Biology:Mescaline

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Mescaline, also known in chemical terms as 3,4,5-trimethoxyphenethylamine, is a naturally occurring psychedelic drug and alkaloid of the phenethylamine and scaline families found in certain cacti like peyote (Lophophora williamsii) and the San Pedro cactus (Echinopsis pachanoi, others).[1][2][3][4][5]

The drug is used recreationally, spiritually, and medically, with psychedelic effects occurring at doses of 100 to 800 mg (as it's hydrochloride salt) orally[5][6] and it can be used in pure form or in the form of mescaline-containing cacti.[1][7][3] Mescaline induces a psychedelic experience characterized by visual changes, altered perception of time, space, and self, synesthesia, and spiritual experiences, with an onset of 30 to 60 minutes, a time to peak of 2 to 4 hours, and a duration that increases with dose and ranges from 6 to 14 hours.[2][5][8]

Mescaline primarily acts as a partial agonist at serotonin 5-HT2A receptors, with varying affinity and efficacy across multiple other receptors and targets.[5][2] The serotonin 5-HT2A receptor antagonist ketanserin blocks mescaline's psychoactive effects.[9][8] Mescaline is a relatively hydrophilic compound structurally related to dopamine,[10][3][4] first synthesized in 1919,[11] with numerous synthetic methods[12] and potent analogues developed since.[10][13] It occurs naturally in various cacti species, with concentrations varying widely, and is biosynthesized in plants from amino acids like phenylalanine and tyrosine.[1][14][12]

The practice of humans consuming mescaline-containing cacti dates back over 6,000 years.[1][11] 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.[11] Mescaline was the first psychedelic compound to be characterized by the Western world and has been referred to as the "first psychedelic".[11][15]

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.[11][16][10] Very few studies of mescaline in people have been conducted since the early 1970s.[11][17] However, the drug is now being studied in terms of its effects and for potential medical use once again as of the early 2020s.[5][17][18]

Use and effects

Mescaline is used recreationally, spiritually, and medically.[1][2] It is typically taken orally.[4] The drug is used as a psychedelic at doses of 100 to 1,000 mg orally.[5][6][19][12] Low doses are 100 to 200 mg, an intermediate or "good effect" dose is 500 mg, and a high (ego-dissolution) dose is 1,000 mg.[5][6] In his book PiHKAL (Phenethylamines I Have Known and Loved), Alexander Shulgin listed a dose range of 200 to 400 mg as the sulfate salt and 178 to 356 mg as the hydrochloride salt.[10][20] Microdosing involves the use of daily mescaline doses of less than 75 mg.[5][6] In addition to pure form, mescaline is used in the form of cacti such as peyote and the San Pedro cactus.[1][7][3] Doses when mescaline is used in the form of fresh or dried cacti have also been described.[21][22][4][7]

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 76 mm (3.0 in) peyote button contains about 25 mg mescaline. Some analyses of traditional preparations of San Pedro cactus have found doses ranging from 34 mg to 159 mg 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.[23]

The onset of the effects of mescaline given orally is 0.5 to 0.9 hours on average with a range of 0.1 to 2.7 hours.[5][8][2][4] Its effects peak after 1.9 to 4.0 hours with a range of 0.5 to 8.0 hours.[5][24][25][8] The duration of mescaline appears to be dose-dependent, varying from 6.4 hours on average (range 3.0–10 hours) at a dose of 100 mg, 9.7 to 11 hours on average (range 5.6–22 hours) at moderate doses of 300 to 500 mg, and 14 hours on average (range 7.2–22 hours) at a dose of 800 mg.[5][8] Cases of mescaline having unusually prolonged or delayed effects have also been described.[26]

Mescaline induces a psychedelic state comparable to those produced by LSD and psilocybin, but with unique characteristics.[17] Subjective effects may include altered thinking processes, an altered sense of time and self-awareness, and closed- and open-eye visual phenomena.[27] In PiHKAL, Shulgin described the effects of mescaline based on a collection of experience reports.[10] The effects included brightened colors, increased visual contrast, open-eye visuals like colors and patterns, pareidolia, increased significance of objects, enhanced music appreciation, feeling intoxicated, self-analysis, insights, increased body awareness, feelings of joy, happiness, and peacefulness, feeling hyper and energized, feelings of empathy, things feeling ridiculous, humor and laughter, religious feelings, restlessness, social discomfort and avoidance, and nausea, among others.[10] Mescaline was one of Shulgin's "magical half-dozen" psychedelic drugs in PiHKAL.[10]

Prominence of color with mescaline is distinctive, appearing brilliant and intense.[1] Recurring visual patterns observed during the mescaline experience include stripes, checkerboards, angular spikes, multicolor dots, and very simple fractals that can turn very complex.[28] 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).[16] Like LSD, mescaline induces distortions of form and kaleidoscopic experiences but they manifest more clearly with eyes closed and under low lighting conditions.[28] 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".[29] The other three are the chessboard design, tunnel, and spiral.[29] Klüver wrote that "many 'atypical' visions are upon close inspection nothing but variations of these form-constants."[29] An unusual but unique characteristic of mescaline use is the "geometrization" of three-dimensional objects.[28][30] The object can appear flattened and distorted, similar to the presentation of a Cubist painting.[28][30] Detailed descriptions of the psychedelic experience induced by mescaline have been given by many authors.[31][12][32][33][34][35][16][10]

The subjective effects of mescaline are qualitatively similar to those of LSD and psilocybin.[5][36][25][37][31] Based on anecdotal evidence however, mescaline is said to be less threatening and to produce less ego dissolution than other psychedelics like LSD.[17][15] This may in part be due its slow onset allowing for a more comfortable ease-in of effects.[17] In addition, mescaline is typically dosed at lower doses than LSD or psilocybin in terms of doses with equivalent or comparable strength.[8][25][5] 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.[38] Mescaline, LSD, and psilocybin appear to produce similar color enhancement in clinical studies, though more research is needed.[39][40][41][42]

Contraindications

Contraindications of psychedelic drugs like mescaline include severe cardiovascular disease, epilepsy or seizures, schizophrenia and other psychotic disorders, bipolar disorder, and pregnancy, among others.[43][44] Serotonin 5-HT2A receptor antagonists such as atypical antipsychotics and certain antidepressants may block psilocybin's hallucinogenic effects and hence may be considered contraindicated in this sense.[45][46]

