The practice of humans consuming mescaline-containing cacti dates back over 6,000years. Peyote cacti were studied scientifically in the 1800s, culminating in the isolation of mescaline as the active psychedelic constituent in cacti, legal recognition of religious use, and ongoing exploration of the therapeutic potential of mescaline and other analogues. Mescaline was the first psychedelic compound to be characterized by the Western world and has been referred to as the "first psychedelic".
Mescaline and the cacti that produce it are largely illegal worldwide, though exceptions exist for religious, scientific, or ornamental use, and the compound has influenced many notable cultural figures, for instance Aldous Huxley and Alexander Shulgin among others. Very few studies of mescaline in people have been conducted since the early 1970s. However, the drug is now being studied in terms of its effects and for potential medical use once again as of the early 2020s.
Mescaline is used recreationally, spiritually, and medically. It is typically taken orally. The drug is used as a psychedelic at doses of 100 to 1,000mg orally. Low doses are 100 to 200mg, an intermediate or "good effect" dose is 500mg, and a high (ego-dissolution) dose is 1,000mg. However, doses of 800mg and above orally are not well-tolerated due to side effects like severe nausea and vomiting. In his book PiHKAL (Phenethylamines I Have Known and Loved), Alexander Shulgin listed a dose range of 200 to 400mg as the sulfatesalt and 178 to 356mg as the hydrochloride salt. Microdosing involves the use of daily mescaline doses of less than 75mg. Mescaline has also been studied via intravenous injection, with assessed doses in the range of 500 to 750mg as the sulfate salt. In addition to pure form, mescaline is used in the form of cacti such as peyote and the San Pedro cactus. Doses when mescaline is used in the form of fresh or dried cacti have also been described.
In traditional peyote preparations, the top of the cactus is cut off, leaving the large tap root along with a ring of green photosynthesizing area to grow new heads. These heads are then dried to make disc-shaped buttons. Buttons are chewed to produce the effects or soaked in water to drink. However, the taste of the cactus is bitter, so modern users will often grind it into a powder and pour it into capsules to avoid having to taste it. The average 76mm (3.0in) peyote button contains about 25mg mescaline.[citation needed] However, another source states that there is about 45mg mescaline per peyote button on average. Some analyses of traditional preparations of San Pedro cactus have found doses ranging from 34mg to 159mg of total alkaloids, a relatively low and barely psychoactive amount. It appears that patients who receive traditional treatments with San Pedro ingest sub-psychoactive doses and do not experience psychedelic effects.
The onset of the effects of mescaline given orally is 0.5 to 0.9hours on average with a range of 0.1 to 2.7hours. Its effects peak after 1.9 to 4.0hours with a range of 0.5 to 8.0hours. The duration of mescaline appears to be dose-dependent, varying from 6.4hours on average (range 3.0–10hours) at a dose of 100mg, 9.7 to 11hours on average (range 5.6–22hours) at moderate doses of 300 to 500mg, and 14hours on average (range 7.2–22hours) at a dose of 800mg. Cases of mescaline having unusually prolonged or delayed effects have also been described. Given intravenously, mescaline has been reported to have an onset of several minutes or within 10minutes, a time to peak of 1 to 2hours, and a duration of approximately 4 to 9hours in different studies.
Prominence of color with mescaline is distinctive, appearing brilliant and intense. Recurring visual patterns observed during the mescaline experience include stripes, checkerboards, angular spikes, multicolor dots, and very simple fractals that can turn very complex. The English writer Aldous Huxley described these self-transforming amorphous shapes as like animated stained glass illuminated from light coming through the eyelids in his autobiographical book The Doors of Perception (1954). Like LSD, mescaline induces distortions of form and kaleidoscopic experiences but they manifest more clearly with eyes closed and under low lighting conditions. Heinrich Klüver coined the term "cobweb figure" in the 1920s to describe one of the four form constant geometric visual hallucinations experienced in the early stage of a mescaline trip: "Colored threads running together in a revolving center, the whole similar to a cobweb". The other three are the chessboard design, tunnel, and spiral. Klüver wrote that "many 'atypical' visions are upon close inspection nothing but variations of these form-constants." An unusual but unique characteristic of mescaline use is the "geometrization" of three-dimensional objects. The object can appear flattened and distorted, similar to the presentation of a Cubist painting. Detailed descriptions of the psychedelic experience induced by mescaline have been given by many authors.
The subjective effects of mescaline are qualitatively similar to those of LSD and psilocybin. Based on anecdotal evidence however, mescaline is said to be less threatening and to produce less ego dissolution than other psychedelics like LSD. This may in part be due its slow onset allowing for a more comfortable ease-in of effects. In addition, mescaline is typically dosed at lower doses than LSD or psilocybin in terms of doses with equivalent or comparable strength. According to a study in the Netherlands, ceremonial San Pedro use seems to be characterized by relatively strong spiritual experiences, and low incidence of challenging experiences. Mescaline, LSD, and psilocybin appear to produce similar color enhancement in clinical studies, though more research is needed.
Mescaline use may rarely lead to hallucinogen-induced psychotic disorder (HIPD). HIPD is a type of substance-induced psychosis. Hallucinogen-induced psychotic disorder symptoms are psychosis with paranoia, delusions, hallucinations, or disorganized thinking that persist beyond the effects of the drug. HIPD due to psychedelics is most commonly seen with LSD use, but may also be caused by mescaline. Hallucinogen-induced psychotic disorder is a medical emergency. Without treatment, the psychotic state can continue for weeks or months. HIPD is treated with an atypical antipsychotic medication such as aripiprazole, quetiapine, olanzapine, or risperidone. Individuals with a personal or family history of mental health issues are at the highest risk for hallucinogen-induced psychotic disorder. The condition occurs in fewer than 1% of people with psychedelics.
Tolerance
Mescaline is associated with rapid tolerance development, including cross-tolerance with other psychedelics like LSD and psilocybin. This tolerance is apparent within a few days and resets after 3 or 4days of abstinence.
Overdose
Only a single case of death due to mescaline, as peyote, has been described, and was likely due to asphyxiation by vomit rather than overdose or toxicity. However, there is also a case report of death due to jumping off a cliff while on a high dose of mescaline. In terms of extrapolated human lethal dose based on animal studies, the lethal dose of mescaline relative to a typical recreational dose has been estimated to be 24-fold or around 8,400mg. However, mescaline has reportedly been taken by humans at doses of up to 8,000mg without apparent toxic reactions. On the other hand, there is one unverified reported case of death due to a dose of 15,000mg intravenously, which would equate to about 150 to 200mg/kg. The median lethal dose (LD50) of mescaline has been determined in various animal species, with the values including 212 to 315mg/kg i.p. in mice, 132 to 410mg/kg i.p. in rats, 328mg/kg i.p. in guinea pigs, 54mg/kg in dogs, and 130mg/kg i.v. in rhesus macaques, among others. It has been said that it would be difficult to take enough mescaline to cause death in humans. No deaths due to peyote use have been reported aside from the asphyxiation case. The highest dose of peyote known to have been taken is 90dried buttons.
It is unclear whether mescaline is metabolized by monoamine oxidase (MAO) enzymes or whether monoamine oxidase inhibitors (MAOIs) might increase the effects of mescaline. No clinical studies of mescaline in combination with MAOIs are known to have been published. However, there are preliminary reports that harmala alkaloids, which are reversible inhibitors of monoamine oxidase A (RIMAs), may potentiate the effects of mescaline in humans, and the combination of mescaline or mescaline-containing cacti with harmala alkaloids has been referred to as "peyohuasca". In accordance with these findings, the harmala alkaloid and RIMA harmine has been reported to augment the effects of mescaline in animals. On the other hand, Daniel Trachsel has stated that mescaline is not metabolized by MAO, instead being metabolized by semicarbazide-sensitive amine oxidase (SSAO), and hence that MAOIs that do not also inhibit SSAO should have no effect on the metabolism of mescaline. Accordingly, the MAOI iproniazid did not potentiate the behavioral effects of mescaline in rats.
