Harmine

Harmine at a Glance

Harmine is a β-carboline (harmala) alkaloid — the principal β-carboline of the South American ayahuasca vine, Banisteriopsis caapi, and one of the main alkaloids of Syrian rue (Peganum harmala) seed. It also turns up as a trace alkaloid in everyday exposures: cooked meat and fish, coffee, and tobacco smoke ^{7Reference 7Herraiz T · 2005Human monoamine oxidase is inhibited by tobacco smoke: beta-carboline alkaloids act as potent and reversible inhibitorsView study →}. Under its old names banisterine, telepathine and yageine, it was one of the first psychoactive-plant alkaloids to reach Western laboratories.

Two facts about the molecule drive almost all of its research interest, and they are chemically independent. First, harmine is a potent, reversible inhibitor of monoamine oxidase A (MAO-A) — a “RIMA” — and this is the pharmacological basis of ayahuasca: it blocks the gut and liver enzyme that would otherwise destroy orally swallowed N,N-DMT, letting the tryptamine survive to reach the brain ^{1,4,5Reference 1Kim H et al. · 1997Inhibition of monoamine oxidase A by beta-carboline derivativesView study →Reference 4Riba J et al. · 2003Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokineticsView study →Reference 5Yritia M et al. · 2002Determination of N,N-dimethyltryptamine and beta-carboline alkaloids in human plasma following oral administration of ayahuascaView study →}. Second, harmine is one of the best-known small-molecule inhibitors of the kinase DYRK1A, which has opened active drug-discovery programmes in diabetes (β-cell regeneration), Alzheimer’s disease and cancer ^{2,13Reference 2Wang P et al. · 2015A high-throughput chemical screen reveals that harmine-mediated inhibition of DYRK1A increases human pancreatic beta cell replicationView study →Reference 13Liu W et al. · 2026AnimalDiscovery of novel harmine derivatives as potent, selective, and brain-permeable GSK-3β inhibitors with effective in vivo anti-AD activityView study →}.

An important honesty note up front: harmine is not, by itself, a classical psychedelic. At the doses that inhibit MAO it is not meaningfully hallucinogenic — the visionary effects of ayahuasca come from the DMT that harmine protects, not from harmine itself. Its headline safety issue is therefore not “tripping” but the drug- and food-interaction profile of an MAO-A inhibitor, shared with its batch-mates harmaline and tetrahydroharmine.

The MAO-A Story — Why Harmine Makes Ayahuasca Work

The single most important thing harmine does pharmacologically is inhibit monoamine oxidase A. It is a reversible, competitive inhibitor selective for MAO-A over MAO-B, with a binding constant (Ki) in the low-nanomolar range — among the most potent naturally occurring MAO inhibitors on record, orders of magnitude stronger than typical flavonoid inhibitors ^{1Reference 1Kim H et al. · 1997Inhibition of monoamine oxidase A by beta-carboline derivativesView study →}. Because the inhibition is reversible (a RIMA), it differs mechanistically from the older irreversible antidepressant MAOIs, though the interaction cautions still apply ^{7Reference 7Herraiz T · 2005Human monoamine oxidase is inhibited by tobacco smoke: beta-carboline alkaloids act as potent and reversible inhibitorsView study →}.

This is the chemistry that makes ayahuasca work. DMT is orally inactive on its own because MAO-A in the gut wall and liver degrades it before it can reach the brain. The Banisteriopsis caapi vine supplies harmine (with harmaline and tetrahydroharmine); the harmine inhibits that MAO-A barrier, so DMT from the companion leaf (chacruna or chaliponga) survives absorption and becomes psychoactive ^{4,5Reference 4Riba J et al. · 2003Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokineticsView study →Reference 5Yritia M et al. · 2002Determination of N,N-dimethyltryptamine and beta-carboline alkaloids in human plasma following oral administration of ayahuascaView study →}. In human pharmacology studies of standardised ayahuasca, harmine and its sister β-carbolines are measurable in plasma alongside DMT, confirming the mechanism operates in people, not just in the test tube ^{4,5Reference 4Riba J et al. · 2003Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokineticsView study →Reference 5Yritia M et al. · 2002Determination of N,N-dimethyltryptamine and beta-carboline alkaloids in human plasma following oral administration of ayahuascaView study →}.

