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Not to be confused with Psilocybin mushrooms.
Summary sheet: Psilocin
Chemical Nomenclature
Common names Psilocin, Psilocine, Psilocyn, Psilotsin, 4-HO-DMT, 4-OH-DMT
Substitutive name 4-Hydroxy-N,N-dimethyltryptamine
Systematic name 3-[2-(Dimethylamino)ethyl]-1H-indol-4-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 5 - 10 mg
Light 10 - 15 mg
Common 15 - 25 mg
Strong 25 - 40 mg
Heavy 40 mg +
Total 4 - 6 hours
Onset 20 - 45 minutes
Peak 2 - 3 hours
Offset 1.5 - 2 hours
After effects 4 - 24 hours

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.


4-Hydroxy-N,N-dimethyltryptamine (also known as 4-HO-DMT, 4-OH-DMT, and psilocin) is a naturally-occurring psychedelic substance of the tryptamine class. Psilocin is the primary psychoactive constituent in certain species of mushrooms, and as a closely related structural analog of the powerful visionary entheogen DMT (also known as N,N-dimethyltryptamine).

Psilocin was first isolated and named by Albert Hofmann in 1958. Its psychoactivity is thought to emerge from the close chemical similarities with the neurotransmitter serotonin, which enables it to interact with a range of serotonin receptor sites throughout the brain that are integral for sensory and cognitive processes.

Notably, while psilocin naturally co-occurs with psilocybin in significant amounts of most psilocybin-containing mushrooms, it is only ever rarely encountered in its synthetic form. Anecdotal reports describe pure psilocin as a more lucid and aggressive version of psilocybin mushrooms.

Unlike other highly prohibited substances, psilocin is not considered to be addictive or physiologically toxic.[1][2] Nevertheless, adverse psychological reactions such as severe anxiety, paranoia and psychosis are always possible, particularly among those predisposed to mental illness.[3] It is highly advised to use harm reduction practices if using this substance.

History and culture

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Psilocin and its phosphorylated inactive precursor (i.e. prodrug) psilocybin were first isolated and named in 1958 by Swiss chemist Albert Hofmann. Hofmann obtained the chemicals from laboratory-grown specimens of the entheogenic mushroom Psilocybe mexicana before proceeding to find their synthetic routes.[4]


Psilocin, or 4-HO-DMT, is an organic indole alkaloid molecule of the tryptamine class of chemicals. Tryptamines share a core structure comprised of a bicyclic indole heterocycle attached at R3 to an amino group via an ethyl side chain. 4-HO-DMT is substituted at R4 of its indole heterocycle with an hydroxyl (-OH) functional group; it also contains two methyl groups CH3- bound to the terminal amine RN of the ethyl side chain. This makes psilocin the 4-hydroxy structural analog of DMT, and dephosphorylated analog of psilocybin.

Psilocin can be obtained by dephosphorylation of natural psilocybin under strongly acidic or under alkaline conditions via hydrolysis,[citation needed] which is how it becomes metabolically active in the human body as well.[citation needed]

In terms of its physical properties, 4-HO-DMT is relatively unstable in solution due to its phenolic hydroxy (-OH) group. In the presence of oxygen it readily forms bluish and dark black degradation products.[citation needed] For this reason it is recommended to store it in optimal chemical storage conditions (i.e. cool, dry, away from light) to avoid excessive degradation.


Further information: Serotonergic psychedelic
Skeletal formula of the psilocybin molecule.
The diagram above demonstrates the neural connections associated with sobriety in comparison to being under the influence of psilocybin as demonstrated through the use of MRI scans. The width of the links is proportional to their weight and the size of the nodes is proportional to their strength. Note that the proportion of heavy links between communities is much higher (and very different) in the psilocybin group, suggesting greater integration[5]

Psilocin's psychedelic effects are believed to come from its interactions at the 5-HT2A receptor as a partial agonist. However, the role of these interactions and how they result in the psychedelic experience remains the subject of ongoing scientific investigation.

