Harmine

Sources

8 strong · 35 moderate · 6 weak

Studies and references cited across this article, graded by evidence strength.

Values approved

49/49 (100%)

Data points an editor reviewed and accepted for publication.

Value Provenance

Dosing

oraltrace

Field	Published	AI Proposed	Confidence
Threshold	50 mg	50 mg	low
Low	50–100 mg	50–100 mg	low
Common	100–200 mg	100–200 mg	low
Strong	200–400 mg	200–400 mg	low
Heavy	400+ mg	400+ mg	low
Editorial	No published oral dose-response data for standalone harmine psychoactivity. Oral bioavailability is very low due to extensive first-pass CYP2D6/CYP1A2 metabolism and MRP2 efflux. Ranges are structural inference from ayahuasca context — typical ayahuasca preparations deliver harmine in the range producing significant MAO-A inhibition (estimated 100-200 mg equivalent). Historical Parkinson's data used 20-70 mg SC, but oral equivalents would be substantially higher due to poor bioavailability. These doses represent MAOI adjunct use context, not standalone psychoactive doses. CYP2D6 poor metabolizers will have substantially different dose-response. SAFETY-CRITICAL: These values are unverified against any controlled dose-response study.
	ReasoningReasoning No published oral dose-response data for standalone harmine psychoactivity. Oral bioavailability is very low due to extensive first-pass CYP2D6/CYP1A2 metabolism and MRP2 efflux. Ranges are structural inference from ayahuasca context — typical ayahuasca preparations deliver harmine in the range producing significant MAO-A inhibition (estimated 100-200 mg equivalent). Historical Parkinson's data used 20-70 mg SC, but oral equivalents would be substantially higher due to poor bioavailability. These doses represent MAOI adjunct use context, not standalone psychoactive doses. CYP2D6 poor metabolizers will have substantially different dose-response. SAFETY-CRITICAL: These values are unverified against any controlled dose-response study. Evidence basis: structural_analogy

buccaltrace

Field	Published	AI Proposed	Confidence
Threshold	20 mg	20 mg	low
Low	20–60 mg	20–60 mg	low
Common	60–120 mg	60–120 mg	low
Strong	120–180 mg	120–180 mg	low
Heavy	180+ mg	180+ mg	low
Editorial	Buccal dose ranges inferred from Egger et al. 2025 factorial dose-finding study (0-180 mg harmine buccal, always co-administered with DMT in 16 healthy participants). 180 mg was the highest buccal dose studied. Dose-response was significant and dose-dependent. Cannot isolate harmine-specific dose-response from combination data — all buccal data are from DMT+harmine co-administration. Ranges are approximations based on the factorial design spread, not established standalone dose tiers. SAFETY-CRITICAL: These values represent combination-context data, not standalone psychoactive doses.
	ReasoningReasoning Buccal dose ranges inferred from Egger et al. 2025 factorial dose-finding study (0-180 mg harmine buccal, always co-administered with DMT in 16 healthy participants). 180 mg was the highest buccal dose studied. Dose-response was significant and dose-dependent. Cannot isolate harmine-specific dose-response from combination data — all buccal data are from DMT+harmine co-administration. Ranges are approximations based on the factorial design spread, not established standalone dose tiers. SAFETY-CRITICAL: These values represent combination-context data, not standalone psychoactive doses. Evidence basis: controlled_human_study

