Mescaline is typically taken orally and used recreationally, spiritually, and medically, with psychedelic effects occurring at doses from 100 to 1,000mg, includingmicrodosing below 75mg, and it can be consumed in pure form or via mescaline-containing cacti. Mescaline induces apsychedelic experience characterized byvivid visual patterns, altered perception of time and self,synesthesia, and spiritual effects, with anonset of 0.5 to 0.9hours and aduration that increases with dose, ranging from about 6 to 14hours. Mescaline has a highmedian lethal dose across species, with the humanLD50 estimated at approximately 880mg/kg, making it very difficult to consume a fatal amount.Ketanserin blocks mescaline’s psychoactive effects, and while it's unclear if mescaline is metabolized bymonoamine oxidase enzymes, preliminary evidence suggestsharmala alkaloids may potentiate its effects.
Mescaline primarily acts as apartial agonist at serotonin5-HT2A receptors, with varying affinity and efficacy across multipleserotonin,adrenergic,dopamine,histamine,muscarinic, andtrace amine receptors, but shows low affinity for most non-serotonergic targets. It is a relativelyhydrophilic psychedelic compound structurally related tocatecholamines but acting on the serotonergic system, first synthesized in 1919, with numerous synthetic methods and potent analogues developed since. Mescaline occurs naturally in various cacti species, with concentrations varying widely, and isbiosynthesized in plants fromphenylalanine via catecholamine pathways likely linked to stress responses.
Mescaline-containing cacti use dates back over 6,000 years.[6] Peyote was studied scientifically in the 19th and 20th centuries, culminating in the isolation of mescaline as its primary psychoactive compound, legal recognition of its religious use, and ongoing exploration of its therapeutic potential. Mescaline is largely illegal worldwide, though exceptions exist for religious, scientific, or ornamental use, and it has influenced many notable cultural figures through its psychoactive effects. Very few studies concerning mescaline's activity and potential therapeutic effects in people have been conducted since the early 1970s.
Mescaline is used as a psychedelic at doses of 100 to 1,000mgorally.[8][14][15] Low doses are 100 to 200mg, an intermediate or "good effect" dose is 500mg, and a high orego-dissolution dose is 1,000mg.[8][14]Microdosing involves the use of subthreshold mescaline doses of less than 75mg.[8][14]
In addition to pure form, mescaline is used in the form of mescaline-containingcacti such aspeyote andSan Pedro.
Mescaline induces apsychedelic state comparable to those produced byLSD andpsilocybin, but with unique characteristics.[16] Subjective effects may include altered thinking processes, an altered sense of time and self-awareness, and closed- and open-eye visual phenomena.[17]
Prominence of color is distinctive, appearing brilliant and intense. Recurring visual patterns observed during the mescaline experience include stripes, checkerboards, angular spikes, multicolor dots, and very simplefractals that turn very complex. The English writerAldous Huxley described these self-transforming amorphous shapes as like animated stained glass illuminated from light coming through the eyelids in his autobiographical bookThe Doors of Perception (1954). Like LSD, mescaline induces distortions of form andkaleidoscopic experiences but they manifest more clearly witheyes closed and under low lighting conditions.[18]
Heinrich Klüver coined the term "cobweb figure" in the 1920s to describe one of the fourform 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."[19]
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 aCubist painting.[20]
Mescaline elicits a pattern of sympathetic arousal, with theperipheral nervous system being a major target for this substance.[21]
According to a research project in the Netherlands, ceremonial San Pedro use seems to be characterized by relatively strong spiritual experiences, and low incidence of challenging experiences.[22]
Theonset of the effects of mescaline givenorally is 0.5 to 0.9hours on average with a range of 0.1 to 2.7hours.[8][9][1][2] Its effects peak after 1.9 to 4.0hours with a range of 0.5 to 8.0hours.[8][24][10][9]
Theduration of mescaline appears to bedose-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.[8][9]