Notes: The smaller the value, the more avidly the drug binds to the site. All proteins are human unless otherwise specified. Refs:
Mescaline acts as an agonist of the serotonin5-HT2A receptor to produce its psychedelic effects. Its EC50Tooltip half-maximal effective concentration at the serotonin 5-HT2A receptor is approximately 10,000nM and at the serotonin 5-HT2B receptor is greater than 20,000nM. How activating the 5-HT2A receptor leads to psychedelic effects is still unknown, but it is likely that somehow it involves excitation of neurons in the prefrontal cortex. In addition to the serotonin 5-HT2A and 5-HT2B receptors, mescaline is also known to bind to the serotonin 5-HT2C receptor and a number of other targets. The drug shows pronounced biased agonism at the serotonin 5-HT2C receptor.
Mescaline is a relatively low-potency psychedelic, with active doses in the hundreds of milligrams and micromolar affinities for the serotonin 5-HT2A receptor. For comparison, psilocybin is approximately 25-fold more potent (doses in the tens of milligrams) and lysergic acid diethylamide (LSD) is approximately 5,000-fold more potent (doses in the tens to hundreds of micrograms). There have been efforts to develop more potent analogues of mescaline. Difluoromescaline and trifluoromescaline are more potent than mescaline, as is its amphetamine homologue TMA. Escaline and proscaline are also both more potent than mescaline, showing the importance of the 4-position substituent with regard to receptor binding.
Mescaline has been uniquely found to robustly produce aggression in rodents, an effect not shared by various other psychedelics. It is unclear why mescaline produces more nausea and vomiting than other psychedelics like LSD and psilocybin in humans. In any case, the serotonin 5-HT2A receptor antagonist ketanserin blocked not only the psychoactive but also the physical side effects of mescaline including nausea and vomiting, suggesting that these effects may be mediated by serotonin 5-HT2A receptor activation. Mescaline has been found to increase oxytocin levels in humans and to a greater extent than LSD or psilocybin at equivalent doses.
There is no evidence of acute tolerance with mescaline. However, tolerance to mescaline builds with repeated use, lasting for a few days. The drug causes cross-tolerance with other psychedelics like LSD and psilocybin.
The cryo-EMstructures of the serotonin 5-HT2A receptor with mescaline, as well as with various other psychedelics and serotonin 5-HT2A receptor agonists, have been solved and published by Bryan L. Roth and colleagues.
Mescaline is usually taken orally, although it may also be insufflated, smoked, or given intravenously. Taken orally, it is rapidly absorbed from the gastrointestinal tract. The oral bioavailability of mescaline is unknown. However, since at least 53% of orally administered mescaline is excreted in urine unchanged, the bioavailability appears to be at least 53%. Peak concentrations of mescaline occur after approximately 1.6 to 2.3hours on average (range 1.0–6.0hours). However, there is a delay of 1 to 2hours following peak levels in terms of the drug producing maximal psychoactive and behavioral effects. The pharmacokinetics of mescaline are dose-proportional over an oral dose range of 100 to 800mg.
Distribution
Mescaline is distributed to the liver, spleen, and kidneys at many times higher levels than blood or brain based on animal studies. It is said that a great proportion of mescaline is combined with hepatic proteins, which is said to delay its onset and elimination half-life. The exact portion bound to plasma proteins seems to be unknown, but appears to be minimal.
Mescaline appears to have relatively poor blood–brain barrierpermeability due to its low lipophilicity. However, it is still able to cross into the central nervous system and produce psychoactive effects at sufficiently high doses. The poor central permeability of mescaline appears to be responsible for its delayed onset of effects and is also thought to contribute to its low potency.
Mescaline given orally appears to be subject to first-pass metabolism of about 50%. Following the first pass, mescaline appears to be subject to relatively limited metabolism.
Mescaline appears not to be subject to metabolism by CYP2D6 based on in-vitro studies with human liver microsomes. Similarly, the in-vitrocytotoxicity of mescaline does not appear to be affected by cytochrome P450 (CYP450) enzyme inhibitors. Conversely, it was potentiated by the MAO-A inhibitor clorgiline but not by the MAO-B inhibitor rasagiline. These findings were in contrast to those with the related compound 2C-B, which was potentiated by rasagiline but not by clorgiline.
Circulating peak and area-under-the-curve concentrations of mescaline and TMPAA are similar with oral administration of mescaline. Conversely, levels of N-acetylmescaline (NAM) are far lower than those of mescaline or TMPAA and are thought not to be of clinical relevance. Intravenous injection of mescaline may result in less hepatic deamination than with oral administration.
It has been theorized that active metabolites of mescaline might contribute to its psychoactive effects. Relatedly, TMPA and TMPE were reported in early research to show pharmacological effects in rats and rabbits with greater potency than mescaline. In addition, co-administration of mescaline with the aldehyde dehydrogenase inhibitor (ALDHI) calcium carbimide, which elevates TMPA and/or TMPE levels, has been reported to produce extreme reactions in rabbits at doses at which mescaline alone was inactive. Similarly, co-administration of TMPE with calcium carbimide markedly potentiated the effects of TMPE. However, subsequent research found that TMPA, TMPE, and NAM all failed to produce mescaline-like effects in rodent drug discrimination tests, and this was the case even when they were co-administered with calcium carbimide. Likewise, another subsequent study found that TMPE and TMPAA were both inactive in producing behavioral effects in rodents, while TMPA was much less potent than mescaline. A further study found TMPAA to be inactive in animals as well. As with animal findings, both TMPAA and NAM have been said to be inactive based on human tests. It has also been noted that metabolites like TMPA and TMPE are rapidly metabolized. As such, metabolites of mescaline like TMPA, TMPE, TMPAA, and NAM do not appear to be involved in the drug's psychedelic-related effects.
3,4,5-Trimethoxyamphetamine (TMA), the α-methylanalogue of mescaline and an MAO-resistant psychedelic, is only about twice as potent as mescaline as a psychedelic in humans despite having similar serotonin receptoraffinity. This suggests that the deamination of mescaline has a relatively limited impact on its potency, compared to for example the 2C series of psychedelics. Another analogue of mescaline, the deuteratedisotopologueAlpha-D (α,α-dideuteromescaline), has been reported to be roughly one-third more potent than mescaline as a psychedelic in humans, albeit based on limited testing. This is consistent with findings of about one-third of a dose of mescaline being metabolized via deamination.
Elimination
Mescaline given orally is excreted 87% in urine within 24hours and 92% in urine within 48hours. During the first hour after administration, 81.4% of mescaline is excreted unchanged while 13.2% is excreted as its deaminated metabolite 3,4,5-trimethoxyphenylacetic acid (TMPAA). However, after the first hour, the percentage excreted as unchanged mescaline declines and the percentage excreted as TMPAA rises. Ultimately, mescaline is excreted in urine 28 to 60% unchanged, 27 to 30% or more as TMPAA, 5% as N-acetyl-3,4-dimethoxy-5-hydroxyphenylethylamine, and less than 0.1% as N-acetylmescaline. Other minor or trace excreted metabolites have also been observed. In a more modern study published in 2025, mescaline was eliminated in urine 53% as unchanged mescaline and 31% as TMPAA.
Mescaline was originally reported to have an elimination half-life of 6hours based on a study conducted in the 1960s. However, subsequent research published in the 2020s found that its half-life is actually about 3.6hours (range 2.6–5.3hours). The previous higher estimate is believed to have been due to small sample numbers and collective measurement of mescaline metabolites. The elimination half-life of mescaline does not appear to be dose-dependent. TMPAA has a half-life of about 3.7 to 4.1hours, similar to that of mescaline. Mescaline has a similar half-life as LSD yet has a longer duration. This is due to mescaline having slower absorption and onset rather than a longer half-life.