In contrast to LSD, this compound has no significant effect on dopamine receptors and only affects the noradrenergic system at very high dosages.[6]

Subjective effects

Anecdotal reports characterize the effects of psilocin as powerful and visionary, with a deep, all-encompassing headspace, immersive visuals with high-level geometry, and a rapid challenging come up that is both reportedly more lucid and anxiety-provoking than orally ingested psilocybin mushrooms; this may make the experience overly intense for those who are not experienced with psychedelics.

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. These effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances of inducing a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects

Visual effects

Cognitive effects

Multi-sensory effects

Transpersonal effects

Combination effects

  • Cannabis - Cannabis intensifies the visual, sensory and cognitive effects of psilocin greatly. This should be used with extreme caution, especially if one is not experienced with psychedelics. This interaction can also amplify the anxiety, confusion and the psychosis risk of cannabis significantly.
  • Dissociatives - Psilocin enhances the the geometry, euphoria, dissociation and hallucinatory effects of dissociatives. Dissociative-induced holes, spaces, and voids while under the influence of psilocin can result in significantly more vivid visuals than dissociatives alone present, along with more intense internal hallucinations, confusion, nausea, delusions and chances of a psychotic reaction.
  • MDMA - Psilocin strongly amplifies the visual, physical and cognitive effects of MDMA. The synergy between these substances is unpredictable, and it is best to start with lower dosages than one would take for both substances individually. The toxicity of this combination is unknown, although there is some evidence that suggests this may increase the the neurotoxic effects of MDMA.[8][9][10]
  • Alcohol - This combination is typically advised against due to alcohol’s ability to cause dehydration, nausea, and physical fatigue which can negatively affect the experience if taken in moderate to high dosages. This combination is, however, considered to be reasonably safe in low doses and when used responsibly, this can often take the edge off the experience as well as dull its psychedelic effects in a fashion somewhat similar to benzodiazepines.
  • Benzodiazepines - Depending on the dosage, benzodiazepines can slightly to completely reduce the intensity of the cognitive, physical and visual effects of a psilocin experience. They can be very efficient at largely stopping or mitigating a bad trip at the cost of amnesia and reduced intensity. Caution is advised when obtaining them for this purpose due to their very high addiction and abuse potential.

Experience reports

Anecdotal reports which describe the effects of this compound within our experience index include:

Additional experience reports can be found here:


Antidepressant effects

While further research is needed to establish the utility of psilocybin and other psychedelics in treating depression, a pilot study has observed significantly decreased depression scores in terminal cancer patients six months after treatment with psilocybin.[11] An open-label study was carried out in 2016 in the UK to investigate the feasibility, safety and efficacy of psilocybin in treating patients with unipolar treatment-resistant depression with promising results; although the study was small and involved only twelve patients, seven of those patients met formal criteria for remission one week following psilocybin treatment and five of those were still in remission from their depression at three months.[12]

The mechanism behind this is not known as of yet, but researchers have suggested that psilocin's deactivation of the medial prefrontal cortex[13] (mPFC) may be relevant to its antidepressant effects, as the mPFC is known to be elevated in depression and normalized after effective treatment.[13] mPFC hyperactivity has been associated with trait rumination.[14] Another possible factor to psilocybin's potential against depression may be that depressed patients with high levels of dysfunctional attitudes were found to have low levels of 5-HT(2A) agonism.[15][16]

Toxicity and harm potential

Psilocin is non-addictive, is not known to cause brain damage, and has an extremely low toxicity relative to dose. Similar to other psychedelic drugs, there are relatively few physical side effects associated with acute psilocin exposure. Various studies have shown that in reasonable doses in a careful context, it presents little to no negative cognitive, psychiatric or toxic physical consequences.[citation needed]

Lethal dosage

The toxicity of psilocybin and psilocin is extremely low. In rats, the median lethal dose (LD50) of psilocybin when administered orally is 280 milligrams per kilogram (mg/kg). Psilocybin comprises approximately 1% of the weight of Psilocybe cubensis mushrooms and so nearly 1.7 kilograms (3.7 lb) of dried mushrooms or 17 kilograms (37 lb) of fresh mushrooms would be required for a 60 kilogram (130 lb) person to reach the 280 mg/kg LD50 value of rats. Based on the results of animal studies, the lethal dose of psilocybin has been extrapolated to be 6 grams, 1000 times greater than the effective dose of 6 milligrams.[citation needed]

Despite its lack of physical toxicity, however, it is still strongly recommended that one use harm reduction practices if choosing to use this substance.

