryofetal developmental in rats (1200 mg/kg/day) is approximately 4 times the maximum recommended human dose (mrhd) of 3000 mg on a body surface area (mg/m2 ) basis. oral administration of levetiracetam (0, 200, 600, or 1800 mg/kg/day) to pregnant rabbits during the period of organogenesis resulted in increased embryofetal mortality and incidence of fetal skeletal variations at the mid and high dose and decreased fetal weights and increased incidence of fetal malformations at the high dose, which was associated with maternal toxicity. the no-effect dose for adverse effects on embryofetal development in rabbits (200 mg/kg/day) is approximately equivalent to the mrhd on a mg/m2 basis. oral administration of levetiracetam (0, 70, 350, or 1800 mg/kg/day) to female rats throughout pregnancy and lactation led to an increased incidence of fetal skeletal variations, reduced fetal body weight, and decreased growth in offspring at the mid and high doses and increased pup mortality and neurobehavioral alterations in offspring at the highest dose tested. there was no evidence of maternal toxicity. the no-effect dose for adverse effects on pre- and postnatal development in rats (70 mg/kg/day) is less than the mrhd on a mg/m2 basis. oral administration of levetiracetam to rats during the latter part of gestation and throughout lactation produced no adverse developmental or maternal effects at doses of up to 1800 mg/kg/day (6 times the mrhd on a mg/m2 basis). risk summary levetiracetam is excreted in human milk. there are no data on the effects of keppra on the breastfed infant, or the effects on milk production. the developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for keppra and any potential adverse effects on the breastfed infant from keppra or from the underlying maternal condition. the safety and effectiveness of keppra for the treatment of partial-onset seizures in patients 1 month to 16 years of age have been established [see clinical pharmacology (12.3) and clinical studies (14.1)] . the dosing recommendation in these pediatric patients varies according to age group and is weight-based [see dosage and administration (2.2)] . the safety and effectiveness of keppra as adjunctive therapy for the treatment of myoclonic seizures in adolescents 12 years of age and older with juvenile myoclonic epilepsy have been established [see clinical studies (14.2)] . the safety and effectiveness of keppra as adjunctive therapy for the treatment of primary generalized tonic-clonic seizures in pediatric patients 6 years of age and older with idiopathic generalized epilepsy have been established [see clinical studies (14.3)] . safety and effectiveness for the treatment of partial-onset seizures in pediatric patients below the age of 1 month; adjunctive therapy for the treatment of myoclonic seizures in pediatric patients below the age of 12 years; and adjunctive therapy for the treatment of primary generalized tonic-clonic seizures in pediatric patients below the age of 6 years have not been established. a 3-month, randomized, double-blind, placebo-controlled study was performed to assess the neurocognitive and behavioral effects of keppra as adjunctive therapy in 98 (keppra n=64, placebo n=34) pediatric patients, ages 4 to 16 years old, with partial seizures that were inadequately controlled. the target dose was 60 mg/kg/day. neurocognitive effects were measured by the leiter-r attention and memory (am) battery, which measures various aspects of a child's memory and attention. although no substantive differences were observed between the placebo and drug treated groups in the median change from baseline in this battery, the study was not adequate to assess formal statistical non-inferiority of the drug and placebo. the achenbach child behavior checklist (cbcl/6-18), a standardized validated tool used to assess a child's competencies and behavioral/emotional problems, was also assessed in this study. an analysis of the cbcl/6-18 indicated on average a worsening in keppra-treated patients in aggressive behavior, one of the eight syndrome scores [see warnings and precautions (5.1)] . juvenile animal toxicity data studies of levetiracetam in juvenile rats (dosed on postnatal days 4 through 52) and dogs (dosed from postnatal weeks 3 through 7) at doses of up to 1800 mg/kg/day (approximately 7 and 24 times, respectively, the maximum recommended pediatric dose of 60 mg/kg/day on a mg/m2 basis) did not demonstrate adverse effects on postnatal development. there were 347 subjects in clinical studies of keppra that were 65 and over. no overall differences in safety were observed between these subjects and younger subjects. there were insufficient numbers of elderly subjects in controlled trials of epilepsy to adequately assess the effectiveness of keppra in these patients. levetiracetam is known to be substantially excreted by the kidney, and the risk of adverse reactions to this drug may be greater in patients with impaired renal function. because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, and it may be useful to monitor renal function [see clinical pharmacology (12.3)] . clearance of levetiracetam is decreased in patients with renal impairment and is correlated with creatinine clearance [see clinical pharmacology (12.3)] . dose adjustment is recommended for patients with impaired renal function and supplemental doses should be given to patients after dialysis [see dosage and administration (2.5)] .

