Vimpat

INSTRUCTION FOR MEDICAL USE OF THE MEDICINAL PRODUCT VIMPAT® (VIMPAT®)

Composition:

Active substance: lacosamide;

1 tablet contains 50 mg, 100 mg, 150 mg, or 200 mg of lacosamide;

Excipients: microcrystalline cellulose, low-substituted hydroxypropylcellulose, silicified microcrystalline cellulose, crospovidone, magnesium stearate, hydroxypropylcellulose;

Coating: Opadry II purple 85F20249 (for 50 mg tablets), Opadry II yellow 85F38040 (for 100 mg tablets), Opadry II yellow-brown 85F27043 (for 150 mg tablets), Opadry II blue 85F30675 (for 200 mg tablets) (polyvinyl alcohol, talc, macrogol 3350, titanium dioxide (E 171), yellow iron oxide (E 172, for 100 mg and 150 mg tablets), red iron oxide (E 172, for 50 mg and 150 mg tablets), black iron oxide (E 172, for 50 mg and 150 mg tablets), FD&C blue 2 indigo carmine aluminum lake (E 132, for 50 mg and 200 mg tablets)).

Pharmaceutical form. Film-coated tablets.

Main physicochemical properties:

50 mg tablets: oval, biconvex tablets, coated with an opaque film coating of pale pink color, engraved with "50" on one side and "SP" on the other side;

100 mg tablets: oval, biconvex tablets, coated with an opaque film coating of dark yellow color, engraved with "100" on one side and "SP" on the other side;

150 mg tablets: oval, biconvex tablets, coated with an opaque film coating of orange-pink color, engraved with "150" on one side and "SP" on the other side;

200 mg tablets: oval, biconvex tablets, coated with an opaque film coating of blue color, engraved with "200" on one side and "SP" on the other side.

Pharmacotherapeutic group. Antiepileptic drugs.

ATC code: N03AX18.

Pharmacological Properties.

Mechanism of action

The active substance, lacosamide (R-2-acetamido-N-benzyl-3-methoxypropionamide), is a functionalized amino acid.

The exact mechanism of the antiepileptic action of lacosamide has not been established. In in vitro electrophysiological studies, lacosamide has been shown to selectively enhance the slow inactivation of voltage-gated sodium channels, leading to stabilization of hyperexcitable neuronal membranes.

Pharmacodynamics.

Anticonvulsant efficacy of lacosamide has been demonstrated in various animal models of partial and primary generalized seizures, as well as in delaying kindling development (an experimental model of epileptogenesis). In preclinical studies, lacosamide showed synergistic or additive anticonvulsant effects when used in combination with levetiracetam, carbamazepine, phenytoin, valproate, lamotrigine, topiramate, or gabapentin.

Clinical efficacy and safety

The efficacy of Vimpat® as adjunctive therapy at recommended doses (200 mg/day, 400 mg/day) was established in three multicenter, randomized, placebo-controlled clinical trials with a 12-week maintenance period. The efficacy of 600 mg lacosamide per day was also established in controlled adjunctive therapy trials. Although efficacy at this dose was similar to that of 400 mg/day, patients tolerated the lower dose better, as higher incidence of adverse reactions from the central nervous system and gastrointestinal tract occurred with 600 mg/day. Therefore, a dose of 600 mg/day is not recommended. The maximum recommended dose is 400 mg/day. These trials included 1308 patients with partial seizures, with a mean history of 23 years, and aimed to evaluate the efficacy and safety of lacosamide when used concomitantly with 1–3 other antiepileptic drugs in patients with uncontrolled partial seizures, with or without secondary generalization. Overall, the percentage of patients achieving a 50% reduction in seizure frequency was 23%, 34%, and 40% in the placebo, 200 mg/day, and 400 mg/day lacosamide groups, respectively.

There are insufficient data on discontinuation of concomitant antiepileptic medication to achieve success with lacosamide monotherapy.

The pharmacokinetics and safety of a single intravenous loading dose of lacosamide were evaluated in a multicenter, open-label study designed to assess the safety and tolerability of rapid initiation of lacosamide using a single intravenous loading dose (up to 200 mg), followed by twice-daily oral administration (equivalent to the intravenous dose) as adjunctive therapy in adult patients aged 16 to 60 years with partial seizures.

Pharmacokinetics.

Absorption

Lacosamide is rapidly and completely absorbed after oral administration. The bioavailability of lacosamide in tablet form is approximately 100%. After oral intake, plasma concentrations of unchanged lacosamide increase rapidly, with Cmax reached within 0.5–4 hours. The dosage forms Vimpat® film-coated tablets and oral syrup are bioequivalent. Food does not affect the rate or extent of absorption.