The same MAO-A inhibition is the source of harmine’s safety headline (see Toxicity & Safety): anything that raises serotonin — SSRIs and other antidepressants, some opioids, other serotonergic drugs — or tyramine-rich foods can become dangerous when MAO-A is blocked.

The DYRK1A Connection

Entirely separate from its effect on MAO, harmine is one of the most-cited chemical inhibitors of DYRK1A (dual-specificity tyrosine-phosphorylation-regulated kinase 1A), an ATP-competitive action at the kinase’s active site ^{2,13Reference 2Wang P et al. · 2015A high-throughput chemical screen reveals that harmine-mediated inhibition of DYRK1A increases human pancreatic beta cell replicationView study →Reference 13Liu W et al. · 2026AnimalDiscovery of novel harmine derivatives as potent, selective, and brain-permeable GSK-3β inhibitors with effective in vivo anti-AD activityView study →}. This one property has spawned three distinct research fields:

• Diabetes / β-cell regeneration. A landmark high-throughput screen found that harmine drives human pancreatic β-cell proliferation by inhibiting DYRK1A, which normally acts as a brake on the cell cycle; harmine increased β-cell mass, insulin content and glycaemic control in diabetic-mouse and human-islet-graft models ^{2Reference 2Wang P et al. · 2015A high-throughput chemical screen reveals that harmine-mediated inhibition of DYRK1A increases human pancreatic beta cell replicationView study →}. This is the finding that moved harmine toward the clinic as a potential diabetes therapy.
• Alzheimer’s disease / tau. DYRK1A phosphorylates the microtubule protein tau, and harmine (and newer harmine-derived dual DYRK1A/GSK-3β inhibitors) reduce tau hyperphosphorylation in cell and animal models — the basis of an Alzheimer’s drug-discovery interest ^{12,13Reference 12Paclibar CG et al. · 2025Towards imaging tau hyperphosphorylation: is DYRK1A a potential target for imaging hyperphosphorylation of tau? Molecules. https://pubmed.ncbi.nlm.nih.gov/40076215/View study →Reference 13Liu W et al. · 2026AnimalDiscovery of novel harmine derivatives as potent, selective, and brain-permeable GSK-3β inhibitors with effective in vivo anti-AD activityView study →}. Harmine’s simultaneous MAO-A binding, however, complicates its use as a clean DYRK1A probe or imaging agent ^{12Reference 12Paclibar CG et al. · 2025Towards imaging tau hyperphosphorylation: is DYRK1A a potential target for imaging hyperphosphorylation of tau? Molecules. https://pubmed.ncbi.nlm.nih.gov/40076215/View study →}.
• Cancer. Through DYRK1A and other targets, harmine shows antiproliferative and anti-metastatic activity across preclinical tumour models ^{10,11Reference 10Bao Y et al. · 2025Harmine inhibits ovarian cancer migration and invasion and epithelial-mesenchymal transition by inhibiting HDAC7 to restore RECK expressionView study →Reference 11He J et al. · 2026Harmine inhibits non-small cell lung cancer growth by targeting phosphodiesterase 4D and inducing ferroptosisView study →}.

The catch is that harmine’s DYRK1A and MAO-A activities travel together, so the medicinal-chemistry effort has focused on building harmine analogues that keep the kinase inhibition while shedding the MAO-A binding ^{12,13Reference 12Paclibar CG et al. · 2025Towards imaging tau hyperphosphorylation: is DYRK1A a potential target for imaging hyperphosphorylation of tau? Molecules. https://pubmed.ncbi.nlm.nih.gov/40076215/View study →Reference 13Liu W et al. · 2026AnimalDiscovery of novel harmine derivatives as potent, selective, and brain-permeable GSK-3β inhibitors with effective in vivo anti-AD activityView study →}.

