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Anadenanthera peregrina

Overview

Yopo (Anadenanthera peregrina, Fabaceae) — cohoba, paricá — is a neotropical tree with one of the highest natural concentrations of bufotenine, a tryptamine alkaloid. Bufotenine is a classical serotonergic psychedelic, chemically related to psilocin and DMT.[1] It activates serotonin receptors in the cortex, generating intense hallucinations and cognitive disruption within minutes.

Yopo (Anadenanthera peregrina, Fabaceae) — cohoba, paricá — is a neotropical tree whose seeds produce one of the highest natural concentrations of the tryptamine alkaloid bufotenine. Its dominant alkaloid, bufotenine, is a classical serotonergic psychedelic active at 5-HT₂A receptors.[1] Bufotenine produces its principal effects by agonizing 5-HT₂A receptors in the cortex, generating intense visual hallucinations and cognitive disruption.

Entity
Anadenanthera peregrina
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NoticeAll →
•6 lethal interactions(all →)
FamilyFabaceae
GenusAnadenanthera
SpeciesAnadenanthera peregrina (L.) Speg.
Native rangeCaribbean and South Tropical America: Bolivia, Brazil, Colombia, Dominican Republic, French Guiana, Guyana, Haiti, Puerto Rico, Suriname, Trinidad-Tobago, Venezuela
CultivationPrimarily wild-harvested; no formal cultivar development documented. Seeds sold commercially online without standardized alkaloid content or quality controls.
→ BUFOTENINE0.6–7.5 %
→ DMT0.009–0.16 %
→ 5-MEO-DMT0.01–0.04 %
traditional alkaline snuff (yopo/cohoba)vaporized free-base bufotenineMAO-inhibitor admixture (yopo + B. caapi)
PsychoactivePsychedelic
ChemicalSubstituted tryptamine
threshold30–30 mg
light65–300 mg
common300–540 mg
strong540–800 mg
heavy800+ mg
Seeds toasted, ground, and mixed with alkaline agent (calcium carbonate or plant ash) to free-base alkaloids for mucosal absorption. Nausea and vomiting near-universal at psychoactive doses. All dose tiers from ICEERS (non-peer-reviewed harm reduction resource); not verified against published primary sources.
common2–8 mg
Purified or semi-purified bufotenine in free-base form. Substantially lower dose than nasal snuff, suggesting higher pulmonary bioavailability. No published pharmacokinetic parameters. Dose range from non-peer-reviewed sources.
Piaroa tradition: yopo snuff combined with Banisteriopsis caapi cuttings or B. caapi consumed prior to insufflation. Harmaline co-administration raises 5-MeO-DMT exposure 3.6–4.4× and bufotenine exposure 9.9× (animal data). Longer, more intense experience with substantially greater serotonin toxicity risk. Classified as severe drug interaction. No standardized dosing exists.
minlowmodhigh
Acute
Chronic
Physical
Psych.
Withdrawal
Builduprapid
Full reset7 days
Cross-tol.
LSD, psilocybin, DMT +2 more
Absolute4 entries
Cardiovascular diseasePsychotic disordersPregnancyMAO inhibitor co-administration
Relative6 entries
Seizure disordersBipolar disorder (manic phase)Severe anxiety disordersHepatic impairmentSSRI/SNRI useCYP2D6 inhibitor use
lethal6
AmphetaminesMDMA, AmphetaminesMDMA, MDAPsychedelics
danger29
5-HTP, TryptophanAlpha-2 adrenergic receptor antagonistAntihistaminesAntipsychotics
caution21
Dosage varies by body weight, tolerance & metabolism · Not medical advice · Terms
See an error? Suggest correction
See an error? Suggest correction

Yopo snuff was first documented in 1496, when Friar Ramón Pané recorded the Taíno of Hispaniola inhaling it during healing and divination ceremonies.[2] Archaeological evidence confirms ritual use across the Caribbean and Orinoco basin dating back roughly 1,000 years.[3] Today the seeds are not internationally scheduled, but their alkaloids are Schedule I in the United States and controlled in most Western countries.

Subjective effects include intense geometric visuals, ego dissolution, disorientation, a racing heart, and nausea. The experience unfolds within one to five minutes and resolves within an hour — short and self-contained, but often overwhelming.[4] Nausea and vomiting are near-universal at psychoactive doses[5] — not incidental side effects, but a consistent part of the experience.

Yopo does not produce physical dependence; rapid serotonin receptor adaptation makes repeated dosing self-limiting.[6] The primary acute risk is cardiovascular — tachycardia and blood pressure spikes are prominent at psychoactive doses — and combining yopo with monoamine oxidase inhibitors multiplies alkaloid exposure up to 9.9-fold,[7] creating serious risk of a life-threatening serotonergic reaction. No controlled human trials have been published for any yopo preparation.

History[edit]

Traditional and historical use

Anadenanthera peregrina seeds have been used as psychoactive snuff — cohoba, yopo, jopo, or paricá — across the Caribbean and northern South America for well over a thousand years. The first European account dates to 1496, when Friar Ramón Pané documented the Taíno of Hispaniola inhaling cohoba through Y-shaped tubes during healing and divination ceremonies.[2] A ritual bundle from Bolivia dated to around 1,000 CE contained bufotenine, DMT, and harmine together — the oldest biochemical confirmation of combined yopo and ayahuasca-like use in the Americas.[3]

Western discovery and research

Western scientific interest began when Richard Spruce collected seeds at Rio Negro in 1854; Holmstedt and Lindgren first identified 5-MeO-DMT and DMT in the seeds in 1967,[8] and the definitive 1977 Schultes monograph documented bufotenine concentrations up to 7.5% of dry seed weight.[9] Traditional preparation — toasting seeds, grinding to powder, mixing with alkaline ash, and insufflating — remained unchanged across these centuries.[10][4] Torres and Repke's 2006 ethnobotanical synthesis consolidated the archaeological and chemical record.[11]

Modern era

DMT was listed as Schedule I under the UN Convention on Psychotropic Substances in 1971; bufotenine and 5-MeO-DMT were not internationally listed.[12] In the United States, bufotenine was separately placed on Schedule I (DEA code 7433); in the United Kingdom, bufotenine and DMT became Class A under the Misuse of Drugs Act 1971. No clinical trials for yopo or bufotenine have been registered.