Duration

oral

Field	Published	AI Proposed	Confidence
Onsettrace	30–60 minutes	30–60 minutes	low
Editorial	Onset 30-60 minutes from typical ayahuasca literature (Riba 2003). This is combination (harmine+DMT) context, not harmine standalone. Work-notes specify oral onset from ayahuasca data.
	ReasoningReasoning Onset 30-60 minutes from typical ayahuasca literature (Riba 2003). This is combination (harmine+DMT) context, not harmine standalone. Work-notes specify oral onset from ayahuasca data. Evidence basis: controlled_human_study
Come uptrace	30–60 minutes	30–60 minutes	low
Editorial	Come-up estimated at 30-60 minutes based on ayahuasca pharmacokinetic timeline — effects build from first alerts to approaching peak (Riba 2003). Combination context.
	ReasoningReasoning Come-up estimated at 30-60 minutes based on ayahuasca pharmacokinetic timeline — effects build from first alerts to approaching peak (Riba 2003). Combination context. Evidence basis: controlled_human_study
Peaktrace	60–90 minutes	60–90 minutes	medium
Editorial	Peak at approximately 1.5-2 hours post-dose from Riba 2003 ayahuasca data. Peak duration estimated at 60-90 minutes. This is the most reliable phase estimate from controlled data, though combination context.
	ReasoningReasoning Peak at approximately 1.5-2 hours post-dose from Riba 2003 ayahuasca data. Peak duration estimated at 60-90 minutes. This is the most reliable phase estimate from controlled data, though combination context. Evidence basis: controlled_human_study
Offsettrace	60–120 minutes	60–120 minutes	low
Editorial	Offset estimated at 1-2 hours based on ayahuasca total duration of 4-6 hours minus onset/come-up/peak phases. No direct measurement of harmine standalone offset.
	ReasoningReasoning Offset estimated at 1-2 hours based on ayahuasca total duration of 4-6 hours minus onset/come-up/peak phases. No direct measurement of harmine standalone offset. Evidence basis: structural_analogy
Totaltrace	4–6 hours	4–6 hours	medium
Editorial	Total duration 4-6 hours from ayahuasca literature consensus (Riba 2003, general ayahuasca clinical data). Work-notes specify this range. Combination context (harmine+DMT), not harmine standalone.
	ReasoningReasoning Total duration 4-6 hours from ayahuasca literature consensus (Riba 2003, general ayahuasca clinical data). Work-notes specify this range. Combination context (harmine+DMT), not harmine standalone. Evidence basis: controlled_human_study
After effectstrace	4–24 hours	4–24 hours	low
Editorial	Aftereffects estimated at 4-24 hours based on ayahuasca reports of reflective, emotionally open state persisting well after primary effects resolve. No harmine-specific data.
	ReasoningReasoning Aftereffects estimated at 4-24 hours based on ayahuasca reports of reflective, emotionally open state persisting well after primary effects resolve. No harmine-specific data. Evidence basis: community_consensus_large

buccal

Field	Published	AI Proposed	Confidence
Totaltrace	4–5 hours	4–5 hours	medium
Editorial	Total duration of 4-5 hours from Egger et al. 2025 buccal DMT+harmine factorial dose-finding study in 16 healthy participants. This is the most directly measured duration value available, though from combination context.
	ReasoningReasoning Total duration of 4-5 hours from Egger et al. 2025 buccal DMT+harmine factorial dose-finding study in 16 healthy participants. This is the most directly measured duration value available, though from combination context. Evidence basis: controlled_human_study

Safety

Toxicity Profiletrace

Field	Published	AI Proposed	Confidence
Acute	low	low	low
Chronic	low	low	low
Organs Affected	gastrointestinal, cardiovascular, neurological	gastrointestinal, cardiovascular, neurological	low
Editorial	Work-notes specify acute=low-to-moderate, chronic=no data, confidence=low. Downgraded to 'low' acute (from 'low-to-moderate') because GI and CV data are from ayahuasca combination context (confounded by DMT), LD50 is unverified, and preclinical data shows no organ toxicity at therapeutic mouse doses. Chronic set to 'low' rather than null — no data but no signals of chronic harm in available animal or observational human data.
	ReasoningReasoning Work-notes specify acute=low-to-moderate, chronic=no data, confidence=low. Downgraded to 'low' acute (from 'low-to-moderate') because GI and CV data are from ayahuasca combination context (confounded by DMT), LD50 is unverified, and preclinical data shows no organ toxicity at therapeutic mouse doses. Chronic set to 'low' rather than null — no data but no signals of chronic harm in available animal or observational human data. Evidence basis: animal_study

Dependence Profiletrace

Field	Published	AI Proposed	Confidence
Physical	none	none	low
Psychological	negligible	negligible	low
Compulsive Redosing	negligible	negligible	low
Dose Escalation	negligible	negligible	low
Editorial	All values inferred from reversible MAOI mechanism and β-carboline class pharmacology per work-notes. No substance-specific dependence data exist. Work-notes specify: physical=none (inferred), psychological=negligible, compulsive redosing=negligible, dose escalation=no data. Confidence low — entirely structural-class inference from RIMA pharmacology.
	ReasoningReasoning All values inferred from reversible MAOI mechanism and β-carboline class pharmacology per work-notes. No substance-specific dependence data exist. Work-notes specify: physical=none (inferred), psychological=negligible, compulsive redosing=negligible, dose escalation=no data. Confidence low — entirely structural-class inference from RIMA pharmacology. Evidence basis: structural_analogy