What It's Used For

Harmine’s evidence base is unusually two-headed: a well-characterised mechanism (MAO-A inhibition, thoroughly documented in humans as part of ayahuasca) alongside a fast-growing but still largely preclinical pharmacology (DYRK1A-driven effects). Almost none of it is isolated-harmine human therapeutics yet.

Evidence by IndicationStrength of support · Beta

Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. The scores mix a well-characterised mechanism with mostly preclinical therapeutic leads, so read the per-row basis.

01MAO-A Inhibition / Enabling Oral DMTPromising62%Enzyme kinetics + human ayahuasca pharmacokinetics ^{1,4,5Reference 1Kim H et al. · 1997Inhibition of monoamine oxidase A by beta-carboline derivativesView study →Reference 4Riba J et al. · 2003Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokineticsView study →Reference 5Yritia M et al. · 2002Determination of N,N-dimethyltryptamine and beta-carboline alkaloids in human plasma following oral administration of ayahuascaView study →}

02DYRK1A Inhibition / β-Cell ProliferationShaky42%High-throughput screen + diabetic-mouse & human-islet models ^{2Reference 2Wang P et al. · 2015A high-throughput chemical screen reveals that harmine-mediated inhibition of DYRK1A increases human pancreatic beta cell replicationView study →}

03Antidepressant-Like EffectsShaky28%Rodent behavioural + BDNF data; human data are brew-level, not isolate ^{6,14Reference 6Fortunato JJ et al. · 2009AnimalAcute harmine administration induces antidepressive-like effects and increases BDNF levels in the rat hippocampusView study →Reference 14Palhano-Fontes F et al. · 2019RCTRapid antidepressant effects of the psychedelic ayahuasca in treatment-resistant depression: a randomized placebo-controlled trialView study →}

04Antiparasitic / AntileishmanialShaky24%In-vitro + rodent Leishmania studies of extract & alkaloids ^{9Reference 9Rahimi-Moghaddam P et al. · 2011In vitroIn vitro and in vivo activities of Peganum harmala extract against Leishmania majorView study →}

05AnticancerShaky20%In-vitro & mouse-xenograft tumour models ^{10,11Reference 10Bao Y et al. · 2025Harmine inhibits ovarian cancer migration and invasion and epithelial-mesenchymal transition by inhibiting HDAC7 to restore RECK expressionView study →Reference 11He J et al. · 2026Harmine inhibits non-small cell lung cancer growth by targeting phosphodiesterase 4D and inducing ferroptosisView study →}

06DYRK1A / Tau — Alzheimer’sShaky16%Cell/animal tau models, largely via harmine derivatives ^{12,13Reference 12Paclibar CG et al. · 2025Towards imaging tau hyperphosphorylation: is DYRK1A a potential target for imaging hyperphosphorylation of tau? Molecules. https://pubmed.ncbi.nlm.nih.gov/40076215/View study →Reference 13Liu W et al. · 2026AnimalDiscovery of novel harmine derivatives as potent, selective, and brain-permeable GSK-3β inhibitors with effective in vivo anti-AD activityView study →}

Mechanisms

The load-bearing point is that the MAO-A and DYRK1A activities are pharmacologically independent but chemically inseparable in the parent molecule — which is exactly why harmine is simultaneously the engine of ayahuasca and a drug-discovery scaffold, and why analogue programmes try to split the two.

Pharmacokinetics

Harmine is a small, lipophilic β-carboline that crosses the blood-brain barrier, but its oral pharmacokinetics are poor and erratic because it is itself an MAO substrate subject to extensive first-pass metabolism — the very enzyme it inhibits also clears it, and it is O-demethylated (to harmol) and conjugated. In human ayahuasca pharmacology, plasma harmine rises within roughly 1–2 hours and clears over a few hours, with substantial inter-individual variability and, at brew doses, only modest peak concentrations ^{4,5Reference 4Riba J et al. · 2003Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokineticsView study →Reference 5Yritia M et al. · 2002Determination of N,N-dimethyltryptamine and beta-carboline alkaloids in human plasma following oral administration of ayahuascaView study →}. Its metabolism intersects CYP2D6, so genetic and drug-induced variation in that enzyme (and MAO saturation by the co-ingested alkaloids) shape exposure ^{4Reference 4Riba J et al. · 2003Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokineticsView study →}. The practical upshot: harmine’s short half-life and heavy first-pass loss are a real translational obstacle for the isolated molecule, and help explain why its potent in-vitro DYRK1A/anticancer effects do not automatically transfer to oral dosing.