Botanical Overview[edit]

Anadenanthera peregrina belongs to the family Fabaceae — the legume family. Linnaeus first described it as Mimosa peregrina in 1753; it passed through Acacia and Piptadenia before Spegazzini established the current binomial in 1923.[14] A closely related species, Anadenanthera colubrina (cebil, vilca), shares similar alkaloid chemistry and traditional use across southern South America.

The tree is native to the Caribbean islands, the Orinoco basin, and the tropical savannas and dry forests of northern South America — from Colombia and Venezuela through Brazil. It grows in open woodland and disturbed forest margins from sea level to roughly 1,000 meters. It is not commercially cultivated but persists in wild and semi-managed populations across its native range.

A. peregrina reaches 15–25 meters in height, with dark, rough bark often covered in conical spines. Leaves are finely compound, resembling those of other mimosoid legumes. The tree produces small spherical clusters of white or pale yellow flowers and flat, dark brown seed pods containing 3–10 glossy, lens-shaped seeds about 1–2 cm across — the only plant part used for psychoactive preparation. Bark, leaves, and roots do not contain psychoactive concentrations of the relevant alkaloids.

Alkaloid Profile[edit]

Bufotenine (5-hydroxy-N,N-dimethyltryptamine) is the dominant psychoactive alkaloid in A. peregrina seeds, present at the highest natural concentration of any documented plant source — up to 7.5% of seed dry weight in Venezuelan specimens.[9] It acts on serotonin receptors through the same pathway as psilocybin and DMT,[1] producing the intense visual and cognitive disruption characteristic of the yopo experience.

The seeds also contain two secondary tryptamines: DMT (N,N-dimethyltryptamine) and 5-MeO-DMT (5-methoxy-N,N-dimethyltryptamine). 5-MeO-DMT acts on a different serotonin pathway from bufotenine, adding an anxiolytic and dissociative dimension to the experience.[15] DMT engages multiple serotonin and other receptor systems simultaneously.[16] All three alkaloids converge downstream on the same cellular signaling cascade that mediates psychedelic effects.[17]

The ratio of bufotenine to DMT to 5-MeO-DMT varies substantially with seed maturity, geographic origin, and storage duration.[9] A batch dominated by bufotenine produces a different experience from one with more 5-MeO-DMT. CYP2D6, a liver enzyme, converts 5-MeO-DMT into bufotenine in the body — individuals with slow-metabolizer genetics show dramatically lower conversion rates.[7] MAO-A is the primary enzyme that clears all three alkaloids.[18]

Neuroscience[edit]

Where it acts

Bufotenine activates 5-HT₂A and 5-HT₂C serotonin receptors in the brain's cortex — the same primary targets as psilocybin and LSD.[1][19] Early researchers doubted bufotenine could even reach the brain; animal studies settled this, showing it accumulates in brain tissue and produces central psychedelic effects.[20] The secondary alkaloids extend the pharmacological reach — 5-MeO-DMT acts on a different serotonin pathway,[15] and DMT activates multiple serotonin systems simultaneously.[16]

What it changes

Bufotenine dampens serotonin's excitatory effects on brainstem neurons — a mechanism shared with LSD.[21] MAO-A breaks down all three seed alkaloids; blocking that enzyme — whether with pharmaceutical MAOIs or with Banisteriopsis caapi, which contains harmine and harmaline — raises bufotenine exposure up to 9.9-fold.[22][7]

Subjective Effects[edit]

Summary

The yopo experience is defined by its compressed arc and somatic weight. The experience arrives within minutes and ends within an hour, but onset is often overwhelming — nausea and a racing heart begin before the visual phase even peaks. Geometric hallucinations, ego dissolution, and intense cognitive disruption unfold while the body is already under significant physical strain. Traditional ritual context consistently shapes psychological outcomes and is reported to substantially reduce panic and disorientation.

Pharmacologically, yopo sits between vaporized DMT and oral ayahuasca. It shares the rapid onset and short duration of smoked DMT, but the dominant bufotenine action and prominent peripheral serotonergic effects give it a heavier somatic character. Preparation method is the primary modifier: alkaline snuff, vaporized free-base bufotenine, and monoamine oxidase-inhibitor admixtures produce pharmacologically distinct states — differing in intensity, duration, and the balance between visual depth and body-load.

Yopo snuff use was first documented by Europeans in 1496 on Hispaniola,[2] with archaeological chemical evidence dating to approximately 1,000 CE.[3] Ritual snuff traditions spread across the Caribbean and Orinoco basin, embedded in indigenous healing and cosmological practice. No clinical trials have been registered for yopo or bufotenine; bufotenine remains Schedule I in the United States.

Subjective effects include intense geometric visuals, ego dissolution, cognitive disruption, nausea, and cardiovascular stimulation, compressed into a 20–60-minute window with onset in 1–5 minutes.[4] The experience varies substantially by preparation — traditional alkaline snuff, vaporized free-base bufotenine, and monoamine oxidase-inhibitor admixtures each produce pharmacologically distinct states. Nausea and vomiting are near-universal at psychoactive doses.[5]

No physical dependence has been documented; rapid 5-HT₂A downregulation makes dose escalation self-limiting.[6] The primary acute risk is cardiovascular — tachycardia, hypertension, and vasoconstriction are prominent at psychoactive doses, and co-administration with MAO inhibitors increases alkaloid exposure up to 9.9-fold.[7] No controlled human pharmacokinetic studies, dose-response studies, or clinical trials have been published for any A. peregrina preparation.

