| Absorption | Amantadine is well absorbed orally from the gastrointestinal tract. |
| Volume of distribution |
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| Protein binding | Approximately 67% bound to plasma proteins over a concentration range of 0.1 to 2.0 µg/mL. |
| Metabolism | No appreciable metabolism, although negligible amounts of an acetyl metabolite have been identified. |
| Route of elimination | It is primarily excreted unchanged in the urine by glomerular filtration and tubular secretion. |
| Half life | Mean half-lives ranged from 10 to 14 hours, however renal function impairment causes a severe increase in half life to 7 to 10 days. |
| Clearance |
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| Toxicity | Deaths have been reported from overdose with amantadine. The lowest reported acute lethal dose was 2 grams. Drug overdose has resulted in cardiac, respiratory, renal or central nervous system toxicity. Cardiac dysfunction includes arrhythmia, tachycardia and hypertension. Pulmonary edema and respiratory distress (including ARDS) have been reported. Renal dysfunction including increased BUN, decreased creatinine clearance and renal insufficiency can occur. Central nervous system effects that have been reported include insomnia, anxiety, aggressive behavior, hypertonia, hyperkinesia, tremor, confusion, disorientation, depersonalization, fear, delirium, hallucination, psychotic reactions, lethargy, somnolence and coma. Seizures may be exacerbated in patients with prior history of seizure disorders. Hyperthermia has also been observed in cases where a drug overdose has occurred. |
| Affected organisms |
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Amantadine
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