Clinical Trials

Human data on isolated harmine are minimal; most human evidence is for ayahuasca (harmine as one component). The DYRK1A/β-cell diabetes programme is the frontier where isolated-harmine-class molecules are advancing toward early-phase trials.

Last checked: July 2026.

Isolate vs. Plant Studies

Harmine’s evidence sits on both sides of the isolate-vs-plant line, and it matters which:

• The MAO-A kinetics are pure-isolate enzyme data ^{1Reference 1Kim H et al. · 1997Inhibition of monoamine oxidase A by beta-carboline derivativesView study →}; the human confirmation of that mechanism is whole-brew (ayahuasca), where harmine acts together with harmaline and tetrahydroharmine, and the psychoactive effect belongs to the co-ingested DMT, not to harmine ^{4,5,14Reference 4Riba J et al. · 2003Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokineticsView study →Reference 5Yritia M et al. · 2002Determination of N,N-dimethyltryptamine and beta-carboline alkaloids in human plasma following oral administration of ayahuascaView study →Reference 14Palhano-Fontes F et al. · 2019RCTRapid antidepressant effects of the psychedelic ayahuasca in treatment-resistant depression: a randomized placebo-controlled trialView study →}.
• The DYRK1A / β-cell, antidepressant and anticancer work is largely isolated harmine as the test article ^{2,6,10Reference 2Wang P et al. · 2015A high-throughput chemical screen reveals that harmine-mediated inhibition of DYRK1A increases human pancreatic beta cell replicationView study →Reference 6Fortunato JJ et al. · 2009AnimalAcute harmine administration induces antidepressive-like effects and increases BDNF levels in the rat hippocampusView study →Reference 10Bao Y et al. · 2025Harmine inhibits ovarian cancer migration and invasion and epithelial-mesenchymal transition by inhibiting HDAC7 to restore RECK expressionView study →} — a genuine strength for translation — but it is preclinical (cells, islets, rodents).
• The antiparasitic data are mostly whole Peganum harmala extract or crude alkaloid fractions, where harmine is one of several β-carbolines ^{9Reference 9Rahimi-Moghaddam P et al. · 2011In vitroIn vitro and in vivo activities of Peganum harmala extract against Leishmania majorView study →}.

So the honest summary is: a well-established mechanism confirmed at the whole-brew level in humans, plus a promising isolate pharmacology that has not yet crossed into proven human therapy.

Prevalence in Nature

Harmine is a β-carboline alkaloid concentrated in two botanically unrelated plants that dominate its story. It is the principal β-carboline of the ayahuasca vine, Banisteriopsis caapi (Malpighiaceae), whose stems carry harmine as the major harmala alkaloid alongside harmaline and tetrahydroharmine ^{4,5Reference 4Riba J et al. · 2003Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokineticsView study →Reference 5Yritia M et al. · 2002Determination of N,N-dimethyltryptamine and beta-carboline alkaloids in human plasma following oral administration of ayahuascaView study →}. It is also a major alkaloid of Syrian rue (Peganum harmala, Nitrariaceae) seed, where the harmala β-carbolines together reach several percent of seed dry weight and harmine is one of the largest fractions ^{3Reference 3Moloudizargari M et al. · 2013Pharmacological and therapeutic effects of Peganum harmala and its main alkaloidsView study →}.

