generation run 2026-04-26
79 min completedmodel pipeline-v5plan not recordedrun/dffe132c…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
none raised on this run
Reproduce
- inputs
- 31 source keys (listed under Sources)
- plan
- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
- streams
- none — agent transcripts are persisted from 2026-09 onward
18 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed · absence | Anadenanthera peregrina bufotenine alkaloid seeds cohoba | 0 | — | No results, will try web search |
| 2 | PubMed | bufotenine blood brain barrier serotonin metabolism | 7 | 4 | Selected articles with direct bufotenine BBB, metabolism, and pharmacology data |
| 3 | ClinicalTrials.gov | bufotenin bufotenine | 10 | 0 | No bufotenine-specific clinical trials found |
| 4 | PubMed | bufotenin pharmacology receptor binding | 15 | 6 | Selected articles with direct bufotenine data; discarded general tryptamine/5-MeO-DMT papers |
| 5 | OpenAlex | bufotenin psychedelic tryptamine | 10 | 2 | Selected reviews containing direct bufotenine pharmacology; discarded 5-MeO-DMT clinical trial papers |
| 6 | PubMed | bufotenine schizophrenia endogenous urine detection psychiatric | 3 | 3 | All directly relevant to endogenous bufotenine and psychiatric hypothesis |
| 7 | PubMed | bufotenine human psychedelic hallucinogen effects | 15 | 4 | All have direct bufotenine data; other results focused on 5-MeO-DMT |
| 8 | PubChem | bufotenin | 1 | 1 | Primary chemical identity confirmation |
| 9 | OpenAlex | bufotenine hallucinogen receptor pharmacology | 10 | 2 | Only items with bufotenine-specific data selected |
| 10 | OpenAlex | bufotenine human study Fabing 1956 psychedelic | 2 | 2 | Both highly relevant - Maitland 2025 is critical new behavioral pharmacology data |
| 11 | ClinicalTrials.gov · absence | bufotenin bufotenine | 0 | 0 | No bufotenine-specific trials |
| 12 | WebSearch | bufotenine legal status schedule controlled substance United States DEA / UK Canada Australia | 10 | 4 | Multiple confirmatory sources converged |
| 13 | HandWiki | — | 1 | 4 | Only web source with quantitative binding data for bufotenine specifically |
| 14 | PubChem + Handwiki | Bufotenine chemical identity SMILES InChIKey CAS MW | 2 | 1 | All chemical identity data confirmed |
| 15 | PubMed | Individual article fetches | 8 | 10 | All confirmed relevant; Almaula 1996, Roth 1997, Berg 2001 also fetched |
| 16 | WebSearch | bufotenine history discovery Handovsky Gonçalves de Lima Phisalix Wieland | 10 | 1 | Corroborated by multiple web sources |
| 17 | PubMed | bufotenine schizophrenia endogenous urine detection psychiatric | 3 | 3 | All directly relevant to endogenous bufotenine in psychiatric disorders |
| 18 | PubMed + Web | Tramadol serotonin syndrome MAO bufotenine interaction | 7 | 2 | Mechanistic basis for tramadol-bufotenine dangerous interaction confirmed |
72 claims by section — every cited sentence, checked against its source
safety19 · 14 ok
The primary safety concern is cardiovascular toxicity: 5-HT₄-mediated positive inotropy and chronotropy confirmed in human atrial preparations, combined with well-documented peripheral vasoconstrictionsupported
Bufotenin acts as agonist at human 5-HT4 receptors, increasing cardiac contractility (pD2=6.77 for left atrium) and heart rate (pD2=7.04 for right atrium) in transgenic mice and human atrial preparations. Demonstrates clinically relevant cardiovascular activity. s00210-023-02414-8
Claim in safety — inconclusiveinconclusiveworking →
Bufotenin produces peripheral vasoconstriction — described as 'a powerful constrictor of blood vessels, causing a rise in blood pressure' — and directly increases cardiac contractility and heart rate via 5-HT₄ receptors in isolated human atrial preparations (positive inotropic effect: pD2 = 6.77; positive chronotropic effect: pD2 = 7.04)supported
Bufotenin acts as agonist at human 5-HT4 receptors, increasing cardiac contractility (pD2=6.77 for left atrium) and heart rate (pD2=7.04 for right atrium) in transgenic mice and human atrial preparations. s00210-023-02414-8
These cardiac effects are potentiated by MAO inhibition.supported
