A prodrug of psilocin, studied in supported clinical settings. Subjective effects, therapeutic outcomes and legal status are distinct questions.
Psilocybin is converted to active psilocin. Modern trials study carefully selected participants and structured support; their results cannot be transferred directly to unsupervised use or variable mushroom preparations. This entry distinguishes parent-compound identity from active-metabolite kinetics.
Included clinical findings come from selected participants receiving psychological support. Comparative benefit, durability and harms need continued assessment.
Assessment belongs to each claim and outcome. An article’s editorial status is not a grade of a substance’s safety or efficacy.Blocking this receptor attenuated acute psilocybin effects in a human experiment. That does not establish a complete mechanism for lasting therapeutic change. [3]
Descriptions of experience in their reported context. Direction does not imply benefit, and these observations do not define a universal intensity score.
Human antagonist experiments support serotonin-receptor involvement in changes to perception and experience; no intensity score is assigned. [3]
What the research measured, for whom, and under which exposure. Findings remain attached to the study’s task or clinical endpoint.
The studied higher-dose arm improved the primary short-term outcome compared with the low-dose control, with adverse events and unresolved durability. [2]
Published exposure records, distinguished by source category. These describe study or reference context and are not personal dosing recommendations.
25 mg [2]
An investigational trial arm, not instructions for personal use or an equivalent mushroom weight.
Absorption, metabolism and elimination depend on the analyte, route, formulation, physiology and other exposures.
Mean elimination of the active metabolite in a small controlled study; this is not the half-life of parent psilocybin or a prediction of experience duration. [1]
The modeled analyte is Psilocin (active metabolite). The curve begins after absorption and distribution; it does not predict onset, felt effects, or an individual’s response.
Route: Oral administration of psilocybin. Formulation: Controlled oral psilocybin preparation. Population: 12 healthy adults in an open-label escalating-exposure study.
Mean elimination of the active metabolite in a small controlled study; this is not the half-life of parent psilocybin or a prediction of experience duration. Source & context
Study mean: 3 hours.
The model uses this single study mean; no range is inferred.
Model: fraction remaining = 2−time / half-life. Assumes a single exposure, instantaneous distribution, and a constant half-life for Psilocin (active metabolite). Formation of metabolites, repeated exposure, and interactions are not modeled. Source & context
3 hoursStudy mean [1]
Mean elimination of the active metabolite in a small controlled study; this is not the half-life of parent psilocybin or a prediction of experience duration.
Adverse effects, interactions, tolerance and withdrawal in the cited contexts. This section is not an exhaustive interaction checker.
The depression trial reported headache, nausea and dizziness. Suicidal ideation, behavior or self-injury occurred across dose groups; the study cannot establish safety for unsupervised use. [2]
The source, the finding and its limitations. Funding information is reported where curated; an unassessed disclosure does not mean a study had no commercial funding.
Measured psilocin elimination after controlled oral psilocybin exposure in 12 healthy adults.
Limitations Small, selected and supported sample. Active-metabolite kinetics are not equivalent to parent-compound kinetics.
Funding / disclosures Not assessed; consult the original disclosure.
A supported clinical protocol improved the primary short-term depression outcome in the higher-dose arm.
Limitations Adverse events occurred; longer and comparative trials are needed. Funded by COMPASS Pathfinder.
Funding / disclosures COMPASS Pathfinder.
Antagonist pretreatment supported a role for serotonin receptors in acute effects.
Limitations Historical terminology and an acute laboratory experiment do not establish a model of schizophrenia or a therapeutic mechanism.
Funding / disclosures Not assessed; consult the original disclosure.
Source for molecular identity, formula, molecular weight and the structure diagram.
Limitations A compound record does not establish a product's purity, identity or clinical benefit.
Funding / disclosures Public database maintained by NCBI.
Each relationship retains its participants, roles and context. Shared membership does not imply that substances should be combined.
Controlled acute human antagonist experiment.
Limitation Acute receptor evidence does not establish a complete mechanism of sustained therapeutic change.
Evidence strength: not formally assessed.
Treatment-resistant depression; standardized preparation and psychological support; assessment at week 3.
Limitation Adverse events occurred and longer comparative trials are needed.
Evidence strength: not formally assessed.
Schedule I under the Controlled Substances Act. State and local rules require separate review. Authority source
Other jurisdictions and activities require separate assessment.
This article is a sourced draft. Editorial review has not been recorded. Content date: Sep 29, 2026.