Beyond those two, harmine appears at trace levels in a scattered range of plants, passionflower (Passiflora spp.) among them — and, strikingly, as a trace dietary and environmental alkaloid in people’s everyday exposure: β-carbolines including harman and harmine form in cooked meat and fish, in coffee, and in tobacco smoke, at levels far too low to be psychoactive but enough to contribute measurably to background MAO inhibition (part of why smokers show reduced MAO activity) ^{7Reference 7Herraiz T · 2005Human monoamine oxidase is inhibited by tobacco smoke: beta-carboline alkaloids act as potent and reversible inhibitorsView study →}.

Major Natural Sources

Source	Part	Harmine level	Note
Syrian rue (Peganum harmala)	Seed	High — a major fraction of the several-percent harmala-alkaloid content 3Reference 3Moloudizargari M et al. · 2013Pharmacological and therapeutic effects of Peganum harmala and its main alkaloidsView study →	Richest common source; also carries harmaline/harmalol
Ayahuasca vine (Banisteriopsis caapi)	Stem / bark	Principal β-carboline of the vine 4,5Reference 4Riba J et al. · 2003Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokineticsView study →Reference 5Yritia M et al. · 2002Determination of N,N-dimethyltryptamine and beta-carboline alkaloids in human plasma following oral administration of ayahuascaView study →	The ayahuasca source; harmine dominates the alkaloid profile
Passionflower (Passiflora spp.)	Aerial	Trace	Minor harmala alkaloid; not the plant’s main actives
Cooked meat/fish, coffee, tobacco smoke	—	Trace	Thermally/environmentally formed β-carbolines; dietary background 7Reference 7Herraiz T · 2005Human monoamine oxidase is inhibited by tobacco smoke: beta-carboline alkaloids act as potent and reversible inhibitorsView study →

Discovery & Synthesis

Harmine was among the earliest plant alkaloids isolated from a psychoactive species. It was obtained from Syrian rue (Peganum harmala) seed in the 1840s (Fritzsche’s work on the harmala alkaloids), and the name traces to harmala. When the same molecule was later identified in the Banisteriopsis caapi vine used for ayahuasca/yagé, it was independently christened banisterine, telepathine and yageine — a tangle of synonyms that was only resolved when the “new” vine alkaloid was shown to be the long-known harmine ^{3Reference 3Moloudizargari M et al. · 2013Pharmacological and therapeutic effects of Peganum harmala and its main alkaloidsView study →}. Its first total synthesis was accomplished by W. H. Perkin Jr. and Robert Robinson in the 1910s, part of Robinson’s foundational work on indole-alkaloid chemistry.

Manufacture today is overwhelmingly by extraction from Peganum harmala seed, a cheap and alkaloid-rich source, rather than by total synthesis; research quantities are also available synthetically, and the medicinal-chemistry interest in DYRK1A has produced numerous semi-synthetic harmine derivatives built from the natural scaffold ^{12,13Reference 12Paclibar CG et al. · 2025Towards imaging tau hyperphosphorylation: is DYRK1A a potential target for imaging hyperphosphorylation of tau? Molecules. https://pubmed.ncbi.nlm.nih.gov/40076215/View study →Reference 13Liu W et al. · 2026AnimalDiscovery of novel harmine derivatives as potent, selective, and brain-permeable GSK-3β inhibitors with effective in vivo anti-AD activityView study →}.

Patents: not yet researched.

Toxicity & Safety

Harmine carries a moderate flag. The dominant reason is that it is a reversible MAO-A inhibitor, and therefore inherits the interaction profile of MAOI drugs — the same class-wide cautions that make antidepressant MAOIs risky. It is also strongly emetic, and tremorigenic/neurotoxic at high doses. Note what it is not: at MAO-inhibiting doses harmine is not a classical hallucinogen — it does not itself produce the visionary state of ayahuasca (that is the DMT it protects), so it is not badged psychedelic here.

