Psilocin
3-[2-(dimethylamino)ethyl]-1H-indol-4-ol
Overview
Psilocin belongs to Psychedelics / Tryptamines.
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.
- A classic serotonergic psychedelic experience: brightened colours, increased visual contrast, open- and closed-eye visuals (geometric patterns, movement, pareidolia) and heightened appreciation of music and scenery.
- Emotional and cognitive shifts: euphoria, peacefulness, emotional amplification, time dilation, ego dissolution and mystical-type experiences, though mood can swing and difficult, anxious or dysphoric states also occur.
- Faster and shorter than LSD or mescaline: onset ≈15–40 minutes and total duration ≈3–6 hours.
- Common physical effects include nausea, dilated pupils, mild tachycardia, shifts in body temperature, sweating or chills and headache. Notably, there is usually no hangover.
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.
Oral. Not a recommendation. Psilocin is only slightly more potent than psilocybin (≈1.4 mg psilocybin ≈ 1.0 mg psilocin, reflecting its ~40% lower molecular weight), but it is rarely taken as the free base. It is almost always used as its prodrugs (psilocybin, 4-AcO-DMT) or as psilocybin mushrooms, whose potency varies widely. Free-base psilocin is also unstable, oxidising to bluish degradation products.
Dose ranges
Common (oral, free base)
≈10–20 mg (Shulgin, TiHKAL)
Duration
onset
≈15–40 min
peak
≈1–2 h
total
≈3–6 h
Chemical & Physical Properties
| Formula | C12H16N2O |
| Molar mass | 204.27 g/mol |
| State | Solid |
| Melting point | 173–176 °C |
| Boiling point | Not reported |
| Density | Not reported |
| Vapor pressure | Not reported |
| pKa | Not reported |
| LogP | 2.1 (predicted, XLogP3) |
| Solubility | Not reported |
| Refractive index | Not reported |
Identifiers & Synonyms
| CAS | 520-53-6 |
| CAS (enantiomer) | |
| PubChem CID | 4980 |
| InChIKey | SPCIYGNTAMCTRO-UHFFFAOYSA-N |
| InChI | InChI=1S/C12H16N2O/c1-14(2)7-6-9-8-13-10-4-3-5-11(15)12(9)10/h3-5,8,13,15H,6-7H2,1-2H3 |
| SMILES | CN(C)CCC1=CNC2=C1C(=CC=C2)O |
Synonyms
- 4-HO-DMT
- 4-hydroxy-DMT
- 4-hydroxy-N,N-dimethyltryptamine
- Psilocyn
- Psilocine
Pharmacodynamics & Biochemistry
Psilocin (4-hydroxy-N,N-dimethyltryptamine, 4-HO-DMT) is the pharmacologically active form of psilocybin: psilocybin is rapidly dephosphorylated to psilocin in the body. A close structural analogue of serotonin, it is a non-selective serotonin-receptor agonist whose psychedelic effects are produced specifically through partial agonism at the 5-HT2A receptor (they are blocked by 5-HT2A antagonists such as ketanserin), with cortical 5-HT2A occupancy correlating with the subjective intensity of the experience. It also activates 5-HT2C (with pronounced biased agonism) and 5-HT1A, and binds broadly across the 5-HT1 and 5-HT2 families as well as 5-HT5A/6/7, with notably high affinity at 5-HT7. It shows functional selectivity, preferentially coupling to phospholipase A2 rather than the phospholipase C pathway used by serotonin itself. Psilocin has essentially no meaningful activity at dopamine receptors and affects noradrenergic signalling only at very high doses, and it is weak-to-inactive at the serotonin, noradrenaline and dopamine transporters: consistent with a classic psychedelic rather than a stimulant. (An early report that psilocin is a potent positive allosteric modulator of the BDNF receptor TrkB was not reproduced by later work.)
