This study (2002) details the pharmacology of psilocybin.
Psilocybin (4-phosphoryloxy-N,N-dimethyltryptamine) is the major psychoactive alkaloid of some species of mushrooms distributed worldwide.These mushrooms represent a growing problem regarding hallucinogenic drug abuse. Despite its experimental medical use in the 1960s, only very few pharmacological data about psilocybin were known until recently. Because of its still growing capacity for abuse and the widely dispersed data this review presents all the available pharmacological data about psilocybin.
Psilocybin-containing mushrooms are described as one of the major hallucinogenic drugs of abuse worldwide, with a growing user population and a range of reported psychiatric complications. Although synthetic psilocybin (Indocybin®) was manufactured and used experimentally in the 1960s, the authors note that until recently pharmacological data were limited and widely dispersed across older and newer studies. Passie and colleagues set out to collate and review the available pharmacological information on psilocybin, emphasising human pharmacokinetic and pharmacodynamic findings from recent psychophysiological studies alongside earlier experimental and clinical reports. The review explicitly excludes a detailed characterisation of the complex psychopathological phenomena induced by the drug and focuses on pharmacology and safety-related data.
The paper is a narrative review that brings together historical and contemporary pharmacological data on psilocybin rather than a systematic review with a described search strategy. The authors draw on a mixture of experimental animal studies, early non-blind human investigations, and more recent double-blind, placebo-controlled human trials and neuroimaging studies. Specific analytic techniques cited in the extracted text include HPLC metabolite assays and PET imaging with radioligands. Detailed inclusion or exclusion criteria, database searches, search dates, and formal risk-of-bias assessment are not reported in the extracted text. Consequently, the synthesis appears to be qualitative and descriptive, integrating pharmacokinetic, pharmacodynamic, somatic toxicity, and receptor-binding information from diverse study designs and species.
Papers cited by this study that are also in Blossom
Delgado, P. L., Moreno, F. A. · Journal of Psychoactive Drugs (1998)
Papers in Blossom that reference this study
Cheng, M., Aboulafia-Brakha, T., Buchard, A. et al. · Psychology International (2025)
Knock, E., Siefried, K. J., Gill Bedi, |. et al. · Addiction (2025)
Chemical identity and history: Psilocybin (4‑phosphoryloxy‑N,N‑dimethyltryptamine) is a substituted indolealkylamine in the tryptamine class. It was isolated from Psilocybe mexicana by Albert Hofmann in 1957 and synthesised in 1958. The compound is found in many mushroom species globally. Psychic effects: At medium oral doses (reported range 12–20 mg), psilocybin produces a controllable altered state characterised by affective stimulation, heightened introspection, perceptual changes (illusions, synaesthesia), altered thought and time sense, and features akin to hypnagogic experiences and dreaming. Onset and duration reported in human studies vary: effects typically last 3–6 hours after oral dosing, with full effects arising within about 70–90 minutes. The review reports threshold and dose ranges: a subjectively detectable sympathomimetic effect may occur at 3–5 mg orally, and full psychotropic effects commonly with 8–25 mg, though interindividual variability is emphasised. Somatic and physiological effects: Animal data include a reported mouse intravenous LD50 of 280 mg/kg. Across multiple species, doses around 10 mg/kg subcutaneously produced autonomic signs such as mydriasis, piloerection, heart and respiratory irregularities, and modest hyperglycaemia and hypertension; motor behaviour was described as muted. Early human EEG studies (small samples) showed reductions in alpha and theta frequencies and changes in visual evoked potentials. Human physiological studies cited (including double-blind trials) document only discrete changes in blood pressure and pulse, and some transient reductions in leukocyte counts between the second and fourth hour after administration. Endocrine measures (cortisol, prolactin, growth hormone) were reported as not significantly affected in a small double-blind study. Mutagenicity testing in mice (micronucleus test) showed no evidence of chromosomal damage, though the authors note that a single test cannot definitively exclude mutagenic potential. Pharmacokinetics: Oral absorption is substantial for labelled psilocybin, with detectable plasma levels within 20–40 minutes on an empty stomach in human studies. The review reports that psilocin (the dephosphorylated derivative) appears in plasma after about 30 minutes and that psychological effects arise with some reported plasma threshold (the extracted text gives an unclear plasma concentration value). A significant first‑pass hepatic effect is described, with most psilocybin converted to