Adverse effects

Side effects of mescaline include fatigue, weakness, impaired concentration, restlessness, tension, anxiety, panic, and social discomfort and avoidance, headache, pupil dilation, nausea, vomiting, sweating, trembling, discomfort, feeling hot or cold, palpitations, chest and neck pains, shortness of breath, increased heart rate and blood pressure, and increased body temperature, among others.[10][2][5][47] Nausea and vomiting are important dose-limiting side effects of mescaline and occur at greater rates than with other psychedelics like LSD and psilocybin.[47][8][25] High doses of mescaline, such as 800 mg and above, are not well-tolerated due to substantial nausea and vomiting.[36][8][47] On the other hand, mescaline appears to induce less fear and anxiety than LSD and psilocybin even at equivalent doses.[5][36][47]

Hallucinogen-induced psychotic disorder (HIPD)

Main article: Medicine:Hallucinogen-induced psychotic disorder

Mescaline use can lead to hallucinogen-induced psychotic disorder (HIPD).[48][49] Hallucinogen-induced psychotic disorder is a type of substance-induced psychosis.[50] HIPD symptoms are psychosis with paranoia, delusions, hallucinations, or disorganized thinking that persist beyond the effects of the drug.[51] Hallucinogen-induced psychotic disorder is most commonly seen with LSD use, but can also be caused by mescaline.[52] Hallucinogen-induced psychotic disorder is a medical emergency. Without treatment, the psychotic state can continue for weeks or months.[53] HIPD is treated with an atypical antipsychotic medication such as aripiprazole, quetiapine, olanzapine, or risperidone.[54] Individuals with a personal or family history of mental health issues are at the highest risk for hallucinogen-induced psychotic disorder.[55]

Tolerance

Mescaline is associated with rapid tolerance development, including cross-tolerance with other psychedelics like LSD and psilocybin.[7][2][4][31] This tolerance is apparent within a few days and resets after 3 or 4 days of abstinence.[2][4][7][31]

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.[56][57][58][59][12] However, there is also a case report of death due to jumping off a cliff while on a high dose of mescaline.[7][60] 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 8,400 mg.[56][57][59] However, mescaline has reportedly been taken by humans at doses of up to 8,000 mg without apparent toxic reactions.[7][12][61][62] On the other hand, there is one unverified reported case of death due to 15,000 mg intravenously, which would equate to about 150 to 200 mg/kg.[12] The median lethal dose (LD50) of mescaline has been determined in various animal species, with the values including 212 to 315 mg/kg i.p. in mice, 132 to 410 mg/kg i.p. in rats, 328 mg/kg i.p. in guinea pigs, 54 mg/kg in dogs, and 130 mg/kg i.v. in rhesus macaques, among others.[4][12][37][63] It has been said that it would be difficult to take enough mescaline to cause death in humans.[4][12] No deaths due to peyote use have been reported aside from the asphyxiation case.[64][12][59] The highest known dose of peyote taken is 90 dried buttons.[65][12][66]

Interactions

The serotonin 5-HT2A receptor antagonist ketanserin has been found to block the psychoactive effects of mescaline.[9][8][67] Similarly, the antipsychotic chlorpromazine, which acts as both a dopamine D2 receptor antagonist and to a lesser extent as a serotonin 5-HT2A receptor antagonist, has been reported to reverse the psychoactive effects of mescaline.[9][68][69][70] Other phenothiazines, such as promethazine and diethazine, have also been reported to antagonize the effects of mescaline in humans, whereas prochlorperazine was much less effective and promazine was ineffective.[37][71] Barbiturates, which are GABAA receptor positive allosteric modulators, have been found to abolish the anxiety induced by mescaline.[37]

It is unclear whether mescaline is metabolized by monoamine oxidase (MAO) enzymes[72][4][31] or whether monoamine oxidase inhibitors (MAOIs) might increase the effects of mescaline.[72][73] No clinical studies of mescaline in combination with MAOIs are known to have been published.[72] 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".[73][12][72] In accordance with these findings, the harmala alkaloid and RIMA harmine has been reported to augment the effects of mescaline in animals.[12][31] 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.[13] Accordingly, the MAOI iproniazid did not potentiate the behavioral effects of mescaline in rats.[13][37][74]

Pharmacology

Pharmacodynamics

Mescaline activities
Target Affinity (Ki, nM)
5-HT1A 1,841–4,600
5-HT1B >10,000
5-HT1D >10,000
5-HT1E 5,205
5-HT1F ND
5-HT2A 550–17,400 (Ki)
88–30,200 (EC50)
33–107% (Emax)
5-HT2B 793–800 (Ki)
1,100–>20,000 (EC50)
91% (Emax)
5-HT2C 300–17,000 (Ki)
20–19,500 (EC50)
22–109% (Emax)
5-HT3 >10,000
5-HT4 ND
5-HT5A >10,000
5-HT6 >10,000
5-HT7 >10,000
α1A >15,000
α1B >10,000
α1D ND
α2A 1,400–8,930
α2B >10,000
α2C 745
β1–β2 >10,000
D1 >10,000
D2 >10,000
D3 >17,000
D4 >10,000
D5 >10,000
H1–H4 >10,000
M1–M5 >10,000
TAAR1 3,300 (Ki) (rat)
11,000 (Ki) (mouse)
3,700–4,800 (EC50) (rodent)
>10,000 (EC50) (human)
I1 2,678
σ1–σ2 >10,000
SERT >30,000 (Ki)
367,000 (IC50)
NET >30,000 (Ki)
>900,000 (IC50)
DAT >30,000 (Ki)
841,000 (IC50)
Notes: The smaller the value, the more avidly the drug binds to the site. All proteins are human unless otherwise specified. Refs: [75][76][5][2]
[77][78][79][80][81][82][83]

Mescaline acts as an agonist of the serotonin 5-HT2A receptor to produce its psychedelic effects.[84][85][86][8] Its EC50 at the serotonin 5-HT2A receptor is approximately 10,000 nM and at the serotonin 5-HT2B receptor is greater than 20,000 nM.[2] 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.[87] 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.[2][79][77] The drug shows pronounced biased agonism at the serotonin 5-HT2C receptor.[88]