Withdrawal Profiletrace

Field	Published	AI Proposed	Confidence
Severity	none	none	low
Symptoms	—	—	low
Fatal	No	No	low
Medical Supervision	Not required	Not required	low
Editorial	No withdrawal syndrome has been described for harmine in any published literature. Inferred from reversible MAOI mechanism — competitive binding with short residence time means MAO-A activity recovers rapidly upon compound clearance, leaving no pharmacodynamic basis for withdrawal.
	ReasoningReasoning No withdrawal syndrome has been described for harmine in any published literature. Inferred from reversible MAOI mechanism — competitive binding with short residence time means MAO-A activity recovers rapidly upon compound clearance, leaving no pharmacodynamic basis for withdrawal. Evidence basis: structural_analogy

Tolerance Profiletrace

Field	Published	AI Proposed	Confidence
Buildup	none	none	low
Half-life	—	—	low
Full Reset	—	—	low
Cross-tolerances	moclobemide	moclobemide	low
Editorial	Work-notes specify: buildup=no data, half-life=no data, full reset=no data, cross-tolerances=theoretically possible with moclobemide but not established. All values inferred from reversible MAOI class pharmacology. Confidence low — no substance-specific data exist. Mechanism note: reversible competitive inhibition means tolerance would require enzyme upregulation, which has not been studied for harmine.
	ReasoningReasoning Work-notes specify: buildup=no data, half-life=no data, full reset=no data, cross-tolerances=theoretically possible with moclobemide but not established. All values inferred from reversible MAOI class pharmacology. Confidence low — no substance-specific data exist. Mechanism note: reversible competitive inhibition means tolerance would require enzyme upregulation, which has not been studied for harmine. Evidence basis: structural_analogy

Effects & Profile

Contraindications

Field	Published	AI Proposed	Confidence
psychiatric Concurrent SSRI/SNRI usetrace	absolute	absolute	high
Editorial	Pharmacological inference supported by PBPK modeling (Ribeiro et al. 2026). No clinical case reports for harmine specifically, but mechanism is well-established for all MAO-A inhibitors including reversible ones.
	ReasoningReasoning Pharmacological inference supported by PBPK modeling (Ribeiro et al. 2026). No clinical case reports for harmine specifically, but mechanism is well-established for all MAO-A inhibitors including reversible ones.
psychiatric Concurrent irreversible MAOI usetrace	absolute	absolute	high
Editorial	Standard MAOI class contraindication. Established pharmacological mechanism — additive MAO-A inhibition is well-documented as dangerous for all MAOI combinations.
	ReasoningReasoning Standard MAOI class contraindication. Established pharmacological mechanism — additive MAO-A inhibition is well-documented as dangerous for all MAOI combinations.
other Concurrent tryptamine use without dose titrationtrace	relative	relative	high
Editorial	Well-established mechanism from McKenna et al. 1984 and confirmed in multiple human PK studies (Riba 2003, Egger 2025). This is the most extensively documented interaction for harmine.
	ReasoningReasoning Well-established mechanism from McKenna et al. 1984 and confirmed in multiple human PK studies (Riba 2003, Egger 2025). This is the most extensively documented interaction for harmine.
cardiovascular Cardiovascular instabilitytrace	relative	relative	medium
Editorial	Riba et al. 2003 documented statistically significant diastolic BP increase in placebo-controlled ayahuasca study. Data is from combination context (harmine+DMT), not harmine alone — confidence reduced accordingly.
	ReasoningReasoning Riba et al. 2003 documented statistically significant diastolic BP increase in placebo-controlled ayahuasca study. Data is from combination context (harmine+DMT), not harmine alone — confidence reduced accordingly.
hepatic Hepatic impairmenttrace	relative	relative	medium
Editorial	Yu et al. 2003 established CYP2D6 and CYP1A2 as the principal metabolic enzymes. Hepatic impairment reducing these enzyme activities will predictably increase harmine exposure. No direct clinical studies in hepatically impaired populations.
	ReasoningReasoning Yu et al. 2003 established CYP2D6 and CYP1A2 as the principal metabolic enzymes. Hepatic impairment reducing these enzyme activities will predictably increase harmine exposure. No direct clinical studies in hepatically impaired populations.
metabolic CYP2D6 poor metabolizer statustrace	relative	relative	medium
Editorial	Yu et al. 2003 confirmed CYP2D6 as the principal metabolic enzyme with exceptionally high turnover numbers. Pharmacogenetic impact is confirmed at the enzyme level but no human outcome studies in poor metabolizers exist.
	ReasoningReasoning Yu et al. 2003 confirmed CYP2D6 as the principal metabolic enzyme with exceptionally high turnover numbers. Pharmacogenetic impact is confirmed at the enzyme level but no human outcome studies in poor metabolizers exist.
pregnancy breastfeeding Pregnancy and lactationtrace	absolute	absolute	low
Editorial	Precautionary default — no reproductive safety data exist. Both MAO-A inhibition and DYRK1A inhibition have theoretical implications for fetal development.
	ReasoningReasoning Precautionary default — no reproductive safety data exist. Both MAO-A inhibition and DYRK1A inhibition have theoretical implications for fetal development.
other Concurrent sympathomimetic usetrace	relative	relative	low
Editorial	Class-level contraindication inherited from reversible MAOI pharmacology as noted in work-notes. No harmine-specific data; inferred from RIMA mechanism.
	ReasoningReasoning Class-level contraindication inherited from reversible MAOI pharmacology as noted in work-notes. No harmine-specific data; inferred from RIMA mechanism.
other High-tyramine foods at significant MAOI dosestrace	relative	relative	medium
Editorial	Standard RIMA class precaution. Dos Santos et al. 2016 review discusses reduced but non-zero tyramine risk with reversible MAO-A inhibitors. Risk is pharmacologically established but substantially lower than irreversible MAOIs.
	ReasoningReasoning Standard RIMA class precaution. Dos Santos et al. 2016 review discusses reduced but non-zero tyramine risk with reversible MAO-A inhibitors. Risk is pharmacologically established but substantially lower than irreversible MAOIs.