psilocin prior to reaching systemic circulation; rodent and human data presented support psilocybin behaving as a prodrug for psilocin. After a rapid rise in psilocin plasma levels, a plateau of roughly 50 minutes was reported followed by a slower decline ending by about 360 minutes in oral studies. The mean elimination half-life of psilocin is reported as approximately 50 minutes, but the review notes considerable interindividual variability and a shorter apparent half-life and subjective effect duration with intravenous administration in one trial (numerical values are reported in the extracted text). Renal excretion includes glucuronidated metabolites and a small proportion (reported as 3–10%) of unchanged psilocybin; about two-thirds of renal excretion of psilocin occurs by three hours in the studies cited. Tolerance and dependence: Early comparative studies cited report that 100 µg (the extracted text indicates 100 m g but appears to refer to microgram/unclear units) of psilocybin was considered equivalent to 1 µg LSD and 1000 µg mescaline in one set of experiments; significant tolerance with repeated use is documented, as is cross‑tolerance with LSD. The authors state that physical dependence does not appear to develop. Pharmacodynamics and neurobiology: Neuroimaging (PET) studies are summarised: one study found no increase in global brain metabolism, while another (Vollenweider et al.) reported regional metabolic increases in frontal cortex (about 24%), anterior cingulate (25%), temporal‑medial cortex (25%) and basal ganglia (19%), with smaller increases in sensorimotor and occipital cortices and a relative decrease in thalamic metabolism; an enhanced frontal–occipital metabolic gradient and pronounced right frontotemporal activation were highlighted. Receptor binding data indicate high affinity at 5‑HT2A receptors (Ki reported as 6 nM) and lower affinity at 5‑HT1A receptors (Ki reported as 190 nM). Unlike LSD, psilocybin and psilocin reportedly show no affinity for dopamine D2 receptors. Pharmacological blockade studies cited include ketanserin (a preferential 5‑HT2A antagonist) which fully blocked psychotomimetic effects in a double‑blind study (n = 15 with ketanserin pre‑treatment), supporting a primary role for 5‑HT2A activation. Pretreatment with the D2 antagonist haloperidol also reduced psychotomimetic effects in other work, suggesting a possible secondary involvement of dopaminergic neurotransmission. Mechanistic hypotheses discussed include inhibition of dorsal raphe serotonergic neurons leading to activation of locus coeruleus noradrenergic neurons (possibly explaining some perceptual alterations) and disrupted cortex–thalamus feedback loops that could ‘‘open’’ thalamic sensory gating and contribute to frontal hyperactivity. Safety and limitations of the evidence: Overall, the review characterises psilocybin as exhibiting low physiological toxicity and being relatively well tolerated in the studies surveyed. However, the authors emphasise that many primary studies are old, frequently small and non‑blinded, and that contemporary safety pharmacology studies are generally lacking. They caution that the main hazards arise from psychotomimetic effects, particularly in vulnerable individuals and in uncontrolled settings.
Passie and colleagues interpret the assembled literature as indicating that psilocybin is principally a prodrug for psilocin, which mediates the compound's psychoactive effects primarily via 5‑HT2A receptor activation. The authors place weight on more recent double‑blind and neuroimaging studies that link subjective effects to regional cortical metabolic changes, notably frontal hyperactivity and altered thalamocortical dynamics. The review situates these findings alongside receptor pharmacology and animal experiments that point to functional interactions among serotonergic, dopaminergic and noradrenergic systems; such interactions may help explain the phenomenology of perceptual changes and the ability of both 5‑HT2A antagonists and dopamine antagonists to attenuate psychotomimetic effects. Clinical safety is viewed cautiously: the physiological toxicity reported is low, but the evidentiary base is limited by old study designs, small sample sizes, variable analytical methods for detecting parent drug, and a paucity of rigorous contemporary safety pharmacology studies. Key limitations acknowledged in the text include the predominance of early non‑blinded studies, variability in plasma concentrations and pharmacokinetics across individuals, and insufficient analytical sensitivity historically to demonstrate the absence of parent psilocybin in plasma. The authors recommend that complications are most likely to arise from psychotomimetic effects in susceptible individuals and that better‑designed safety and pharmacological investigations are required to firm up conclusions about clinical risk and mechanism. They also note the relevance of emerging therapeutic research (for example in compulsive disorders) as a reason to clarify psilocybin's pharmacology and safety profile.