Mescaline lacks affinity for the monoamine transporters, including the serotonin transporter (SERT), norepinephrine transporter (NET), and dopamine transporter (DAT) (Ki > 30,000 nM).[2] However, it has been found to increase levels of the major serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) at high doses in rodents.[2][3][4][89] This finding suggests that mescaline might inhibit the reuptake and/or induce the release of serotonin at such doses.[2][3][90] In any case, this possibility has not yet been further assessed or demonstrated.[2] Besides serotonin, mescaline might also weakly induce the release of dopamine, but this is probably of modest significance, if it occurs.[3][4][91] In accordance, there is no evidence of the drug showing addiction or dependence.[4][3] Mescaline appears to be inactive in terms of norepinephrine release induction and indirect sympathomimetic activity.[92] Other psychedelic phenethylamines, including the closely related 2C, DOx, and TMA drugs, are inactive as monoamine releasing agents and reuptake inhibitors.[93][94] However, an exception is trimethoxyamphetamine (TMA), the amphetamine analogue of mescaline, which is a very low-potency serotonin releasing agent (EC50 = 16,000 nM).[93] The possible monoamine-releasing effects of mescaline would likely be related to the compound's phenethylamine backbone[4][3]

Mescaline is a relatively low-potency psychedelic, with active doses in the hundreds of milligrams and micromolar affinities for the serotonin 5-HT2A receptor.[1][2] 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).[36][2] There have been efforts to develop more potent analogues of mescaline.[1][10][95][13][96] Difluoromescaline and trifluoromescaline are more potent than mescaline, as is its amphetamine homologue TMA.[95][13][97] Escaline and proscaline are also both more potent than mescaline, showing the importance of the 4-position substituent with regard to receptor binding.[10][13][98]

It is unclear why mescaline produces more nausea and vomiting than other psychedelics like LSD and psilocybin.[47] 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.[8]

Mescaline has been found to increase oxytocin levels in humans and to a greater extent than LSD or psilocybin at equivalent doses.[99][100][25]

There is no evidence of acute tolerance with mescaline.[101] However, tolerance to mescaline builds with repeated use, lasting for a few days.[2][4][7][31] The drug causes cross-tolerance with other psychedelics like LSD and psilocybin.[2][4][7][31]

The cryo-EM structures 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.[102][103]

Mescaline has been found to bind to tubulin and act as a highly potent mitotic inhibitor similarly to its cyclized derivatives colchicine and demecolcine.[7][104][105] Aside from the identification of this action however, it does not appear to have been further studied.[104]

Pharmacokinetics

Absorption

Mescaline is usually taken orally, although it may also be insufflated, smoked, or given intravenously.[4] Taken orally, it is rapidly absorbed from the gastrointestinal tract.[4][37] The oral bioavailability of mescaline is unknown.[106] However, since at least 53% of orally administered mescaline is excreted in urine unchanged, the bioavailability appears to be at least 53%.[101] Peak concentrations of mescaline occur after approximately 1.6 to 2.3 hours on average (range 1.0–6.0 hours).[5][25][8] However, there is a delay of 1 to 2 hours following peak levels in terms of the drug producing maximal psychoactive and behavioral effects.[13] The pharmacokinetics of mescaline are dose-proportional over an oral dose range of 100 to 800 mg.[5][8]

Distribution

Mescaline is distributed to the liver, spleen, and kidneys at many times higher levels than blood or brain based on animal studies.[37][4][2] 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.[4][2] The exact portion bound to plasma proteins seems to be unknown, but appears to be minimal.[106][58][107]

Mescaline appears to have relatively poor blood–brain barrier permeability due to its low lipophilicity.[3][4][101][36] However, it is still able to cross into the central nervous system and produce psychoactive effects at sufficiently high doses.[3][4][101] 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.[101][13][36][108]

Metabolism

Metabolism of mescaline in humans and/or animals.[4]

Mescaline given orally appears to be subject to first-pass metabolism of about 50%.[101] Following the first pass, mescaline appears to be subject to relatively limited metabolism.[101]

The primary metabolic pathway of mescaline is oxidative deamination.[4][72][1][2][31] The specific enzymes mediating the deamination of mescaline are controversial however.[4][72][31][109] Monoamine oxidase (MAO), diamine oxidase (DAO; histamine oxidase), semicarbazide-sensitive amine oxidase (SSAO), and/or other enzymes may be responsible.[4][13][31][109] Preclinical studies of mescaline given in combination with inhibitors of MAO and/or DAO, such as iproniazid, pargyline, and semicarbazide, have been conducted, but findings have been conflicting.[4][72][13][31][37][110][109] Mescaline has been reported to be a poor or negligible substrate of highly purified human MAO in-vitro.[31][37][111] Mescaline is converted via deamination into 3,4,5-trimethoxyphenylacetaldehyde (TMPA) as an intermediate and then into 3,4,5-trimethoxyphenylacetic acid (TMPAA) or 3,4,5-trimethoxyphenylethanol (TMPE).[4][2][3][26] β-Hydroxymescaline may also be a minor metabolite of mescaline formed by dopamine β-hydroxylase (DBH), though this remains unclear.[4][13][112][113]

Mescaline appears not to be subject to metabolism by CYP2D6 based on in-vitro studies with human liver microsomes.[114] Similarly, the in-vitro cytotoxicity of mescaline does not appear to be affected by cytochrome P450 (CYP450) enzyme inhibitors.[115] Conversely, it was potentiated by the MAO-A inhibitor clorgiline but not by the MAO-B inhibitor rasagiline.[115] These findings were in contrast to those with the related compound 2C-B, which was potentiated by rasagiline but not by clorgiline.[115]

Circulating peak and area-under-the-curve concentrations of mescaline and TMPAA are similar with oral administration of mescaline.[8][101] Conversely, levels of N-acetylmescaline (NAM) are far lower than those of mescaline or TMPAA and are thought not to be of clinical relevance.[8][101] Intravenous injection of mescaline may result in less hepatic deamination than with oral administration.[2][101]

It has been theorized that active metabolites of mescaline might contribute to its psychoactive effects.[3][4][1][13][116][117][26][74] Relatedly, TMPA and TMPE were reported in early research to show pharmacological effects in rats and rabbits with greater potency than mescaline.[26][74] 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.[26] Similarly, co-administration of TMPE with calcium carbimide markedly potentiated the effects of TMPE.[74] 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.[1][116][118] 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.[117] A further study found TMPAA to be inactive in animals as well.[26][119] As with animal findings, both TMPAA and NAM have been said to be inactive based on human tests.[10][120] It has also been noted that metabolites like TMPA and TMPE are rapidly metabolized.[117] As such, metabolites of mescaline like TMPA, TMPE, TMPAA, and NAM do not appear to be involved in the drug's psychedelic-related effects.[116][118][120]