Timeline Phases

oral

Field	Published	AI Proposed	Confidence
Onsettrace	1800–3600 sec(i=0.10)	1800–3600 sec(i=0.10)	low
Editorial	All timeline data is from the ayahuasca (harmine+DMT) combination context per Riba et al. 2003 and general ayahuasca literature consensus. Harmine-specific standalone timeline cannot be characterized from available data. Peak timing (~1.5-2 hours) from Riba 2003; total duration 4-6 hours from ayahuasca literature. Work-notes specify all phases derived from combination context, not harmine alone.
	ReasoningReasoning All timeline data is from the ayahuasca (harmine+DMT) combination context per Riba et al. 2003 and general ayahuasca literature consensus. Harmine-specific standalone timeline cannot be characterized from available data. Peak timing (~1.5-2 hours) from Riba 2003; total duration 4-6 hours from ayahuasca literature. Work-notes specify all phases derived from combination context, not harmine alone. Evidence basis: published_case_series
Come uptrace	1800–3600 sec(i=0.40)	1800–3600 sec(i=0.40)	low
Editorial	All timeline data is from the ayahuasca (harmine+DMT) combination context per Riba et al. 2003 and general ayahuasca literature consensus. Harmine-specific standalone timeline cannot be characterized from available data. Peak timing (~1.5-2 hours) from Riba 2003; total duration 4-6 hours from ayahuasca literature. Work-notes specify all phases derived from combination context, not harmine alone.
	ReasoningReasoning All timeline data is from the ayahuasca (harmine+DMT) combination context per Riba et al. 2003 and general ayahuasca literature consensus. Harmine-specific standalone timeline cannot be characterized from available data. Peak timing (~1.5-2 hours) from Riba 2003; total duration 4-6 hours from ayahuasca literature. Work-notes specify all phases derived from combination context, not harmine alone. Evidence basis: published_case_series
Peaktrace	3600–5400 sec(i=1.00)	3600–5400 sec(i=1.00)	low
Editorial	All timeline data is from the ayahuasca (harmine+DMT) combination context per Riba et al. 2003 and general ayahuasca literature consensus. Harmine-specific standalone timeline cannot be characterized from available data. Peak timing (~1.5-2 hours) from Riba 2003; total duration 4-6 hours from ayahuasca literature. Work-notes specify all phases derived from combination context, not harmine alone.
	ReasoningReasoning All timeline data is from the ayahuasca (harmine+DMT) combination context per Riba et al. 2003 and general ayahuasca literature consensus. Harmine-specific standalone timeline cannot be characterized from available data. Peak timing (~1.5-2 hours) from Riba 2003; total duration 4-6 hours from ayahuasca literature. Work-notes specify all phases derived from combination context, not harmine alone. Evidence basis: published_case_series
Resolutiontrace	3600–7200 sec(i=0.40)	3600–7200 sec(i=0.40)	low
Editorial	All timeline data is from the ayahuasca (harmine+DMT) combination context per Riba et al. 2003 and general ayahuasca literature consensus. Harmine-specific standalone timeline cannot be characterized from available data. Peak timing (~1.5-2 hours) from Riba 2003; total duration 4-6 hours from ayahuasca literature. Work-notes specify all phases derived from combination context, not harmine alone.
	ReasoningReasoning All timeline data is from the ayahuasca (harmine+DMT) combination context per Riba et al. 2003 and general ayahuasca literature consensus. Harmine-specific standalone timeline cannot be characterized from available data. Peak timing (~1.5-2 hours) from Riba 2003; total duration 4-6 hours from ayahuasca literature. Work-notes specify all phases derived from combination context, not harmine alone. Evidence basis: published_case_series
Afterglowtrace	14400–72000 sec(i=0.10)	14400–72000 sec(i=0.10)	low
Editorial	All timeline data is from the ayahuasca (harmine+DMT) combination context per Riba et al. 2003 and general ayahuasca literature consensus. Harmine-specific standalone timeline cannot be characterized from available data. Peak timing (~1.5-2 hours) from Riba 2003; total duration 4-6 hours from ayahuasca literature. Work-notes specify all phases derived from combination context, not harmine alone.
	ReasoningReasoning All timeline data is from the ayahuasca (harmine+DMT) combination context per Riba et al. 2003 and general ayahuasca literature consensus. Harmine-specific standalone timeline cannot be characterized from available data. Peak timing (~1.5-2 hours) from Riba 2003; total duration 4-6 hours from ayahuasca literature. Work-notes specify all phases derived from combination context, not harmine alone. Evidence basis: published_case_series