TheLD50 of mescaline has been measured in various animals: 212–315mg/kg i.p. (mice), 132–410mg/kg i.p. (rats), 328mg/kg i.p. (guinea pigs), 54mg/kg in dogs, and 130mg/kg i.v. inrhesus macaques.[2][25] For humans, theLD50 of mescaline has been reported to be approximately 880mg/kg.[25] It has been said that it would be very difficult to consume enough mescaline to cause death in humans.[2]
Notes: The smaller the value, the more avidly the drug binds to the site. All proteins are human unless otherwise specified.Refs:[30][31][8][1] [32][33][34][35][36][37][38]
In humans, mescaline acts similarly to other psychedelic agents.[39] It acts as an agonist,[40] binding to and activating theserotonin5-HT2A receptor.[41][9] ItsEC50Tooltip 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.[1] 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 theprefrontal cortex.[42] In addition to the serotonin 5-HT2A and 5-HT2B receptors, mescaline is also known to bind to the serotonin5-HT2C receptor and a number of othertargets.[1][34][32][43]
Mescaline is a relatively low-potency psychedelic, with active doses in the hundreds of milligrams and micromolar affinities for the serotonin 5-HT2A receptor.[6][1] For comparison,psilocybin is approximately 20-fold more potent (doses in the tens of milligrams) andlysergic acid diethylamide (LSD) is approximately 2,000-fold more potent (doses in the tens to hundreds of micrograms).[1] There have been efforts to develop more potentanalogues of mescaline.[6] Difluoromescaline andtrifluoromescaline are more potent than mescaline, as is its amphetaminehomologue TMA.[50][51]Escaline andproscaline are also both more potent than mescaline, showing the importance of the 4-position substituent with regard to receptor binding.[52]
Thecryo-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 byBryan L. Roth and colleagues.[54][55]
Mescaline is usually takenorally, although it may also beinsufflated,smoked, or givenintravenously.[2] Taken orally, it is rapidlyabsorbed from thegastrointestinal tract.[2][11] The oralbioavailability of mescaline is unknown.[5] However, since at least 53% of orally administered mescaline is excreted inurine unchanged, the bioavailability appears to be at least 53%.[4]Peak concentrations of mescaline occur after approximately 1.6 to 2.3hours on average (range 1.0–6.0hours).[8][10][9] Thepharmacokinetics of mescaline are dose-proportional over anoral dose range of 100 to 800mg.[8][9]
Metabolism of mescaline in humans and/or animals.[2]
Mescaline given orally appears to be subject tofirst-pass metabolism of about 50%.[4] Following the first pass, mescaline appears to be subject to relatively limitedmetabolism.[4]
Mescaline appears not to be subject to metabolism byCYP2D6 based onin-vitro studies with human liver microsomes.[60] Similarly, thein-vitrocytotoxicity of mescaline does not appear to be affected bycytochrome P450 (CYP450)enzyme inhibitors.[61] Conversely, it was potentiated by theMAO-A inhibitorclorgiline but not by theMAO-B inhibitorrasagiline.[61] These findings were in contrast to those with the related compound2C-B, which was potentiated by rasagiline but not by clorgiline.[61]
Circulatingpeak andarea-under-the-curve concentrations of mescaline and 3,4,5-trimethoxyphenylacetic acid (TMPAA) are similar with oral administration of mescaline.[9][4] Conversely, levels ofN-acetylmescaline (NAM) are far lower than those of mescaline or TMPAA and are thought not to be of clinical relevance.[9][4]Intravenous injection of mescaline may result in less hepatic deamination than with oral administration.[1][4]
Active metabolites of mescaline might contribute to its psychoactive effects.[7][2][6] However, both TMPAA and NAM have been said to be inactive based on human tests.[12] Similarly, 3,4,5-trimethoxyphenylethanol (TMPE), 3,4,5-trimethoxyphenylacetaldehyde (TMPA), and NAM all failed to produce mescaline-like effects in rodentdrug discrimination tests.[6][62][63]
3,4,5-Trimethoxyamphetamine (TMA), the α-methylanalogue of mescaline and an MAO-resistant psychedelic, is only about twice aspotent as mescaline as a psychedelic in humans despite having similarserotonin receptoraffinity.[62] This suggests that the deamination of mescaline has a relatively limited impact on its potency, compared to for example the2C series of psychedelics.[62]
Mescaline given orally isexcreted 87% inurine within 24hours and 92% in urine within 48hours.[1][11][64][12] 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).[2][1][12] However, after the first hour, the percentage excreted as unchanged mescaline declines and the percentage excreted as TMPAA rises.[1][12] Ultimately, mescaline is excreted in urine 28 to 60% unchanged, 27 to 30% or more as TMPAA, 5% asN-acetyl-3,4-dimethoxy-5-hydroxyphenylethylamine, and less than 0.1% asN-acetylmescaline.[2][11][12] Other minor or trace excreted metabolites have also been observed.[2][12] In a more modern study published in 2025, mescaline was eliminated in urine 53% as unchanged mescaline and 31% as TMPAA.[4]