Psilocybin-containing mushrooms are one of the major hallucinogenic drugs of abuse today. These mushroom species are distributed worldwideand their abuse potential produces partially harmful effects in a growing population of psychedelic drug users.No physical damage but many psychiatric complications have been reported worldwide.Recent research has been reported on the treatment of compulsive disorders in humans with psilocybin; 4 therefore, it is important to know the essential pharmacological data about psilocybin. Despite the fact that pure synthetic psilocybin (Indocybin ® Sandoz) was used and marketed for experimental and psychotherapeutic purposes in the 1960s, until recently only limited pharmacological data were available. In recent years some experimental psychophysiological studies were performed in which human pharmacokinetic and pharmacodynamic data of psilocybin were explored further.Because of the widely dispersed material about the pharmacological properties of psilocybin, old and new data are reviewed here. It should be noted that characterization of the complex psychopathological phenomena inudced is not in the focus of this review.
Psilocybin (4-phosphoryloxy-N,N-dimethyltryptamine) is a substituted indolealkylamine and belongs to the group of hallucinogenic tryptamines. Psilocybin was isolated from Central American mushrooms (Psilocybe mexicana) by the renowned Swiss chemist Albert Hofmann in 1957, and in 1958 was produced synthetically for the first time.It has been found in many species of mushrooms worldwide 1 (Fig.).
In a medium dosage (12-20 mg p.o.), psilocybin was found to produce a well-controllable altered state of consciousness. This state is marked by stimulation of affect, enhanced ability for introspection and altered psychological functioning in the direction of Freudian primary processes, known otherwise as hypnagogic experience and dreams.Especially noteworthy are perceptual changes such as illusions, synaestesias, affective activation, and alterations of thought and time sense. The effects last from 3 to 6 hours. After extensive tests in animals and humans, psilocybin was distributed worldwide under the name Indocybin ® (Sandoz) as a short-acting and more compatible substance (than, for example, LSD) to support psychotherapeutic procedures.Experimental and therapeutic use was extensive and without complications.
Cerlettireported an LD 50 for mice with intravenous application of 280 mg/kg which may imply an LD 50 of some grams of psilocybin in humans. In some in vitro experiments, except for an inhibitory effect on the neurotransmitter serotonin, psilocybin showed no specific effects on isolated organs (intestines, heart) of guinea pigs and rats.Characteristic autonomic effects of the neurovegetative system that were notable for the whole animal (mice, rats, rabbits, cats and dogs) with doses of 10 mg/kg s.c. included: mydriasis, piloerection, irregularities in heart and breathing rate and discrete hyperglycaemic and hypertonic effects.Cerletti interpreted these effects as an excitatory syndrome caused by central stimulation of the sympathetic system. In contrast to an autonomic excitatory syndrome, motor behaviour was muted.Experiments with Rhesus monkeys (2-4 mg/kg i. p.) confirmed the above changes of physiological parameters and a central excitatory syndrome. After 20-40 minutes the EEG showed a disappearance of alpha activity and an increase of beta activity in the neocortex.In two early non-blind studies in healthy volunteers (n = 12, 0.12-0.15 mg/kg p.o.),(n = 22, 10 mg p.o.)the EEG showed variations of visual evoked potentials and decrease in alpha and theta frequencies. There were no changes in the electroretinogram.The somatic effects in humans were investigated first by Quetinin a non-blind study in healthy volunteers (n = 29, 8-12 mg p.o., i.m.). The physiological changes which were noted regularly are listed in Table. These effects were confirmed qualitatively by another early nonblind study (n = 16, 0.11 mg/kg p.o.).Discrete changes of RR and pulse were also confirmed in a recent double-blind placebo-controlled study (n = 8, 0.2 mg/kg p.o.), as shown in Table.The effects described were barely noticeable and should be interpreted as secondary pharmacological effects, induced mainly by the sympathomimetic excitation syndrome.Hollister et al.found no significant aberrations of the aforementioned parameters in one subject after adminstration of psilocybin for 21 consecutive days with increasing dosages (1.5 mg increased to 25 mg p.o. in three doses per day). Electrolyte levels, liver toxicity tests and blood sugar levels remained unaffected.Human leucocytes were found by Quetin(n = 29, 8-12 mg p.o., i.m.) and Hollister et al.