Dose Tier Summaries

thresholdtrace

low

At threshold doses, harmine produces no appreciable psychoactive effects as a standalone agent. The relevant threshold is pharmacological rather than experiential — the dose at which measurable peripheral MAO-A inhibition begins, reducing the enzymatic breakdown of dietary and endogenous monoamines. Users may notice a subtle shift in somatic awareness or faint gastrointestinal stirring, but these effects are difficult to distinguish from placebo. Physical effects are minimal. Slight nausea may occur in sensitive individuals. No perceptual, cognitive, or emotional changes are expected at this level. Note: Harmine is primarily used as an MAOI adjunct to DMT, not as a standalone psychoactive. Threshold doses for MAOI activity are substantially lower than doses that would produce direct CNS effects. CYP2D6 poor metabolizers may experience effects at lower doses due to reduced metabolic clearance.

Editorial

No published threshold dose data for standalone harmine psychoactivity. Work-notes specify this tier should describe MAOI threshold rather than psychoactive threshold. All inference from RIMA pharmacology and ayahuasca combination context.

Reasoning

Evidence basis: structural_analogy

lighttrace

low

At light doses, harmine produces partial MAO-A inhibition with subtle subjective effects. As a standalone agent, users may notice mild sedation, slight bodily heaviness, and a gentle introspective quality. In combination with DMT, light harmine doses produce modest potentiation — extending DMT's duration and mildly intensifying its effects without fully enabling oral bioavailability. Physical effects may include mild nausea, slight dizziness, and gentle sedation. The gastrointestinal effects that characterize higher doses are typically absent or mild at this level. Oral bioavailability of harmine is very low due to extensive first-pass metabolism. Buccal or sublingual administration achieves substantially higher systemic exposure at equivalent doses. CYP2D6 poor metabolizers will experience stronger effects than typical.

Editorial

No published dose-response data for harmine as standalone psychoactive. Light tier description inferred from RIMA pharmacology, ayahuasca combination data, and work-notes guidance. Egger 2025 studied harmine 0-180 mg buccal but always co-administered with DMT.

Reasoning

Evidence basis: structural_analogy

commontrace

low

At common doses, harmine produces significant MAO-A inhibition sufficient to enable oral DMT bioavailability in the ayahuasca context. As a standalone agent, effects may include moderate sedation, enhanced introspection, mild emotional enhancement, and subtle dreaming enhancement. Creativity enhancement and divergent thinking facilitation have been documented in the ayahuasca context at these dose ranges. Physical effects typically include nausea (reported by most users in the ayahuasca context), bodily heaviness, mild dizziness, and possible trembling. Temperature dysregulation may occur. Gastrointestinal effects are the most consistently reported adverse response at this level. Standalone psychoactive effects of harmine at common doses have not been characterized in controlled studies. All experiential descriptions are derived from the ayahuasca (harmine+DMT) combination context, where DMT drives the primary phenomenology.