Effects potentiated by MAO inhibitor. s00210-023-02414-8
Historical human IV experiments in the 1950s consistently produced alarming cardiovascular effects at doses intended to achieve psychedelic effects — facial flushing, tachycardia, and hypertension were prominent and dose-limiting.supported
Comprehensive review of Bufo toad mythology and bufotenine science. Investigates alleged psychedelic properties. Reviews human experiments. pmid:8895112
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
The transmethylation hypothesis proposes that endogenous bufotenin overproduction may contribute to psychotic symptoms, but whether exogenous administration reliably induces psychosis or psychosis-adjacent states is undetermined from the available evidence.supported
Reviews transmethylation hypothesis of schizophrenia. Bufotenin (N,N-dimethylserotonin) as endogenous psychotomimetic. Reviews conflicting data on MIA excretion in psychotic patients. pmid:9468359
The transmethylation hypothesis proposes that endogenous bufotenin overproduction may contribute to psychotic symptoms, but whether exogenous administration reliably induces psychosis or psychosis-adjacent states is undetermined from the available evidence.supported
Concludes too early to use as biomarker. Endogenous bufotenine may be implicated in schizophrenia and ASD pathophysiology. cureus.84510
Tramadol is a weak serotonin reuptake inhibitor implicated in serotonin toxicity when combined with MAO inhibitors, including fatal casessupported
Tramadol is a weak serotonin reuptake inhibitor; involved in serotonin toxicity with MAOIs (including fatalities). pmid:16051647
Tramadol is a weak serotonin reuptake inhibitor implicated in serotonin toxicity when combined with MAO inhibitors, including fatal casessupported
Tramadol has serotonergic effects; in combination with MAOIs, risk of life-threatening serotonin syndrome. s00482-015-1512-0
Bufotenin contributes direct serotonin receptor agonism (5-HT₁A, 5-HT₂A/C, 5-HT₄) and is itself a MAO-A substratesupported
Metabolized primarily by MAO-A (not MAO-B). pmid:8532147
MAO-A is bufotenin's primary metabolic enzyme; inhibition dramatically reduces clearance, prolongs duration of action, and increases plasma levelssupported
Metabolized primarily by MAO-A (not MAO-B). pmid:8532147
In isolated human atrial preparations, the MAO inhibitor pargyline potentiated bufotenin's cardiac 5-HT₄ effectssupported
Effects potentiated by MAO inhibitor. Demonstrates clinically relevant cardiovascular activity. s00210-023-02414-8
Historical forensic analysis documented that street bufotenin in New York City was typically smoked with marijuana, indicating co-use occurs, but no safety data on this combination have been published.supported
Bufotenine identified in 42 NYC Police Lab case samples (sold as 'hashish', smoked with marijuana) since 1992. pmid:26270149
Cardiovascular disease, hypertension, and cardiac arrhythmia represent the most significant contraindication. 5-HT₄-mediated positive inotropy and chronotropy confirmed in human cardiac tissue, combined with peripheral vasoconstriction, create substantial cardiovascular risk for individuals with pre-existing cardiac conditions.supported
Bufotenin acts as agonist at human 5-HT4 receptors, increasing cardiac contractility (pD2=6.77 for left atrium) and heart rate (pD2=7.04 for right atrium) in transgenic mice and human atrial preparations. Demonstrates clinically relevant cardiovascular activity. s00210-023-02414-8
Concurrent MAOI use is contraindicated due to bufotenin's MAO-A-dependent metabolismsupported
Metabolized primarily by MAO-A (not MAO-B). pmid:8532147
pharmacology16 · 16 ok
Bufotenin acts as an agonist at multiple serotonin receptor subtypes, but its psychedelic profile is pharmacologically constrained by two converging factors: poor blood-brain barrier (BBB) penetration via systemic routes and balanced 5-HT₁A/5-HT₂A activity in which 5-HT₁A agonism suppresses 5-HT₂A-mediated psychedelic effects.supported
Evidence is reviewed that the reported lack of classic hallucinogenic response in human experiments is due to poor BBB penetration, not lack of receptor activation. pmid:11061684