Tolerance and addiction potential

Psilocin 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 psilocin are built almost immediately after ingestion. After that, it takes about 3 days for the tolerance to be reduced to half and 7 days to be back at baseline (in the absence of further consumption). Psilocin presents cross-tolerance with all psychedelics, meaning that after the consumption of psilocin all psychedelics will have a reduced effect.

Legal status

Psilocin is a Schedule I drug under the Convention on Psychotropic Substances, meaning the possession and sale of it (including psilocin and psilocybin-containing mushrooms) is prohibited in most countries.[17]

  • Brazil - Possession, production and sale is illegal as it is listed on Portaria SVS/MS nº 344[18], but mushrooms fall under religious use laws.
  • British Virgin Isles: The sale of mushrooms is illegal, but possession and consumption is legal.
  • Bulgaria: The sale of mushrooms is illegal, but possession and consumption is legal.
  • Belgium: Possession and sale of mushrooms have been illegal since 1988.
  • Canada: Psilocybin and psilocin are illegal to possess, obtain or produce without a prescription or license as they are Schedule III under the Controlled Drugs and Substances Act.[19]
  • Czech Republic: The distribution (including sale) of mushrooms is illegal, but consumption is legal. The possession of over 40 hallucinogenic caps is considered a crime if they contain more than 50mg of psilocin or the corresponding amount of psilocybin. The possession of more than 40g of hallucinogenic mycelium is considered a crime. If these limits are not exceeded, the act is considered a minor offence and a fine of up to 15 thousand CZK may be imposed.
  • Cyprus The possession, sale and consumption of mushrooms is illegal.
  • Denmark: The possession, growth, sale and consumption of mushrooms is illegal.
  • Finland: The possession, growth, sale and consumption of mushrooms is illegal.
  • Germany: Psilocin is controlled under BtMG Anlage I, making it illegal to manufacture, import, possess, sell, or transfer it without a license.[20]
  • Greece: The possession, growth, sale and consumption of mushrooms is illegal.
  • Ireland: The possession, growth, sale and consumption of mushrooms is illegal.
  • Japan: The possession, growth, sale and consumption of mushrooms is illegal.
  • Latvia: Hallucinogenic mushrooms, psilocin and psilocibyn are Schedule I controlled substances.[21]
  • Mexico: The possession, growth, sale and consumption of mushrooms is illegal. Rules are relaxed regarding religious use however.
  • The Netherlands: The possession, growth, sale and consumption of mushrooms is illegal. However, due to a legal loophole, psilocybin truffles can be legally possessed, grown, sold and consumed.
  • New Zealand: Psilocybin is Class A.
  • Norway: Possession, growth, sale and consumption of mushrooms is illegal. Spores, even though not containing psilocybin, are also illegal.
  • Turkey: The possession, growth, sale and consumption of mushrooms is illegal.
  • United Kingdom: According to the 2005 Drugs Act, fresh and prepared psilocybin mushrooms are Class A.[22]
  • United States: Psilocybin and psilocin are illegal Schedule I drugs.[23]

