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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


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



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

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.[1] 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.[2] 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


Physical effects

Visual effects

Experience reports


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.[3] These parotoid glands also produce the 5-MeO-DMT[4] 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.


Tolerance and addiction potential


Tolerance to the effects of bufotenin are 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


  • Tramadol - Tramadol lowers the seizure threshold[5] and psychedelics may act as triggers for seizures in susceptible individuals.[citation needed]

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[6][7] that are easily avoidable and could have been otherwise prevented.

Legal issues

  • USA: Bufotenin is a Schedule I substance.[citation needed]
  • United Kingdom - Bufotenin is a Class A drug.[8]

See also

External links


  1. The roles of 5-HT1A and 5-HT2 receptors in the effects of 5-MeO-DMT on locomotor activity and prepulse inhibition in rats (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/17013638
  2. The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/17223101
  3. Phillips, Steven J. and Wentworth Comus, Patricia, ed. (2000). A Natural History of the Sonoran Desert. University of California Press. p. 537. ISBN 0-520-21980-5.
  4. http://www.erowid.org/archive/sonoran_desert_toad/erspamer.htm
  6. http://www.ncbi.nlm.nih.gov/pubmed/15214625
  7. http://www.ncbi.nlm.nih.gov/pubmed/16356341