Distribution

The volume of distribution is approximately 0.6 L/kg, and the plasma protein binding is less than 15%.

Biotransformation

Approximately 95% of the dose is excreted in urine as lacosamide and its metabolites. The metabolism of lacosamide has not been fully characterized.

The main compounds excreted in urine are unchanged lacosamide (approximately 40% of the dose) and its O-desmethyl metabolite (less than 30%).

The proportion of polar fraction in urine (likely serine derivatives) was approximately 20%, although only small amounts (0–2%) were detected in plasma of some patients. Small quantities of other metabolites found in urine account for 0.5–2%.

In vitro data indicate that CYP2C9, CYP2C19, and CYP3A4 are capable of catalyzing the formation of the O-desmethyl metabolite, but the primary contributing isoenzyme has not been confirmed in vivo. No clinically relevant differences in lacosamide exposure were observed when comparing pharmacokinetics between extensive metabolizers (individuals with functional CYP2C19) and poor metabolizers (individuals with deficient functional CYP2C19). Furthermore, interaction studies with omeprazole (a CYP2C19 inhibitor) demonstrated no clinically significant changes in lacosamide plasma concentrations, indicating minimal relevance of this metabolic pathway.

The plasma concentration of the O-desmethyl metabolite is approximately 15% of the lacosamide concentration. This major metabolite has no known pharmacological activity.

Elimination

Lacosamide is primarily eliminated from systemic circulation via renal excretion and biotransformation. After oral and intravenous administration of radiolabeled lacosamide, approximately 95% of radioactivity was recovered in urine and less than 0.5% in feces. The elimination half-life of unchanged lacosamide is approximately 13 hours. Pharmacokinetics are dose-proportional, time-independent, and characterized by low inter- and intra-individual variability. Steady-state plasma concentrations are achieved within 3 days with twice-daily dosing. Accumulation results in approximately a two-fold increase in plasma concentration.

A single 200 mg loading dose brings plasma lacosamide concentrations close to those achieved with 100 mg twice daily oral dosing.

Pharmacokinetics in special patient populations

Gender

Clinical studies have shown that gender has no clinically significant effect on lacosamide plasma concentrations.

Renal impairment

AUC values for lacosamide increased by approximately 30% in patients with mild to moderate renal impairment, and by 60% in patients with severe renal impairment and those with end-stage renal disease requiring hemodialysis. However, these conditions do not affect Cmax.

Lacosamide is effectively removed from plasma by hemodialysis. After 4 hours of hemodialysis, lacosamide AUC is reduced by approximately 50%. Therefore, a supplemental dose is recommended after hemodialysis. Exposure to the O-desmethyl metabolite increases several-fold in patients with moderate to severe renal impairment. If hemodialysis is not performed in patients with end-stage renal disease, these values remain elevated and continuously increase, as shown by analyses conducted over 24 hours. It is unknown whether increased exposure to the metabolite in patients with end-stage renal disease may lead to adverse reactions, although no pharmacological activity of this metabolite has been identified.

Hepatic impairment

Increased lacosamide concentrations (approximately 50% higher AUCnorm) were observed in patients with moderate hepatic impairment (Child-Pugh class B). The increased exposure is partially attributed to reduced renal function in the study participants. Reduced non-renal clearance in these patients resulted in a 20% increase in lacosamide AUC. The pharmacokinetics of lacosamide in patients with severe hepatic impairment have not been studied.

Elderly patients (aged 65 years and older)

In studies involving elderly men and women, including 4 patients aged 75 years and older, AUC levels were approximately 30% and 50% higher, respectively, compared to younger patients. This difference is partly due to lower body weight. The difference was 26% and 23%, respectively, when adjusted for body weight. Increased variability in drug exposure was also observed. These studies showed that renal clearance of lacosamide in elderly patients was only slightly reduced.

The total dose of the drug should not be reduced, except when indicated due to impaired renal function.

Clinical characteristics.

Indications.

As adjunctive therapy for the treatment of partial-onset seizures, with or without secondary generalization, in patients aged 16 years and older with epilepsy.

Contraindications.

Hypersensitivity to the active substance or to any of the excipients.

Second- or third-degree atrioventricular block in medical history.

Interaction with other medicinal products and other forms of interactions.

Lacosamide should be used with caution in patients receiving drugs that may cause PR interval prolongation (including antiepileptic drugs that are sodium channel blockers), and in patients receiving antiarrhythmic agents.