See also

External links



  1. Lüscher, C., & Ungless, M. A. (2006). The Mechanistic Classification of Addictive Drugs, 3(11).
  2. Nichols, D. E. (2016). "Psychedelics." Pharmacological Reviews, 68(2), 264-355.
  3. Strassman, R. J. (1984). Adverse Reactions to Psychedelic Drugs: A Review of the Literature. The Journal of Nervous and Mental Disease, 172(10), 577-595. PMID: 6384428
  4. Hofmann, A., Heim, R., Brack, A., Kobel, H., Frey, A., Ott, H., Petrzilka, Th. and Troxler, F. (1959), Psilocybin und Psilocin, zwei psychotrope Wirkstoffe aus mexikanischen Rauschpilzen. HCA, 42: 1557–1572.
  5. Petri, G., Expert, P., Turkheimer, F., Nutt, D., Hellyer, P. J., & Vaccarino, F. (2014). Homological scaffolds of brain functional networks, 14–18.
  6. Psilocybin Investigator’s Brochure |
  7. Johnson, M. W., Garcia-Romeu, A., Cosimano, M. P., & Griffiths, R. R. (2014). Pilot study of the 5-HT2AR agonist psilocybin in the treatment of tobacco addiction. Journal of Psychopharmacology, 28(11), 983-992.
  8. Armstrong, B. D., Paik, E., Chhith, S., Lelievre, V., Waschek, J. A., & Howard, S. G. (2004). Potentiation of (DL)‐3, 4‐methylenedioxymethamphetamine (MDMA)‐induced toxicity by the serotonin 2A receptior partial agonist d‐lysergic acid diethylamide (LSD), and the protection of same by the serotonin 2A/2C receptor antagonist MDL 11,939. Neuroscience Research Communications, 35(2), 83-95.
  9. Potentiation of MDMA-induced dopamine release and serotonin neurotoxicity by 5-HT2 receptor agonists |
  10. Ecstasy induces apoptosis via 5-HT(2A)-receptor stimulation in cortical neurons. |
  11. Grob, C. S., Danforth, A. L., Chopra, G. S., Hagerty, M., McKay, C. R., Halberstadt, A. L., & Greer, G. R. (2011). Pilot study of psilocybin treatment for anxiety in patients with advanced-stage cancer. Archives of General Psychiatry, 68(1), 71-78.
  12. Carhart-Harris, R. L., Bolstridge, M., Rucker, J., Day, C. M., Erritzoe, D., Kaelen, M., ... & Taylor, D. (2016). Psilocybin with psychological support for treatment-resistant depression: an open-label feasibility study. The Lancet Psychiatry, 3(7), 619-627.
  13. 13.0 13.1 Carhart-Harris, R. L., Erritzoe, D., Williams, T., Stone, J. M., Reed, L. J., Colasanti, A., ... & Hobden, P. (2012). Neural correlates of the psychedelic state as determined by fMRI studies with psilocybin. Proceedings of the National Academy of Sciences, 109(6), 2138-2143.
  14. Farb, N. A. S., Anderson, A. K., Bloch, R. T., & Segal, Z. V. (2011). Mood Linked Responses in Medial Prefrontal Cortex Predict Relapse in Patients with Recurrent Unipolar Depression. Biological Psychiatry, 70(4), 366–372.
  15. Bhagwagar, Z., Hinz, R., Taylor, M., Fancy, S., Cowen, P., & Grasby, P. (2006). Increased 5-HT 2A receptor binding in euthymic, medication-free patients recovered from depression: a positron emission study with [11 C] MDL 100,907. American Journal of Psychiatry, 163(9), 1580-1587.
  16. Meyer, J. H., McMain, S., Kennedy, S. H., Korman, L., Brown, G. M., DaSilva, J. N., ... & Houle, S. (2003). Dysfunctional attitudes and 5-HT2 receptors during depression and self-harm. American Journal of Psychiatry, 160(1), 90-99.
  17. "Green list" (PDF). INCB. Retrieved 2017-10-11.
  19. Controlled Drugs and Substances Act of Canada
  20. BtMG Anlage I |
  21. Noteikumi par Latvijā kontrolējamajām narkotiskajām vielām, psihotropajām vielām un prekursoriem (I saraksts) |
  22. Legislation - Drugs Act 2005|
  23. FDA - Controlled Substances Act|