3,4,5-Trimethoxyamphetamine (TMA), the α-methyl analogue of mescaline and an MAO-resistant psychedelic, is only about twice as potent as mescaline as a psychedelic in humans despite having similar serotonin receptor affinity.[13][116] This suggests that the deamination of mescaline has a relatively limited impact on its potency, compared to for example the 2C series of psychedelics.[116] Another analogue of mescaline, the deuterated isotopologue Alpha-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.[13] This is consistent with findings of about one-third of a dose of mescaline being metabolized via deamination.[13]

Elimination

Mescaline given orally is excreted 87% in urine within 24 hours and 92% in urine within 48 hours.[2][37][121][120] 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).[4][2][120] However, after the first hour, the percentage excreted as unchanged mescaline declines and the percentage excreted as TMPAA rises.[2][120] 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.[4][37][120] Other minor or trace excreted metabolites have also been observed.[4][120] In a more modern study published in 2025, mescaline was eliminated in urine 53% as unchanged mescaline and 31% as TMPAA.[101]

Mescaline was originally reported to have an elimination half-life of 6 hours based on a study conducted in the 1960s.[4][2][25][120] However, subsequent research published in the 2020s found that its half-life is actually about 3.6 hours (range 2.6–5.3 hours).[5][25][8][101] The previous higher estimate is believed to have been due to small sample numbers and collective measurement of mescaline metabolites.[25] The elimination half-life of mescaline does not appear to be dose-dependent.[5][25] TMPAA has a half-life of about 3.7 to 4.1 hours, similar to that of mescaline.[101] Mescaline has a similar half-life as LSD yet has a longer duration.[5] This is due to mescaline having slower absorption and onset rather than a longer half-life.[5][25]

Chemistry

Mescaline, also known as 3,4,5-trimethoxyphenethylamine (3,4,5-TMPEA), is a substituted phenethylamine derivative.[122][3] It is closely structurally related to the dopamine (3,4-dihydroxyphenethylamine), norepinephrine (3,4,β-trihydroxyphenethylamine), and epinephrine (3,4,β-trihydroxy-N-methylphenethylamine).[122] In contrast to the catecholamine neurotransmitters however, mescaline acts primarily on the serotonergic system rather than on the dopaminergic or adrenergic systems.[1]

Properties

A sample of pure mescaline.

The physical properties and general chemistry of mescaline have been reviewed.[37] The compound is relatively hydrophilic with low fat solubility.[3] Its predicted log P (XLogP3) is 0.7.[122]

Synthesis

Mescaline was first ever psychedelic drug synthesized by chemists.[11] Ernst Späth's 1919 total synthesis started from 3,4,5-trimethoxy­benzoyl chloride.[123] Several approaches using different starting materials have been developed since, including the following:[12][31]

Analogues

A large number of structural analogues of mescaline that act as psychedelics have been developed.[10][13] These drugs often have far greater potency than mescaline itself.[10][13] Examples include scalines like escaline, 3Cs like 3,4,5-trimethoxyamphetamine (TMA or TMA-1; α-methylmescaline), 2Cs like 2C-B, and DOx drugs like DOM, among others.[10][13] Other notable analogues of mescaline include N-methylmescaline (found in Pachycereus pringlei), trichocereine (N,N-dimethylmescaline), mescaline-FLY, and NBOMe-mescaline, among others.[10][13] Deuterated isotopologues of mescaline include α-D (α,α-dideuteromescaline), β-D (β,β-dideuteromescaline), α,β-D (α,β-dideuteromescaline), and 4-D (4-trideuteromescaline), among others.[10][13]

Natural occurrence

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.[12] 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.[12] Levels of mescaline are much lower in other Lophophora species.[12] 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.[12] Mescaline occurs in only small or trace amounts in most other cactus species in which it has been detected.[12]

Mescaline content in selected cactus species[12]
Plant source Amount of mescaline (% of dry weight)
Echinopsis lageniformis (Bolivian torch cactus, syns. Echinopsis scopulicola, Trichocereus bridgesii)[138] Average 0.56%; 0.85% in one cultivar of Echinopsis scopulicola[138][139]
Leucostele terscheckii (syns Echinopsis terscheckii, Trichocereus terscheckii)[140] 0.005–2.375%[141][142]
Lophophora williamsii (peyote)[143] 0.01–5.5%[144]
Trichocereus macrogonus var. macrogonus (Peruvian torch, syns Echinopsis peruviana, Trichocereus peruvianus)[139] 0.01–0.05%;[141] 0.24–0.81%[139]
Trichocereus macrogonus var. pachanoi (San Pedro cactus, syns Echinopsis pachanoi, Echinopsis santaensis, Trichocereus pachanoi)[145] 0.23–4.7%;[139] 0.32% under its synonym Echinopsis santaensis[139]
Trichocereus uyupampensis (syn. Echinopsis uyupampensis) 0.05%[139]
Trichocereus tacaquirensis (subsp. taquimbalensis syn. Trichocereus taquimbalensis) 0.005–2.7%[146]

As shown in the accompanying table, the concentration of mescaline in different specimens can vary largely within a single species.[12] Moreover, the concentration of mescaline within a single specimen varies as well.[147]

In peyote, mescaline constitutes about 30% of total alkaloid content.[148][149][3][150] For comparison, the alkaloid contents of other major constituents include pellotine 17%, anhalonidine 14%, anhalamine 8%, hordenine 8%, and lophophorine 5%.[148][149][3][150]

It has also reported to be found in small amounts in certain members of the bean family, Fabaceae, including Senegalia berlandieri (syn. Acacia berlandieri),[151] although these reports have been challenged and have been unsupported in any additional analyses.[12][152]

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.[153]

Biosynthesis

Biosynthesis of mescaline.

Mescaline is biosynthesized from tyrosine, which, in turn, is derived from phenylalanine by the enzyme phenylalanine hydroxylase.[1][14][12] In Lophophora williamsii (peyote), dopamine converts into mescaline in a biosynthetic pathway involving m-O-methylation and aromatic hydroxylation.[154]

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 monophenol hydroxylase 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.[153][155]

History

The stela of the cactus bearer, a piece of ancient Peruvian art depicting the San Pedro cactus.

Archaeological evidence from sites in the United States, Mexico, and Peru indicates that mescaline-containing cacti have been used for over 6,000 years.[1] Europeans recorded use of peyote in Native American religious ceremonies upon early contact with the Huichol people in Mexico.[156] Other mescaline-containing cacti such as the San Pedro cactus have a long history of use in South America, from Peru to Ecuador.[157][158][159][160] While religious and ceremonial peyote use was widespread in the Aztec 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.[161]

Arthur Heffter, the chemist who isolated mescaline and discovered its effects.