The physical properties and general chemistry of mescaline have been reviewed. The compound is relatively hydrophilic with low fat solubility. Its predicted log P (XLogP3) is 0.7.
Synthesis
Mescaline was the first ever psychedelic drug synthesized by chemists. Ernst Späth's 1919 total synthesis started from 3,4,5-trimethoxybenzoyl chloride. Several approaches using different starting materials have been developed since, including the following:
Reduction of 3,4,5-trimethoxy(2-nitrovinyl)benzene with lithium aluminum hydride.
Treatment of tricarbonyl-(η6-1,2,3-trimethoxybenzene) chromium complex with acetonitrile carbanion in THF and iodine, followed by reduction of the nitrile with lithium aluminum hydride.
Trichocereus pachanoi (San Pedro cactus) in Peru.Dried peyote (Lophophora williamsii), containing ~5 to 6% mescaline by weight.
Mescaline has been isolated from numerous cactus species, including Echinopsis (Trichocereus), Gymnocalycium, Lophophora, Opuntia, Stenocereus, and Turbinicarpus species, among others. It occurs at the highest known concentrations in Lophophora williamsii (peyote), where it is highly variable but makes up 0.1 to 0.255% fresh weight and 0.9 to 6.3% of dry weight. Levels of mescaline are much lower in other Lophophora species. The compound also occurs in relatively high concentrations in various Echinopsis species, for instance Echinopsis pachanoi (San Pedro cactus), ranging from 0.02 to 0.12% fresh weight and 0.331 to 2.0% dry weight in this species. Mescaline occurs in only small or trace amounts in most other cactus species in which it has been detected.
As shown in the accompanying table, the concentration of mescaline in different specimens can vary largely within a single species. Moreover, the concentration of mescaline within a single specimen varies as well.
In peyote, mescaline constitutes about 30% of total alkaloid content. For comparison, the alkaloid contents of other major constituents include pellotine 17%, anhalonidine 14%, anhalamine 8%, hordenine 8%, and lophophorine 5%.
It has also reported to be found in small amounts in certain members of the bean family, Fabaceae, including Senegalia berlandieri (syn. Acacia berlandieri), although these reports have been challenged and have been unsupported in any additional analyses.
In plants, mescaline may be the end-product of a pathway utilizing catecholamines as a method of stress response, similar to how animals may release such compounds and others such as cortisol when stressed. The in vivo function of catecholamines in plants has not been investigated, but they may function as antioxidants, as developmental signals, and as integral cell wall components that resist degradation from pathogens. The deactivation of catecholamines via methylation produces alkaloids such as mescaline.
Tyrosine and phenylalanine serve as metabolic precursors towards the synthesis of mescaline. Tyrosine can either undergo a decarboxylation via tyrosine decarboxylase to generate tyramine and subsequently undergo an oxidation at carbon 3 by a monophenolhydroxylase or first be hydroxylated by tyrosine hydroxylase to form L-DOPA and decarboxylated by DOPA decarboxylase. These create dopamine, which then experiences methylation by a catechol-O-methyltransferase (COMT) by an S-adenosyl methionine (SAM)-dependent mechanism. The resulting intermediate is then oxidized again by a hydroxylase enzyme, likely monophenol hydroxylase again, at carbon 5, and methylated by COMT. The product, methylated at the two meta positions with respect to the alkyl substituent, experiences a final methylation at the 4 carbon by a guaiacol-O-methyltransferase, which also operates by a SAM-dependent mechanism. This final methylation step results in the production of mescaline.
Phenylalanine serves as a precursor by first being converted to L-tyrosine by L-amino acid hydroxylase. Once converted, it follows the same pathway as described above.
Arthur Heffter, the chemist who isolated mescaline and discovered its effects.
Peyote was first described by Bernardino de Sahagún in 1560. It was first scientifically named as Peyotl zacatensis by Francisco Hernández in 1638. Botanical studies of peyote began in the 1840s and the drug was listed in the Mexican pharmacopeia. The first use of mescal buttons was published by John Raleigh Briggs in 1887. However, he took a very low dose of the drug, and in the modern literature, the symptoms he experienced have been attributed to a severe panic attack in response to the drug. In 1887, the German pharmacologist Louis Lewin received his first sample of the peyote cactus, found numerous new alkaloids and later published the first methodical analysis of it. The effects of mescaline in humans were first properly described by D. W. Prentiss and Francis P. Morgan in 1895. Mescaline was first isolated and identified in 1897 by the German chemist Arthur Heffter. He showed that mescaline was exclusively responsible for the psychoactive or hallucinogenic effects of peyote. However, other components of peyote, such as hordenine, pellotine, and anhalinine, are also active. Mescaline was first synthesized in 1919 by Ernst Späth.
Studies of the potential therapeutic effects of mescaline started in the 1950s. It was studied as part of psychedelic-assisted psychotherapy by Walter Frederking by 1953. Aldous Huxley's book The Doors of Perception, about his experience with mescaline, was published in 1954. In 1955, English politician Christopher Mayhew took part in an experiment for BBC's Panorama, in which he ingested 400mg of mescaline under the supervision of psychiatrist Humphry Osmond. Though the recording was deemed too controversial and ultimately omitted from the show, Mayhew praised the experience, calling it "the most interesting thing I ever did" and saying that it was "profoundly thought-provoking".
The mechanism of action of mescaline, activation of the serotonin5-HT2A receptors, became fully known in the 1990s. A serotonin 5-HT2A receptor antagonist, specifically ketanserin, was first clearly shown to block the psychedelic effects of mescaline in humans by Matthias Liechti and colleagues in 2024.
Arthur Heffter isolated mescaline from peyote and discovered its psychedelic effects via self-experimentation. He published these findings in 1898. Heffter was the first person to experience psychedelic effects with a pure psychedelic compound.
Silas Weir Mitchell was one of the first to experiment with mescaline, as peyote, and published his experience in 1896.
Havelock Ellis was the author of one of the first written reports to the public about an experience with mescaline (1898).
William James was one of the first to experiment with mescaline, as peyote. However, he took a low dose (1 peyote button), became violently ill for 2days, and experienced no other effects. He opted not to retry the drug. James tried peyote in 1896 but his experience was not published until decades later.
Jean-Paul Sartre took mescaline shortly before the publication of his book, L'Imaginaire (1940); he had a bad trip during which he imagined that he was menaced by sea creatures. For many years following this, he persistently imagined that he was being followed by lobster- or crab-like creatures, and became a patient of Jacques Lacan in hopes of being rid of them. Lobsters and crabs figure in his novel Nausea (1938).
Salvador Dalí has been persistently rumored to have taken psychedelics such as mescaline. However, in response to these rumors, Dalí famously exclaimed "I don't do drugs. I am drugs!" in 1982.
Antonin Artaud wrote 1947's The Peyote Dance, where he describes his peyote experiences in Mexico a decade earlier.
Allen Ginsberg took peyote. Part II of his poem "Howl" was inspired by a peyote vision that he had in San Francisco.
Stanisław Ignacy Witkiewicz, Polish writer, artist and philosopher, experimented with mescaline and described his experience in a 1932 book Nikotyna Alkohol Kokaina Peyotl Morfina Eter.
Quanah Parker, appointed by the federal government as principal chief of the entire Comanche Nation, advocated the syncretic Native American Church alternative, and fought for the legal use of peyote in the movement's religious practices.
Alexander Shulgin, the prolific psychedelic chemist, said that he was first inspired to explore psychedelic compounds by a mescaline experience in 1960. In 1974, Shulgin synthesized 2C-B, a psychedelic phenylethylamine derivative, structurally similar to mescaline, and one of Shulgin's self-rated most important phenethylamine compounds together with mescaline, 2C-E, 2C-T-7, and 2C-T-2.
