Molecular target
Monoamine Oxidase A
Mitochondrial enzyme that degrades serotonin, norepinephrine, and dopamine. Inhibition raises monoamine availability.
Educational use only. This page summarizes published research and traditional-use records for educational purposes. It does not diagnose, treat, cure, or prevent any disease. Do not start, stop, or change medications based on this information. Discuss any decisions about therapies — pharmaceutical or botanical — with a qualified clinician who knows your medical history.
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Pharmaceutical agents
Drugs that act on Monoamine Oxidase A
These medications have Monoamine Oxidase A among their molecular targets. Sharing a target is a mechanistic relationship — it does not make any plant below an alternative to, or substitute for, these drugs.
Botanical connections
Plants whose compounds act on Monoamine Oxidase A
Each plant below contains a named compound documented to act on Monoamine Oxidase A. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.
- Harmineβ-Carboline alkaloid
Reversible, selective MAO-A inhibitor from Banisteriopsis caapi vine. Allows orally-ingested DMT (from chacruna leaf) to escape gut MAO-A metabolism and reach the brain — the deliberate pharmacological pairing that defines ayahuasca.
- Harmalineβ-Carboline alkaloid
Auxiliary β-carboline with similar MAO-A inhibition; structurally distinct from harmine by hydrogenation state.
- Tetrahydroharmineβ-Carboline alkaloid
Adds mild SERT inhibition to the β-carboline MAOI profile.
- Rosmarinic acidHydroxycinnamic acid ester
The al-Sereiti et al. (1999) review — one of the cited papers — reports that rosmarinic acid modulates prostaglandin E2 and leukotriene B4 production and inhibits the complement system. MAO inhibitory and COX-specific inhibitory designations are drawn from the broader pharmacological literature and are not directly described in the cited abstracts; clinical translation is not established.
- ApigeninFlavone
Preclinical data in the broader literature suggest weak MAO-A inhibitory activity; this specific target is not described in the cited abstracts and functional significance in rosemary preparations is unclear.
- PiperineAlkamide (isobutylamide alkaloid)
Meghwal et al. (2013) report piperine has demonstrated activity at TRPV1 receptors, inhibition of NF-κB and COX-2-related inflammatory pathways, and monoamine oxidase inhibitory effects in preclinical models. Piperine is also reported to inhibit P-glycoprotein and CYP enzyme systems, with consequent effects on drug bioavailability. Turrini et al. (2020) additionally describe preclinical anticancer pathway modulation, including effects on cell-cycle and apoptotic signalling.
- β-Carbolines (harman, norharman)β-Carboline alkaloid
Tobacco-specific MAO inhibitors found in tobacco smoke (formed during combustion). Contributes to smoking's antidepressant subjective effect and complicates the addiction profile beyond pure nicotine pharmacology.
- MyristicinPhenylpropanoid
Preclinical studies report myristicin may inhibit monoamine oxidase and modulate monoamine reuptake transporters; psychotomimetic and potential serotonergic effects have been documented at higher exposures. Safrole is a structural analogue and known hepatotoxin/carcinogen in animals.
- SalidrosidePhenylpropanoid glycoside
Primary adaptogenic constituent; weak MAO-A inhibition and BDNF modulation contribute to mood/fatigue effects.
- PalmatineIsoquinoline alkaloid (protoberberine)
Protoberberine-class alkaloid; in vitro and preclinical data suggest interactions with dopaminergic and serotonergic systems. Direct relevance to Calumba's digestive actions has not been established in clinical trials.