Peyote was first described by Bernardino de Sahagún in 1560.[37][31] It was first scientifically named as Peyotl zacatensis by Francisco Hernández in 1638.[31] Botanical studies of peyote began in the 1840s and the drug was listed in the Mexican pharmacopeia.[3] The first use of mescal buttons was published by John Raleigh Briggs in 1887.[3][149][162] 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.[163][162] 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.[7] The effects of mescaline in humans were first properly described by D. W. Prentiss and Francis P. Morgan in 1895.[149][32] Mescaline was first isolated and identified in 1897 by the German chemist Arthur Heffter.[3][4][164] He showed that mescaline was exclusively responsible for the psychoactive or hallucinogenic effects of peyote.[3] However, other components of peyote, such as hordenine, pellotine, and anhalinine, are also active.[3] Mescaline was first synthesized in 1919 by Ernst Späth.[4][123]

Three major books on mescaline and/or peyote were published in the mid-to-late 1920s.[11][165] These included French pharmacist Alexandre Rouhier's Le Peyotl: La Plante Qui Fait les Yeux Émerveillés (Peyote: The Plant That Fills the Eyes with Marvels) in 1927,[11][166][163][35] the German psychiatrist Kurt Beringer's Der Meskalinrausch, seine Geschichte und Erscheinungsweise (Mescaline Intoxication, its History and Manifestation) in 1927,[11][165][33] and German–American psychologist Heinrich Klüver's Mescal: The Divine Plant and Its Psychological Effects in 1928.[11][165][34]

Studies of the potential therapeutic effects of mescaline started in the 1950s.[3] It was studied as part of psychedelic-assisted psychotherapy by Walter Frederking by 1953.[37][31][167][168] Aldous Huxley's book The Doors of Perception, about his experience with mescaline, was published in 1954.[169] In 1955, English politician Christopher Mayhew took part in an experiment for BBC's Panorama, in which he ingested 400 mg of mescaline under the supervision of psychiatrist Humphry Osmond.[11][170][171][172] 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".[11][170][171][172]

The mechanism of action of mescaline, activation of the serotonin 5-HT2A receptors, became fully known in the 1990s.[3] 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.[8]

The history of mescaline was reviewed in the 2019 book Mescaline: A Global History of the First Psychedelic by cultural historian Mike Jay.[173][11]

Society and culture

Religious use

Mescaline-containing cacti are used as entheogens for religious purposes by certain Latin American and Native American and groups.[174][11] The Huichol (Wixárika) people of Mexico and the Native American Church use peyote, while the native people of Peru use the San Pedro cactus (huachuma).[174][11] The use of mescaline-containing cacti for such purposes by Mexican and South American people dates back thousands of years.[174][11] The use of peyote spread from the Huichol people into Native American tribes such as the Kiowa and Comanche in the late 1800s.[174][11]

Notable individuals

  • Arthur Heffter isolated mescaline from peyote and discovered its psychedelic effects via self-experimentation.[11][163][175] He published these findings in 1898.[11][163][175] Heffter was the first person to experience psychedelic effects with a pure psychedelic compound.[11][12]
  • Silas Weir Mitchell was one of the first to experiment with mescaline, as peyote, and published his experience in 1896.[176][177]
  • Havelock Ellis was the author of one of the first written reports to the public about an experience with mescaline (1898).[178][179][180]
  • William James was one of the first to experiment with mescaline, as peyote.[181][182] However, he took a low dose (1 peyote button), became violently ill for 2 days, and experienced no other effects.[181][182] He opted not to retry the drug.[181][182] James tried peyote in 1896 but his experience was not published until decades later.[181][182]
  • 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.[183][184] 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.[183][184] Lobsters and crabs figure in his novel Nausea (1938).[184][183]
  • Salvador Dalí has been persistently rumored to have taken psychedelics such as mescaline.[11] However, in response to these rumors, Dalí famously exclaimed "I don't do drugs. I am drugs!" in 1982.[11]
  • Antonin Artaud wrote 1947's The Peyote Dance, where he describes his peyote experiences in Mexico a decade earlier.[185][15]
  • Allen Ginsberg took peyote. Part II of his poem "Howl" was inspired by a peyote vision that he had in San Francisco.[186]
  • Aldous Huxley described his experience with mescaline in the essay "The Doors of Perception" (1954).
  • Ken Kesey took peyote prior to writing One Flew Over the Cuckoo's Nest.
  • 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.[187]
  • Jim Carroll in The Basketball Diaries described using peyote that a friend smuggled from Mexico.
  • 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.
  • Hunter S. Thompson wrote an extremely detailed account of his first use of mescaline in "First Visit with Mescalito", and it appeared in his book Songs of the Doomed, as well as featuring heavily in his novel Fear and Loathing in Las Vegas.
  • Alexander Shulgin, the prolific psychedelic chemist, said that he was first inspired to explore psychedelic compounds by a mescaline experience in 1960.[11][10][188] In 1974, Shulgin synthesized 2C-B, a psychedelic phenylethylamine derivative, structurally similar to mescaline,[189] and one of Shulgin's self-rated most important phenethylamine compounds together with mescaline, 2C-E, 2C-T-7, and 2C-T-2.[190]
  • Bryan Wynter produced Mars Ascends after trying the substance for the first time.[191]
  • George Carlin mentioned mescaline use during his youth while being interviewed in 2008.[192]
  • Carlos Santana told about his mescaline use in a 1989 Rolling Stone interview.[193]
  • Disney animator Ward Kimball described participating in a study of mescaline and peyote conducted by UCLA in the 1960s.[194]
  • Michael Cera used real mescaline for the movie Crystal Fairy & the Magical Cactus, as expressed in an interview.[195]
  • Philip K. Dick was inspired to write Flow My Tears, the Policeman Said after taking mescaline.[196]
  • 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 500 mg. He experienced a psychedelic trip that caused profound changes in his life and outlook. * Michael Pollan has described his experiences with mescaline and San Pedro cactus.[15]

Media representations

Movies

  • Fantasia (1940), with lead visualist Oskar Fischinger, may have been inspired by mescaline-induced visuals.[197]
  • Fear and Loathing in Las Vegas (1998) starring Johnny Depp and Benicio del Toro featured mescaline use.
  • The Matrix (1999) by the Wachowskis included a brief mention of mescaline.[198]
  • The Royal Tenenbaums (2001) features a character named Eli Cash (Owen Wilson) who regularly takes mescaline.
  • Crystal Fairy & the Magical Cactus (2013) starring Michael Cera and Gaby Hoffmann was about taking mescaline in the form of the San Pedro cactus.

