Fluoxetine
Serotonin-transporter inhibition; the active norfluoxetine metabolite contributes to prolonged persistence.
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Structured references cover selected adult formulations. Brief entries provide limited context; neither is an exhaustive monograph.
Serotonin-transporter inhibition; the active norfluoxetine metabolite contributes to prolonged persistence.
Selective serotonin-transporter inhibition, followed by downstream adaptive changes.
Selective serotonin-transporter inhibition by the S-enantiomer of citalopram.
Selective serotonin-transporter inhibition.
Serotonin-transporter inhibition with clinically relevant anticholinergic and CYP2D6 effects.
Selective serotonin-transporter inhibition.
Serotonin and noradrenaline reuptake inhibition; the relative contribution depends on exposure.
Serotonin and noradrenaline reuptake inhibition; an active metabolite of venlafaxine.
Serotonin and noradrenaline reuptake inhibition.
Serotonin/noradrenaline reuptake inhibitor.
Serotonin/noradrenaline reuptake inhibitor.
Tricyclic monoamine-reuptake inhibition with muscarinic, histamine and adrenergic effects.
Tricyclic antidepressant with prominent noradrenaline-reuptake inhibition.
Tricyclic antidepressant.
Tricyclic antidepressant with strong serotonergic reuptake effects and an active metabolite.
Tricyclic antidepressant.
Tricyclic antidepressant; formulations span different indications.
Tricyclic antidepressant.
Tricyclic antidepressant.
Noradrenaline and dopamine reuptake effects; it is not an SSRI.
Presynaptic alpha-2 antagonism and serotonin-receptor effects; H1 antagonism contributes to sedation.
Tetracyclic; alpha-adrenoceptor and antihistamine actions.
Serotonin-reuptake inhibition and receptor antagonism; effects vary with exposure.
Serotonin-transporter inhibition combined with several serotonin-receptor actions.
Serotonin reuptake inhibition and 5-HT1A partial agonism.
MT1/MT2 agonism and 5-HT2C antagonism.
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Monoamine oxidase inhibitor.
Irreversible monoamine oxidase inhibition.
Reversible monoamine oxidase-A inhibitor.
Monoamine oxidase inhibition; selectivity depends on exposure.
NMDA/sigma-1 activity from dextromethorphan; bupropion inhibits CYP2D6 and raises its exposure.
S-enantiomer of ketamine; NMDA receptor antagonism.
Neuroactive steroid; full product source remains to verify.
Positive allosteric modulation of GABA-A receptors.
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Potent dopamine D2 receptor antagonism.
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Broad receptor effects with a clinical role in appropriately assessed treatment resistance.
Dopamine D2 and serotonin 5-HT2 receptor antagonism.
Dopamine D2/serotonin 5-HT2 antagonism; active risperidone metabolite.
Dopamine and serotonin receptor antagonism with additional histamine, muscarinic and adrenergic effects.
Dopamine/serotonin receptor effects; the active metabolite has additional pharmacological actions.
Partial dopamine D2/D3 and serotonin 5-HT1A agonism with 5-HT2A antagonism.
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Dopamine D2 and serotonin receptor antagonism.
Selective dopamine D2/D3 antagonism.
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Multiple intracellular signaling effects; clinical action is not explained by a single receptor.
Multiple effects on inhibitory signaling and ion channels.
Voltage-sensitive sodium-channel blockade with substantial metabolic enzyme induction.
Voltage-sensitive sodium-channel effects with reduced excitatory neurotransmission.
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Benzodiazepine enhancement of GABA-A signaling.
Positive allosteric modulation of GABA-A receptors; active metabolites contribute to prolonged effects.
Positive allosteric modulation of GABA-A receptors.
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Inhibition of dopamine and noradrenaline reuptake.
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Selective noradrenaline-transporter inhibition.
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Opioid receptor antagonism.
Modulates neurotransmission associated with alcohol dependence; mechanism is not fully established.
Inhibits aldehyde dehydrogenase, causing acetaldehyde accumulation with alcohol.
Partial mu-opioid receptor agonism.
Buprenorphine partial agonism with naloxone to discourage parenteral misuse.
Full mu-opioid receptor agonism with prolonged, variable elimination.
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Nicotine receptor agonism reduces tobacco withdrawal.
Partial agonism at alpha4beta2 nicotinic receptors.
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Competitive opioid receptor antagonism.
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Acetylcholinesterase inhibition; it is symptomatic treatment rather than a cure for neurodegeneration.
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Uncompetitive NMDA receptor antagonism.
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