However, subgroup analyses from clinical trials did not show additional PR interval prolongation in patients who received lacosamide concomitantly with carbamazepine or lamotrigine.

In vitro data

Overall study results indicate a low likelihood of lacosamide interactions with other drugs. In vitro studies show that lacosamide does not induce CYP1A2, 2B6, or 2C9 enzymes and does not inhibit CYP1A1, 1A2, 2A6, 2B6, 2C8, 2C9, 2D6, or 2E1 at plasma concentrations observed during clinical trials. In vitro studies indicate that lacosamide is not transported by P-glycoprotein in the intestine. In vitro data suggest that CYP2C9, CYP2C19, and CYP3A4 are capable of catalyzing the formation of the O-desmethyl metabolite.

In vivo data

In vivo, lacosamide does not clinically significantly inhibit or induce CYP2C19 and 3A4 enzymes.

Lacosamide did not affect the AUC of midazolam (metabolized by CYP3A4, lacosamide administered at a dose of 200 mg twice daily), although the Cmax of midazolam was slightly increased (by 30%). Lacosamide did not affect the pharmacokinetics of omeprazole (metabolized by CYP2C19 and 3A4, lacosamide administered at a dose of 300 mg twice daily).

The CYP2C19 inhibitor omeprazole (40 mg once daily) did not cause clinically significant changes in lacosamide exposure. Therefore, it is unlikely that moderately potent CYP2C19 inhibitors will have a clinically significant effect on systemic lacosamide exposure. Concomitant use of potent CYP2C9 inhibitors (e.g., fluconazole) and CYP3A4 inhibitors (e.g., itraconazole, ketoconazole, ritonavir, clarithromycin), which may increase systemic lacosamide exposure, is recommended with caution. Such interactions have not been established in vivo, but their likelihood is based on in vitro data.

Strong enzyme inducers such as rifampicin or St John’s wort (Hypericum perforatum) may cause a moderate decrease in systemic lacosamide exposure. Therefore, caution is advised when initiating or discontinuing such medications.

Antiepileptic drugs

In interaction studies, lacosamide did not cause significant changes in plasma concentrations of carbamazepine or valproic acid. In turn, carbamazepine and valproic acid did not affect plasma levels of lacosamide. According to population pharmacokinetic analysis, concomitant therapy with other enzyme-inducing antiepileptic drugs (carbamazepine, phenytoin, phenobarbital at various doses) reduced total systemic exposure to lacosamide by 25%.

Oral contraceptives

An interaction study did not reveal signs of a clinically significant interaction between lacosamide and oral contraceptives containing ethinylestradiol and levonorgestrel. Progesterone concentrations were not altered when the drugs were used concomitantly.

Others

Lacosamide did not affect the pharmacokinetics of digoxin. No clinically significant interaction between lacosamide and metformin was observed.

Concomitant administration of warfarin with lacosamide did not reveal clinically significant changes in the pharmacokinetics or pharmacodynamics of warfarin.

Although pharmacokinetic data on the interaction of lacosamide with alcohol are lacking, a pharmacodynamic effect cannot be excluded.

The extent of lacosamide protein binding is low, less than 15%. Therefore, clinically significant interactions with other drugs that bind to plasma proteins are unlikely.

Special precautions for use.

Dizziness

Treatment with lacosamide is associated with dizziness, which may lead to an increased incidence of accidental injuries and falls. Therefore, patients should be advised to exercise caution until they become familiar with the potential effects of the medicinal product (see section "Adverse reactions").

Cardiac rhythm and conduction

In clinical trials, dose-dependent prolongation of the PR interval was observed during lacosamide administration. Lacosamide should be used with caution in patients with known proarrhythmic conditions such as cardiac conduction disorders or serious cardiac diseases (e.g. ischemia/myocardial infarction, heart failure, structural heart disease, or cardiac sodium channelopathies), in patients taking medicinal products that affect cardiac conduction, including antiarrhythmic agents and antiepileptic sodium channel blockers (see section "Interaction with other medicinal products and other forms of interaction"), and in elderly patients.

In placebo-controlled studies of lacosamide in patients with epilepsy, no reports of atrial fibrillation or flutter were observed; however, such events were reported during open-label epilepsy studies and in post-marketing surveillance.

During post-marketing surveillance, cases of second- or higher-degree atrioventricular block have been reported. Ventricular tachyarrhythmias have been reported in patients with proarrhythmic conditions. Rarely, these events led to asystole, cardiac arrest, or death in patients with known proarrhythmic conditions.