Bryan Wynter produced Mars Ascends after trying the substance for the first time.
George Carlin mentioned mescaline use during his youth while being interviewed in 2008.
Arthur Kleps, a psychologist turned drug legalization advocate and writer whose Neo-American Church defended use of marijuana and hallucinogens such as LSD and peyote for spiritual enlightenment and exploration, bought, in 1960, by mail from Delta Chemical Company in New York 1 g of mescaline sulfate and took 500mg. He experienced a psychedelic trip that caused profound changes in his life and outlook.[citation needed]
Michael Pollan has described his experiences with mescaline and San Pedro cactus.
Media representations
Movies
Fantasia (1940), with lead visualist Oskar Fischinger, may have been inspired by mescaline-induced visuals.
In the United States, mescaline was made illegal in 1970 by the Comprehensive Drug Abuse Prevention and Control Act, categorized as a Schedule I hallucinogen. The drug is prohibited internationally by the 1971 Convention on Psychotropic Substances. Mescaline is legal only for certain religious groups (such as the Native American Church by the American Indian Religious Freedom Act of 1978) and in scientific and medical research. In 1990, the Supreme Court ruled that the state of Oregon could ban the use of mescaline in Native American religious ceremonies. The Religious Freedom Restoration Act (RFRA) in 1993 allowed the use of peyote in religious ceremony, but in 1997, the Supreme Court ruled that the RFRA is unconstitutional when applied against states. Many states, including the state of Utah, have legalized peyote usage with "sincere religious intent", or within a religious organization,[citation needed] regardless of race. Synthetic mescaline, but not mescaline derived from cacti, was officially decriminalized in the state of Colorado by ballot measure Proposition 122 in November 2022.
In the United Kingdom, mescaline in purified powder form is a Class A drug. However, dried cactus can be bought and sold legally.
Australia
Mescaline is considered a schedule 9 substance in Australia under the Poisons Standard (February 2020). A schedule 9 substance is classified as "Substances with a high potential for causing harm at low exposure and which require special precautions during manufacture, handling or use. These poisons should be available only to specialised or authorised users who have the skills necessary to handle them safely. Special regulations restricting their availability, possession, storage or use may apply."
Other countries
In Canada, France, the Netherlands, and Germany, mescaline in raw form and dried mescaline-containing cacti are considered illegal drugs. However, anyone may grow and use peyote (Lophophora williamsii) as well as Echinopsis pachanoi and Echinopsis peruviana (San Pedro cactus) without restriction, as they are specifically exempt from legislation. In Canada, mescaline is classified as a schedule III drug under the Controlled Drugs and Substances Act, whereas peyote is exempt. In Russia, mescaline, its derivatives, and mescaline-containing plants are banned as narcotic drugs (Schedule I).
Mescaline has a wide array of suggested medical usage, including treatment of depression, anxiety, PTSD, nicotine dependence, and alcoholism. However, its status as a Schedule Icontrolled substance in the Convention on Psychotropic Substances limits availability of the drug to researchers. Because of this, very few studies concerning mescaline's activity and potential therapeutic effects in people have been conducted since the early 1970s. However, the drug is under development by Journey Colab under the code name JOUR-5700 and by Biomind Labs under the code names BMND04, BMND06, and BMND09 for various medical applications, such as treatment of alcoholism.
12345678910111213141516Mueller L, Klaiber A, Ley L, Becker AM, Thomann J, Luethi D, etal. (July 2025). "Pharmacokinetics, Pharmacodynamics, and Urinary Recovery of Oral Mescaline Hydrochloride in Healthy Participants". Clinical Pharmacokinetics. 64 (10): 1495–1506. doi:10.1007/s40262-025-01544-x. PMC12479620. PMID40658345. The low affinity of mescaline for 5-HT2A receptors [3] and poor blood–brain barrier permeability [20] contribute to the comparatively high oral doses of 300–800 mg of mescaline hydrochloride (HCl) that are typically required to induce a full psychedelic experience in humans compared with psilocybin dihydrate (20–40 mg) and LSD base (100–200 µg) [5, 21]. [...] We found that acute subjective efects of mescaline were closely linked to the plasma mescaline concentrations but occurred with a delay as seen in the counterclockwise hysteresis. Accordingly, our modeling approach that used an efect compartment that was connected to the plasma mescaline concentration using a frst-order equilibrium rate constant (ke0) adequately described the observed acute efects. This finding is consistent with a delayed central distribution of mescaline.
123Dart RC (2004). Medical Toxicology (3ed.). Lippincott Williams & Wilkins. p.1706. ISBN978-0-7817-2845-4. Archived from the original on 29 March 2022. Mescaline binds to liver proteins but not to plasma proteins. It is rapidly and widely distributed into the peripheral tissues. The volume of distribution is not specifically known but is believed to be on the order of several L/kg.
12Oh YH, Leitch WE, Axelrod S, Small SM, Winzler RJ, Sanders BE (May 1967). "Binding of biologically active amines to plasma protein fractions". Biochemical Pharmacology. 16 (5): 849–861. doi:10.1016/0006-2952(67)90058-5. PMID6036735. Studies have been initiated to provide information on biochemical relationships between biogenic amines and plasma proteins. The binding in vitro of several biogenic amines, i.e. 3,4-dimethoxyphenylethylamine, mescaline, tyramine, and normetanephrine, labeled with 14C or 3H to human plasma protein fractions have been studied. [...] No appreciable binding to any of the plasma protein fractions was observed with mescaline or normetanephrine. [...]
12345678910111213141516171819Kapadia GJ, Fayez MB (December 1970). "Peyote constituents: chemistry, biogenesis, and biological effects". Journal of Pharmaceutical Sciences. 59 (12): 1699–1727. Bibcode:1970JPhmS..59.1699K. doi:10.1002/jps.2600591202. PMID5499699. Some authors (398) postulated that mescaline oxidase is identical with diamine oxidase, while others (399-401) believe that the oxidative deamination of mescaline can be effected by monoamine oxidase or diamine oxidase or both. However, mescaline was found to be a poor substrate for highly purified human plasma monoamine oxidase (402) and for dopamine-β-oxidase (403). According to Seiler (404), who treated mescaline with mouse brain homogenates, the oxidation is not caused by diamine oxidase but by a monoamine oxidase leading to 3,4,5-trimethoxyphenylacetic acid (LXXIII). [...] rabbit liver preparations caused O-demethylation to VII and LX along with oxidation to LXXIII (407). The formation of this acid (LXXIII) was inhibited by iproniazid, semicarbazide, nicotinamide, and triphosphopyridine nucleotide. [...] Harmine was found to augment the effect of mescaline (260). [...] (260) H. Hoshikawa, Nippon Yakurigaku Zasshi, 58, 241, 261 (1962); through Chem. Abstr., 60, 7338(1964).
123Denber HC (1958). "The Mescaline Psychosis: II. Clinical Considerations of the Mescaline-Induced State". In Rinkel M (ed.). Chemical Concepts of Psychosis: Proceedings of the Symposium on Chemical Concepts of Psychosis held at the Second International Congress of Psychiatry in Zurich, Switzerland, September 1 to 7, 1957. New York: McDowell, Obolensky. pp.120–126. doi:10.1037/11190-009.
