Mechanism of action In Lambert–Eaton myasthenic syndrome, acetylcholine release is inhibited as antibodies involved in the host response against certain cancers cross-react with Ca2+ channels on the prejunctional membrane.<unk>  works by blocking potassium channel efflux in nerve terminals so that action potential duration is increased. Ca2+ channels can then be open for a longer time and allow greater acetylcholine release to stimulate muscle at the end plate. Pharmacokinetics N-(4-Amino-3-pyridinyl)acetamide or 3-N-acetylamifampridine, the thumb<unk>  is quickly and almost completely (93–100%) absorbed from the gut. In a study with 91 healthy subjects, maximum<unk>  concentrations in blood plasma were reached after 0.6 (±0.25) hours when taken without food, or after 1.3 (±0.9) hours after a fatty meal, meaning that the speed of absorption varies widely. Biological half-life (2.5±0.7 hrs) and the area under the curve (AUC = 117±77 ng∙h/ml) also vary widely between subjects, but are nearly independent of food intake. The substance is deactivated by acetylation via N-acetyltransferases to the single metabolite 3-N-acetylamifampridine. Activity of these enzymes (primarily N-acetyltransferase 2) in different individuals seems to be primarily responsible for the mentioned differences in half-life and AUC: the latter is increased up to 9-fold in slow metabolizers as compared to fast metabolizers.<unk>  is eliminated via the kidneys and urine to 74–81% as N-acetylamifampridine and to 19% in unchanged form.
Amifampridine
Secnidazole
Rifampicin
Miproxifene phosphate
Tinidazole
Rifabutin
Azficel-T
Piretanide