Bufotenin

3-[2-(dimethylamino)ethyl]-1H-indol-5-ol

Overview

Bufotenin belongs to Psychedelics.

Key safety note: Bufotenin can produce powerful and potentially dangerous peripheral cardiovascular effects that may dominate the experience, especially by injection: intense facial and neck flushing or purpling, a rapid heart rate (with reports of arrhythmia), chest tightness and cyanosis.[2][1]
Effects
Subjective effects vary. What a substance feels like depends on dose, individual physiology, mindset, and setting. The points below describe commonly reported effects, not guaranteed, uniform, or desirable outcomes.
  • Physical effects tend to dominate and can be very intense: a heavy, sometimes overwhelming body load with strong tactile sensations, flushing, nausea and cardiovascular effects
  • Visionary effects (via insufflation or vaporisation) are described as swirling, brightly coloured, arabesque tryptamine patterns, often with comparatively mild open-eye visuals
  • Effects are short-lived, particularly when vaporised (often 15–90 minutes total)
Dosing & duration
Harm-reduction note: These are commonly cited reference ranges, not a recommendation or a “safe” dose. Potency, purity, body chemistry, tolerance, and drug combinations vary widely. Start low, go slow, wait for full effects before redosing, and never assume an unknown product matches these figures. Missing data is not evidence of safety.

Insufflated, Vaporised, Oral, Intravenous. Bufotenin is strongly route-dependent and poorly active orally (heavy first-pass metabolism: roughly 10× the parenteral dose is needed). Insufflated, ~40 mg is a 'visionary threshold' and ~100 mg produces effects within ~5 minutes, peaking at 35–40 minutes. Vaporised, it is active from ~2–8 mg with a very fast onset. Intravenous injection produces severe and potentially dangerous peripheral cardiovascular effects and is not advised. The tiered figures below are for the vaporised/smoked route.

Dose ranges

Threshold

~2 mg (vaporised)

Light

5–20 mg (vaporised)

Common

20–40 mg (vaporised)

Strong

40–60 mg (vaporised)

Duration

onset

15–30 s (vaporised), ~5 min (insufflated)

peak

1–5 min (vaporised), 35–40 min (insufflated)

total

15–90 min

Chemical & Physical Properties
FormulaC12H16N2O
Molar mass204.27 g/mol
StateSolid
Melting point146.5 °C
Boiling pointNot reported
DensityNot reported
Vapor pressureNot reported
pKaNot reported
LogP1.2 (predicted, XLogP3)
SolubilityNot reported
Refractive indexNot reported
Identifiers & Synonyms
CAS487-93-4
CAS (enantiomer)
PubChem CID10257
InChIKeyVTTONGPRPXSUTJ-UHFFFAOYSA-N
InChIInChI=1S/C12H16N2O/c1-14(2)6-5-9-8-13-12-4-3-10(15)7-11(9)12/h3-4,7-8,13,15H,5-6H2,1-2H3
SMILESCN(C)CCC1=CNC2=C1C=C(C=C2)O

Synonyms

  • 5-HO-DMT
  • 5-Hydroxy-N,N-dimethyltryptamine
  • N,N-Dimethylserotonin
  • Mappine
  • Cebilcin
Pharmacodynamics & Biochemistry

A naturally occurring tryptamine: 5-hydroxy-N,N-dimethyltryptamine (5-HO-DMT), the 5-hydroxy positional isomer of psilocin and a close relative of 5-MeO-DMT. It is a potent, non-selective serotonin-receptor agonist (5-HT1A, 5-HT2A, 5-HT2C, 5-HT6, 5-HT7 and others) and also acts as a selective serotonin-releasing agent (EC₅₀ ≈ 30 nM) without releasing dopamine or noradrenaline. Its 5-hydroxy group makes it a hydrophilic zwitterion that crosses the blood–brain barrier poorly, so it is far more peripherally selective than 5-MeO-DMT, although roughly 3× more potent than 5-MeO-DMT once in the brain, much less of it reaches the CNS, which is why its psychoactivity was historically disputed and is strongly route-dependent. High affinity at 5-HT3 receptors (comparable to serotonin itself) drives prominent nausea and vomiting. Robust central psychedelic effects have been confirmed via insufflation and vaporisation.