History[edit]

Traditional and historical use

Anadenanthera peregrina seeds have been used as psychoactive snuff — known as cohoba, yopo, jopo, and paricá — across the Caribbean and northern South America in one of the oldest documented ritual drug practices in the Americas. The first European account dates to 1496, when Friar Ramón Pané documented the Taíno of Hispaniola inhaling cohoba through Y-shaped tubes during healing and divination ceremonies.[2]

Archaeological residue analysis from a ritual bundle in the Lípez Altiplano, Bolivia (approximately 1,000 CE) identified bufotenine and DMT alongside harmine and cocaine, providing the oldest biochemically confirmed evidence of combined Anadenanthera and ayahuasca-like admixture use.[3] Traditional preparation involves toasting seeds over low heat, grinding them to fine powder, and mixing with alkaline material — calcium carbonate from shells or plant ash — then insufflating through tubes.[8][4]

Western discovery and research

Richard Spruce collected A. peregrina seeds at Rio Negro in 1854; these specimens were analyzed roughly 120 years later as part of the foundational alkaloid quantification study.[9] Holmstedt and Lindgren first detected 5-MeO-DMT and DMT in the seeds in 1967.[10]

The 1977 monograph by Schultes, Holmstedt, Lindgren, and Rivier remains the definitive alkaloid quantification reference, reporting bufotenine concentrations up to 7.5% in Venezuelan seeds.[9] Torres and Repke consolidated the archaeological, ethnobotanical, and alkaloid chemistry of the genus in Anadenanthera: Visionary Plant of Ancient South America (2006).[11]

Modern era

DMT was listed as Schedule I under the UN Convention on Psychotropic Substances in 1971; bufotenine and 5-MeO-DMT were not internationally scheduled.[12] In the United States, bufotenine was placed on Schedule I (DEA code 7433). In the United Kingdom, bufotenine and DMT were classified as Class A under the Misuse of Drugs Act 1971. No clinical trials for A. peregrina, yopo, or bufotenine have been registered.

Botanical Overview[edit]

Anadenanthera peregrina belongs to the family Fabaceae (legume family). Originally described by Linnaeus as Mimosa peregrina in Species Plantarum (1753), the species was transferred through Acacia and Piptadenia before Spegazzini established the current binomial in 1923.[14] A closely related species, Anadenanthera colubrina (cebil, vilca), shares similar alkaloid chemistry and traditional use patterns in southern South America.

The tree is native to the Caribbean islands, the Orinoco basin, and the tropical savannas and dry forests of northern South America, from Colombia and Venezuela through Brazil. It grows in open woodland, cerrado, and disturbed forest margins at elevations from sea level to approximately 1,000 meters. A. peregrina is not cultivated commercially but persists in wild and semi-managed populations across its native range.

A. peregrina is a medium to large deciduous tree reaching 15–25 meters in height, with dark, rough bark often covered in conical spines. Leaves are bipinnately compound with numerous small leaflets, resembling those of other mimosoid legumes. The tree produces spherical clusters of white or pale yellow flowers and flat, dark brown seed pods containing 3–10 glossy, lens-shaped seeds approximately 1–2 cm in diameter.

Seeds are harvested when mature pods darken and split open. The seeds are the only plant part used for psychoactive preparation — bark, leaves, and roots do not contain psychoactive concentrations of the relevant tryptamines. Detailed preparation methods are described in the Preparations section.

Alkaloid Profile[edit]

bufotenine (5-hydroxy-N,N-dimethyltryptamine) is the dominant psychoactive alkaloid in A. peregrina seeds, present at the highest natural concentration of any documented plant source. The definitive quantification study reported bufotenine at up to 7.5% of seed dry weight in Venezuelan specimens.[9] Bufotenine acts as a 5-HT₂A receptor agonist, producing classical psychedelic effects through the same serotonergic pathway as psilocybin and DMT.[1]

The seeds contain two secondary tryptamine alkaloids — DMT (N,N-dimethyltryptamine) and 5-MeO-DMT (5-methoxy-N,N-dimethyltryptamine) — that contribute additional psychoactive effects. 5-MeO-DMT has primary affinity for 5-HT₁A receptors,[15] adding an anxiolytic and dissociative dimension. DMT acts across 5-HT₁A, 5-HT₂A, 5-HT₂C, sigma-1 receptor, and TAAR1 receptor systems.[16] All three alkaloids converge downstream on the Gq/phosphoinositide hydrolysis cascade that mediates psychedelic effects.[17]

The ratio of bufotenine to DMT to 5-MeO-DMT varies dramatically with seed maturity, geographic origin, and storage duration.[9] Seeds from different provenances produce pharmacologically distinct preparations — a batch dominated by bufotenine will produce a different experience from one with a higher proportion of 5-MeO-DMT. No commercial standardization or alkaloid content testing exists for seeds sold online.

CYP2D6 catalyzes the O-demethylation of 5-MeO-DMT to bufotenine in vivo, a metabolic conversion significantly affected by genetic polymorphism: poor metabolizers show 2.6–40-fold lower catalytic efficiency.[7] MAO-A is the primary degradation pathway for all three alkaloids.[18]

Neuroscience[edit]

Where it acts

Bufotenine binds the 5-HT₂A receptor through a hydrogen bond with residue L229 and a stable salt bridge with residue D155.[1] It also activates 5-HT₂C.[19] The secondary alkaloids extend the pharmacological reach: 5-MeO-DMT acts primarily at 5-HT₁A,[15] while DMT engages 5-HT₁A, 5-HT₂A, 5-HT₂C, sigma-1 receptor, and TAAR1.[16]

What it changes

Early researchers questioned whether bufotenine crossed the blood-brain barrier, attributing its effects to peripheral cardiovascular actions. This has been resolved: chronic administration in mice demonstrated bufotenine accumulation in brain tissue,[20] and 5-HT₂A binding with head twitch confirmation establishes central psychedelic activity.[1] Microiontophoretic studies show bufotenine antagonizes serotonin excitatory effects on brainstem neurons — a mechanism of psychotomimetic action shared with LSD.[21]

Monoamine oxidase inhibitor co-administration dramatically reshapes the pharmacokinetic profile: harmaline increases systemic 5-MeO-DMT exposure 3.6–4.4-fold and bufotenine exposure 9.9-fold,[22] providing the pharmacokinetic basis for the traditional Piaroa practice of combining yopo with B. caapi.[7]

Subjective Effects[edit]

Summary

The yopo experience is defined by its compressed temporal arc and somatic intensity. Nausea, vomiting, and cardiovascular stimulation are not incidental adverse effects but integral to the experience — they precede and overlap with the perceptual phase, shaping its overall character. Onset is rapid and often overwhelming; geometric visuals, cognitive disruption, and ego dissolution unfold within minutes, then resolve within an hour. Set and setting sensitivity is high, and traditional ritual context is reported to substantially modulate psychological outcomes.

Pharmacologically, yopo sits between vaporized DMT and oral ayahuasca. It shares the rapid onset and short duration of smoked DMT, but the dominant bufotenine action, prominent peripheral serotonergic effects, and somatic weight of onset distinguish it from other tryptamine preparations. The preparation method is the primary modifier: alkaline snuff, vaporized free-base, and monoamine oxidase-inhibitor admixtures each produce pharmacologically distinct states.

