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Summary sheet: Bufotenin
Chemical Nomenclature
Common names Bufotenin, 5-HO-DMT
Substitutive name N,N-dimethylserotonin
Systematic name 3-[2-(Dimethylamino)ethyl]-1H-indol-5-ol
Class Membership
Psychoactive class Psychedelic
Chemical class Tryptamine
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.

Threshold 2 mg
Light 5 - 20 mg
Common 20 - 40 mg
Strong 40 - 60 mg
Heavy 60 mg +
Total 15 - 90 minutes
Onset 15 - 30 seconds
Come up 15 - 30 seconds
Peak 1 - 5 minutes
Offset 5 - 10 minutes
After effects 10 - 60 minutes

DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.


Bufotenin (5-HO-DMT, N,N-dimethylserotonin, bufotenine) is a naturally occurring substituted tryptamine alkaloid and a serotonergic psychedelic drug. Bufotenin is a structural derivative of tryptamine and serotonin. Bufotenin is found in a wide array of flora and fauna, including several species of psychoactive toads, most notably the Colorado River toad. The overall effects of bufotenin are generally described as less pleasant than those of other psychedelics such as LSD.


Generic structure of a tryptamine molecule.

Bufotenin, 5-HO-DMT or 5-hydroxy-N,N-dimethyltryptamine is a ring-substituted indole alkaloid molecule of the tryptamine class. Tryptamines share a core structure comprised of a bicylic indole heterocycle attached at R3 to a terminal amine group via an ethyl side chain. Bufotenin is substituted at R5 of its indole heterocycle with a hydroxy (OH) functional group; it also contains two methyl groups CH3- bound to the terminal amine RN of its tryptamine backbone (DMT).


Further information: Serotonergic psychedelic

In rats, subcutaneously administered bufotenin (1–100 μg/kg) distributes mainly to the lungs, heart, and blood, and to a much lesser extent, the brain (hypothalamus, brain stem, striatum, and cerebral cortex), and liver. It reaches peak concentrations at one hour and is nearly completely eliminated within 8 hours.[1] In humans, intravenous administration of bufotenin results in excretion of (70%) of injected drug in the form of 5-HIAA, an endogenous metabolite of serotonin, while roughly 4% is eliminated unmetabolized in the urine. Orally administered bufotenin undergoes extensive first-pass metabolism by the enzyme monoamine oxidase.

Bufotenin's psychedelic effects are primarily believed to come from its efficacy at the 5-HT2A receptor as a partial agonist. Specifically, this molecule shows high binding affinity for the 5-HT2A and 5-HT1A subtypes.[2] However, the role of these interactions and how they result in the psychedelic experience continues to remain elusive.

Additional mechanisms of action such as reuptake inhibition of neurotransmitters such as serotonin, noradrenaline and dopamine are also thought to be involved to an extent.[3] This can result in bufotenin becoming dangerously toxic when combined with MAOIs, RIMAs, SSRIs, stimulants or any substance which acts as a releasing agent or reuptake inhibitor of monoamine neurotransmitters.

Subjective effects

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.

Physical effects

Visual effects

Experience reports

There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:

Natural sources

Colorado River toad

Status iucn3.1 LC.svg.png

The Colorado River toad (Incilius alvarius), also known as the Sonoran Desert toad, is a psychoactive toad found in northern Mexico and the southwestern United States. Its skin and venom contain 5-MeO-DMT and bufotenin.

The toad's primary defense system are glands that produce a poison that may be potent enough to kill a grown dog.[4] These parotoid glands also produce the 5-MeO-DMT[5] and bufotenin for which the toad is known. Fresh venom can easily be collected from these glands without harm to the toad. To do this, obtain a flat glass plate or any other smooth, nonporous surface of at least 12-inches square and hold the toad in front of the plate (which is fixed in a vertical position). When the desert toad is stroked near the parotid glands in the neck region, there is a squirting out of this venom. When it is allowed to dry on a hard surface it takes on the texture of rubber cement. It contains up to 15% 5-MeO-DMT, as well as N-methyl-5-methoxytryptamine, 5-MeO-NMT and Bufotenin, which have their own entries. In this manner, the venom can be collected on the glass plate, free of dirt and liquid released when the toad is handled.

Toxicity and harm potential

The toxicity and long-term health effects of recreational bufotenin do not seem to have been studied in any scientific context and the exact toxic dose is unknown. This is because bufotenin is a research chemical with very little history of human usage. Anecdotal evidence from people within the psychonaut community who have tried bufotenin suggests that there are no negative health effects attributed to simply trying the drug by itself at low to moderate doses and using it very sparingly (but nothing can be completely guaranteed). Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.

It is strongly recommended that one use harm reduction practices when using this drug.

Tolerance and addiction potential

Bufotenin is not habit-forming and the desire to use it can actually decrease with use. It is most often self-regulating.

Tolerance to the effects of bufotenin is built almost immediately after ingestion. After that, it takes about 1 hour for the tolerance to be reduced to half and 2 hours to be back at baseline (in the absence of further consumption). Bufotenin does not have a cross-tolerance with other psychedelics, meaning that after the consumption of bufotenin psychedelics will not have a reduced effect.