(n = 16, 0.06-0.2 mg/ kg p.o., s.c.) to be reduced in number temporarily between the second and fourth hour after psilocybin. In a recent double-blind placebo-controlled study (n = 8, 0.2 mg/kg p.o.) endocrine activity (cortisol, prolactin, growth hormone) was found not to be affected significantly by psilocybin.Experiments in mice (4, 8 and 16 mg/kg) with the micronucleus test, highly sensitive to the chromosome-breaking potential of substances, found no evidence for genetic aberrations through psilocybin.In mutagenicity testing it is not possible at present to prove the mutagenic potential of a compound in a single test system. Results of other tests are required to confirm these negative results.
Pharmacokinetic studies showed that 50% of 14 C-labelled psilocybin was absorbed following oral administration. The isotope is distributed almost uniformly throughout the whole body.As part of a recent double-blind placebo-controlled psychopathological study (n = 13, 0.2 mg/kg p.o.), Holzmann 5 assayed psilocybin metabolites in human plasma and urine by HPLC as part of an investigation of the pharmacokinetics of psilocybin and psilocin. In another recent double-blind placebo-controlled study (n = 6, 0.5-3 mg i.v.; n = 6 0.22mg/kg p.o.) Hasler et al.used HPLC with column-switching coupled with the electrochemical detection procedure for reliable quantitative determination of psilocybin metabolites. Altogether, four metabolites of psilocybin have been identified (Fig.): According to the two above-mentioned pharmacokinetic studies in humans it was found that after oral administration (on an empty stomach), psilocybin is detectable in significant amounts in the plasma within 20-40 minutes. Psychological effects occur with plasma levels of 4-6 m g/ml.The threshold dose depends on interindividual differences, but may be in the range of 3-5 mg p.o. for a subjectively detectable sympathomimetic, but not hallucinogenic, effect as found in double-blind placebo-controlled trials.The full effects occur with doses of 8-25 mg p.o. within 70-90 minutes. Psilocin appears in the plasma after 30 minutes. A significant first-pass effect with the vast majority of psilocybin converted into psilocin mainly by hepatic metabolism can be assumed.Another early biochemical study showed psilocin to be the main, if not the solely pharmacologically active substance by decreasing the dephosphorylation of psilocybin to psilocin using a competetive substrate (beta-glycerophosphate) for blocking the alkaline phosphatase.Recent experimentation on rodent tissue presented more evidence for complete conversion of psilocybin to psilocin before entering systemic circulation.This assumption is also supported by the finding that equimolar amounts of psilocybin and psilocin evoke qualitatively and quantitatively similar psychotropic effects in humans.Psilocybin could therefore be referred to as a prodrug. However, because of the lack of reliable analytical methods for the determination of psilocybin in human plasma, it was not possible to prove this assumption by showing the absence of the parent drug in plasma after psilocybin administration. After a rapid increase of psilocin plasma levels a plateau of about 50 minutes follows, after which there is a relatively slow decline of the curve, ending at about 360 minutes. This is confirmed by the subjective impressions of the subjects and Leuner's diagram of the clinical course (Fig.).An interesting fact may be the much shorter half-life (mean 74.1 ± 19.6 minutes i.v. compared to 163 ± 64 minutes p.o.) and duration of action (subjective effects lasting only 15-30 minutes) when psilocybin is given intravenously, as performed in a