Patients should be informed about symptoms of cardiac arrhythmia (e.g. slow, fast, or irregular pulse, palpitations, shortness of breath, confusion, or loss of consciousness). Patients should seek immediate medical attention if such symptoms occur.

Suicidal thoughts and behaviour

Suicidal thoughts and behaviour have been observed in patients treated with antiepileptic medicinal products for various conditions. A meta-analysis of randomized, placebo-controlled clinical trials of antiepileptic medicinal products also demonstrated a small increased risk of suicidal thoughts and behaviour. The mechanism of this risk is unknown, and available data do not exclude a possible increased risk with lacosamide use.

Therefore, patients should be monitored for signs of suicidal thoughts and behaviour, and appropriate treatment should be initiated if necessary. Patients (and caregivers) should be advised to seek medical advice promptly if signs of suicidal thoughts or behaviour emerge (see section "Adverse reactions").

Use during pregnancy or breastfeeding.

Women of childbearing potential

Physicians should discuss family planning and contraceptive methods with women of childbearing potential who are taking lacosamide (see "Pregnancy" below).

If a woman plans to become pregnant, the continued use of lacosamide should be re-evaluated.

Pregnancy

Risk associated with epilepsy and use of antiepileptic drugs in general. The incidence of congenital malformations in newborns of mothers receiving treatment for epilepsy is 2–3 times higher than in the general population (approximately 3%). Polytherapy in pregnant women has been associated with an increased frequency of congenital malformations in offspring, although it remains unclear to what extent this is due to treatment and/or the underlying disease. Moreover, effective antiepileptic therapy should not be discontinued during pregnancy, as worsening of the disease may have serious consequences for both mother and fetus.

Risk associated with use of lacosamide. There are no adequate data on the use of lacosamide in pregnant women. Animal studies (in rats and rabbits) did not reveal teratogenic effects of the drug, but embryotoxicity was observed when the drug was administered at maternal toxic doses. The possibility of risk in humans is unknown. Lacosamide should not be used during pregnancy except when treatment is necessary (i.e. when benefit to the pregnant woman clearly outweighs the potential risk to the fetus). If a woman plans pregnancy, careful consideration of the appropriateness of using this drug is required.

Breastfeeding

Lacosamide is excreted in human breast milk. Risk to newborns/infants cannot be excluded. Breastfeeding is recommended to be discontinued during lacosamide treatment.

Fertility

Adverse effects on fertility and reproductive function in male and female rats were not observed at doses where plasma drug exposure (AUC) was approximately twice that of human plasma AUC at the maximum recommended dose.

Ability to affect reaction speed when driving or operating machinery.

Vimpat® has a minor or moderate influence on the ability to drive or operate machinery. Treatment with this medicinal product has been associated with dizziness or blurred vision. Therefore, patients should not drive or operate potentially hazardous machinery until their individual response to Vimpat® is known.

Dosage and Administration

Vimpat® should be administered twice daily (usually once in the morning and once in the evening). If a dose is missed, patients should be advised to take the missed dose immediately, and then continue with the next dose according to the prescribed schedule. However, if the missed dose is noticed within 6 hours before the next scheduled dose, patients should be advised to wait and take the next dose at the regular time. Patients must not take a double dose.

The recommended initial dose is 50 mg twice daily. After 1 week, the dose should be increased to the initial therapeutic dose of 100 mg twice daily.

Depending on therapeutic response and tolerability, the maintenance dose may be further increased at weekly intervals by 50 mg twice daily (100 mg per day) up to the maximum recommended daily dose of 400 mg (200 mg twice daily).

Initiation of treatment with a loading dose of lacosamide

Treatment may also be initiated with a single loading dose of 200 mg, followed approximately 12 hours later by a maintenance dose of 100 mg twice daily (200 mg/day). Subsequent dose adjustments should be made according to individual response and tolerability, as described above. A loading dose may be considered for patients when the physician determines that rapid achievement of steady-state plasma concentrations of lacosamide and therapeutic effect is justified. Administration should be performed under medical supervision due to the potential for increased frequency of serious cardiac arrhythmias and central nervous system adverse reactions (see section "Adverse Reactions"). The administration of a loading dose has not been studied in acute conditions such as status epilepticus.

Discontinuation of treatment

According to current clinical practice, Vimpat® should be discontinued gradually (by reducing the dose by 200 mg per week).