Biological targets

  • 5-HT2A
  • 5-HT1A
  • 5-HT2C

Binding & functional measurements

TargetMeasurementSpecies
5-HT1A receptorKi 2.5 nMHuman
5-HT1D receptorKi 3.7 nMHuman
5-HT6 receptorKi 4.5 nMHuman
5-HT2B receptorKi 6.2 nMHuman
5-HT7 receptorKi 7.9 nMHuman
5-HT2A receptorKi 15 nMHuman
5-HT2C receptorKi 16 nMHuman
5-HT1E receptorKi 25 nMHuman
5-HT1F receptorKi 32 nMHuman
5-HT3 receptorKi 34 nMHuman
5-HT1B receptorKi 41 nMHuman
5-HT5A receptorKi 302 nMHuman
D3 receptorKi 692 nMHuman
Serotonin transporterKi 1,120 nMHuman
5-HT5B receptorKi 1,585 nMHuman
Pharmacokinetics
BioavailabilityNot reported
TmaxNot reported
Half-lifeShort (rapidly deaminated by MAO-A, peak ≈1 h, largely cleared within ≈8 h)
VdNot reported
Protein bindingNot reported
MetabolismRapidly deaminated by monoamine oxidase A to 5-HIAA (~70% of an intravenous dose) with glucuronide and sulfate conjugation. It undergoes a strong first-pass effect and is poorly active orally (roughly 10× the parenteral dose is needed). Circulating levels peak within about an hour and it is largely eliminated within ~8 hours
ExcretionNot reported
Toxicology & Safety
Harm-reduction note: Toxicity and risk depend on dose, route, purity, combinations, setting, and individual health factors. Missing harms should never be interpreted as evidence of safety.

Not reported

Bufotenin can produce powerful and potentially dangerous peripheral cardiovascular effects that may dominate the experience, especially by injection: intense facial and neck flushing or purpling, a rapid heart rate (with reports of arrhythmia), chest tightness and cyanosis. In one clinical study a 40 mg intramuscular dose produced an extremely rapid heart rate with no obtainable pulse and extreme cyanosis. Strong 5-HT3 activity causes marked nausea and vomiting. Eating bufotenin-containing toads has caused fatal poisonings, and this is not the same as the smoked secretion of the Colorado River toad, whose main psychedelic is 5-MeO-DMT. As with all serotonergic drugs, combining it with MAOIs or other serotonergic agents raises the risk of serotonin toxicity, and MAOIs also greatly potentiate and prolong its effects. Limited and historically conflicting human data must never be read as evidence of safety.[2][1]

Legal Status
Legal note: Legal status can change over time and may vary by country, region, formulation, analogue status, prescription context, and enforcement practice. Always confirm with current official sources before relying on this section.
Interactions & Contraindications

Drug interactions

MAOIs Greatly potentiate and prolong effects and, with other serotonergics, raise the risk of serotonin toxicity (the basis of yopo snuff combined with beta-carboline plants).
SSRIs, SNRIs, Lithium, Tramadol, Other serotonergic drugs Add to serotonergic load.
Stimulants (amphetamines, cocaine), Drugs that raise blood pressure or heart rate Compound bufotenin's already strong pressor and cardiac effects, a particular concern given its peripheral toxicity.
Cannabis Can heighten anxiety and disorientation.

Contraindications

Cardiovascular disease, hypertension or arrhythmia bufotenin has powerful, potentially dangerous cardiovascular effects.
Personal or family history of psychosis, schizophrenia or bipolar disorder
Concurrent MAOI, SSRI/SNRI or other serotonergic medication MAOIs or other strongly serotonergic drugs.
Settings where impairment or dissociation risks injury (driving, water, heights) unsupervised use, given the intensity and peripheral risk.
Usage & Context
  • Research.
  • Traditional.
Sources & Evidence

Further Information