123456789101112Ley L, Holze F, Arikci D, Becker AM, Straumann I, Klaiber A, etal. (October 2023). "Comparative acute effects of mescaline, lysergic acid diethylamide, and psilocybin in a randomized, double-blind, placebo-controlled cross-over study in healthy participants". Neuropsychopharmacology. 48 (11): 1659–1667. doi:10.1038/s41386-023-01607-2. PMC10517157. PMID37231080. In the present study, both 500 mg mescaline and LSD, but not psilocybin, enhanced circulating oxytocin. Therefore, the present study was the first to document elevated plasma oxytocin levels in response to mescaline as it was previously shown for LSD [24, 27, 28] and psilocybin [24]. In fact, 500 mg mescaline was the strongest releaser of oxytocin among the psychedelics that were tested herein. [...] As for its limitations; we failed to achieve instant dose equivalence, leading to a subsequent increase in the mescaline dose from 300 to 500 mg. The study thus tested two doses of mescaline against LSD and psilocybin. [...] Figure S4. Effects on plasma levels of oxytocin and brain-derived neurotrophic factor (BDNF). Mescaline and LSD significantly increased plasma oxytocin levels compared with placebo. Oxytocin levels were significantly higher after mescaline (n = 32) compared with psilocybin.
12Denber HC, Merlis S (July 1955). "Studies on mescaline. I. Action in schizophrenic patients; clinical observations and brain wave patterns, showing effects before and after electric convulsive treatments". Psychiatr Q. 29 (3): 421–429. doi:10.1007/BF01567467. PMID13266921.
12Mokrasch LC, Stevenson I (August 1959). "The metabolism of mescaline with a note on correlations between metabolism and psychological effects". J Nerv Ment Dis. 129 (2): 177–183. doi:10.1097/00005053-195908000-00007. PMID14423321.
123456789Charalampous KD, Walker KE, Kinross-Wright J (1966). "Metabolic fate of mescaline in man". Psychopharmacologia. 9 (1): 48–63. doi:10.1007/BF00427703. PMID5989103.
1234567891011Anderson EF (1996). Peyote: The Divine Cactus (2ed.). University of Arizona Press. ISBN978-0-8165-1654-4. Archived from the original on 22 September 2022. Ruth Underhill (1952, 148) reported that humans have taken 8 grams of mescaline powder—more than ten times the usual dose—without apparent toxic reactions.
123Tabaac BJ, Shinozuka K, Fadel M, Jones G, Worchel J, Muir OS (June 2026). "Psychedelic Therapy: A Primer for Primary Care Clinicians-Mescaline". American Journal of Therapeutics. 33 (4): e318–e323. doi:10.1097/MJT.0000000000002160. PMID42299720.
12Wang Y, Wang H, Lin C, Wang X (June 2026). "Chemical ecology and convergent evolution of natural hallucinogens: From ecological defense to conserved neural targets". Proceedings of the National Academy of Sciences of the United States of America. 123 (26) e2535785123. doi:10.1073/pnas.2535785123. PMC13321363. PMID42341036.
123456Klaiber A, Humbert-Droz M, Ley L, Schmid Y, Liechti ME (November 2024). "Safety pharmacology of acute mescaline administration in healthy participants". British Journal of Clinical Pharmacology bcp.16349. doi:10.1111/bcp.16349. PMID39587436.
↑Engel LB, Low M (2025). "The Trouble with Psychedelic Cacti: Conflicting Meanings of San Pedro and Peyote". Contemporary Drug Problems. 52 (1): 104–117. doi:10.1177/00914509251318751.
↑Engel LB, Thal S, Bright SJ, Low M (2024). "Psychedelic Trip Sitting, Dosages and Intensities: Supplementing Clinical Studies with Anecdotal Reports". Journal of Psychedelic Studies. 8 (3): 313–323. doi:10.1556/2054.2024.00377.
123456Neff N, Rossi GV (September 1963). "Mescaline". American Journal of Pharmacy and the Sciences Supporting Public Health. 135 (9): 319–327. PMID14061276.
12Beringer K (1927) [1927]. Der Meskalinrausch, seine Geschichte und Erscheinungsweise[Mescaline Intoxication, its History and Manifestation]. Monographien aus dem Gesamtgebiete der Neurologie und Psychiatrie (in German). Vol.49. Julius Springer. doi:10.1007/978-3-662-11451-3. ISBN978-3-540-04660-8. OCLC2536666.{{cite book}}: ISBN / Date incompatibility (help)
↑Aday JS, Wood JR, Bloesch EK, Davoli CC (July 2021). "Psychedelic drugs and perception: a narrative review of the first era of research". Reviews in the Neurosciences. 32 (5): 559–571. doi:10.1515/revneuro-2020-0094. PMID33550787. Alan M. Hartman and Leo E. Hollister conducted what seemed to be the most focused studies on psychedelics' effects on color perception from this era, as they systematically compared the effects of LSD, psilocybin, and mescaline on a variety of color perception measures. [...] the authors concluded that the similarities of LSD, psilocybin, and mescaline's effects on color perception are more prominent than any differences. [...]
↑Kometer M, Vollenweider FX (2018). "Serotonergic Hallucinogen-Induced Visual Perceptual Alterations". Current Topics in Behavioral Neurosciences. Behavioral Neurobiology of Psychedelic Drugs. Vol.36. pp.257–282. doi:10.1007/7854_2016_461. ISBN978-3-662-55878-2. PMID27900674. Interestingly, classical hallucinogens, including psilocybin, mescaline and LSD, frequently induced form constants of the lattice and tunnel types. Furthermore, hallucinogen-induced visual experiences were dominated by red, orange, or yellow colors, while blue colors were most commonly observed after the administration of delta-9-THC. [...] Thus, visual experiences showed marked consistency across various classical hallucinogens, not only in terms of specific form constants, but also in terms of the color and movement categories.
↑Hollister LE, Hartman AM (August 1962). "Mescaline, lysergic acid diethylamide and psilocybin comparison of clinical syndromes, effects on color perception and biochemical measures". Comprehensive Psychiatry. 3 (4): 235–242. doi:10.1016/s0010-440x(62)80024-8. PMID13908449.
↑Hartman AM, Hollister LE (August 1963). "Effect of Mescaline, Lysergic Acid Diethylamide and Psilocybin on Color Perception". Psychopharmacologia. 4 (6): 441–451. doi:10.1007/BF00403349. PMID14048565.
↑Sulstarova A, Scheuerlein L, Monari S, Seragnoli F, Gabriel T, Preller K, etal. (August 2025). "Treatment approaches and efficacy in psychedelic-induced psychosis: A systematic review". Asian Journal of Psychiatry. 110 104604. doi:10.1016/j.ajp.2025.104604. PMID40614615.
↑Duraković D, Silić A, Peitl V, Vlahović D, Vojnović D, Karlović D (23 October 2022). "Acute Mescaline Intoxication Followed by Catatonia". Archives of Psychiatry Research: An International Journal of Psychiatry and Related Sciences. 58 (2): 287–292. doi:10.20471/dec.2022.58.02.12. ISSN2671-1079.
↑Fiorentini A, Volonteri LS, Dragogna F, Rovera C, Maffini M, Mauri MC, etal. (December 2011). "Substance-induced psychoses: a critical review of the literature". Current Drug Abuse Reviews. 4 (4): 228–240. doi:10.2174/1874473711104040228. PMID21999698.
↑Bowers MB, Swigar ME (June 1983). "Vulnerability to psychosis associated with hallucinogen use". Psychiatry Research. 9 (2): 91–97. doi:10.1016/0165-1781(83)90030-6. PMID6578530.
12Thomas K (2024). "Toxicology and Pharmacological Interactions of Classic Psychedelics". Psychedelic Harm Reduction. Current Topics in Behavioral Neurosciences. Vol.77. Berlin, Heidelberg: Springer Berlin Heidelberg. pp.43–62. doi:10.1007/7854_2024_508. ISBN978-3-032-21106-4. PMID39042251.
↑Reynolds PC, Jindrich EJ (1985). "A mescaline associated fatality". Journal of Analytical Toxicology. 9 (4): 183–184. doi:10.1093/jat/9.4.183. PMID4033076.