Bufotenin acts as an agonist at multiple serotonin receptor subtypes, but its psychedelic profile is pharmacologically constrained by two converging factors: poor blood-brain barrier (BBB) penetration via systemic routes and balanced 5-HT₁A/5-HT₂A activity in which 5-HT₁A agonism suppresses 5-HT₂A-mediated psychedelic effects.supported
Bufotenine only induced elevated HTRs (ED50=0.99 mg/kg, max=24 counts) when 5-HT1A receptors were pharmacologically blocked. Without 5-HT1A blockade, bufotenine failed to produce significant HTR. 2025.04.28.650242
Roth et al. (1997) showed that bufotenin labeled approximately 22% of high-affinity 5-HT₂A agonist binding sites yet was devoid of detectable agonist activity in phosphoinositide hydrolysis assays — evidence favoring a modified ternary complex model where high-affinity binding alone is insufficient for receptor activationsupported
Bufotenine labels ~22% high-affinity agonist binding sites at 5-HT2A but is devoid of detectable agonist activity (phosphoinositide hydrolysis). Demonstrates dissociation between high-affinity binding and functional efficacy. pmid:9023266
The molecular basis was elucidated by Almaula et al. (1996): N,N-dimethylation creates steric hindrance preventing a critical hydrogen bond with Ser3.36(159) in transmembrane helix 3, altering the ligand's orientation in the binding pocketsupported
N,N-dimethylation causes steric hindrance preventing Ser3.36 hydrogen bond interaction. Reveals molecular basis of bufotenin's altered receptor interaction. pmid:8663249
Ebersole et al. (2003) confirmed that ligand position within the binding pocket determines degree of receptor activation.supported
Ser3.36 and Ser5.46 interactions determine ligand position in binding pocket, which determines receptor activation. pmid:12488534
Maitland et al. (2025, preprint) tested bufotenin in the mouse head-twitch response (HTR) paradigm and found that bufotenin produced elevated HTRs only when 5-HT₁A receptors were pharmacologically blocked (ED50 = 0.99 mg/kg, maximum counts = 24)supported
Bufotenine only induced elevated HTRs (ED50=0.99 mg/kg, max=24 counts) when 5-HT1A receptors were pharmacologically blocked. 2025.04.28.650242
Without 5-HT₁A blockade, bufotenin showed no significant HTR activity — paralleling findings with 5-MeO-DMT analogs.supported
5-HT1A agonist activity can dampen 5-HT2A-mediated HTRs. 5-HT1A blockade markedly increases HTR responses (40-90 HTRs/30 min). Structure-activity relationships for N,N-dialkyl tryptamines. acschemneuro.4c00513
At the 5-HT₂C receptor (Ki = 16–209 nM), bufotenin exhibits agonist-directed trafficking: its relative efficacy for arachidonic acid release versus inositol phosphate accumulation is reversed compared to other agonists such as TFMPPsupported
Bufotenin and TFMPP show reversed efficacy order (AA release vs IP accumulation) at non-edited 5-HT2C receptor, demonstrating agonist-directed trafficking. pmid:11564657
RNA editing of the 5-HT₂C receptor's second intracellular loop eliminates this biased signaling.supported
RNA editing eliminates this trafficking difference. pmid:11564657
Bufotenin is also an agonist at human cardiac 5-HT₄ receptors (pD2 = 6.77–7.04), producing positive inotropic and chronotropic effects in isolated human atrial preparationssupported
Bufotenin acts as agonist at human 5-HT4 receptors, increasing cardiac contractility (pD2=6.77 for left atrium) and heart rate (pD2=7.04 for right atrium) in transgenic mice and human atrial preparations. s00210-023-02414-8
In rats, subcutaneous bufotenin reaches peak tissue concentration approximately 1 hour post-injection, with high concentrations in lung, heart, and blood but significantly lower levels in brain and liver — brain-to-blood ratios are approximately 15-fold lower than those of 5-MeO-DMTpartially supported
High in lung, heart, blood; low in brain and liver. Poor BBB penetration confirmed. pmid:8532147
The primary metabolic enzyme is MAO-A (not MAO-B), confirmed by differential effects of the selective inhibitors LY51641 (MAO-A selective) and deprenyl (MAO-B selective)supported