Editorial

No standalone dose-response data. Common tier inferred from ayahuasca combination studies (Riba 2003, Durante 2021) and work-notes guidance. Effects at this tier are primarily from combination context and cannot be attributed to harmine alone.

Reasoning

Evidence basis: structural_analogy

strongtrace

low

At strong doses, harmine produces near-complete peripheral MAO-A inhibition. In combination with DMT, this tier produces intense subjective effects including vivid internal hallucinations, profound emotional enhancement, strong introspection enhancement, and marked time alteration. Cognitive euphoria and catharsis are commonly reported. The experience becomes immersive and may include thought connectivity and multiple thought streams. Physical effects intensify significantly: nausea and vomiting become likely, bodily heaviness is pronounced, and trembling may occur. Dizziness and motor control impairment are common. Cardiovascular effects include modest blood pressure elevation (+9 mmHg diastolic documented in controlled study). The experience requires a dedicated setting with no obligations for 6+ hours. Higher doses in the Egger 2025 factorial design (up to 180 mg buccal) produced stronger effects but always with co-administered DMT. Historical subcutaneous doses of 40-70 mg in Parkinson's trials produced mood elevation and motor effects.

Editorial

No standalone dose-response data. Strong tier inferred from higher-dose ayahuasca studies (Riba 2003 high dose, Egger 2025 factorial design up to 180 mg buccal) and historical Parkinson's trial data (20-70 mg SC). Work-notes flag that all effect descriptions are from combination context.

Reasoning

Evidence basis: structural_analogy

heavytrace

low

At heavy doses, harmine saturates peripheral MAO-A capacity and may achieve sufficient CNS penetration for direct psychoactive effects beyond MAOI activity. Historical Parkinson's trials using subcutaneous doses up to 70 mg reported significant mood elevation alongside motor effects including tremor worsening. In combination with DMT, heavy harmine doses produce maximally intense experiences with potential for overwhelming visionary states, confusion, and significant anxiety. Physical effects at this level are pronounced: vomiting is likely, trembling and motor control impairment are expected, and cardiovascular effects become more concerning. The gastrointestinal burden may be substantial and debilitating. Seizure threshold considerations arise at extreme doses based on class pharmacology. This dose range carries significant safety concerns. Serotonin syndrome risk increases with any concurrent serotonergic exposure. CYP2D6 poor metabolizers may reach heavy-equivalent exposure at nominally strong doses. No controlled human data characterize harmine's standalone effects at these levels.

Editorial

No controlled standalone dose-response data. Heavy tier inferred from historical Parkinson's SC data (70 mg as upper clinical range), Egger 2025 buccal data (180 mg maximum studied), and work-notes guidance. All effect descriptions extrapolated from combination context and historical reports.

Reasoning

Evidence basis: structural_analogy

History

current version

published Oct 2, 2026system—

versions

2 total · since previous: +0 / −0 citations

publication ledger

publish Oct 2, 2026

backfill Jun 4, 2026

Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.