Biological targets
- 5-HT2A
- 5-HT2C
- 5-HT2B
- 5-HT1A
- 5-HT7
Binding & functional measurements
| Target | Measurement | Species |
|---|---|---|
| 5-HT7 receptor | Ki 75 nM | Human |
| 5-HT2B receptor | Ki 8.0 nM | Human |
| 5-HT2A receptor | Ki 49 ± 10 nM | Human |
| 5-HT2C receptor | Ki 94 ± 9.0 nM | Human |
| 5-HT1D receptor | Ki 130 nM | Human |
| D1 | Ki 20 nM | Human |
| 5-HT1B receptor | Ki 580 nM | Human |
| 5-HT1E receptor | Ki 155 nM | Human |
| 5-HT1A receptor | Ki 123 ± 20 nM | Human |
| 5-HT6 receptor | Ki 38 nM | Human |
| 5-HT5A receptor | Ki 116 nM | Human |
| D3 receptor | Ki 8,900 ± 800 nM | Human |
| I2 | Ki 792 nM | Human |
| α2-adrenoceptor | Ki 2,100 ± 10 nM | Human |
| TAAR1 | Ki 1,400 ± 200 nM | Rat |
| H1 receptor | Ki 1,600 ± 200 nM | Human |
| Serotonin transporter | Ki 6,000 ± 300 nM | Human |
| D2 receptor | Ki 3,700 ± 600 nM | Human |
| DAT | Ki 6,000 nM | Human |
| 5-HT1A receptor | Ki 118 nM | Mouse |
| 5-HT2A receptor | EC50 2.4 nM Emax 98.4 ± 1.3% | Human |
| 5-HT2A receptor | EC50 13 nM Emax 67% | Mouse |
| 5-HT2A receptor | Ki 235 nM | Mouse |
| 5-HT2B receptor | EC50 8.0 nM Emax 38% | Human |
| 5-HT2C receptor | EC50 34 nM Emax 84% | Human |
| α1A-adrenoceptor | Ki 6,700 ± 1,100 nM | Human |
Pharmacokinetics
| Bioavailability | ≈53% oral (as psilocin, from psilocybin) |
| Tmax | ≈80–105 min (onset 15–40 min) |
| Half-life | ≈2.3–3 h oral, ≈1.2 h after IV (as psilocin) |
| Vd | Not reported |
| Protein binding | Not reported |
| Metabolism | Glucuronidation (UGT) → psilocin-O-glucuronide. MAO demethylation/deamination and ALDH oxidation → 4-hydroxyindole-3-acetic acid (4-HIAA). Minor 4-hydroxytryptophol |
| Excretion | Renal: mainly as psilocin-O-glucuronide. ~2–4% excreted unchanged |
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
Psilocin has low physiological toxicity, no established lethal dose and no withdrawal syndrome, so its principal risks are psychological: anxiety, confusion or a frightening ('bad trip') experience and, rarely, prolonged perceptual disturbances (HPPD). It produces mild sympathomimetic effects (raised heart rate, blood pressure and body temperature, dilated pupils). As with other serotonergic psychedelics, people with a personal or family history of psychosis, schizophrenia or bipolar disorder, or significant cardiovascular disease, are at higher risk, and combining it with lithium has been linked to seizures. Tolerance builds quickly, with well-documented cross-tolerance to LSD and mescaline. It is the active moiety behind psilocybin-assisted therapy research. Limited data must never be read as evidence of safety.[4][5]
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.
US: Schedule I. UK: Class A. DE: BtMG Anlage I
Interactions & Contraindications
Drug interactions
Contraindications
Personal or family history of psychosis, schizophrenia or bipolar disorder[4]
Cardiovascular disease, hypertension or arrhythmia significant disease or uncontrolled hypertension.
Concurrent MAOI, SSRI/SNRI or other serotonergic medication concurrent lithium therapy (seizure risk).[4]
Pregnancy or breastfeeding
No interactions or contraindications listed.
Usage & Context
- Used spiritually and shamanically for centuries as psilocybin mushrooms, notably in Mesoamerican (Mazatec) traditions, and re-introduced to the West after 1955.
- Widely used recreationally and for self-exploration: almost always as psilocybin mushrooms or ester prodrugs (psilocybin, 4-AcO-DMT) rather than as isolated psilocin.
- The active moiety behind the current wave of psilocybin-assisted psychotherapy research (e.g. for depression). Psilocybin was approved for supervised therapeutic use in Australia in 2023.
Sources & Evidence
- PubChem: Psilocin (CID 4980) — identifiers & experimental properties
- IUPHAR/BPS Guide to PHARMACOLOGY: psilocin (ligand 11291) CC BY-SA 4.0
- McKenna DJ, Repke DB, Lo L, et al. (1990). Differential interactions of indolealkylamines with 5-hydroxytryptamine receptor subtypes. Neuropharmacology 29:193-8.
PMID 2139186 · doi:10.1016/0028-3908(90)90001-8
- Wikipedia: Psilocin — pharmacology (PDSP/BindingDB binding table), effects, dosing & pharmacokinetics CC BY-SA 4.0
- Dinis-Oliveira RJ (2017). Metabolism of psilocybin and psilocin: clinical and forensic toxicological relevance. Drug Metab Rev 49:84-91.
PMID 28074670 · doi:10.1080/03602532.2016.1278228
- DEA Diversion Control Division: Controlled Substance Schedules (psilocin — Schedule I, US)
- GOV.UK: Controlled drugs list — psilocin is Class A (UK) OGL v3.0
- Glatfelter GC, Pottie E, Partilla JS, et al. (2022). Structure-Activity Relationships for Psilocybin, Baeocystin, Aeruginascin, and Related Analogues to Produce Pharmacological Effects in Mice. ACS Pharmacol Transl Sci 5:1181-1196.
PMID 36407948 · doi:10.1021/acsptsci.2c00177
- Rickli A, Moning OD, Hoener MC, et al. (2016). Receptor interaction profiles of novel psychoactive tryptamines compared with classic hallucinogens. Eur Neuropsychopharmacol 26:1327-37.
PMID 27216487 · doi:10.1016/j.euroneuro.2016.05.001
- Klein AK, Chatha M, Laskowski LJ, et al. (2020). Investigation of the Structure-Activity Relationships of Psilocybin Analogues. ACS Pharmacol Transl Sci 4:533-542.
PMID 33860183 · doi:10.1021/acsptsci.0c00176