Documentaries

  • Peyote to LSD: A Psychedelic Odyssey (2008), a History Channel documentary, covers mescaline.
  • Hamilton's Pharmacopeia (2016–2021) has multiple episodes on mescaline in the form of peyote and the San Pedro cactus.
  • How to Change Your Mind (2022) features an episode on mescaline.
See also: Medicine:Legal status of psychedelic drugs and Legal status of psychoactive cacti by country

United States

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.[199] The drug is prohibited internationally by the 1971 Convention on Psychotropic Substances.[200] 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.[201] Many states, including the state of Utah, have legalized peyote usage with "sincere religious intent", or within a religious organization, regardless of race.[202] Synthetic mescaline, but not mescaline derived from cacti, was officially decriminalized in the state of Colorado by ballot measure Proposition 122 in November 2022.[203]

While mescaline-containing cacti of the genus Echinopsis are technically controlled substances under the Controlled Substances Act, they are commonly sold publicly as ornamental plants.[204]

United Kingdom

In the United Kingdom, mescaline in purified powder form is a Class A drug. However, dried cactus can be bought and sold legally.[205]

Australia

Mescaline is considered a schedule 9 substance in Australia under the Poisons Standard (February 2020).[206] 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."[206]

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.[143] In Canada, mescaline is classified as a schedule III drug under the Controlled Drugs and Substances Act, whereas peyote is exempt.[207] In Russia, mescaline, its derivatives, and mescaline-containing plants are banned as narcotic drugs (Schedule I).[208]

Research

See also: Unsolved:Psychedelic therapy and List of investigational hallucinogens and entactogens

Mescaline has a wide array of suggested medical usage, including treatment of depression, anxiety, PTSD,[209] nicotine dependence, and alcoholism.[210][211] However, its status as a Schedule I controlled 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.[212][209][17] 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.[17][213][214][215][216][217][18][218]