recent double-blind placebo controlled trial.Despite weight-specific dosage used in recent human studies, the plasma concentration-time curves indicate highly variable plasma concentrations. However, the timing of the maximum plasma concentration is after approximately 80 minutes (Fig.).The elimination of glucuronidated metabolites as well as unaltered psilocybin (3-10%) was found to occur through the kidneys. Approximately two-thirds of the renal excretion of psilocin is completed after 3 hours, but with great interindividual differences. The mean elimination half-life of psilocin is 50 minutes (Fig., Table).In two early single-blind randomized comparative studies a dose of 100 m g psilocybin was reported as equivalent to 1 m g LSD and 1000 m g mescaline.Even though significant tolerance is known to occur with repeated use of psilocybin, the development of physical dependence does not occur.Other early single-blind experiments showed cross-tolerance of psilocybin and LSD.Pharmacodynamics Two recent double-blind placebo controlled PET (positron emission tomography) studies using [F-18]-fluorodeoxyglucose showed brain metabolic activation under the influence of psilocybin. Gouzoulis et al.(n = 8, 0.20 mg/kg p.o.) found no increase of global brain metabolism, while Vollenweider et al.cortex (24%), as well as in the anterior cingulate gyrus (25%), the temporal-medial cortex (25%) and the basal ganglia (19%). The smallest increases were found in the sensorimotor (15%) and the occipital cortex (14%). Furthermore, an increase of the frontal-occipital metabolic gradient occurs.Regional activation was especially high in the right hemispheric frontotemporal cortical regions and decreased in the thalamus.Psilocybin interacts mainly with serotonergic neurotransmission (5-HT1A, 5-HT1D, 5-HT2A and 5-HT2C receptor subtypes). It binds with high affinity at 5-HT2A (Ki = 6 nM) and to a lesser extent at 5-HT1A (Ki = 190 nM) receptors.It should be noted that psilocybin and its active metabolite psilocin havein contrast to the indoleamine LSD -no affinity for dopamine D2 receptors.A recent double-blind placebocontrolled study (n = 15, 0.25 mg/kg p.o.) with ketanserin pre-treatment (20 mg/40 mg p.o.) showed that the psychotomimetic effects of psilocybin can be blocked completely using the preferential 5HT2A receptor antagonist ketanserin.It is probable, therefore, that the effects of psilocybin are mediated mainly via activation of presynaptic 5HT2A receptors. However, pretreatment with the D2 receptor antagonist haloperidol also reduces psilocybin-induced psychotomimesis, which raises the possibility that psilocybin-induced psychotomimesis is a secondary response to increased dopaminergic transmission, as demonstrated recently in a double-blind placebo-controlled PET study in humans (n = 7, 0.25 mg/kg p.o.) using the D2-receptor ligand [11C] raclopride.Functional interactions of central dopaminergic and serotoninergic systems have been well demonstrated.In experiments with rats, Aghajanianshowed psilocybin to interact mainly with serotonin receptors of the dorsal raphe nucleus. Because of its inhibiting influence on neurones of the dorsal raphe nucleus an activation of noradrenergic neurones of the nearby locus coeruleus is induced. The locus coeruleus represents a major center for the integration of sensory input. This may explain some forms of perceptual alterations such as synaesthesias. Another hypothesis generated in the course of recent human studies with psilocybin assumed that alterations of different feedback-loops between cortex and thalamus are responsible for an "opening of the thalamic filter for sensory input" as the cause of the psilocybin induced frontal hyperfrontality, as shown in PET studies.The evidence reviewed suggests psilocybin to exhibit low toxicity and may be seen as physiologically well tolerated. However, most studies are old and do not meet contemporary standards for safety studies. In particular, properly conducted safety pharmacology studies are lacking. Complications may result mainly from its psychotomimetic effects in vulnerable individuals, especially under uncontrolled conditions.
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