↑Underhill RM (1952). "Peyote". Proceedings of the Thirtieth International Congress of Americanists, Held in Cambridge, 18-23 August 1952. London: Royal Anthropological Institute. pp.143–148. Archived from the original on 30 June 2026. [Our workers] intend to work with mescaline and not with peyote, which contains very little of it—1/10 gramme to a hundred buttons. The Indians at a meeting usually take eight buttons or 1/200 gramme. Even the greatest peyote user never boasts of more than thirty, or 1/33 gramme, while white experimenters with mescaline have taken eight whole grammes.
↑Underhill R (1 May 1957). "Religion Among American Indians". The Annals of the American Academy of Political and Social Science. 311 (1): 127–136. doi:10.1177/000271625731100114. To produce any bad effects such as shortened respiration, at least 350 mgs. of mescaline are needed; white experimenters have taken as many as 700 without harm. The standard buttons (eight) taken at meetings contain only some 107 mgs.
↑Buckingham J (2014). "Mescaline". Dictionary of Natural Products: 254–260.
↑Slothower JD, Wiegand TJ (2014). "Mescaline". In Wexler P (ed.). Encyclopedia of Toxicology (3rded.). Academic Press. pp.221–222. doi:10.1016/B978-0-12-386454-3.00747-8. ISBN978-0-12-386455-0. There have been no reported deaths due to the physiological effects of peyote/mescaline. Traumatic deaths have occurred secondary to hallucinations.
↑Schultes RE (1938). "The Appeal of Peyote (Lophophora Williamsii) as a Medicine". American Anthropologist. 40 (4): 698–715. doi:10.1525/aa.1938.40.4.02a00100. In the ceremony, peyote is eaten dry, but occasionally fresh plants are consumed.16 The dried mescal buttons keep indefinitely and are stored in bags for use. They possess a very bitter taste, but in spite of this, they are chewed and swallowed in great number by peyotists. The smallest consumption by a single person is about four buttons at each meeting. It is impossible to estimate the largest, but I have seen an Indian eat more than thirty at one ceremony. Other investigators17 report doses as large as ninety buttons. An estimate of the average consumption, however, would probably be about twelve buttons by each person at a single meeting.
↑Mooney J (15 January 1896). "The Mescal Plant and Ceremony". Therapeutic Gazette. 12 (1): 7–11. Archived from the original on 10 June 2026. The Indians say that no mental effect is produced by less than ten, which is probably true of the seasoned initiates. From twelve to twenty is a common number for one person in the course of the night, and many have eaten thirty or more on occasions. The man with the highest record among the Kiowas is said to have once eaten more than ninety at a single sitting, or nearly a pound and a half. I do not vouch for this, but believe it possible, as he is a recognized leader in the ceremony and powerfully built. The Indians themselves, however, admit that such a quantity is excessive and extraordinary. I have myself seen this man chew up ten, one after another, like so many lozenges, without pausing. I have never heard of any serious results from over-indulgence, and it may be that vomiting relieves the stomach in such cases.
↑Denber HC, Merlis S (November 1955). "Studies on mescaline. VI. Therapeutic aspects of the mescaline-chlorpromazine combination". The Journal of Nervous and Mental Disease. 122 (5): 463–469. doi:10.1097/00005053-195511000-00008. PMID13320144. The effects of the injection of chlorpromazine have already been reported elsewhere (3). Tension and anxiety began to subside within minutes following the injection. In most pаtients the whole mescaline-induced state disappeared in one hour. One patient required a second injection of 50 mg. of chlorpromazine to terminate the state. The intense push and flow of thought abated slowly, and many patients became lethargic, drowsy and sleepy.
↑Denber HC, Merlis S (1956). "Studies on mescaline IV: Antagonism between mescaline and chlorpromazine". In Kline NS (ed.). Psychopharmacology. Publication No. 42. Washington: American Association for the Advancement of Science. pp.141–144. Archived from the original on 28 May 2023. One hour after the injection of chlorpromazine hydrochloride all the signs and symptoms of the mescaline-induced state had disappeared. [...] Chlorpromazine hydrochloride directly antagonizes the effects of mescaline sulfate in non-epileptic patients as evidenced by changes in alpha activity, pulse, blood pressure, and pupillary diameters, as well as by the reversal of the abnormal psychic state due to mescaline.
↑Merlis S, Denber HC (June 1956). "Studies on mescaline. V. Electroencephalgraphic evidence for the antagonism between mescaline and chlorpromazine hydrochloride". The Journal of Nervous and Mental Disease. 123 (6): 542–545. doi:10.1097/00005053-195606000-00005. PMID13406579.
1234567Rached G, Campana A, Fiani D, Nguyen C, Van den Eynde V, Gillman PK, etal. (January 2026). "Safety and Efficacy of Monoamine Oxidase Inhibitors in Patients Who Use Psychoactive Substances: Potential Drug Interactions and Substance Use Disorder Treatment Data". CNS Drugs. 40 (3): 359–417. doi:10.1007/s40263-025-01256-7. PMID41546846.
12Ott J. "Pharmahuasca: On Phenethylamines and Potentiation"(PDF). MAPS Newsletter. 6 (3): 32–35. [...] there is circumstantial evidence for traditional use of ayahuasca containing mescaline and/or other β-phenethylamines in Amazonian Peru. [...] preliminary human bioassays suggest that the β-carboline harmaline might in fact potentiate mescaline - low doses of 60 and 100 mg mescaline hydrochloride, corresponding to 51 and 86 mg base or 0.78 and 1.32 mg/kg respectively, were decidedly psychoactive. The combination of mescaline or mescaline-containing cacti with β-carbolines has been dubbed peyohuasca.(5,18)
↑Monte AP, Waldman SR, Marona-Lewicka D, Wainscott DB, Nelson DL, Sanders-Bush E, etal. (September 1997). "Dihydrobenzofuran analogues of hallucinogens. 4. Mescaline derivatives". Journal of Medicinal Chemistry. 40 (19): 2997–3008. doi:10.1021/jm970219x. PMID9301661.
↑Appel JB, Callahan PM (January 1989). "Involvement of 5-HT receptor subtypes in the discriminative stimulus properties of mescaline". European Journal of Pharmacology. 159 (1): 41–46. doi:10.1016/0014-2999(89)90041-1. PMID2707301.
↑Trulson ME, Crisp T, Henderson LJ (December 1983). "Mescaline elicits behavioral effects in cats by an action at both serotonin and dopamine receptors". European Journal of Pharmacology. 96 (1–2): 151–154. doi:10.1016/0014-2999(83)90544-7. PMID6581976.
12Nagai F, Nonaka R, Satoh Hisashi Kamimura K (March 2007). "The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain". European Journal of Pharmacology. 559 (2–3): 132–137. doi:10.1016/j.ejphar.2006.11.075. PMID17223101.
↑Nichols DE (February 1986). "Studies of the relationship between molecular structure and hallucinogenic activity". Pharmacology, Biochemistry, and Behavior. 24 (2): 335–340. doi:10.1016/0091-3057(86)90362-x. PMID3952123. S2CID30796368.
↑Sbordone RJ, Wingard JA, Elliott MK, Jervey J (May 1978). "Mescaline produces pathological aggression in rats regardless of age or strain". Pharmacology, Biochemistry, and Behavior. 8 (5): 543–546. doi:10.1016/0091-3057(78)90385-4. PMID566933.
↑Sbordone RJ, Wingard JA, Gorelick DA, Elliott ML (1979). "Severe aggression in rats induced by mescaline but not other hallucinogens". Psychopharmacology. 66 (3). Berl: 275–280. doi:10.1007/BF00428319. PMID119274.
↑Shull RN, Sbordone RJ, Gorelick DA (1981). "EEG correlates of mescaline-induced pathological aggression in rats". Physiological Psychology. 9 (2): 208–212. doi:10.3758/BF03332925. ISSN0090-5046.