Effect Grid

Dose Level:
Description

Full psychedelic effects emerge. Geometry — colored geometric patterns, both open-eye and closed-eye — becomes prominent. Color enhancement and color alteration are vivid. Visual drifting and visual breathing are clearly perceptible. Internal hallucinations may feature structured imagery. Time alteration is marked; minutes may feel substantially longer or shorter.

Nausea and vomiting are likely at this level — vomiting is considered a normal component of the experience in traditional contexts. Cardiovascular stimulation is significant: tachycardia, facial flushing, and vasoconstriction are expected. Dizziness, muscle tension, and stimulation accompany the perceptual effects. Pupil dilation is probable.

Cognitive disruption includes confusion and thought disorganization, particularly during onset. Introspection enhancement and emotional enhancement emerge as the peak develops. This is the characteristic yopo experience. Functional impairment is substantial; a sitter is advisable. Primary effects last 20–60 minutes.

Modeled from the effect's dose-dependence curve — not per-substance measurements.

Perception(47)likelihood · intensity
Holotropic state
likely
Ganzfeld effect
likely
Color alteration
likely
Geometry
likely
Brightness alteration
possible
Color enhancement
possible
Spatial disorientation
possible
Vestibular distortion
possible
Visual drifting
possible

Color enhancement · Spatial disorientation · Vestibular distortion · Visual drifting · Auditory distortion · Depth perception distortion · Environmental patterning · Light sensitivity · Peripheral vision distortion · Perspective distortion · Proprioceptive distortion · Sound sensitivity · Symmetrical texture repetition · Tracers · Visual breathing · Visual morphing · After-images · Auditory misinterpretation · Visual diffraction · Visual haze / noise · Visual melting · Auditory enhancement · Peripheral misidentification · Synesthesia · Tinnitus · Touch enhancement · Visual magnification · Visual processing acceleration · Flashbacks · Internal hallucinations · External hallucinations · Auditory hallucinations · Environmental orbism / cubism · Object transformations · Perspective hallucinations · Visual processing suppression · Visual recursion · Visual scenery slicing · Object activation · Visual flipping · Shadow people · Persisting hallucinations

Auditory distortion · Depth perception distortion · Environmental patterning · Light sensitivity · Peripheral vision distortion · Perspective distortion · Proprioceptive distortion · Sound sensitivity · Symmetrical texture repetition · Tracers · Visual breathing · Visual morphing · After-images · Auditory misinterpretation · Visual diffraction · Visual haze / noise · Visual melting · Auditory enhancement · Peripheral misidentification · Synesthesia · Tinnitus · Touch enhancement · Visual magnification · Visual processing acceleration · Flashbacks · Internal hallucinations · External hallucinations · Auditory hallucinations · Environmental orbism / cubism · Object transformations · Perspective hallucinations · Visual processing suppression · Visual recursion · Visual scenery slicing · Object activation · Visual flipping · Shadow people · Persisting hallucinations

Body(33)likelihood · intensity
Nausea
likely
Body scan awareness
likely
Dizziness
likely
Excessive sweating
likely
Motor control impairment!
likely
Pupil dilation
likely
Body high
possible
Temperature dysregulation!
possible
Vasoconstriction!
possible

Excessive sweating · Pupil dilation · Body high · Nasal congestion · Physical fatigue · Salivation · Spontaneous body sensations · Trembling · Vomiting · Watery eyes · Appetite suppression · Bodily pressures · Breathing alteration · Heart rate perception changes · Involuntary body movements · Vibrations / buzzing · Nystagmus (eye wobbles) · Sedation · Stimulation · Tingling / electric sensations · Vasoconstriction · Bodily heaviness · Body schema distortion · Headache · Muscle tension · Restlessness · Bodily dissociation · Tactile hallucination

Nasal congestion · Physical fatigue · Salivation · Spontaneous body sensations · Trembling · Vomiting · Watery eyes · Appetite suppression · Bodily pressures · Breathing alteration · Heart rate perception changes · Involuntary body movements · Vibrations / buzzing · Nystagmus (eye wobbles) · Sedation · Stimulation · Tingling / electric sensations · Bodily heaviness · Body schema distortion · Headache · Muscle tension · Restlessness · Bodily dissociation · Tactile hallucination

Thinking(36)likelihood · intensity
Cognitive impairment
possible
Confusion
possible
Decision impairment!
possible
Focus suppression
possible
Thought disorganization
possible
Aesthetic enhancement
possible
Analysis suppression
possible
Suggestibility enhancement!
possible
Amnesia!
rare

Thought disorganization · Aesthetic enhancement · Analysis suppression · Cognitive fatigue · Immersion enhancement · Information processing suppression · Introspection enhancement · Memory fragmentation · Novelty enhancement · Openness enhancement · Pattern recognition enhancement · Cognitive dysphoria · Cognitive euphoria · Cognitive flexibility · Conceptual thinking · Increased nature relatedness · Language suppression · Memory replays · Memory suppression · Motivation suppression · Multiple thought streams · Thought connectivity · Thought deceleration · Thought loops · Creativity enhancement · Synchronicity · Thought acceleration · Analysis enhancement · Amnesia · Delirium · Delusions

Cognitive fatigue · Immersion enhancement · Information processing suppression · Introspection enhancement · Memory fragmentation · Novelty enhancement · Openness enhancement · Pattern recognition enhancement · Cognitive dysphoria · Cognitive euphoria · Cognitive flexibility · Conceptual thinking · Increased nature relatedness · Language suppression · Memory replays · Memory suppression · Motivation suppression · Multiple thought streams · Thought connectivity · Thought deceleration · Thought loops · Creativity enhancement · Synchronicity · Thought acceleration · Analysis enhancement · Delirium · Delusions

Feeling(9)likelihood · intensity
Anxiety
possible
Emotional enhancement
possible
Catharsis
possible
Emotional lability
possible
Simultaneous emotions
possible
Dysphoria
possible
Euphoria
possible
Empathy enhancement
possible
Paranoia!
possible

Simultaneous emotions · Dysphoria · Euphoria · Empathy enhancement

Self(14)likelihood · intensity
Derealization
possible
Communication suppression
possible
Depersonalization
possible
Emotional susceptibility
possible
Social disconnection
possible
Disinhibition
possible
Sociability suppression
possible
Flow state
rare
Self-control suppression!
rare