Safety at a Glance

⚠️ Moderate toxicity

• Not intrinsically hallucinogenic. At the doses that inhibit MAO, harmine is not a classical psychedelic; ayahuasca’s visions come from the co-ingested DMT, not from harmine.
• MAO-A inhibitor — serotonin-toxicity risk. Combining harmine with SSRIs/SNRIs, other antidepressants, certain opioids (e.g. tramadol, meperidine) or other serotonergic agents can precipitate potentially life-threatening serotonin syndrome.
• Tyramine / hypertensive risk. As with other MAO-A inhibitors, tyramine-rich foods (aged cheeses, cured meats, fermented products) can provoke a hypertensive reaction.
• Emetic and, at high doses, tremorigenic/neurotoxic. Nausea and vomiting are common; the harmala alkaloids drive rhythmic inferior-olive firing and tremor at high exposure, and Peganum harmala overdose can cause neuro-behavioural and cardiovascular toxicity.
• Reproductive caution. Peganum harmala has a traditional reputation as an emmenagogue/abortifacient, and its alkaloids show uterine-stimulant and reproductive-toxicity signals in animal studies — relevant to pregnancy.

Full Safety & Interactions Detail

MAOI interaction profile (the headline). Because harmine reversibly inhibits MAO-A, it removes a key route for clearing serotonin and other monoamines. Co-exposure to serotonergic drugs (SSRIs, SNRIs, MAOIs, tricyclics, some triptans, and serotonergic opioids such as tramadol, meperidine/pethidine and dextromethorphan) can drive serotonin toxicity/serotonin syndrome; tyramine-rich foods can drive a hypertensive (“cheese”) reaction ^{7Reference 7Herraiz T · 2005Human monoamine oxidase is inhibited by tobacco smoke: beta-carboline alkaloids act as potent and reversible inhibitorsView study →}. That reversible inhibition is shorter-lived than an irreversible MAOI, but the interaction hazard is real, and it is the practical reason ayahuasca is dangerous to combine with antidepressants.

Acute/high-dose toxicity. Harmine is reliably emetic. At high doses the harmala alkaloids are tremorigenic and neurotoxic: harmine and harmaline induce rhythmic burst-firing in the inferior olive that propagates through the olivocerebellar circuit to produce tremor, a phenomenon used to model essential tremor in animals ^{8Reference 8Handforth A · 2012AnimalHarmaline tremor: underlying mechanisms in a potential animal model of essential tremorView study →}. Human Peganum harmala poisonings (from seed overdoses taken for their effects or as folk medicine) report neuro-sensory, gastrointestinal and cardiovascular toxicity, and the plant’s total alkaloid load — not harmine alone — is responsible ^{3Reference 3Moloudizargari M et al. · 2013Pharmacological and therapeutic effects of Peganum harmala and its main alkaloidsView study →}.

Reproductive. Peganum harmala is a documented emmenagogue/abortifacient in traditional use, and reviews of its pharmacology note uterine-stimulant and reproductive/developmental-toxicity findings for its alkaloids in animal studies ^{3Reference 3Moloudizargari M et al. · 2013Pharmacological and therapeutic effects of Peganum harmala and its main alkaloidsView study →}. Pregnancy and lactation decisions belong to the herb or product page where intake is decided; the finding is stated here as a cited risk, not a per-molecule verdict.

Legality & framing. Harmine itself is not a scheduled controlled substance in most jurisdictions, but it is inseparable from contexts that are regulated: DMT (which harmine activates in ayahuasca) is widely controlled, and Syrian rue and ayahuasca sit in a shifting legal grey zone that varies by country. Nothing here is use guidance — the material above is the research and toxicology literature, framed educationally.

Dosage

There is no established therapeutic dose of isolated harmine. What the literature documents are research and ethnographic exposures, not recommendations:

Isolated harmine’s poor, MAO-limited oral pharmacokinetics (see Pharmacokinetics) mean that in-vitro-active concentrations do not map simply onto oral doses. These are doses studied in research or estimated from traditional preparations, and are not a personal recommendation — and the MAOI interaction cautions above apply to any exposure.

