Treatment-Resistant Depression (TRD)Depressive DisordersAnxiety DisordersSubstance Use Disorders (SUD)Palliative & End-of-Life DistressHealthy VolunteersSafety & Risk ManagementMedicinal Chemistry & Drug DevelopmentPsilocybin

Pharmacokinetics of Escalating Doses of Oral Psilocybin in Healthy Adults

This open-label study (n=12) gave healthy participants increasing doses of psilocybin (21-42mg/70kg). The study found the half-life to be about 3 hours, this was not predicted by body weight, and no adverse effects were observed.

Authors

  • Christopher Nicholas
  • Nicholas Cozzi
  • Paul Hutson

Published

Clinical Pharmacokinetics
individual Study

Abstract

Introduction

Psilocybin is a psychedelic tryptamine that has shown promise in recent clinical trials for the treatment of depression and substance use disorders. This open-label study of the pharmacokinetics of psilocybin was performed to describe the pharmacokinetics and safety profile of psilocybin in sequential, escalating oral doses of 0.3, 0.45, and 0.6 mg/kg in 12 healthy adults.

Methods

Eligible healthy adults received 6-8 h of preparatory counseling in anticipation of the first dose of psilocybin. The escalating oral psilocybin doses were administered at approximately monthly intervals in a controlled setting and subjects were monitored for 24 h. Blood and urine samples were collected over 24 h and assayed by a validated liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay for psilocybin and psilocin, the active metabolite. The pharmacokinetics of psilocin were determined using both compartmental (NONMEM) and noncompartmental (WinNonlin) methods.

Results

No psilocybin was found in plasma or urine, and renal clearance of intact psilocin accounted for less than 2% of the total clearance. The pharmacokinetics of psilocin were linear within the twofold range of doses, and the elimination half-life of psilocin was 3 h (standard deviation 1.1). An extended elimination phase in some subjects suggests hydrolysis of the psilocin glucuronide metabolite. Variation in psilocin clearance was not predicted by body weight, and no serious adverse events occurred in the subjects studied.

Conclusions

The small amount of psilocin renally excreted suggests that no dose reduction is needed for subjects with mild-moderate renal impairment. Simulation of fixed doses using the pharmacokinetic parameters suggest that an oral dose of 25 mg should approximate the drug exposure of a 0.3 mg/kg oral dose of psilocybin. Although doses of 0.6 mg/kg are in excess of likely therapeutic doses, no serious physical or psychological events occurred during or within 30 days of any dose.

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Research Summary of 'Pharmacokinetics of Escalating Doses of Oral Psilocybin in Healthy Adults'

Introduction

Psilocybin is a naturally occurring psychedelic tryptamine that is rapidly dephosphorylated in vivo to the active compound psilocin, which mediates psychoactive effects primarily via serotonin 5‑HT2A receptor agonism. Renewed clinical interest in psilocybin arises from trials showing potential therapeutic effects in anxiety and depression, including single-dose and multi-dose studies in terminal illness and treatment‑resistant depression. Previous human pharmacokinetic (PK) studies of oral psilocybin were small, sampled for relatively short durations, and used assays with higher limits of quantitation, leaving questions about the full 24‑hour PK profile, renal excretion, metabolite handling, and the influence of covariates such as renal function and body weight. Brown and colleagues designed this open‑label, sequentially escalating dose pharmacokinetic study in healthy adults to characterise psilocybin/psilocin PK under contemporary cGCP/cGLP conditions. The primary aim was to build a population PK model for psilocin after oral psilocybin administered at 0.3, 0.45, and 0.6 mg/kg. Secondary aims included assessment of covariates potentially predictive of PK behaviour (for example renal function and weight), determination of renal excretion of psilocin, safety characterisation, and simulation of fixed oral doses to evaluate whether a fixed dosing strategy (e.g. 25 mg) could approximate weight‑based exposures used in prior studies.

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Study Details

References (9)

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