Social disconnection · Disinhibition · Sociability suppression · Flow state · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings

Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings

Time(4)likelihood · intensity
Time alteration
likely
Present-moment absorption
possible
Temporal disorientation
possible
Time cessation
v.rare
Transpersonal(12)likelihood · intensity
Unity and interconnectedness
possible
Entity contact
rare
Existential realization
rare
Noetic insight
rare
Transpersonal feelings
rare
Transpersonal visions
rare
Death-rebirth sequence
rare
Near-death experience
v.rare
Non-dual awareness
v.rare

Transpersonal visions · Death-rebirth sequence · Near-death experience · Non-dual awareness · Transpersonal memory access · Cessation · Voidness

Transpersonal memory access · Cessation · Voidness

Awareness(4)likelihood · intensity
Personal insight
possible
Cognitive dissonance
possible
Reality testing impairment!
rare
Recursive awareness
rare
report missing effect
Likelihood: how common this effect is at the selected dose level.This effect has safety implications — review before use.

Timeline · by preparation

traditional alkaline snuff (yopo/cohoba) (insufflated)
onset1 min – 5 min
peak5 min – 20 min
offset20 min – 1 h
afterglow1 h – 2 h
vaporized free-base bufotenine (vaporized)
onset0 s – 1 min
peak5 min – 20 min
offset20 min – 1 h
MAO-inhibitor admixture (yopo + B. caapi) (insufflated)
onset1 min – 5 min

Preparations[edit]

Traditional alkaline snuff

Seeds are toasted until they crack, ground to fine powder, and blended with an alkaline agent — typically calcium carbonate from snail shells or plant ash. The alkaline additive converts the alkaloids into free-base form for efficient absorption through nasal tissue.[4] The snuff is blown into the nose through a long tube by an assistant, or self-administered through a Y-shaped tube.[10]

Onset: 1–5 minutes.[4] Duration: 20–60 minutes. Nausea and vomiting are near-universal at psychoactive doses. This is the traditional and most widely documented preparation.

Vaporized free-base bufotenine

Purified or semi-purified bufotenine in free-base form can be vaporized and inhaled. Active doses are reported at 2–8 mgcitation needed — substantially lower than the snuff route, suggesting more efficient pulmonary absorption. Onset is near-instantaneous. Duration is comparable: 20–60 minutes. No published pharmacokinetic data exist for this route.

MAO-inhibitor admixture

Some indigenous traditions, notably the Piaroa of southern Venezuela, combine yopo with Banisteriopsis caapi or consume it prior to insufflation.[10] The harmine and harmaline in B. caapi block MAO-A — the primary pathway for alkaloid breakdown — raising 5-MeO-DMT exposure 3.6–4.4-fold and bufotenine exposure 9.9-fold in animal models.[22][7]

The resulting experience is longer, more intense, and carries substantially greater serotonin syndrome risk. This combination is classified as severe for drug interaction purposes.

Per-preparation dose tiers, timelines, and bioavailability data are in the Dose · by preparation card on this page.

Safety[edit]

Harm
Acute toxicity
Moderate
Chronic toxicity
Low
Withdrawal
None
Tolerance buildup
rapid
Tolerance reset
7 days
Dependence
Physical
None
Psychological
Negligible
Compulsive redosing
Negligible
Dose escalation
Negligible
Cross-tol.
LSD · psilo · DMT
Risk Shape
TOXPHYPSYWDRREDTOL

Toxicity

No human fatality attributed to yopo or bufotenine has been found in peer-reviewed literature. Animal studies administering bufotenine daily for 21 days found dose-dependent behavioral changes but no organ damage at lower doses; the alkaloid accumulated in the heart and kidney, and at higher doses in the lungs and brain.[20]

Cardiovascular effects are clinically significant at psychoactive doses: tachycardia, hypertension, intense vasoconstriction, facial purpling, chest heaviness, and respiratory stimulation have been documented in historical human administration studies.safety citation needed Nausea and vomiting are near-universal, triggered by serotonin receptor activation in the gut.[5]

No published studies examine contaminant profiles — pesticides, heavy metals, mycotoxins, or microbial load — in commercially sold seeds or prepared snuff. Alkaloid concentrations vary substantially by provenance, and no standardized testing requirement exists for this market.

Psychological Risks

Rapid onset and intense perceptual disruption create a high risk of acute anxiety and panic, especially for unprepared individuals outside ritual contexts. The risk of acute psychotic episodes is elevated in people with a personal or family history of psychotic disorders.[17]

Persistent visual disturbances after the experience ends (HPPD) are a documented risk of serotonergic psychedelic use; yopo-specific risk has not been studied but is extrapolated from LSD and psilocybin data.[23]

Tolerance & Dependence

No physical dependence, compulsive use pattern, or withdrawal has been documented for bufotenine or yopo.[17] Serotonin downregulation after each dose makes tolerance build quickly[6] — this is why self-escalating use is pharmacologically self-limiting. Cross-tolerance with psilocybin, LSD, and other serotonergic psychedelics is established.[6] Traditional cultural frameworks further structure and limit use patterns.[13]

Drug Interactions

MAO-A inhibitors are the most dangerous interaction class. Harmaline blocks the body's primary pathway for breaking down the seed alkaloids, raising bufotenine exposure 9.9-fold[7][22] and creating conditions for a potentially fatal serotonergic reaction. This includes pharmaceutical MAOIs (phenelzine, tranylcypromine, moclobemide) and botanical sources (B. caapi, Syrian rue). Severity: severe.[18]

SSRIs and SNRIs add serotonergic load, raising the risk of a dangerous overheating and seizure response. Chronic SSRI use also downregulates the serotonin receptor bufotenine targets, potentially blunting effects in unpredictable ways. Severity: moderate to severe.[24]

CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion) reduce the conversion of 5-MeO-DMT into bufotenine, altering alkaloid exposure unpredictably. Severity: moderate.[7][24]

Additional serotonergic agents — triptans, tramadol, fentanyl, linezolid — carry additive serotonin syndrome risk.[24]

All severity classifications are based on animal data and pharmacodynamic class effects. No clinical case report of serotonin syndrome from yopo combined with any pharmaceutical has been published.