↑Dave M, Shore R, Cupido T, Haley C, Clinkard D (May 2025). "Anaesthetic implications of psilocybin and lysergic acid diethylamide: what is old is now new: A narrative review on psychedelics and anaesthesia". European Journal of Anaesthesiology. 42 (5): 430–434. doi:10.1097/EJA.0000000000002138. PMID39967455. Biochemically, mescaline is associated with a larger release of oxytocin [than LSD or psilocybin], which can precipitate increased serum levels of insulin and glucagon, and a positive inotropic effect on the cardiovascular system.27
↑Thuery G, Crossen F, Mc Loone D, Hinds C, Duffy R, Jairaj C, etal. (2026). "Psychedelic therapy and postpartum depression: priorities and prospects". Therapeutic Advances in Psychopharmacology. 16 20451253251408280. doi:10.1177/20451253251408280. PMC12972557. PMID41816502. Psychedelics and peptide hormones. DOI administration in rats acutely increases oxytocin and prolactin release in a 5-HT2AR-dependent manner.59 In healthy humans, circulating oxytocin and prolactin are acutely increased by LSD60 and psilocybin.61 Ley et al.62 additionally found that mescaline increased circulating oxytocin levels, although they found no effect of psilocybin. LSD-mediated increases in oxytocin were abrogated by co-administration of the 5-HT2AR antagonist ketanserin, providing human evidence that the effect is largely 5-HT2AR-mediated.60 Interestingly, Straumann et al.63 found that the increase in oxytocin induced by LSD, although statistically significant, was minimal compared with that induced by MDMA. Similarly, Holze et al.64 found that MDMA, but not LSD, significantly increased plasma oxytocin concentrations. These data may help explain why pro-social effects are particularly pronounced during MDMA experiences, whereas they are less intense, though still reliably observed, with LSD.
12De Abreu IR, Barkdull A, Munoz JR, Smith RP, Craddock TJ (September 2023). "A molecular analysis of substituted phenylethylamines as potential microtubule targeting agents through in silico methods and in vitro microtubule-polymerization activity". Scientific Reports. 13 (1) 14406. Bibcode:2023NatSR..1314406D. doi:10.1038/s41598-023-41600-9. PMC10474033. PMID37658096. Beyond these targets, phenethylamine compounds, such as mescaline and its derivatives, are also structurally similar to the microtubule-destabilizing agent colchicine8 and may exert effects via direct modulation of cytoskeletal dynamics. Like colchicine mescaline binds to the microtubule constituent protein tubulin, inhibits microtubule dependent axonal transport, and inhibits microtubule and mitotic spindle formation9. Conversely, 2-phenethylamine shows a concentration dependent stabilization of microtubules and suggests a biochemical basis for neuromodulation via direct effect on tubulin of phenethylamines10–12. The effect of phenethylamines on the microtubule cytoskeleton does not appear to have been studied further than this13.
↑Pálenícek T, Balíková M, Bubeníková-Valesová V, Horácek J (January 2008). "Mescaline effects on rat behavior and its time profile in serum and brain tissue after a single subcutaneous dose". Psychopharmacology. 196 (1). Berl: 51–62. doi:10.1007/s00213-007-0926-5. PMID17922234.
123Smythies JR, Johnston VS, Bradley RJ (October 1967). "Alteration by pretreatment with iproniazid and an inactive mescaline analogue of a behaviour change induced by mescaline". Nature. 216 (5111): 196–197. Bibcode:1967Natur.216..196S. doi:10.1038/216196a0. PMID6057240.
↑Musacchio JM, Goldstein M (June 1967). "The metabolism of mescaline-14-C in rats". Biochemical Pharmacology. 16 (6): 963–970. doi:10.1016/0006-2952(67)90268-7. PMID6040403.
↑Tang Y, Xu L, Guo Z, Zhao J, Xiao Y, Xiang P, etal. (June 2025). "Metabolism study of two phenethylamine - derived new psychoactive substances using in silico, in vivo, and in vitro approaches". Archives of Toxicology. 99 (6): 2367–2378. Bibcode:2025ArTox..99.2367T. doi:10.1007/s00204-025-04010-6. PMID40064698. Previous studies have suggested that mescaline could be bioactivated by dopamine-β-hydroxylase, similar to the activation of some biogenic amines, which would lead to the formation of β-hydroxymescaline (Goldstein and Contrera 1962). Taking both the literature results and the actual results from this study into consideration, the reaction position of monohydroxylation of proscaline and methallylescaline was concluded to be on the β-carbon, which was consistent with the fragment ion analysis.
↑Creveling CR, Daly JW, Witkop B, Undenfriend S (October 1962). "Substrates and inhibitors of dopamine-beta-oxidase". Biochimica et Biophysica Acta. 64: 125–134. doi:10.1016/0006-3002(62)90765-5. PMID14023834.
↑Wu D, Otton SV, Inaba T, Kalow W, Sellers EM (June 1997). "Interactions of amphetamine analogs with human liver CYP2D6". Biochemical Pharmacology. 53 (11): 1605–1612. doi:10.1016/S0006-2952(97)00014-2. PMID9264312.
123Watanabe K, Kayano Y, Matsunaga T, Yamamoto I, Yoshimura H (May 1995). "3,4,5-Trimethoxyphenylacetaldehyde, an intermediate metabolite of mescaline, is a substrate for microsomal aldehyde oxygenase in the mouse liver". Biological & Pharmaceutical Bulletin. 18 (5): 696–699. doi:10.1248/bpb.18.696. PMID7492985.
12Browne RG, Ho BT (1975). "Discriminative stimulus properties of mescaline: mescaline or metabolite?". Pharmacology, Biochemistry, and Behavior. 3 (1): 109–114. doi:10.1016/0091-3057(75)90088-x. PMID1129346.
↑Leth-Petersen S, Bundgaard C, Hansen M, Carnerup MA, Kehler J, Kristensen JL (October 2014). "Correlating the metabolic stability of psychedelic 5-HT₂A agonists with anecdotal reports of human oral bioavailability". Neurochemical Research. 39 (10): 2018–2023. doi:10.1007/s11064-014-1253-y. PMID24519542. Mescaline (11a in Fig. 4) is known to be metabolized very slowly in humans, with more than 87% of the ingested dose being excreted [...] with the urine within 24 h [36].
123PubChem. "Mescaline". PubChem. Retrieved 6 November 2024.
12Späth E (February 1919). "Über dieAnhalonium-Alkaloide I. Anhalin und Mezcalin". Monatshefte für Chemie und Verwandte Teile Anderer Wissenschaften (in German). 40 (2): 129–154. doi:10.1007/BF01524590. ISSN0343-7329. S2CID104408477.
↑Slotta KH, Heller H (1930). "Über β-Phenyl-äthylamine, I. Mitteil.: Mezcalin und mezcalin-ähnliche Substanzen". Berichte der Deutschen Chemischen Gesellschaft (A and B Series). 63 (11): 3029–3044. doi:10.1002/cber.19300631117.
↑Kindler K, Peschke W (1932). "Über neue und über verbesserte Wege zum Aufbau von pharmakologisch wichtigen Aminen VI. Über Synthesen des Meskalins". Archiv der Pharmazie. 270 (7): 410–413. doi:10.1002/ardp.19322700709. S2CID93188741.
↑Hahn G, Rumpf F (1938). "Über β-[Oxy-phenyl]-äthylamine und ihre Umwandlungen, V. Mitteil.: Kondensation von Oxyphenyl-äthylaminen mit α-Ketonsäuren". Berichte der Deutschen Chemischen Gesellschaft (A and B Series). 71 (10): 2141–2153. doi:10.1002/cber.19380711022.
↑Szyszka G, Slotta KH (1933). "Über β-Phenyl-äthylamine.III. Mitteilung: Neue Darstellung von Mescalin". Journal für Praktische Chemie. 137 (9–12): 339–350. doi:10.1002/prac.19331370907.