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

glenmark pharmaceuticals inc. usa - lacosamide (unii: 563ks2pqy5) (lacosamide - unii:563ks2pqy5) - lacosamide tablets are 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) tablets. however, due to ucb, inc.’s marketing exclusivity rights, this drug product is not labeled with that information. none. pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as lacosamide, during pregnancy. encourage women who are taking lacosamide 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 available data from the north american antiepileptic drug (naaed) pregnancy registry, a prospective cohort study, case reports, and a case series with lacosamide use in pregnant women are insufficient to identify a drug associated risk of major birth defects, miscarriage or other

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

indoco remedies limited - lacosamide (unii: 563ks2pqy5) (lacosamide - unii:563ks2pqy5) - lacosamide tablets 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) tablets. however, due to ucb, inc.’s marketing exclusivity rights, this drug product is not labeled with that pediatric information. none. pregnancy exposure registry  there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as lacosamide, during pregnancy. encourage women who are taking lacosamide 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 there are no adequate data on the developmental risks associated with the use of lacosamide in pregnant women. lacosamide produced developmental toxicity (increased embryofetal and perinatal mortality, growth deficit) in rats following administration during pregn

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

sagent pharmaceuticals - lacosamide (unii: 563ks2pqy5) (lacosamide - unii:563ks2pqy5) - lacosamide injection is indicated for the treatment of partial-onset seizures in patients 17 years of age and older. pediatric use information is approved for ucb, inc.'s vimpat ® (lacosamide) injection. however, due to ucb, inc.'s marketing exclusivity rights, this drug product is not labeled with that pediatric information. none. pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as lacosamide, during pregnancy. encourage women who are taking lacosamide 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 available data from the north american antiepileptic drug (naaed) pregnancy registry, a prospective cohort study, case reports, and a case series with lacosamide use in pregnant women are insufficient to identify a drug associated risk of major birth defects, miscarriage or o

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

avkare - lacosamide (unii: 563ks2pqy5) (lacosamide - unii:563ks2pqy5) - lacosamide tablets are 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) tablets. however, due to ucb, inc.’s marketing exclusivity rights, this drug product is not labeled with that pediatric information. none.  pregnancy exposure registry  there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as lacosamide, during pregnancy. encourage women who are taking lacosamide 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  there are no adequate data on the developmental risks associated with the use of lacosamide in pregnant women.  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) .  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. the background risk of major birth defects and miscarriage for the indicated population is unknown.  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  there are no data on the presence of lacosamide in human milk, the effects on the breastfed infant, or the effects on milk production. studies in lactating rats have shown excretion of lacosamide and/or its metabolites in milk.  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.  partial-onset seizures safety and effectiveness of lacosamide 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 in this age group is supported by evidence from adequate and well-controlled studies of lacosamide 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. 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) tablets. however, due to ucb, inc.’s marketing exclusivity rights, this drug product is not labeled with that pediatric 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 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,  2.3,  2.4)  and   clinical pharmacology (12.3)] .  based on data in adults, no dose adjustment is necessary in adult and pediatric patients with mild to moderate renal impairment (cl cr ≥30 ml/min). in adult and pediatric patients with severe renal impairment (cl cr <30 ml/min) and in those with end-stage renal disease, a reduction of 25% of the maximum dosage is recommended  [see dosage and administration (2.3)  and   clinical pharmacology (12.3)] .  in all patients with renal impairment, dose titration should be performed with caution.  lacosamide is effectively removed from plasma by hemodialysis. dosage supplementation of up to 50% following hemodialysis should be considered.  based on data in adults, 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 during dose titration  [see dosage and administration (2.4),  clinical pharmacology (12.3)] . the pharmacokinetics of lacosamide has not been evaluated in severe hepatic impairment. lacosamide use is not recommended in patients with severe hepatic impairment.  lacosamide is a schedule v controlled substance. in a human abuse potential study, single doses of 200 mg and 800 mg lacosamide 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%.  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. 

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

zydus pharmaceuticals usa inc. - lacosamide (unii: 563ks2pqy5) (lacosamide - unii:563ks2pqy5) - lacosamide is indicated for the treatment of partial-onset seizures in patients 4 years of age and older. pediatric use information is approved for ucb, inc.'s vimpat® (lacosamide) injection. however, due to ucb, inc.'s marketing exclusivity rights, this drug product is not labeled with that information. lacosamide is indicated as adjunctive therapy in the treatment of primary generalized tonic-clonic seizures in patients 4 years of age and older. none. pregnancy exposure registry there is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to antiepileptic drugs (aeds), such as lacosamide, during pregnancy. encourage women who are taking lacosamide 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 available data from the north american antiepileptic drug (naaed) pregnancy registry, a prospective cohort study, case reports, and a case series with la