Contraindications

MAO inhibitor co-administration is absolutely contraindicated — multi-fold increases in alkaloid exposure make serotonin toxicity risk severe.[7]

Cardiovascular disease — ischemic heart disease, arrhythmias, uncontrolled hypertension — is absolutely contraindicated given prominent cardiovascular stimulation at psychoactive doses.[5]

Psychotic disorders or strong family history of psychosis are absolutely contraindicated; serotonergic psychedelics can trigger or worsen psychotic episodes.[17]

Pregnancy is contraindicated; tryptamine alkaloids are expected to cross the placenta.safety citation needed

Hepatic impairment may reduce MAO-A clearance, increasing systemic alkaloid exposure.safety citation needed

SSRI or SNRI use requires physician-supervised taper and washout before use due to serotonin syndrome risk.[24]

Harm Reduction[edit]

Forms & Identification

Reagent ResultsNot recorded+ add reagent results
AppearanceNot recorded+ add appearance
Red FlagsNot recorded+ add red flags

A. peregrina seeds are sold online as whole dried seeds, pre-ground powder, or prepared snuff. No Certificate of Analysis program or alkaloid content labeling requirement exists for any commercial product. Because bufotenine, DMT, and 5-MeO-DMT concentrations vary dramatically by seed provenance and maturity, identical-looking seeds from different batches may produce substantially different experiences.

Reagent testing can confirm tryptamine presence but cannot quantify individual alkaloid ratios. Starting with a small test dose from each new batch is the only reliable safeguard against unexpected potency.

Full identification analysis →

Guidelines

  • Start with a fraction of a typical dose from any new seed batch — alkaloid content is unstandardized and varies by provenance.
  • Have a basin or bag nearby; nausea and vomiting are near-universal and onset is rapid.
  • Do not use alone. A sober companion should be present for the duration.
  • Do not combine with monoamine oxidase inhibitors (pharmaceutical or botanical) unless the pharmacokinetic consequences are fully understood — alkaloid exposure increases up to 9.9-fold.
  • Do not use if taking SSRIs, SNRIs, or any serotonergic medication.
  • Avoid use with any cardiovascular condition, including uncontrolled hypertension.
  • Allow at minimum 7 days between sessions to permit 5-HT₂A receptor resensitization.
  • Ensure the alkaline preparation agent is food-grade calcium carbonate or verified plant ash — unidentified alkaline substitutes may introduce contaminants.

Set & Setting

Yopo's rapid onset and intense somatic effects — nausea, vomiting, cardiovascular stimulation — make environment especially important. A calm, private, indoor setting with soft surfaces reduces injury risk during the disorienting onset phase.

A sober, trusted companion should be present, ideally someone familiar with the substance and its somatic intensity. The companion's primary role is physical safety during the first 10 minutes, when nausea and perceptual disruption are most acute. Individuals experiencing significant anxiety, depression, or emotional lability should not use yopo.

Aftercare & integration. The 1–2 hours following a yopo experience may include residual nausea, fatigue, and emotional sensitivity. Hydrate and rest. Avoid operating vehicles or machinery for at least 2 hours after effects resolve.

Nausea may persist beyond the psychoactive window — ginger tea or bland food can help settle the stomach. If distressing content arose during the experience, allow several days before attempting to interpret or analyze it. Persistent anxiety or perceptual disturbances beyond 48 hours warrant professional consultation.

Recovery & Support

Yopo does not produce physical dependence, and compulsive use is rare due to the self-limiting tolerance mechanism and the intensity of somatic onset. Any pattern of escalating use frequency or use despite negative consequences warrants self-assessment.

For individuals experiencing psychological difficulty after yopo use — persistent anxiety, depersonalization, or perceptual disturbances — professional support is available:

  • SAMHSA National Helpline (US): 1-800-662-4357 (free, confidential, 24/7)
  • Fireside Project (psychedelic peer support): 62-FIRESIDE (623-473-7433)
  • Crisis Text Line: Text HOME to 741741

Integration therapists with psychedelic experience can provide structured processing for difficult experiences.

Recovery resources, crisis lines, and support pathways → View all

Emergency Response

Recognizing an emergency

Immediate steps

  • 1. Stay with the person. Do not leave them alone.
  • 2. Call emergency services if any red flag above is present.
  • 3. Place the person in a recovery position if they are vomiting and unable to sit upright.
  • 4. Monitor breathing and pulse continuously.
  • 5. Keep the environment calm — reduce noise, dim lights, speak in short reassuring statements.

What to tell the dispatcher

State: "This person has inhaled a tryptamine-containing plant snuff (yopo). Estimated dose: [amount]. Time of administration: [time]. Symptoms: [describe]." Good Samaritan laws protect callers from prosecution in many jurisdictions.

Reversal agents

No specific reversal agent exists for bufotenine or tryptamine psychedelics. Treatment is supportive. Benzodiazepines may be administered by medical personnel for severe agitation.

Preparations[edit]

Traditional alkaline snuff

The traditional and most widely documented preparation. Seeds are toasted over low heat until they crack, ground to fine powder, and blended with an alkaline agent — typically calcium carbonate from snail shells or plant ash. The alkaline additive free-bases the tryptamine alkaloids, converting them from their salt form for efficient mucosal absorption.[4] The snuff is insufflated nasally, traditionally blown through a long tube by an assistant or self-administered via a Y-shaped tube.[8]

Onset occurs within 1–5 minutes.[4] Duration is 20–60 minutes. Nausea and vomiting are near-universal at psychoactive doses. The experience is intense and self-limiting; intensity peaks within minutes and subsides rapidly.

Vaporized free-base bufotenine

Purified or semi-purified bufotenine in free-base form can be vaporized and inhaled. This route is reported active at 2–8 mg,citation needed substantially below the nasal snuff dose, suggesting higher bioavailability through pulmonary absorption. Onset is near-instantaneous. Duration is comparable to the snuff route (20–60 minutes). No published pharmacokinetic parameters exist for this route.

MAO-inhibitor admixture

Some indigenous traditions, notably the Piaroa of southern Venezuela, combine yopo with Banisteriopsis caapi cuttings or consume B. caapi prior to insufflation.[8] The harmine and harmaline in B. caapi inhibit MAO-A, the primary degradation pathway for all three seed alkaloids.[18] This increases systemic exposure dramatically — harmaline co-administration raises 5-MeO-DMT exposure 3.6–4.4-fold and bufotenine exposure 9.9-fold in animal models.[22][7]

The resulting experience is longer, more intense, and carries substantially greater serotonin syndrome risk. This combination is classified as severe for drug interaction purposes.