↑Burger A, Ramirez FA (1950). "The Reduction of Phenolic β-Nitrostyrenes by Lithium Aluminum Hydride". Journal of the American Chemical Society. 72 (6): 2781–2782. Bibcode:1950JAChS..72.2781R. doi:10.1021/ja01162a521.
↑Hahn G, Wassmuth H (1934). "Über β-[Oxyphenyl]-äthylamine und ihre Umwandlungen, I. Mitteil.: Synthese des Mezcalins". Berichte der Deutschen Chemischen Gesellschaft (A and B Series). 67 (4): 696–708. doi:10.1002/cber.19340670430.
↑Banholzer K, Campbell TW, Schmid H (1952). "Notiz über eine neue Synthese von Mezcalin, N-Methyl- und N-Dimethylmezcalin". Helvetica Chimica Acta. 35 (5): 1577–1581. Bibcode:1952HChAc..35.1577B. doi:10.1002/hlca.19520350519.
↑Engel L, Hall DR, Skene D, Gaur P, Li CG, Low M (14 October 2026), "Mescaline distribution and concentration in Trichocereus bridgesii", Research Square, doi:10.21203/rs.3.rs-10696166/v1
123456Ogunbodede O, McCombs D, Trout K, Daley P, Terry M (September 2010). "New mescaline concentrations from 14 taxa/cultivars of Echinopsis spp. (Cactaceae) ("San Pedro") and their relevance to shamanic practice". Journal of Ethnopharmacology. 131 (2): 356–362. doi:10.1016/j.jep.2010.07.021. PMID20637277.
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↑Klein MT, Kalam M, Trout K, Fowler N, Terry M (2015). "Mescaline Concentrations in Three Principal Tissues of Lophophora williamsii (Cactaceae): Implications for Sustainable Harvesting Practices". Haseltonia. 131 (2). Elsevier BV: 34–42. Bibcode:2015Hasel..20...34K. doi:10.2985/026.020.0107. S2CID32474292.
1234Bruhn JG, Holmstedt B (1973). "Early peyote research an interdisciplinary study". Economic Botany. 28 (4): 353–390. Bibcode:1973EcBot..28..353B. doi:10.1007/BF02862854. ISSN0013-0001. The spark that was to ignite the "peyote boom" was not lit until 1887 when Briggs published the first study of the effects of "muscale buttons". [...] Early peyote research is closely connected with the name of Louis Lewin. However, he was not the discoverer of the drug. Credit for having brought peyote to the attention of the medical world of the 1880's must go to Dr. John Raleigh Briggs of Dallas, Texas. An instrumental role was also played by the pharmaceutical manufacturers Parke, Davis & Company of Detroit. [...] Mrs. Nickels was long considered to be the first supplier of "mescal buttons" for scientific study, but Slotkin (1955, p. 222, note 7) rejected this and pointed out that Briggs was the pioneer (cf. Bender, 1968). [...] In 1894, however, Prentiss and Morgan (1895) of the Medical Department of Columbian University in Washington obtained a large supply of mescal buttons through James Mooney, "agent among the Indians". They described six experiments in man with the crude drug. "The production of visions" was the most interesting effect found, and the authors concluded that the action of Anhalonium lewinii was not identical with that of any other drug. Except for Briggs' early (and somewhat dubious) self-experiment, these were the first reported studies of the drug in man. [...] The first person to draw the attention of the scientific world to peyote was doubtless Dr. J. R. Briggs, and not Mrs. A. B. Nickels as is often stated.
12Lundström J (June 1971). "Biosynthetic studies on mescaline and related cactus alkaloids". Acta Pharmaceutica Suecica. 8 (3): 275–302. PMID5560272.
↑Dewick PM (2009). Medicinal Natural Products: A Biosynthetic Approach. United Kingdom: John Wiley & Sons. pp.335–336. ISBN978-0-471-49641-0.
↑Rosengarten H, Friedhoff AJ (1976). "A review of recent studies of the biosynthesis and excretion of hallucinogens formed by methylation of neurotransmitters or related substances". Schizophrenia Bulletin. 2 (1): 90–105. doi:10.1093/schbul/2.1.90. PMID779022.
↑Ruiz de Alarcón H (1984). Treatise on the Heathen Superstitions that Today Live Among the Indians Native to this New Spain, 1629. University of Oklahoma Press. ISBN978-0-8061-2031-7.
↑El-Seedi HR, De Smet PA, Beck O, Possnert G, Bruhn JG (October 2005). "Prehistoric peyote use: alkaloid analysis and radiocarbon dating of archaeological specimens of Lophophora from Texas". Journal of Ethnopharmacology. 101 (1–3): 238–242. doi:10.1016/j.jep.2005.04.022. PMID15990261.
↑Dubus Z, Grandgeorge E, Verroust V (2023). "History of the administration of psychedelics in France". Frontiers in Psychology. 14 1131565. doi:10.3389/fpsyg.2023.1131565. PMC10513055. PMID37744588. In the 1920s, the pharmacologist Alexandre Rouhier captured the attention of the French and international scientific communities, first through his important monograph on the uses of peyote, which was translated several times, and later through his pharmaceutical preparations. [...] Alexandre Rouhier: the totality of peyote's alkaloids, for a polyvalent therapeutic action: The 1927 appearance of pharmacist Alexandre Rouhier's Le Peyotl: la plante qui fait les yeux émerveillés (Peyote: The Plant That Fills the Eyes with Marvels) was a success considering its somewhat obscure subject matter (Rouhier, 1927). [...]
↑Frederking W (March 1955). "Intoxicant drugs (mescaline and lysergic acid diethylamide) in psychotherapy". The Journal of Nervous and Mental Disease. 121 (3): 262–266. doi:10.1097/00005053-195503000-00010. PMID14381913.
12Walker SR, Pullella GA, Piggott MJ, Duggan PJ (17 July 2023). "Introduction to the chemistry and pharmacology of psychedelic drugs". Australian Journal of Chemistry. 76 (5): 236–257. doi:10.1071/CH23050. ISSN0004-9425. In 1955, mescaline (4) even gained the attention of British politician Christopher Mayhew, who participated in an 'experiment' in which he was recorded after being administered mescaline (4). The footage of Mayhew was to be televised on the BBC programme Panorama; however, the broadcaster decided against airing it. Mayhew later described the experiment as 'the most interesting thing [he has] ever done' and 'profoundly thought-provoking'.[80]
↑Metzer WS (February 1989). "The experimentation of S. Weir Mitchell with mescal". Neurology. 39 (2 Pt 1): 303–304. doi:10.1212/wnl.39.2.303. PMID2644583.
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↑"FLOW MY Tears". www.philipkdickfans.com. Retrieved 4 May 2018.
↑Doblin R (June 2001). Regulation of the Medical Use of Psychedelics and Marijuana (Ph.D. thesis). Harvard University. In 1927, German physician Kurt Beringer published a description of his mescaline studies in research subjects.70 One subject of his, who reportedly felt that the remarkable visual images he experienced should be captured in film, was subsequently hired by Walt Disney as the chief visualist for the Disney film, Fantasia.71
↑"The Matrix Quotes". imdb.com. Neo: You ever have that feeling where you're not sure if you're awake or still dreaming? Choi: All the time. It's called mescaline, it's the only way to fly.
↑Copes H, Hochstetler A, Ragland J, Hendricks PS (2026). "Hitting the Reset Button: Ceremonial Use of Peyote and Experiences of Personal Change". Journal of Drug Issues. 56 (1): 150–170. doi:10.1177/00220426241274737. ISSN0022-0426.
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Notes: (1) TAAR1 activity of ligands varies significantly between species. Some agents that are TAAR1 ligands in some species are not in other species. This navbox includes all TAAR1 ligands regardless of species. (2) See the individual pages for references, as well as the List of trace amines, TAAR, and TAAR1 pages. See also:Receptor/signaling modulators