References

1. Kim H, Sablin SO, Ramsay RR (1997). Inhibition of monoamine oxidase A by beta-carboline derivatives. Archives of Biochemistry and Biophysics, 337(1), 137–142. https://pubmed.ncbi.nlm.nih.gov/8990278/
2. Wang P, Alvarez-Perez JC, Felsenfeld DP, et al. (2015). A high-throughput chemical screen reveals that harmine-mediated inhibition of DYRK1A increases human pancreatic beta cell replication. Nature Medicine, 21(4), 383–388. https://pubmed.ncbi.nlm.nih.gov/25751815/
3. Moloudizargari M, Mikaili P, Aghajanshakeri S, et al. (2013). Pharmacological and therapeutic effects of Peganum harmala and its main alkaloids. Pharmacognosy Reviews, 7(14), 199–212. https://pubmed.ncbi.nlm.nih.gov/24347928/
4. Riba J, Valle M, Urbano G, et al. (2003). Human pharmacology of ayahuasca: subjective and cardiovascular effects, monoamine metabolite excretion, and pharmacokinetics. Journal of Pharmacology and Experimental Therapeutics, 306(1), 73–83. https://pubmed.ncbi.nlm.nih.gov/12660312/
5. Yritia M, Riba J, Ortuño J, et al. (2002). Determination of N,N-dimethyltryptamine and beta-carboline alkaloids in human plasma following oral administration of ayahuasca. Journal of Chromatography B, 779(2), 271–281. https://pubmed.ncbi.nlm.nih.gov/12361741/
6. Fortunato JJ, Réus GZ, Kirsch TR, et al. (2009). Acute harmine administration induces antidepressive-like effects and increases BDNF levels in the rat hippocampus. Progress in Neuro-Psychopharmacology & Biological Psychiatry, 33(8), 1425–1430. https://pubmed.ncbi.nlm.nih.gov/19632287/
7. Herraiz T, Chaparro C (2005). Human monoamine oxidase is inhibited by tobacco smoke: beta-carboline alkaloids act as potent and reversible inhibitors. Biochemical and Biophysical Research Communications, 326(2), 378–386. https://pubmed.ncbi.nlm.nih.gov/15582589/
8. Handforth A (2012). Harmaline tremor: underlying mechanisms in a potential animal model of essential tremor. Tremor and Other Hyperkinetic Movements, 2, tre-02-92-769-1. https://pubmed.ncbi.nlm.nih.gov/23440018/
9. Rahimi-Moghaddam P, Ebrahimi SA, Ourmazdi H, et al. (2011). In vitro and in vivo activities of Peganum harmala extract against Leishmania major. Journal of Research in Medical Sciences, 16(8), 1032–1039. https://pubmed.ncbi.nlm.nih.gov/22279479/
10. Bao Y, et al. (2025). Harmine inhibits ovarian cancer migration and invasion and epithelial-mesenchymal transition by inhibiting HDAC7 to restore RECK expression. Biochemical Pharmacology. https://pubmed.ncbi.nlm.nih.gov/41061932/
11. He J, et al. (2026). Harmine inhibits non-small cell lung cancer growth by targeting phosphodiesterase 4D and inducing ferroptosis. Phytomedicine. https://pubmed.ncbi.nlm.nih.gov/41344272/
12. Paclibar CG, et al. (2025). Towards imaging tau hyperphosphorylation: is DYRK1A a potential target for imaging hyperphosphorylation of tau? Molecules. https://pubmed.ncbi.nlm.nih.gov/40076215/
13. Liu W, et al. (2026). Discovery of novel harmine derivatives as potent, selective, and brain-permeable GSK-3β inhibitors with effective in vivo anti-AD activity. European Journal of Medicinal Chemistry. https://pubmed.ncbi.nlm.nih.gov/41313964/
14. Palhano-Fontes F, Barreto D, Onias H, et al. (2019). Rapid antidepressant effects of the psychedelic ayahuasca in treatment-resistant depression: a randomized placebo-controlled trial. Psychological Medicine, 49(4), 655–663. https://pubmed.ncbi.nlm.nih.gov/29903051/

View all 14 references▾