Per-preparation dose tiers, timelines, and bioavailability data are in the Dose · by preparation card on this page.

Safety[edit]

Harm
Acute toxicity
Moderate
Chronic toxicity
Low
Withdrawal
None
Tolerance buildup
rapid
Tolerance reset
7 days
Dependence
Physical
None
Psychological
Negligible
Compulsive redosing
Negligible
Dose escalation
Negligible
Cross-tol.
LSD · psilo · DMT
Risk Shape
TOXPHYPSYWDRREDTOL

Toxicity

No human fatality attributed to yopo snuff or bufotenine has been identified in peer-reviewed literature. In chronic mouse studies, intraperitoneal bufotenine at doses of 0.63, 1.05, and 2.1 mg/animal/day for 21 days produced dose-dependent mild behavioral changes with no histological organ damage; the lowest effective dose was assessed as safe.[20] The alkaloid accumulated in heart and kidney at all doses, and in lungs and brain at higher doses.[20]

Cardiovascular effects are prominent and clinically significant at psychoactive doses. Historical human administration studies documented tachycardia, hypertension, intense peripheral vasoconstriction producing facial purpling and cyanosis, chest heaviness, and increased respiratory rate.safety citation needed Nausea and vomiting are near-universal, mediated by peripheral serotonin₃ and 5-HT₄ receptor activation.[5]

No published analytical studies examine contaminant profiles — pesticide residues, heavy metals (lead, cadmium, arsenic, mercury), mycotoxins, or microbial load — in commercially sold A. peregrina seeds or prepared snuff. Seeds are sold online without standardized alkaloid content testing, and alkaloid concentrations vary substantially by provenance. Preparation with unverified alkaline substitutes may introduce additional contaminants. No Certificate of Analysis requirement or ISO/IEC-accredited laboratory program exists for this market.

Psychological Risks

The rapid onset (1–5 minutes) and intense perceptual disruption create a high risk of acute anxiety and panic, particularly for unprepared individuals outside ritual contexts. Bufotenine is psychotomimetic at psychoactive doses; the risk of acute psychotic episodes is elevated in individuals with personal or family history of psychotic disorders.[17]

Hallucinogen-persisting perception disorder (HPPD) is a documented risk of serotonergic psychedelic use; yopo-specific risk has not been studied but is extrapolated from LSD and psilocybin data.[23] No peer-reviewed case reports of adverse psychiatric events specific to yopo snuff have been published.

Tolerance & Dependence

Classical serotonergic psychedelics produce rapid tolerance via 5-HT₂A downregulation; tolerance to the head twitch response is observed after repeated dosing, with single-dose tolerance detectable at 24 hours.[6] Cross-tolerance between serotonergic psychedelics has been documented.[6]

No physical dependence, compulsive use pattern, dose-escalation syndrome, or withdrawal has been documented for bufotenine or yopo.[17] The 5-HT₂A downregulation mechanism makes self-escalating use pharmacologically self-limiting. Traditional cultural frameworks further structure and limit use patterns.[13]

Drug Interactions

MAO-A inhibitors represent the most dangerous interaction class. Harmaline co-administration increases systemic 5-MeO-DMT exposure 3.6–4.4-fold and bufotenine exposure 9.9-fold by inhibiting MAO-A deamination — the primary metabolic inactivation pathway for all three seed alkaloids.[7][22] This includes botanical sources (B. caapi, Syrian rue) and pharmaceutical MAOIs (phenelzine, tranylcypromine, moclobemide). Severity: severe.[18]

SSRIs and SNRIs present a dual risk: pharmacodynamic serotonergic load addition raises serotonin syndrome risk, while chronic SSRI-induced 5-HT₂A downregulation may blunt effects unpredictably. Severity: moderate to severe.[24]

CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion) reduce 5-MeO-DMT conversion to bufotenine, altering alkaloid exposure in unpredictable ways. Severity: moderate.[7][24]

Additional serotonergic agents — triptans, tramadol, fentanyl, linezolid — carry additive serotonin toxicity risk.[24]

All severity classifications are based on pharmacokinetic mechanism from animal data and pharmacodynamic class effects. No clinical case report of serotonin syndrome from yopo combined with any pharmaceutical has been published.

Contraindications

MAO inhibitor co-administration is absolutely contraindicated due to multi-fold increases in alkaloid exposure and serotonin toxicity risk.[7]

Cardiovascular disease — including ischemic heart disease, arrhythmias, and uncontrolled hypertension — is absolutely contraindicated given prominent cardiovascular stimulation at psychoactive doses.[5]

Psychotic disorders or strong family history of psychosis are absolutely contraindicated; serotonergic psychedelics can precipitate or exacerbate psychotic episodes.[17]

Pregnancy is contraindicated; tryptamine alkaloids are expected to cross the placenta based on structural properties.safety citation needed

Hepatic impairment may reduce MAO-A clearance, increasing systemic alkaloid exposure.safety citation needed

SSRI or SNRI use requires taper and physician-supervised washout prior to use due to serotonin syndrome risk.[24]

Harm Reduction[edit]

Forms & Identification

Reagent ResultsNot recorded+ add reagent results
AppearanceNot recorded+ add appearance
Red FlagsNot recorded+ add red flags

A. peregrina seeds are sold online as whole dried seeds, pre-ground powder, or prepared snuff. No Certificate of Analysis program, ISO-accredited laboratory testing standard, or alkaloid content labeling requirement exists for any commercial product. Because bufotenine, DMT, and 5-MeO-DMT concentrations vary dramatically by seed provenance and maturity, identical-looking seeds from different batches may produce substantially different experiences.

Reagent testing can confirm tryptamine presence but cannot quantify individual alkaloid ratios. This means dosing decisions carry inherent uncertainty — starting with a small test dose from each new batch is the only reliable safeguard.

Full identification analysis →

Guidelines

  • Start with a fraction of a typical dose from any new seed batch — alkaloid content is unstandardized and varies by provenance.
  • Have a basin or bag nearby; nausea and vomiting are near-universal and onset is rapid.
  • Do not use alone. A sober companion should be present for the duration.
  • Do not combine with monoamine oxidase inhibitors (pharmaceutical or botanical) unless the pharmacokinetic consequences are fully understood — alkaloid exposure increases up to 9.9-fold.
  • Do not use if taking SSRIs, SNRIs, or any serotonergic medication.
  • Avoid use with any cardiovascular condition, including uncontrolled hypertension.
  • Allow at minimum 7 days between sessions to permit 5-HT₂A receptor resensitization.
  • Ensure the alkaline preparation agent is food-grade calcium carbonate or verified plant ash — unidentified alkaline substitutes may introduce contaminants.