Mescaline was originally reported to have anelimination half-life of 6hours based on a study conducted in the 1960s.[2][1][10][12] However, subsequent research published in the 2020s found that its half-life is actually about 3.6hours (range 2.6–5.3hours).[8][10][9][4] The previous higher estimate is believed to have been due to smallsample numbers and collective measurement of mescaline metabolites.[10] The elimination half-life of mescaline does not appear to bedose-dependent.[8][10] TMPAA has a half-life of about 3.7 to 4.1hours, similar to that of mescaline.[4] Mescaline has a similar half-life as LSD yet has a longerduration.[8] This is due to mescaline having slowerabsorption andonset rather than a longer half-life.[8][10]
Laboratory synthetic mescaline biosynthesized[clarification needed] frompeyote — this was the first psychedelic compound to be extracted and isolated[66]Dried Peyote (Lophophora williamsii), containing around 5-6% mescaline by weight
Mescaline was first synthesized in 1919 byErnst Späth from 3,4,5-trimethoxybenzoyl chloride.[67] 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.[17]
Treatment of tricarbonyl-(η6-1,2,3-trimethoxybenzene) chromium complex with acetonitrile carbanion inTHF and iodine, followed by reduction of the nitrile with lithium aluminum hydride.[78]
It occurs naturally in several species ofcacti. It is also reported to be found in small amounts in certain members of the bean family,Fabaceae, includingSenegalia berlandieri (syn.Acacia berlandieri),[82] although these reports have been challenged and have been unsupported in any additional analyses.[83]
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.[94]
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 ascortisol when stressed. Thein vivo function of catecholamines in plants has not been investigated, but they may function asantioxidants, 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.[95]
Mescaline isbiosynthesized fromtyrosine, which, in turn, is derived fromphenylalanine by the enzyme phenylalanine hydroxylase. InLophophora williamsii (Peyote),dopamine converts into mescaline in a biosynthetic pathway involvingm-O-methylation and aromatic hydroxylation.[96]
Tyrosine and phenylalanine serve as metabolic precursors towards the synthesis of mescaline. Tyrosine can either undergo a decarboxylation viatyrosine decarboxylase to generatetyramine and subsequently undergo an oxidation at carbon 3 by a monophenol hydroxylase or first be hydroxylated bytyrosine hydroxylase to formL-DOPA and decarboxylated byDOPA decarboxylase. These create dopamine, which then experiences methylation by acatechol-O-methyltransferase (COMT) by anS-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 toL-tyrosine byL-amino acid hydroxylase. Once converted, it follows the same pathway as described above.[95][97]
Archaeological evidence from sites in the United States, Mexico, and Peru indicates that mescaline-containing cacti have been used for over 6,000 years.[6] Europeans recorded use of peyote in Native American religious ceremonies upon early contact with theHuichol people in Mexico.[98] Other mescaline-containing cacti such as the San Pedro have a long history of use in South America, from Peru to Ecuador.[99][100][101][102] While religious and ceremonial peyote use was widespread in theAztec Empire and northern Mexico at the time of the Spanish conquest, religious persecution confined it to areas near the Pacific coast and up to southwest Texas. However, by 1880, peyote use began to spread north of South-Central America with "a new kind of peyote ceremony" inaugurated by the Kiowa and Comanche people. These religious practices, incorporated legally in the United States in 1920 as the Native American Church, have since spread as far as Saskatchewan, Canada.[103]
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 typical dose is 200 to 400mg of mescaline sulfate or 178 to 356mg of mescaline hydrochloride.[23][104] The average 76 mm (3.0 in) peyote button contains about 25mg mescaline.[105] 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.[106]