Metabolized primarily by MAO-A (not MAO-B). pmid:8532147
The principal metabolite is 5-hydroxyindoleacetic acid (5-HIAA), accounting for approximately 70% of the administered dose — the same metabolite produced from serotoninpartially supported
Metabolite 5-HIAA detected. pmid:8532147
Bufotenin N-oxide is a secondary metabolitesupported
N-oxide metabolites of methylated tryptamines measured in rat urine. pmid:3475068
Unlike serotonin, bufotenin is not stored in platelets: greater than 99% is found in platelet-poor plasma compared to 2% for serotonin.supported
Bufotenine not stored in platelets. pmid:8532147
Molecular dynamics simulations provide a molecular-level explanation for poor BBB penetration: bufotenin partitions into lipid bilayers but does not spontaneously cross the membrane, unlike DMT and 5-MeO-DMT, which cross spontaneously under identical simulation conditions.supported
All partition into bilayer. Bufotenine does NOT cross membrane spontaneously (unlike DMT and 5-MeO-DMT), consistent with BBB impermeability. j.chemphyslip.2023.105279
history8 · 8 ok
Bufotenin has been reported in several Amanita mushroom species, including A. muscaria, A. citrina, A. porphyria, and A. tomentellasupported
Natural sources: Anadenanthera seeds, toad species, mushrooms. pmid:26270149
In 1893, French pharmacologist Césaire Phisalix and biochemist Gabriel Bertrand first isolated a toxic component from the cutaneous secretion of Bufo vulgaris (common toad)supported
Comprehensive review of Bufo toad mythology and bufotenine science. Discovery traced to 1893. pmid:8895112
Bufotenin is a major alkaloid in seeds of Anadenanthera peregrina (formerly Piptadenia peregrina), native to South America and the West Indiessupported
Natural sources: Anadenanthera seeds, toad species, mushrooms. Historical use as snuff by South American indigenous peoples. pmid:26270149
Archaeological evidence confirms deep antiquity: bufotenin has been identified in 1,200-year-old samples of Anadenanthera material from excavated tombs in northern Chile.supported
Archaeological samples found in 1200-year-old Andean tomb. pmid:26270149
Beyond Anadenanthera, bufotenin occurs in the skin and parotid glands of multiple toad species — Bufo marinus, B. vulgaris, B. viridis, and Rhinella marinasupported
Identifies novel indolethylamine N-methyltransferase (RmNMT) in cane toad (Rhinella marina) and related NMT in Bufo bufo. RmNMT biosynthesizes bufotenin and other tryptamines. j.jbc.2023.105231
Bufotenin is produced endogenously in humans, detectable in urine under normal physiological conditions, presumably via indolethylamine N-methyltransferase (INMT) — the same enzyme implicated in endogenous DMT production.supported
Urinary bufotenine detected in 82% of psychiatric patients vs 29% of healthy controls. cureus.84510
In 1956, Fabing and Hawkins administered intravenous bufotenin to psychiatric patients, reporting prominent cardiovascular effects — facial flushing, tachycardia, hypertension — with some visual phenomena at higher dosessupported
Comprehensive review of Bufo toad mythology and bufotenine science. Investigates alleged psychedelic properties. Reviews human experiments. pmid:8895112
McBride (2000) reexamined the historical data and concluded that the absence of clear psychedelic effects in intravenous experiments reflects bufotenin's poor blood-brain barrier penetration rather than failure to activate relevant CNS receptorssupported
Evidence is reviewed that the reported lack of classic hallucinogenic response in human experiments is due to poor BBB penetration, not lack of receptor activation. pmid:11061684
summary7 · 5 ok
Claim in summary — inconclusiveinconclusiveworking →
Intravenous experiments in psychiatric patients during the 1950s produced prominent cardiovascular effects but equivocal psychedelic responses, fueling decades of debate over whether the compound is genuinely hallucinogenicsupported
Comprehensive review of Bufo toad mythology and bufotenine science. Investigates alleged psychedelic properties. Reviews human experiments. pmid:8895112