Set & Setting

Yopo's rapid onset (1–5 minutes) and intense somatic effects — nausea, vomiting, cardiovascular stimulation — make environment especially important. A calm, private, indoor setting with soft surfaces reduces injury risk during the disorienting onset phase.

A sober, trusted companion should be present, ideally someone familiar with the substance and its somatic intensity. The companion's primary role is physical safety during the first 10 minutes, when nausea and perceptual disruption are most acute. Individuals experiencing significant anxiety, depression, or emotional lability should not use yopo.

Aftercare & integration. The 1–2 hours following a yopo experience may include residual nausea, fatigue, and emotional sensitivity. Hydrate and rest. Avoid operating vehicles or machinery for at least 2 hours after effects resolve.

Nausea may persist beyond the psychoactive window — ginger tea or bland food can help settle the stomach. Emotional processing is common after intense psychedelic experiences; journaling or quiet reflection is often more useful than immediate social engagement.

If distressing content arose during the experience, allow several days before attempting to interpret or analyze it. Persistent anxiety or perceptual disturbances beyond 48 hours warrant professional consultation.

Recovery & Support

Yopo does not produce physical dependence, and compulsive use is rare due to the self-limiting tolerance mechanism and the intensity of the somatic onset. However, any pattern of escalating use frequency or use despite negative consequences warrants self-assessment.

For individuals experiencing psychological difficulty after yopo use — persistent anxiety, depersonalization, or perceptual disturbances — professional support is available:

  • SAMHSA National Helpline (US): 1-800-662-4357 (free, confidential, 24/7)
  • Fireside Project (psychedelic peer support): 62-FIRESIDE (623-473-7433)
  • Crisis Text Line: Text HOME to 741741

Integration therapists with psychedelic experience can provide structured processing for difficult experiences.

Recovery resources, crisis lines, and support pathways → View all

Emergency Response

Recognizing an emergency

Immediate steps

  • 1. Stay with the person. Do not leave them alone.
  • 2. Call emergency services if any red flag above is present.
  • 3. Place the person in a recovery position if they are vomiting and unable to sit upright.
  • 4. Monitor breathing and pulse continuously.
  • 5. Keep the environment calm — reduce noise, dim lights, speak in short reassuring statements.

What to tell the dispatcher

State: "This person has inhaled a tryptamine-containing plant snuff (yopo). Estimated dose: [amount]. Time of administration: [time]. Symptoms: [describe]." Good Samaritan laws protect callers from prosecution in many jurisdictions.

Reversal agents

No specific reversal agent exists for bufotenine or tryptamine psychedelics. Treatment is supportive. Benzodiazepines may be administered by medical personnel for severe agitation.

Frequently asked questions

What is Anadenanthera peregrina?

Anadenanthera peregrina (yopo) is a South American tree whose seeds yield a bufotenine-rich psychedelic snuff used ritually since at least 1000 CE. Its primary alkaloid, bufotenine, acts as a 5-HT₂A receptor agonist; no controlled human studies have been published.

What are dangerous combinations with Anadenanthera peregrina?

The highest-severity documented interactions for Anadenanthera peregrina: Amphetamines (Lethal), MDMA, Amphetamines (Lethal), MDMA, MDA (Lethal), Psychedelics (Lethal), SNRIs (Lethal). See the interactions section for the full list with mechanisms and severity levels.

Is Anadenanthera peregrina addictive?

Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for Anadenanthera peregrina: tolerance builds rapid; full reset takes 7 days; cross-tolerance develops with LSD, psilocybin, DMT, mescaline, DOI. See the article's dependence and safety sections for recorded dependence data.

experience reports

No experience reports yet. Be the first to contribute.

First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.

references

  1. [1] 
    ^abcZhang M, Yang Y, Yang Z, et al. (2025) Structural insights into tryptamine psychedelics: The role of hydroxyl indole ring site in 5-HT2A receptor activation and psychedelic-like activity — European Journal of Medicinal Chemistry doi:10.1016/j.ejmech.2024.117049
  2. [2] 
    ^abPane R (1496) Relación acerca de las antigüedades de los indios
  3. [3] 
    ^abMiller MJ, Albarracin-Jordan J, Moore C, Capriles JM (2019) Chemical evidence for the use of multiple psychotropic plants in a 1,000-year-old ritual bundle from South America — Proceedings of the National Academy of Sciences doi:10.1073/pnas.1902174116
  4. [4] 
    ^abcdICEERS (2023) Yopo: Basic Info
  5. [5] 
    ^abcTittarelli R, Mannocchi G, Pantano F, Romolo FS (2015) Recreational use, analysis and toxicity of tryptamines. — Current neuropharmacology doi:10.2174/1570159x13666141210222409
  6. [6] 
    ^abcde la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J (2022) Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice — ACS Chemical Neuroscience doi:10.1021/acschemneuro.2c00170

references

  1. [1] 
    ^abcdZhang M, Yang Y, Yang Z, et al. (2025) Structural insights into tryptamine psychedelics: The role of hydroxyl indole ring site in 5-HT2A receptor activation and psychedelic-like activity — European Journal of Medicinal Chemistry doi:10.1016/j.ejmech.2024.117049
  2. [2] 
    ^abPane R (1496) Relación acerca de las antigüedades de los indios
  3. [3] 
    ^abMiller MJ, Albarracin-Jordan J, Moore C, Capriles JM (2019) Chemical evidence for the use of multiple psychotropic plants in a 1,000-year-old ritual bundle from South America — Proceedings of the National Academy of Sciences doi:10.1073/pnas.1902174116
  4. [4] 
    ^abcdICEERS (2023) Yopo: Basic Info
  5. [5] 
    ^abcTittarelli R, Mannocchi G, Pantano F, Romolo FS (2015) Recreational use, analysis and toxicity of tryptamines. — Current neuropharmacology doi:10.2174/1570159x13666141210222409
  6. [6] 
    ^abcde la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J (2022) Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice — ACS Chemical Neuroscience doi:10.1021/acschemneuro.2c00170
Last updated Jun 4, 2026