For management of depression and for Obsessive Compulsive Disorder (OCD). Has also been used in the management of bulimia nervosa.
The exact mechanism of action of fluvoxamine has not been fully determined, but appears to be linked to its inhibition of CNS neuronal uptake of serotonin. Fluvoxamine blocks the reuptake of serotonin at the serotonin reuptake pump of the neuronal membrane, enhancing the actions of serotonin on 5HT<sub>1A</sub> autoreceptors. In-vitro studies suggest that fluvoxamine is more potent than clomipramine, fluoxetine, and desipramine as a serotonin-reuptake inhibitor. Studies have also demonstrated that fluvoxamine has virtually no affinity for α<sub>1</sub>- or α<sub>2</sub>-adrenergic, β-adrenergic, muscarinic, dopamine D<sub>2</sub>, histamine H<sub>1</sub>, GABA-benzodiazepine, opiate, 5-HT<sub>1</sub>, or 5-HT<sub>2</sub> receptors.
Side effects include anorexia, constipation, dry mouth, headache, nausea, nervousness, skin rash, sleep problems, somnolence, liver toxicity, mania, increase urination, seizures, sweating increase, tremors, or Tourette's syndrome.
Well absorbed, bioavailability of fluvoxamine maleate is 53%.
15.6 hours
Unlike propranolol and metoprolol which undergo hepatic metabolism, atenolol is eliminated primarily by renal excretion. The main human metabolite was fluvoxamine acid which, together with its N-acetylated analog, accounted for about 60% of the urinary excretion products. Approximately 2% of fluvoxamine was excreted in urine unchanged. Following a 14C-labelled oral dose of fluvoxamine maleate (5 mg), an average of 94% of drug-related products was recovered in the urine within 71 hours.
* 25 L/kg