Modern research interest centers on the transmethylation hypothesis — elevated urinary bufotenin in schizophrenia and autism spectrum disorder — and on the pharmacological mechanisms constraining its psychedelic activity.supported
Urinary bufotenine detected in 82% of psychiatric patients vs 29% of healthy controls. 5/8 studies found higher bufotenine in mental illness. Endogenous bufotenine may be implicated in schizophrenia and ASD pathophysiology. cureus.84510
Bufotenin binds 5-HT₂A receptors (Ki = 15–>10,000 nM) but exhibits near-zero functional efficacy at that target — a dissociation attributable to steric hindrance from N,N-dimethylation, which prevents a critical hydrogen bond with Ser3.36(159) in transmembrane helix 3supported
N,N-dimethylation causes steric hindrance preventing Ser3.36 hydrogen bond interaction. Reveals molecular basis of bufotenin's altered receptor interaction. pmid:8663249
Concurrent 5-HT₁A agonism (Ki = 2.5–1,023 nM) actively suppresses residual 5-HT₂A-mediated effects; mouse head-twitch response data show psychedelic-like activity emerges only under 5-HT₁A blockade (ED50 = 0.99 mg/kg)supported
Bufotenine only induced elevated HTRs (ED50=0.99 mg/kg, max=24 counts) when 5-HT1A receptors were pharmacologically blocked. 2025.04.28.650242
Bufotenin also acts as an agonist at human cardiac 5-HT₄ receptors (pD2 = 6.77–7.04).supported
Bufotenin acts as agonist at human 5-HT4 receptors, increasing cardiac contractility (pD2=6.77 for left atrium) and heart rate (pD2=7.04 for right atrium) in transgenic mice and human atrial preparations. s00210-023-02414-8
Claim in summary — inconclusiveinconclusiveworking →
chemistry6 · 5 ok
Claim in chemistry — inconclusiveinconclusiveworking →
This hydrophilicity directly underlies the compound's poor blood-brain barrier penetrationsupported
Evidence is reviewed that the reported lack of classic hallucinogenic response in human experiments is due to poor BBB penetration, not lack of receptor activation. pmid:11061684
Molecular dynamics simulations confirm that bufotenin partitions into lipid bilayers but does not cross membranes spontaneously — unlike DMT and 5-MeO-DMT, which traverse model membranes during simulation timescales.supported
All partition into bilayer. Bufotenine does NOT cross membrane spontaneously (unlike DMT and 5-MeO-DMT), consistent with BBB impermeability. j.chemphyslip.2023.105279
In animals, it is biosynthesized in the parotid glands and skin of toads via a toad-specific indolethylamine N-methyltransferase (RmNMT) that converts serotonin to bufotenin through sequential methylationsupported
Identifies novel indolethylamine N-methyltransferase (RmNMT) in cane toad (Rhinella marina). RmNMT biosynthesizes bufotenin and other tryptamines. j.jbc.2023.105231
In plants, it is a major alkaloid of Anadenanthera peregrina seeds and has been isolated from Desmodium elegans leavessupported
Bufotenin isolated from Desmodium elegans leaves alongside new MAO inhibitor alkaloid. j.fitote.2014.07.022
Bufotenin is also produced endogenously in humans, detectable in urine under normal physiological conditions, presumably via indolethylamine N-methyltransferase (INMT)supported
Urinary bufotenine detected in 82% of psychiatric patients vs 29% of healthy controls. cureus.84510
clinical-evidence4 · 4 ok
The only human dosing data come from uncontrolled experiments conducted in the 1950s–60s, reviewed in secondary sourcessupported
Comprehensive review of Bufo toad mythology and bufotenine science. Reviews human experiments. Provides bibliography of Bufo toad and bufotenine history. pmid:8895112
Clarke (2025) conducted a systematic review of studies measuring urinary bufotenin in patients with schizophrenia and autism spectrum disorder, finding consistently elevated levels compared to controlssupported
Systematic review of 8 papers (609 participants). Urinary bufotenine detected in 82% of psychiatric patients vs 29% of healthy controls. 5/8 studies found higher bufotenine in mental illness. cureus.84510
Ciprian-Ollivier (1997) proposed a common molecular pathway linking altered methylation to endogenous psychosissupported