Botanical studies of peyote began in the 1840s and the drug was listed in the Mexicanpharmacopeia.[7] The first use of mescal buttons was published by John Raleigh Briggs in 1887.[7] In 1887, the German pharmacologistLouis Lewin received his first sample of the peyote cactus, found numerous new alkaloids and later published the first methodical analysis of it.[107] Mescaline was first isolated and identified in 1897 by the German chemistArthur Heffter.[7][2][108] He showed that mescaline was exclusively responsible for the psychoactive or hallucinogenic effects of peyote.[7] However, other components of peyote, such ashordenine,pellotine, andanhalinine, are alsoactive.[7] Mescaline was firstsynthesized in 1919 byErnst Späth.[2][67]
In 1955, English politicianChristopher Mayhew took part in an experiment forBBC'sPanorama, in which he ingested 400mg of mescaline under the supervision of psychiatristHumphry 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".[109]
Studies of the potential therapeutic effects of mescaline started in the 1950s.[7]
In the United States, mescaline was made illegal in 1970 by theComprehensive Drug Abuse Prevention and Control Act, categorized as a Schedule I hallucinogen.[110] The drug is prohibited internationally by the 1971Convention on Psychotropic Substances.[111] Mescaline is legal only for certain religious groups (such as theNative American Church by the American Indian Religious Freedom Act of 1978) and in scientific and medical research. In 1990, theSupreme Court ruled that the state of Oregon could ban the use of mescaline in Native American religious ceremonies. TheReligious 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.[112] Many states, including the state ofUtah, have legalized peyote usage with "sincere religious intent", or within a religious organization,[citation needed] regardless of race.[113] Synthetic mescaline, but not mescaline derived from cacti, was officially decriminalized in the state of Colorado by ballot measure Proposition 122 in November 2022.[114]
Mescaline is considered a schedule 9 substance in Australia under thePoisons Standard (February 2020).[117] 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."[117]
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, orLophophora williamsii, as well asEchinopsis pachanoi andEchinopsis peruviana without restriction, as it is specifically exempt from legislation.[89] In Canada, mescaline is classified as a schedule III drug under theControlled Drugs and Substances Act, whereas peyote is exempt.[118]
In Russia mescaline, its derivatives and mescaline-containing plants are banned as narcotic drugs (Schedule I).[119]
Jean-Paul Sartre took mescaline shortly before the publication of his first book,L'Imaginaire; he had a bad trip during which he imagined that he was menaced by sea creatures. For many years following this, he persistently thought that he was being followed by lobsters, and became a patient ofJacques Lacan in hopes of being rid of them. Lobsters and crabs figure in his novelNausea.
Havelock Ellis was the author of one of the first written reports to the public about an experience with mescaline (1898).[122][123][124]
Stanisław Ignacy Witkiewicz, Polish writer, artist and philosopher, experimented with mescaline and described his experience in a 1932 bookNikotyna Alkohol Kokaina Peyotl Morfina Eter.[125]
Quanah Parker, appointed by the federal government as principal chief of the entireComanche Nation, advocated the syncretic Native American Church alternative, and fought for the legal use of peyote in the movement's religious practices.
Psychedelic research pioneerAlexander Shulgin said he was first inspired to explore psychedelic compounds by a mescaline experience.[126] In 1974, Shulgin synthesized2C-B, a psychedelic phenylethylamine derivative, structurally similar to mescaline,[127] and one of Shulgin's self-rated most important phenethylamine compounds together with Mescaline,2C-E,2C-T-7, and2C-T-2.[128]
Bryan Wynter producedMars Ascends after trying the substance for the first time.[129]
George Carlin mentioned mescaline use during his youth while being interviewed in 2008.[130]
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]
Mescaline has a wide array of suggested medical usage, including treatment of depression, anxiety, PTSD,[135] andalcoholism.[136] However, its status as a Schedule I controlled substance in theConvention 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.[137][135][16]
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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 theList of trace amines,TAAR, andTAAR1 pages. See also:Receptor/signaling modulators