full version history suggest a correction contact@psychedex.org

Sources

8 strong · 35 moderate · 6 weak

[1]
moderate
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[2]
moderate
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McKenna DJ, Towers GH, Abbott F · 1984 · Journal of Ethnopharmacology
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[3]
strong
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linkno claims checked
[6]
moderate
A high-throughput chemical screen reveals that harmine-mediated inhibition of DYRK1A increases human pancreatic beta cell replication
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[7]
moderate
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[8]
moderate
Exposure Characteristics of the Analogous Beta-Carboline Alkaloids Harmaline and Harmine Based on the Efflux Transporter of Multidrug Resistance Protein 2
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moderate
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linkno claims checked
[12]
moderate
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[23]
moderate
Inhibition of DYRK1A Stimulates Human β-Cell Proliferation
Dirice E, Walpita D, Vetere A, Meier BC, Kahraman S, et al. · 2016 · Diabetes
doi.org/10.2337/db15-1127 pubmed 26953159no claims checked
[24]
moderate
Harmine and its derivatives: A promising multi-target therapeutic avenue for Alzheimer's disease
Shen X, Dong X, Nao J · 2026 · Neuroscience
doi.org/10.1016/j.neuroscience.2026.03.006 pubmed 41812815no claims checked
[25]
moderate
Design, synthesis and biological evaluation of harmine derivatives as potent GSK-3β/DYRK1A dual inhibitors for the treatment of Alzheimer's disease
Liu W, Liu X, Tian L, Gao Y, Liu W, Chen H, et al. · 2021 · European Journal of Medicinal Chemistry
doi.org/10.1016/j.ejmech.2021.113554 pubmed 34098466no claims checked
[26]
moderate
Inhibition of Dyrk1A Attenuates LPS-Induced Neuroinflammation via the TLR4/NF-κB P65 Signaling Pathway
Ju C, Wang Y, Zang C, Liu H, Yuan F, et al. · 2022 · Inflammation
doi.org/10.1007/s10753-022-01699-w pubmed 35917097no claims checked
[27]
moderate
The alkaloids of Banisteriopsis caapi, the plant source of the Amazonian hallucinogen Ayahuasca, stimulate adult neurogenesis in vitro
Morales-Garcia JA, de la Fuente Revenga M, Alonso-Gil S, et al. · 2017 · Scientific Reports
doi.org/10.1038/s41598-017-05407-9 pubmed 28706205no claims checked
[28]
moderate
Harmine produces antidepressant-like effects via restoration of astrocytic functions
Liu F, Wu J, Gong Y, Wang P, Zhu L, et al. · 2017 · Progress in Neuro-Psychopharmacology & Biological Psychiatry
doi.org/10.1016/j.pnpbp.2017.06.012 pubmed 28625859no claims checked
[29]
moderate
Harmine alleviates LPS-induced acute lung injury by inhibiting CSF3-mediated MAPK/NF-κB signaling pathway
Zhai Y, Chen K, Xu Z, Chen X, Tong J, He Y, et al. · 2025 · Respiratory Research
doi.org/10.1186/s12931-025-03196-8 pubmed 40156005no claims checked
[30]
moderate
Harmine exerts anticancer effects through the ROS/p38 axis to induce autophagy and apoptosis in osteosarcoma
Yu L, Bi K, Gu J, Yu Z, Li S, Chen Y · 2025 · Bioorganic Chemistry
doi.org/10.1016/j.bioorg.2025.108557 pubmed 40345123no claims checked
[31]
moderate
Harmine induces anticancer activity in breast cancer cells via targeting TAZ
Ding Y, He J, Huang J, Yu T, Shi X, Zhang T, et al. · 2019 · International Journal of Oncology
doi.org/10.3892/ijo.2019.4777 pubmed 31081045no claims checked
[32]
strong
Predicting drug-drug interactions between ayahuasca alkaloids and SSRIs using physiologically based pharmacokinetic modeling
Ribeiro GSG, Paranhos BAPB, Dörr F, et al. · 2026 · Frontiers in Molecular Biosciences
doi.org/10.3389/fmolb.2026.1768402 pubmed 41788629no claims checked
[33]
strong
Population pharmacokinetic-pharmacodynamic modeling of co-administered N,N-dimethyltryptamine and harmine in healthy subjects
Äbelö A, Smallridge JW, von Rotz R, et al. · 2025 · Biomedicine & Pharmacotherapy
doi.org/10.1016/j.biopha.2025.118329 pubmed 40639043no claims checked
[34]
moderate
[3H]harman binding experiments: a reversible and selective radioligand for monoamine oxidase subtype A in the CNS of the rat
May T, Rommelspacher H, Pawlik M · 1991 · Journal of Neurochemistry
pubmed 1988552no claims checked
[35]
moderate