See also

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 "Dark Classics in Chemical Neuroscience: Mescaline". ACS Chemical Neuroscience 9 (10): 2448–2458. October 2018. doi:10.1021/acschemneuro.8b00215. PMID 29847089. https://repositorio.uchile.cl/handle/2250/155746. 
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 2.23 2.24 2.25 2.26 2.27 "Mescaline: The forgotten psychedelic". Neuropharmacology 222. January 2023. doi:10.1016/j.neuropharm.2022.109294. PMID 36252614. 
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 3.21 3.22 3.23 "An Overview on the Hallucinogenic Peyote and Its Alkaloid Mescaline: The Importance of Context, Ceremony and Culture". Molecules (Basel, Switzerland) 28 (24): 7942. December 2023. doi:10.3390/molecules28247942. PMID 38138432. 
  4. ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 4.15 4.16 4.17 4.18 4.19 4.20 4.21 4.22 4.23 4.24 4.25 4.26 4.27 4.28 4.29 4.30 4.31 4.32 4.33 4.34 4.35 "Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions". Current Molecular Pharmacology 12 (3): 184–194. 2019. doi:10.2174/1874467211666181010154139. PMID 30318013. 
  5. ↑ 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 5.10 5.11 5.12 5.13 5.14 5.15 5.16 5.17 5.18 5.19 5.20 5.21 "Serotonergic Psychedelics: A Comparative Review of Efficacy, Safety, Pharmacokinetics, and Binding Profile". Biological Psychiatry. Cognitive Neuroscience and Neuroimaging 9 (5): 472–489. May 2024. doi:10.1016/j.bpsc.2024.01.007. PMID 38301886. 
  6. ↑ 6.0 6.1 6.2 6.3 "Dosing Psychedelics and MDMA". Disruptive Psychopharmacology. Curr Top Behav Neurosci. 56. 2022. pp. 3–21. doi:10.1007/7854_2021_270. ISBN 978-3-031-12183-8. https://www.researchgate.net/publication/355943062. 
  7. ↑ 7.00 7.01 7.02 7.03 7.04 7.05 7.06 7.07 7.08 7.09 7.10 Peyote: The Divine Cactus (2 ed.). University of Arizona Press. 1996. ISBN 978-0-8165-1654-4. https://books.google.com/books?id=p-YzEAAAQBAJ. "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." 
  8. ↑ 8.00 8.01 8.02 8.03 8.04 8.05 8.06 8.07 8.08 8.09 8.10 8.11 8.12 8.13 8.14 8.15 8.16 "Acute dose-dependent effects of mescaline in a double-blind placebo-controlled study in healthy subjects". Translational Psychiatry 14 (1). September 2024. doi:10.1038/s41398-024-03116-2. PMID 39349427. "[...] a 500 mg dose of mescaline hydrochloride produced comparable effects to 100 µg LSD base or 20 mg psilocybin dihydrate when they were compared within the same study and subjects [14]; [...] Dosages ranging from 178 to 356 mg of mescaline hydrochloride are considered moderate [36].". 
  9. ↑ 9.0 9.1 9.2 "Psychedelic Therapy: A Primer for Primary Care Clinicians-Mescaline". American Journal of Therapeutics. June 2026. doi:10.1097/MJT.0000000000002160. PMID 42299720. 
  10. ↑ 10.00 10.01 10.02 10.03 10.04 10.05 10.06 10.07 10.08 10.09 10.10 10.11 10.12 10.13 10.14 10.15 10.16 10.17 10.18 10.19 Shulgin, Alexander; Shulgin, Ann (September 1991). PiHKAL: A Chemical Love Story. Berkeley, California: Transform Press. ISBN 0-9630096-0-5. OCLC 25627628. http://www.erowid.org/library/books_online/pihkal/pihkal.shtml.  https://erowid.org/library/books_online/pihkal/pihkal096.shtml
  11. ↑ 11.00 11.01 11.02 11.03 11.04 11.05 11.06 11.07 11.08 11.09 11.10 11.11 11.12 11.13 11.14 11.15 11.16 11.17 11.18 11.19 11.20 11.21 11.22 11.23 Mescaline: A Global History of the First Psychedelic. Yale University Press. 18 June 2019. ISBN 978-0-300-23107-6. https://books.google.com/books?id=6IKVDwAAQBAJ. 
  12. ↑ 12.00 12.01 12.02 12.03 12.04 12.05 12.06 12.07 12.08 12.09 12.10 12.11 12.12 12.13 12.14 12.15 12.16 12.17 12.18 12.19 12.20 12.21 12.22 12.23 Keeper Trout & friends (2013). "Chapter 2: Mescaline and Chapter 3: Pharmacology & Metabolism of Mescaline". Trout's Notes on The Cactus Alkaloids Nomenclature, Physical properties, Pharmacology & Occurrences (Sacred Cacti Fourth Edition, Part C: Cactus Chemistry: Section 1). Mydriatic Productions/Better Days Publishing. pp. 81–104, 105–146. https://isomerdesign.com/bitnest/external/TCA/81-146. 
  13. ↑ 13.00 13.01 13.02 13.03 13.04 13.05 13.06 13.07 13.08 13.09 13.10 13.11 13.12 13.13 13.14 13.15 13.16 13.17 13.18 13.19 (in de) Phenethylamine: von der Struktur zur Funktion. Nachtschatten-Science (1 ed.). Solothurn: Nachtschatten-Verlag. 2013. pp. 677–705. ISBN 978-3-03788-700-4. OCLC 858805226. https://books.google.com/books?id=-Us1kgEACAAJ. 
  14. ↑ 14.0 14.1 "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). June 2026. doi:10.1073/pnas.2535785123. PMID 42341036. 
  15. ↑ 15.0 15.1 15.2 15.3 This Is Your Mind on Plants. New York: Penguin Press. 2021. pp. 161–248. ISBN 978-0-593-29690-5. https://books.google.com/books?id=Fxs3EAAAQBAJ. 
  16. ↑ 16.0 16.1 16.2 The Doors of Perception. Classics To Go. Otbebookpublishing. 2020. ISBN 978-3-96537-009-8. https://books.google.com/books?id=ziNdEQAAQBAJ. Retrieved 26 November 2025. 
  17. ↑ 17.0 17.1 17.2 17.3 17.4 17.5 17.6 "Finding medical value in mescaline". Nature 609 (7929): S90–S91. September 2022. doi:10.1038/d41586-022-02873-8. PMID 36171368. Bibcode: 2022Natur.609S..90B. 
  18. ↑ 18.0 18.1 "Mental Health Startup Journey Colab Aims To Develop Mescaline As An FDA-Approved Treatment For Alcohol Use Disorder". Forbes. 26 April 2022. https://www.forbes.com/sites/louismetzgeriv/2022/04/26/mental-health-startup-journey-colab-aims-to-develop-mescaline-as-an-fda-approved-treatment-for-alcohol-use-disorder/. 
  19. ↑ "Monoamine Transporter and Receptor Interaction Profiles in Vitro Predict Reported Human Doses of Novel Psychoactive Stimulants and Psychedelics". The International Journal of Neuropsychopharmacology 21 (10): 926–931. October 2018. doi:10.1093/ijnp/pyy047. PMID 29850881. 
  20. ↑ "The epidemiology of mescaline use: Pattern of use, motivations for consumption, and perceived consequences, benefits, and acute and enduring subjective effects". Journal of Psychopharmacology (Oxford, England) 36 (3): 309–320. March 2022. doi:10.1177/02698811211013583. PMID 33949246. 
  21. ↑ "The Trouble with Psychedelic Cacti: Conflicting Meanings of San Pedro and Peyote". Contemporary Drug Problems 52 (1): 104–117. 2025. doi:10.1177/00914509251318751. 
  22. ↑ "Psychedelic Trip Sitting, Dosages and Intensities: Supplementing Clinical Studies with Anecdotal Reports". Journal of Psychedelic Studies 8 (3): 313–323. 2024. doi:10.1556/2054.2024.00377. 
  23. ↑ "San Pedro: Basic Info" (in en-US). 2019-09-20. https://www.iceers.org/san-pedro-basic-info/. 
  24. ↑ "Pharmacological Properties of Psychedelics with a Special Focus on Potential Harms". Current Topics in Behavioral Neurosciences. Psychedelic Harm Reduction 77: 25–42. July 2024. doi:10.1007/7854_2024_510. ISBN 978-3-032-21106-4. PMID 39080236. https://www.researchgate.net/publication/382715259. 