Dangerous Interactions

Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).

Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.

Deaths from bufotenin are rare but, as a powerful monoamine reuptake inhibitor (MRI), injury can occur when excessive doses are taken or when taken with drugs such as MAOIs, RIMAs, stimulants and any substance which act as a releasing agent or reuptake inhibitor of neurotransmitters such as serotonin and dopamine. This has resulted in well documented deaths[7][8] that are easily avoidable and could have been otherwise prevented.

Legal status

  • Germany: Bufotenin is controlled under the NpSG[9] (New Psychoactive Substances Act) as of July 18, 2019.[10] Production and import with the aim to place it on the market, administration to another person, placing it on the market and trading is punishable. Possession is illegal but not punishable.[11][12] The legislator considers it possible that orders of Bufotenin are punishable as an incitement to place it on the market.[13]
  • Switzerland: Bufotenin is not controlled under Buchstabe A, B, C and D. It could be considered legal.[14]
  • United Kingdom: Bufotenin is a Class A drug.[15]
  • United States: Bufotenin is a Schedule I substance.[citation needed]

See also

External links


  1. Fuller, R. W., Snoddy, H. D., Perry, K. W. (July 1995). "Tissue distribution, metabolism and effects of bufotenine administered to rats". Neuropharmacology. 34 (7): 799–804. doi:10.1016/0028-3908(95)00049-C. ISSN 0028-3908. 
  2. Krebs-Thomson, K.; Ruiz, E. M.; Masten, V.; Buell, M.; Geyer, M. A. (2006). "The roles of 5-HT1A and 5-HT2 receptors in the effects of 5-MeO-DMT on locomotor activity and prepulse inhibition in rats". Psychopharmacology. 189 (3): 319–329. doi:10.1007/s00213-006-0566-1. eISSN 1432-2072. ISSN 0033-3158. OCLC 2409222. PMID 17013638. 
  3. Nagai, F.; Nonaka, R.; Satoh, K.; Kamimura, H. (2007). "The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain". European Journal of Pharmacology. 559 (2–3): 132–137. doi:10.1016/j.ejphar.2006.11.075. eISSN 1879-0712. ISSN 0014-2999. OCLC 01568459. PMID 17223101. 
  4. Steven J. Phillips (2000). Patricia Wentworth Comus, ed. A Natural History of the Sonoran Desert. University of California Press. p. 537. ISBN 0-520-21980-5. OCLC 837703609. 
  5. "The Sonoran Desert Toad: Bufo alvarius". Erowid. Retrieved August 27, 2020. 
  6. Talaie, H.; Panahandeh, R.; Fayaznouri, M. R.; Asadi, Z.; Abdollahi, M. (2009). "Dose-independent occurrence of seizure with tramadol". Journal of Medical Toxicology. 5 (2): 63–67. doi:10.1007/BF03161089. ISSN 1556-9039. 
  7. Brush, D. E.; Bird, S. B.; Boyer, E. W. (2004). "Monoamine oxidase inhibitor poisoning resulting from Internet misinformation on illicit substances". Journal of Toxicology: Clinical Toxicology. 42 (2): 191–195. doi:10.1081/clt-120030949. eISSN 1556-9519. ISSN 1556-3650. PMID 15214625. 
  8. Sklerov, J.; Levine, B.; Moore, K. A.; King, T.; Fowler, D. (2005). "A fatal intoxication following the ingestion of 5-methoxy-N,N-dimethyltryptamine in an ayahuasca preparation". Journal of Analytical Toxicology. 29 (8): 838–841. doi:10.1093/jat/29.8.838. eISSN 1945-2403. ISSN 0146-4760. OCLC 02942106. PMID 16356341. 
  9. "Anlage NpSG" (in German). Bundesamt für Justiz [Federal Office of Justice]. Retrieved December 10, 2019. 
  10. "Verordnung zur Änderung der Anlage des Neue-psychoaktive-Stoffe-Gesetzes und von Anlagen des Betäubungsmittelgesetzes" (PDF). Bundesgesetzblatt Jahrgang 2019 Teil I Nr. 27 (in German). Bundesanzeiger Verlag. July 17, 2019. pp. 1083–1094. ISSN 0341-1095. 
  11. "§ 4 NpSG" (in German). Bundesamt für Justiz [Federal Office of Justice]. Retrieved December 10, 2019. 
  12. "§ 3 NpSG" (in German). Bundesamt für Justiz [Federal Office of Justice]. Retrieved December 10, 2019. 
  13. "Gesetzentwurf der Bundesregierung: Entwurf eines Gesetzes zur Bekämpfung der Verbreitung neuer psychoaktiver Stoffe" (PDF) (in German). Deutscher Bundestag. May 30, 2016. p. 20. Drucksache 18/8579. 
  14. "Verordnung des EDI über die Verzeichnisse der Betäubungsmittel, psychotropen Stoffe, Vorläuferstoffe und Hilfschemikalien" (in German). Bundeskanzlei [Federal Chancellery of Switzerland]. Retrieved January 1, 2020. 
  15. "Schedule 2: Part I: Class A Drugs". "Misuse of Drugs Act 1971". UK Government. Retrieved August 20, 2020.