In patients who develop a serious cardiac arrhythmia, a clinical benefit/risk assessment should be performed and lacosamide should be discontinued if necessary.

Special populations

Use in elderly patients (aged 65 years and older)

No dose adjustment is required for elderly patients. Experience with the use of lacosamide in elderly patients with epilepsy is limited. For elderly patients, the possibility of age-related reduction in renal clearance and increased AUC should be considered (see sections "Use in patients with renal impairment" and "Pharmacokinetics").

Use in patients with renal impairment

No dose adjustment is required for patients with mild or moderate renal impairment (creatinine clearance > 30 mL/min).

A loading dose (200 mg) may be administered to patients with mild or moderate renal impairment, but subsequent dose titration (> 200 mg/day) should be performed with caution. For patients with severe renal impairment (creatinine clearance ≤ 30 mL/min) and those with end-stage renal disease, a maximum dose of 250 mg/day is recommended. Dose titration in these patients should be performed cautiously. If a loading dose is administered, an initial single dose of 100 mg/day followed by 50 mg twice daily should be used during the first week.

For patients undergoing hemodialysis, it is recommended to administer an additional 50% of the daily dose immediately at the end of the hemodialysis procedure. Treatment of patients with end-stage renal disease should be performed with caution due to limited clinical experience and the potential accumulation of a metabolite with no known pharmacological activity.

Use in patients with hepatic impairment

For patients with mild or moderate hepatic impairment, a maximum dose of 300 mg/day is recommended.

Dose titration in these patients should be performed with caution, considering the possibility of concomitant renal impairment. A loading dose (200 mg) may be administered, but subsequent dose titration (> 200 mg/day) should be performed with caution. The pharmacokinetics of lacosamide have not been studied in patients with severe hepatic impairment. Lacosamide should be prescribed to patients with severe hepatic impairment only if the expected therapeutic benefit outweighs the potential risks.

Dose adjustment may be necessary based on careful monitoring of disease activity and consideration of potential adverse effects in the patient.

Pediatric use

The drug is not recommended for children under 16 years of age, as safety and efficacy have not been established in these age groups.

Administration method

Lacosamide film-coated tablets are intended for oral administration. Lacosamide may be taken independently of food intake.

Pediatric use.

The use of the drug is not recommended in children under 16 years of age, as safety and efficacy have not been studied in these age groups.

Overdose.

Symptoms

Symptoms observed following accidental or intentional overdose of lacosamide are primarily related to the central nervous system (CNS) and gastrointestinal tract.

• No clinically significant differences in the type of adverse reactions were observed between patients receiving doses above 400 mg up to 800 mg and those receiving therapeutic doses of lacosamide.
• Reactions reported after ingestion of more than 800 mg include dizziness, nausea, vomiting, seizures (generalized tonic-clonic seizures, status epilepticus). Cardiac conduction disturbances, shock, and coma have also been observed. Fatal outcomes have been reported in patients following acute single overdose (ingestion of several grams of lacosamide).

Treatment

There is no specific antidote for lacosamide overdose. Management of overdose includes general supportive measures and, if necessary, hemodialysis.

Adverse Reactions

Based on pooled results from placebo-controlled clinical trials as adjunctive therapy involving 1308 patients with partial-onset seizures, it was established that 61.9% of patients randomized to the lacosamide group and 35.2% of patients randomized to the placebo group experienced at least one adverse reaction. The most common adverse reactions (≥ 10%) with lacosamide were dizziness, headache, nausea, and diplopia. These were generally mild or moderate in severity. Some of these reactions were dose-dependent, and dose reduction led to their alleviation. The frequency and severity of central nervous system and gastrointestinal adverse reactions generally decreased over time.

In all these controlled clinical trials, treatment discontinuation due to adverse reactions occurred in 12.2% of patients in the lacosamide group compared to 1.6% in the placebo group. Dizziness was the most frequent reason for discontinuation of lacosamide treatment.

The frequency of central nervous system adverse reactions (such as dizziness) may increase after administration of a loading dose.

The adverse reactions listed below were identified during clinical trials and post-marketing surveillance. Adverse reaction frequencies are defined as follows: very common (≥ 1/10), common (≥ 1/100 to < 1/10), uncommon (≥ 1/1000 to < 1/100), frequency not known (cannot be estimated from available data). Within each category, adverse reactions are listed in order of decreasing severity.

Blood and lymphatic system disorders: frequency not known – agranulocytosis¹.

Immune system disorders: uncommon – drug hypersensitivity¹; frequency not known – drug reaction with eosinophilia and systemic symptoms (DRESS)¹,².

