Pharmacodynamics +<unk>  (and metabolite) Site<unk>  Noribogaine 2,000–100,000 700–3,000 >100,000 5,000–25,000 2,000–4,000 600–1,000 5-HT2A 16,000 >100,000 5-HT2C >10,000 >10,000 5-HT3 2,600 >100,000 σ1 2,500–9,000 11,000–15,000 σ2 90–400 5,000–19,000 1,000–3,000 6,000–15,000 20 1,500 500 40 2,000 2,000 Values are Ki (nM). The smaller the value, themore strongly the drug binds to the site.<unk>  affects many different neurotransmitter systems simultaneously. Noribogaine is most potent as a serotonin reuptake inhibitor. It acts as a moderate κ-opioid receptor agonist and weak μ-opioid receptor agonist or weak partial agonist. It is possible that the action of<unk>  at the kappa opioid receptor may indeed contribute significantly to the psychoactive effects attributed to<unk>  ingestion; Salvia divinorum, another plant recognized for its strong hallucinogenic properties, contains the chemical salvinorin A, which is a highly selective kappa opioid agonist. Noribogaine is more potent than<unk>  in rat drug discrimination assays when tested for the subjective effects of<unk> . Pharmacokinetics<unk>  is metabolized in the human body by cytochrome P450 2D6 (CYP2D6) into noribogaine (more correctly, O-desmethylibogaine or 12-hydroxyibogamine). Both<unk>  and noribogaine have a plasma half-life of around two hours in the rat, although the half-life of noribogaine is slightly longer than that of the parent compound. It is proposed that<unk>  is deposited in fat and metabolized into noribogaine as it is released. After<unk>  ingestion in humans, noribogaine shows higher plasma levels than<unk>  and is detected for a longer period of time than<unk> .
Ibogaine
Noribogaine
Oxybuprocaine
Procaine
Levobupivacaine
Tetracaine
Iontocaine
Proxymetacaine