Molecular target
Monoamine Oxidase B
Enzyme that preferentially degrades dopamine, phenethylamine, and benzylamine. Selective inhibition (selegiline, rasagiline) prolongs dopamine availability — the mechanism of MAO-B inhibitors in Parkinson's disease.
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 B
These medications have Monoamine Oxidase B 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 B
Each plant below contains a named compound documented to act on Monoamine Oxidase B. The compound and the reason for the connection are shown on every edge — a shared mechanism, not a therapeutic equivalence.
- SarmentosinIsoquinoline alkaloid
A clinical crossover study (Lomiwes et al. 2024) identified sarmentosin as a key bioactive driving MAO-B inhibition in human platelets following consumption of blackcurrant powder or juice, with anthocyanins playing a secondary role. Platelet MAO-B inhibition was reported at ~89–91% in that study population.
- AnthocyaninsFlavonoids
Earlier clinical work suggested anthocyanins contributed to MAO-B inhibition; however, Lomiwes et al. 2024 reported that MAO-B inhibition must be predominantly attributed to other bioactives (notably sarmentosin), with anthocyanins playing a lesser role.
- MAO-B–inhibitory chalcones / 5-hydroxyflavanoneChalcone / flavanone
Three compounds isolated by Haraguchi et al. (2004) demonstrated competitive MAO-B inhibition in vitro, with selectivity for MAO-B over MAO-A. In vitro findings only; no human pharmacokinetic or pharmacodynamic data available.
- 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.
- Kavalactones (P. methysticum)Lactone / pyranone
Kavalactones are reported to modulate GABAergic transmission and have been investigated for interactions with 5-HT2A and serotonin reuptake pathways; MAO-B inhibitory activity has been proposed in preclinical models. Clinical anxiolytic signals reported in one RCT (Sarris et al. 2009).
- 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.
- Rosiroside / Salidroside
In vitro screening of Rhodiola rosea extracts and isolated constituents has shown inhibition of MAO-B as well, of interest for neuroprotective/anti-Parkinsonian relevance. Compound-specific inhibitory data reported.