Harmine Selectively Drives Human Beta Cell Differentiation and Function Via Protein Kinase A Pathways
Wang P, Kumar K, Lambertini L, Liu H, Wood O, et al. · 2025 · bioRxiv
doi.org/10.64898/2025.12.07.692818 pubmed 41573826no claims checked
[36]
moderate
Increased frontal and paralimbic activation following ayahuasca, the pan-amazonian inebriant
Riba J, Romero S, Grasa E, Mena E, Carrio I · 2006 · Psychopharmacology
doi.org/10.1007/s00213-006-0358-7 pubmed 16575552no claims checked
[37]
moderate
The psychedelic state induced by ayahuasca modulates the activity and connectivity of the default mode network
Palhano-Fontes F, Andrade KC, Tofoli LF, et al. · 2015 · PLoS ONE
doi.org/10.1371/journal.pone.0118143 pubmed 25693169no claims checked
[38]
strong
Rapid antidepressant effects of the psychedelic ayahuasca in treatment-resistant depression: a randomized placebo-controlled trial
Palhano-Fontes F, Barreto D, Onias H, Andrade KC, Novaes MM, et al. · 2018 · Psychological Medicine
doi.org/10.1017/s0033291718001356 pubmed 29903051no claims checked
[39]
moderate
Ayahuasca enhances creative divergent thinking while decreasing conventional convergent thinking
Kuypers KPC, Riba J, de la Fuente Revenga M, Barker SA, Theunissen EL, et al. · 2016 · Psychopharmacology
doi.org/10.1007/s00213-016-4377-8 pubmed 27435062no claims checked
[40]
moderate
Antidepressant effects of a single dose of ayahuasca in patients with recurrent depression: a preliminary report
Osório FL, Sanches RF, Macedo LR, Santos RG, et al. · 2015 · Revista brasileira de psiquiatria
doi.org/10.1590/1516-4446-2014-1496 pubmed 25806551no claims checked
[41]
moderate
Acute experiences and persisting psychological effects of DMT-harmala alkaloid combination: phase 1 study
Perkins D, Halman A, Urokohara A, Palumbo J, Low M, Ruffell S, et al. · 2025 · Scientific Reports
doi.org/10.1038/s41598-025-25767-x pubmed 41266565no claims checked
[42]
strong
Pharmacokinetics and pharmacodynamics of an innovative psychedelic N,N-dimethyltryptamine/harmine formulation in healthy participants: a randomized controlled trial
Mueller MJ, Aicher HD, Dornbierer DA, et al. · 2024 · International Journal of Neuropsychopharmacology
doi.org/10.1093/ijnp/pyaf001 pubmed 39774840no claims checked
[43]
strong
Pre-clinical investigations of β-carboline alkaloids as antidepressant agents: A systematic review
Ferraz CAA, de Oliveira Júnior RG, Picot L, da Silva Almeida JRG, Nunes XP · 2019 · Fitoterapia
doi.org/10.1016/j.fitote.2019.104196 pubmed 31175948no claims checked
[44]
weak
Harmine Guide: Effects, Benefits, Risks, and Legality
ACS Laboratory · 2024
linkno claims checked
[45]
moderate
Risk assessment of ayahuasca use in a religious context: self-reported risk factors and adverse effects
Durante I, Dos Santos RG, Bouso JC, Hallak JE · 2021 · Brazilian Journal of Psychiatry
doi.org/10.1590/1516-4446-2020-0913 pubmed 33146343no claims checked
[46]
moderate
Beta-carbolines (harman/norharman) are increased in heroin dependent patients
Stohler R, Rommelspacher H, Ladewig D, Dammann G · 1993 · Therapeutische Umschau
pubmed 8475471no claims checked
[47]
moderate
Peganum harmala seed extract attenuates anxiety and depression in rats via BDNF/TrkB signaling pathway
Tekşen Y, Gündüz MK, Berikten D, Özatik FY, Aydın HE · 2024 · Metabolic Brain Disease
doi.org/10.1007/s11011-024-01416-6 pubmed 39172328no claims checked
[48]
moderate
The Therapeutic Potentials of Ayahuasca: Possible Effects against Various Diseases of Civilization
Frecska E, Bokor P, Winkelman M · 2016 · Frontiers in Pharmacology
doi.org/10.3389/fphar.2016.00035 pubmed 26973523no claims checked
[49]
weak
Legal Status of Syrian Rue and Harmala Alkaloids
SyrianRue.org · 2024
linkno claims checked

Claim Verification

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Coverage & Gaps

effect links

17 links · 17 approved · 0 audited0/17 with evidence basis

Harmine

Value Provenance

Dosing

oraltrace →

buccaltrace →

Duration

oral

buccal

Safety

Toxicity Profiletrace →

Dependence Profiletrace →

Withdrawal Profiletrace →

Tolerance Profiletrace →

Effects & Profile

Contraindications

Timeline Phases

oral

Dose Tier Summaries

History

Sources

Claim Verification

Coverage & Gaps

oraltrace

buccaltrace

Toxicity Profiletrace

Dependence Profiletrace

Withdrawal Profiletrace

Tolerance Profiletrace