Collated from TripSit, Pharmacology, DrugCentral, DailyMed. Where sources differ (e.g. dosing), Compare shows them side by side.
Also known as luvox, faverinTS
🧬 Receptor activityPHDC
| Target | Action | Affinity | Source | |
|---|---|---|---|---|
| Sodium-dependent dopamine transporter | — | Ki 1.46 nM | CHEMBL | TargetSodium-dependent dopamine transporter Action— AffinityKi 1.46 nM SourceCHEMBL |
| Sodium-dependent serotonin transporter | — | Ki 3.08 nM | CHEMBL | TargetSodium-dependent serotonin transporter Action— AffinityKi 3.08 nM SourceCHEMBL |
| Sigma non-opioid intracellular receptor 1 | — | Ki 36 nM | CHEMBL | TargetSigma non-opioid intracellular receptor 1 Action— AffinityKi 36 nM SourceCHEMBL |
| Cytochrome P450 2D6 | — | Ki 8000 nM | CHEMBL | TargetCytochrome P450 2D6 Action— AffinityKi 8000 nM SourceCHEMBL |
| Sigma intracellular receptor 2 | — | Ki 8439 nM | CHEMBL | TargetSigma intracellular receptor 2 Action— AffinityKi 8439 nM SourceCHEMBL |
| Unchecked | — | Ki 8439 nM | CHEMBL | TargetUnchecked Action— AffinityKi 8439 nM SourceCHEMBL |
| Cytochrome P450 2C9 | — | Ki 8500 nM | CHEMBL | TargetCytochrome P450 2C9 Action— AffinityKi 8500 nM SourceCHEMBL |
| Cytochrome P450 1A2 | — | Ki 57400 nM | CHEMBL | TargetCytochrome P450 1A2 Action— AffinityKi 57400 nM SourceCHEMBL |
| Sodium-dependent serotonin transporter (SLC6A4) | Inhibitor | 8.51 Ki | DRUGCENTRAL | TargetSodium-dependent serotonin transporter (SLC6A4) ActionInhibitor Affinity8.51 Ki SourceDRUGCENTRAL |
| Cytochrome P450 1A2 (CYP1A2) | — | 5.07 Ki | DRUGCENTRAL | TargetCytochrome P450 1A2 (CYP1A2) Action— Affinity5.07 Ki SourceDRUGCENTRAL |
| Sigma non-opioid intracellular receptor 1 (SIGMAR1) | — | 7.44 Ki | DRUGCENTRAL | TargetSigma non-opioid intracellular receptor 1 (SIGMAR1) Action— Affinity7.44 Ki SourceDRUGCENTRAL |
| Sodium-dependent dopamine transporter (SLC6A3) | — | 8.84 Ki | DRUGCENTRAL | TargetSodium-dependent dopamine transporter (SLC6A3) Action— Affinity8.84 Ki SourceDRUGCENTRAL |
| Sodium-dependent noradrenaline transporter (SLC6A2) | — | 5.951 Ki | DRUGCENTRAL | TargetSodium-dependent noradrenaline transporter (SLC6A2) Action— Affinity5.951 Ki SourceDRUGCENTRAL |
Mechanism of actionPHDM
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. 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, despite having an affinity for binding to σ1 receptors.
PharmacodynamicsPHDM
Fluvoxamine, an aralkylketone-derivative agent, is one of a class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs) that differs structurally from other SSRIs. It is used to treat the depression associated with mood disorders. It is also used on occassion in the treatment of body dysmorphic disorder and anxiety. The antidepressant, antiobsessive-compulsive, and antibulimic actions of Fluvoxamine are presumed to be linked to its inhibition of CNS neuronal uptake of serotonin. <i>In vitro</i> studies show that Fluvoxamine is a potent and selective inhibitor of neuronal serotonin reuptake and has only very weak effects on norepinephrine and dopamine neuronal reuptake. Moreover, apart from binding to σ1 receptors, fluvoxamine has no significant affinity for adrenergic (alpha1, alpha2, beta), cholinergic, GABA, dopaminergic, histaminergic, serotonergic (5HT<sub>1A</sub>, 5HT<sub>1B</sub>, 5HT<sub>2</sub>), or benzodiazepine receptors; antagonism of such receptors has been hypothesized to be associated with various anticholinergic, sedative, and cardiovascular effects for other psychotropic drugs. Furthermore, some studies have demonstrated that the chronic administration of Fluvoxamine was found to downregulate brain norepinephrine receptors (as has been observed with other drugs effective in the treatment of major depressive disorder), while others suggest the opposite.
Pharmacokinetics
Half-lifePH
15.6 hours.
AbsorptionPHDM
Well absorbed, bioavailability of fluvoxamine maleate is 53%.
Nine metabolites were identified following a 5 mg radio labelled dose of fluvoxamine maleate, constituting approximately 85% of the urinary excretion products of fluvoxamine. 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.
MetabolismPH
Fluvoxamine is metabolized extensively by the liver.
Fluvoxamine has known human metabolites that include Fluvoxamino alcohol.
Hepatic
Route of Elimination: 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.
Half Life: 15.6 hours
Protein bindingPH
~77-80% (plasma protein).
External links
Fact-sheets from PsychonautWiki. Harm-reduction reference only — not medical advice.