Monograph
N03AX18 - Lacosamide |
Propably not porphyrinogenic |
PNP |
Rationale
Clinically insignificant CYP interaction potential.
Chemical description
Functionalized aminoacid: optical antipode of the naturally occurring amino acid L-serine.
Therapeutic characteristics
Adjunctive therapy in partial seizures with or without secondary generalization in patients aged 16 years and above. Lacosamide selectively enhances sodium channel slow inactivation, without affecting fast inactivation. The maximum therapeutic dose is 400 mg per day. In higher doses there is an increased risk for side effects from the central nervous system and the gastrointestinal channel such as dizziness, headache, nausea, vomiting, constipation etc.
Hepatic exposure
No conclusive data. Negligible liver first pass effect.
Metabolism and pharmacokinetics
Metabolism is not fully elucidated. About 95% of a dose is excreted in the urine, about 40% as unchanged drug and less than 30% as the inactive O-desmethyl metabolite. Studies in vitro and in human clinical use show that lacosamide has a low CYP interaction potential. Weak inducer of CYP 3A4 and weak inhibitor of CYP 2C19 in vitro, without clinical significance in therapeutic doses. No other enzymes are involved in the metabolism.
Preclinical data
None.
References
| # |
Citation details |
PMID |
|---|
| * | Scientific articles |
| 1. |
J.J.Kuszczki. Third generation antiepileptic drugs: mechanisms of action, pharmacokinetics and interactions. Pharmacological Reports 2009; 61:197-216.
|
19443931 |
| * | Drug reference publications |
| 2. |
Martindale
|
|
| * | Other sources |
| 3. |
National Formularies ( Swedish, Norwegian and British )
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