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| Names | |
|---|---|
| IUPAC name 1,2-Dimethoxy-6aβ-aporphine | |
| Systematic IUPAC name (6aR)-1,2-Dimethoxy-6-methyl-5,6,6a,7-tetrahydro-4H-dibenzo[de,g]quinoline | |
| Other names (R)-1,2-Dimethoxyaporphine | |
| Identifiers | |
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3D model (JSmol) | |
| ChEMBL | |
| ChemSpider |
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| UNII | |
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| Properties | |
| C19H21NO2 | |
| Molar mass | 295.376 g/mol |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
Nuciferine is analkaloid found within the plantsNymphaea caerulea andNelumbo nucifera.[1][2]
Nuciferine, anaporphine derivative structurally related toapomorphine, exhibits complex pharmacological effects: early studies show it had effect demonstratingdopamine blockade, producingneuroleptic effects, while its degradation product, atherosperminine,stimulates dopamine receptors. More recent research indicates nuciferine acts on multipleserotonin and dopamine receptors (as anantagonist,partial agonist,inverse agonist, or fullagonist depending on the receptor) and inhibits thedopamine transporter. In rodent models, it demonstrates antipsychotic-like effects, modulates locomotor activity, restoresPCP-inducedsensory gating deficits, and may enhancemorphine analgesia without causingcatalepsy. It also shows potential anti-inflammatory effects, possibly throughPPAR delta activation, with a reportedmedian lethal dose of 289 mg/kg in mice.
A 1978 study found that nuciferine acts as a dopamine-receptor blocker producing neuroleptic effects, whereas itsHofmann degradation product atherosperminine stimulates dopamine receptors, producing opposing psychopharmacological effects.[3]
According to a newer study from 2016, Nuciferine acts as anantagonist at5-HT2A,5-HT2C, and5-HT2B receptors, aninverse agonist at the5-HT7 receptor, apartial agonist atD2,D5, and5-HT6 receptors, and anagonist at5-HT1A andD4 receptors. Additionally, it inhibits the dopamine transporter (DAT).[4]
In rodent models relating to antipsychotic drug effects, Nuciferine has shown various actions such as blockinghead-twitch responses and discriminative stimulus effects of a5-HT2A agonist, enhancing amphetamine-induced locomotor activity, inhibitingphencyclidine (PCP)-induced locomotor activity, and restoringPCP-induced disruption ofpre-pulse inhibition without inducingcatalepsy.[4]
Nuciferine may also potentiatemorphineanalgesia. Themedian lethal dose in mice is 289 mg/kg. It is structurally related toapomorphine and otheraporphine derivatives.[5][6]
Nuciferine has been reported to have variousanti-inflammatory effects, possibly mediated viaPPAR delta activation.[7]