Reviews transmethylation hypothesis of schizophrenia. Bufotenin (N,N-dimethylserotonin) as endogenous psychotomimetic. Ayahuasca model for understanding hallucinogenic symptoms in schizophrenia. pmid:9468359
Zhao et al. (2021) identified analgesic properties of bufotenin and its derivatives through computational target prediction and behavioral assays in animal modelssupported
Reverse docking identified AChE and alpha4beta2 nAChR as analgesic targets. Bufotenine+morphine shows synergistic analgesia. s1875-5364(21)60044-4
comparative-pharmacology4 · 3 ok
Its polarity reduces lipophilicity (log P = 0.89–2.04), directly impairing membrane permeability and BBB penetrationsupported
Bufotenine does NOT cross membrane spontaneously (unlike DMT and 5-MeO-DMT), consistent with BBB impermeability. j.chemphyslip.2023.105279
At the receptor level, bufotenin's 5-hydroxyl group creates additional constraints on binding orientation at 5-HT₂A that virtually eliminate functional efficacy.supported
Bufotenine labels ~22% high-affinity agonist binding sites at 5-HT2A but is devoid of detectable agonist activity (phosphoinositide hydrolysis). Demonstrates dissociation between high-affinity binding and functional efficacy. pmid:9023266
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
The Maitland et al. (2025, preprint) findings with bufotenin — where HTR activity emerged only under 5-HT₁A blockade — extend this principle to a 5-hydroxylated tryptaminesupported
Bufotenine only induced elevated HTRs (ED50=0.99 mg/kg, max=24 counts) when 5-HT1A receptors were pharmacologically blocked. Without 5-HT1A blockade, bufotenine failed to produce significant HTR. 2025.04.28.650242
receptor-pharmacology4 · 4 ok
Bufotenin labels approximately 22% of high-affinity agonist binding sites — comparable to the 26% labeled by the full agonist DOI — but produces no detectable phosphoinositide hydrolysissupported
Bufotenine labels ~22% high-affinity agonist binding sites at 5-HT2A but is devoid of detectable agonist activity (phosphoinositide hydrolysis). pmid:9023266
Serotonin's primary amine forms hydrogen bonds with both Asp3.32 and Ser3.36(159) in the 5-HT₂A binding pocket; bufotenin's bulkier tertiary amine maintains the Asp3.32 interaction but cannot access Ser3.36, resulting in an altered binding orientation that fails to trigger the activation cascade.supported
Ser3.36 and Ser5.46 interactions determine ligand position in binding pocket, which determines receptor activation. Relevant to bufotenine's partial agonist behavior. pmid:12488534
This functional selectivity is abolished by RNA editing of the second intracellular loop, indicating that receptor isoform determines the downstream signaling pattern.supported
RNA editing eliminates this trafficking difference. pmid:11564657
Reverse docking analyses have implicated bufotenin as a ligand at sigma-1 and 5-HT₃A receptors, potentially contributing to anti-inflammatory effectssupported
Sigma-1 receptor and 5-HT3A receptor binding implicated. Anti-inflammatory and analgesic mechanisms described. j.biopha.2021.111749
neuroscience2 · 2 ok
Bufotenin, like DMT and 5-MeO-DMT, antagonized 5-HT excitations on single neurons, demonstrating direct CNS activity when the blood-brain barrier is bypassedsupported
Bufotenine (5-HODMT), like DMT and 5-MeO-DMT, specifically antagonized 5-HT excitations on single neurons. All three psychotomimetic tryptamines mimicked 5-HT actions on neurons. pmid:4277490
Proposed in the mid-20th century and refined by Ciprian-Ollivier (1997), it posits that endogenous overproduction of methylated tryptamines — including bufotenin, DMT, and their precursors — contributes to psychotic symptomatologysupported
Reviews transmethylation hypothesis of schizophrenia. Bufotenin (N,N-dimethylserotonin) as endogenous psychotomimetic. Ayahuasca model for understanding hallucinogenic symptoms in schizophrenia. pmid:9468359
pharmacokinetic-detail2 · 2 ok
The only systematic pharmacokinetic data derive from Fuller et al. (1995) in rats following subcutaneous injection:supported
Bufotenine concentrations measured in rats after s.c. injection. pmid:8532147
Bufotenin is primarily metabolized by MAO-Asupported
Metabolized primarily by MAO-A (not MAO-B). pmid:8532147