Nervous system disorders: very common – dizziness, headache; common – balance disorder, memory impairment, cognitive disorder, somnolence, tremor, nystagmus, hypoaesthesia, dysarthria, attention disturbance, paraesthesia; uncommon – loss of consciousness², incoordination, dyskinesia; frequency not known – convulsions.

Psychiatric disorders: common – depression, confusional state, insomnia¹; uncommon – aggression, agitation¹, euphoric mood¹, psychotic disorder¹, suicide attempt¹, suicidal ideation, hallucinations¹.

Eye disorders: very common – diplopia; common – blurred vision.

Ear and labyrinth disorders: common – vertigo, tinnitus.

Cardiac disorders: uncommon – atrioventricular block¹,², bradycardia¹,², atrial fibrillation¹,², atrial flutter¹,²; frequency not known – ventricular tachyarrhythmia¹.

Gastrointestinal disorders: very common – nausea; common – vomiting, constipation, flatulence, dyspepsia, dry mouth, diarrhoea.

Hepatobiliary disorders: uncommon – liver function test abnormalities¹, increased liver enzymes (> 2 × ULN)¹.

Skin and subcutaneous tissue disorders: common – pruritus, rash¹; uncommon – angioneurotic oedema¹, urticaria¹; frequency not known – Stevens-Johnson syndrome¹, toxic epidermal necrolysis¹.

Musculoskeletal and connective tissue disorders: common – muscle spasm.

General disorders and administration site conditions: common – gait disturbance, asthenia, fatigue, irritability, feeling drunk.

Injury, poisoning and procedural complications: common – fall, skin fissures, contusion.

Notes:

1 Adverse reactions reported during the post-marketing period;

2 See description of individual adverse reactions.

Individual Adverse Reactions

Lacosamide administration is associated with dose-dependent prolongation of the PR interval. Adverse reactions related to PR interval prolongation (atrioventricular block, loss of consciousness, bradycardia) are possible.

In additional clinical trials of patients with epilepsy, first-degree atrioventricular block was observed uncommonly, in 0.7% and 0.5% of patients receiving lacosamide 200 mg and 600 mg, respectively, and was not observed at the 400 mg dose or with placebo. In patients receiving lacosamide in these trials, second- or higher-degree atrioventricular block was not observed. However, cases of second- and third-degree atrioventricular block associated with lacosamide treatment have been reported during post-marketing surveillance.

In pooled adjunctive therapy clinical trials, loss of consciousness occurred uncommonly, and its frequency did not differ between patients with epilepsy receiving lacosamide (0.1%, n = 944) and those receiving placebo (0.3%, n = 364).

Atrial fibrillation or flutter was not reported during short-term clinical trials; however, both events have been observed in open-label epilepsy trials and during post-marketing monitoring.

Laboratory parameter abnormalities

Abnormalities in liver function parameters were observed during placebo-controlled lacosamide trials in adult patients with partial-onset seizures who were concurrently taking 1 to 3 antiepileptic drugs. ALT levels increased to ≥ 3 × ULN (upper limit of normal) in 0.7% (7/935) of patients receiving Vimpat® and in 0% (0/356) of patients in the placebo group.

Multi-organ hypersensitivity reactions

Multi-organ hypersensitivity reactions (also known as drug reaction with eosinophilia and systemic symptoms (DRESS)) have been reported in patients taking certain antiepileptic drugs. These reactions varied in presentation but typically included fever and rash, and were associated with multi-organ involvement. If a multi-organ hypersensitivity reaction is suspected, lacosamide should be discontinued.

Children

The frequency, type, and severity of adverse reactions in patients aged 16 years and older are expected to be similar to those in adults. Safety in children under 16 years of age has not been established. No data available.

Reporting of suspected adverse reactions

Reporting suspected adverse reactions after medicinal product authorization is important. It allows continued monitoring of the benefit-risk balance of the medicinal product. Healthcare professionals, pharmacists, patients, and their legal representatives should report all suspected adverse reactions and lack of efficacy via the Automated Pharmacovigilance Information System at: https://aisf.dec.gov.ua.

Shelf life. 5 years.

Storage conditions.

Keep out of the reach of children. No special storage conditions required.

Packaging.

14 tablets per blister. 1 or 4 blisters per cardboard box.

Prescription status. Prescription only.

Manufacturer.

SciCan Pharmaceuticals GmbH.

Manufacturer's location and address of place of business.

Alfred-Nobel-Str. 10, 40789 Monheim am Rhein, Germany.