  25. ↑ 25.00 25.01 25.02 25.03 25.04 25.05 25.06 25.07 25.08 25.09 25.10 "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. October 2023. doi:10.1038/s41386-023-01607-2. PMID 37231080. "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.". 
  26. ↑ 26.0 26.1 26.2 26.3 26.4 26.5 "Mescaline". American Journal of Pharmacy and the Sciences Supporting Public Health 135 (9): 319–327. September 1963. PMID 14061276. https://archive.org/details/mescaline-neff-rossi-1963. 
  27. ↑ 27.0 27.1 "Novel, unifying mechanism for mescaline in the central nervous system: electrochemistry, catechol redox metabolite, receptor, cell signaling and structure activity relationships". Oxidative Medicine and Cellular Longevity 2 (4): 181–190. 1 January 2009. doi:10.4161/oxim.2.4.9380. PMID 20716904. 
  28. ↑ 28.0 28.1 28.2 28.3 "Peyote, a Mescaline-Containing Cactus". Pharmacology and Abuse of Cocaine, Amphetamines, Ecstasy and Related Designer Drugs. Dordrecht: Springer Netherlands. 2009. pp. 227–228. doi:10.1007/978-90-481-2448-0_38. ISBN 978-90-481-2447-3. http://link.springer.com/10.1007/978-90-481-2448-0_38. 
  29. ↑ 29.0 29.1 29.2 "C". A Dictionary of Hallucinations. New York, NY: Springer New York. 2010. pp. 81–123. doi:10.1007/978-1-4419-1223-7_3. ISBN 978-1-4419-1222-0. http://link.springer.com/10.1007/978-1-4419-1223-7_3. Retrieved 26 November 2025. 
  30. ↑ 30.0 30.1 Drugs of Abuse. Oradell, NJ.: Medical Economics Books. 1989. pp. 207–239. ISBN 978-0-87489-499-8. 
  31. ↑ 31.00 31.01 31.02 31.03 31.04 31.05 31.06 31.07 31.08 31.09 31.10 31.11 31.12 31.13 31.14 31.15 31.16 "Peyote constituents: chemistry, biogenesis, and biological effects". Journal of Pharmaceutical Sciences 59 (12): 1699–1727. December 1970. doi:10.1002/jps.2600591202. PMID 5499699. Bibcode: 1970JPhmS..59.1699K. "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).". 
  32. ↑ 32.0 32.1 "Anhalonium Lewinii (Mescal Buttons). A Study of the Drug, With Especial Reference to its Physiological Action Upon Man, With Report of Experiments". Therapeutic Gazette 19: 577–585. 16 September 1895. https://collections.nlm.nih.gov/catalog/nlm:nlmuid-101751140-bk. 
  33. ↑ 33.0 33.1 (in de) Der Meskalinrausch, seine Geschichte und Erscheinungsweise. Monographien aus dem Gesamtgebiete der Neurologie und Psychiatrie. 49. Julius Springer. 1927. doi:10.1007/978-3-662-11451-3. ISBN 978-3-540-04660-8. OCLC 2536666. 
  34. ↑ 34.0 34.1 Mescal: The ʻDivine' Plant and Its Psychological Effects. K. Paul, Trench, Trubner & Company Limited. 1928. https://books.google.com/books?id=oZYaAAAAIAAJ. 
  35. ↑ 35.0 35.1 (in fr) Le Peyotl: La Plante Qui Fait les Yeux Émerveillés. Doin. 1927. https://books.google.com/books?id=aQqJHAAACAAJ. Retrieved 26 June 2026. 
  36. ↑ 36.0 36.1 36.2 36.3 36.4 36.5 "Clinical Pharmacology". Psychedelics in Psychiatry. International Review of Neurobiology. 181. London: Academic Press. 2025. pp. 99–148. doi:10.1016/bs.irn.2025.02.003. ISBN 978-0-443-34386-5. https://books.google.com/books?id=zNcmEQAAQBAJ&pg=PA99. 
  37. ↑ 37.00 37.01 37.02 37.03 37.04 37.05 37.06 37.07 37.08 37.09 37.10 37.11 37.12 37.13 "Mescaline and related compounds". Fortschritte Der Arzneimittelforschung. Progress in Drug Research. Progres Des Recherches Pharmaceutiques 11: 11–47. 1968. doi:10.1007/978-3-0348-7062-7_1. PMID 4873202. 
  38. ↑ "Altered States of Consciousness During Ceremonial San Pedro Use". The International Journal for the Psychology of Religion 33 (4): 309–331. 2022-12-05. doi:10.1080/10508619.2022.2139502. ISSN 1050-8619. 
  39. ↑ "Psychedelic drugs and perception: a narrative review of the first era of research". Reviews in the Neurosciences 32 (5): 559–571. July 2021. doi:10.1515/revneuro-2020-0094. PMID 33550787. "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. [...]". 
  40. ↑ "Serotonergic Hallucinogen-Induced Visual Perceptual Alterations". Current Topics in Behavioral Neurosciences 36: 257–282. 2018. doi:10.1007/7854_2016_461. PMID 27900674. "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.". 
  41. ↑ "Mescaline, lysergic acid diethylamide and psilocybin comparison of clinical syndromes, effects on color perception and biochemical measures". Comprehensive Psychiatry 3: 235–242. August 1962. doi:10.1016/s0010-440x(62)80024-8. PMID 13908449. 
  42. ↑ "Effect of Mescaline, Lysergic Acid Diethylamide and Psilocybin on Color Perception". Psychopharmacologia 4: 441–451. August 1963. doi:10.1007/BF00403349. PMID 14048565. 
  43. ↑ "Medical Contraindications to "Classic" Psychedelic Use". University of California, San Francisco. 22 March 2022. https://psychedelics.ucsf.edu/blog/medical-contraindications-to-classic-psychedelic-use. 
  44. ↑ "Reconsidering evidence for psychedelic-induced psychosis: an overview of reviews, a systematic review, and meta-analysis of human studies". Molecular Psychiatry 30 (3): 1223–1255. March 2025. doi:10.1038/s41380-024-02800-5. PMID 39592825. 
  45. ↑ "Drug-drug interactions involving classic psychedelics: A systematic review". Journal of Psychopharmacology (Oxford, England) 38 (1): 3–18. January 2024. doi:10.1177/02698811231211219. PMID 37982394. 
  46. ↑ "Trip-killers: a concerning practice associated with psychedelic drug use". Emergency Medicine Journal 41 (2): 112–113. January 2024. doi:10.1136/emermed-2023-213377. PMID 38123961. https://isomerdesign.com/bitnest/external/10.1136/emermed-2023-213377. 
  47. ↑ 47.0 47.1 47.2 47.3 47.4 "Safety pharmacology of acute mescaline administration in healthy participants". British Journal of Clinical Pharmacology. November 2024. doi:10.1111/bcp.16349. PMID 39587436. 
  48. ↑ Sulstarova, Adi; Scheuerlein, Luise; Monari, Silvia; Seragnoli, Federico; Gabriel, Thorens; Preller, Katrin; Böge, Kerem; Sentissi, Othman et al. (2025-08-01). "Treatment approaches and efficacy in psychedelic-induced psychosis: A systematic review". Asian Journal of Psychiatry 110. doi:10.1016/j.ajp.2025.104604. ISSN 1876-2018. https://www.sciencedirect.com/science/article/pii/S1876201825002473. 
  49. ↑ "Adverse effects of psychedelics: From anecdotes and misinformation to systematic science". Journal of Psychopharmacology (Oxford, England) 36 (3): 258–272. March 2022. doi:10.1177/02698811211069100. PMID 35107059. 
  50. ↑ Tomašić, Lea; Peček, Mirta; Petrović, Zrnka Kovačić (2024-02-01). "Substance-Induced Psychosis: a Narrative Review" (in en). Current Addiction Reports 11 (1): 55–67. doi:10.1007/s40429-023-00528-w. ISSN 2196-2952. https://doi.org/10.1007/s40429-023-00528-w. 
  51. ↑ Mauri, Massimo Carlo; Paletta, Silvia; Di Pace, Chiara (2018), Brambilla, Paolo; Mauri, Massimo Carlo; Altamura, Alfredo Carlo, eds., "Hallucinations in the Substance-Induced Psychosis" (in en), Hallucinations in Psychoses and Affective Disorders: A Clinical and Biological Approach (Cham: Springer International Publishing): pp. 57–83, doi:10.1007/978-3-319-75124-5_5, ISBN 978-3-319-75124-5, https://doi.org/10.1007/978-3-319-75124-5_5, retrieved 2026-08-03 
  52. ↑ Duraković, Din; Silić, Ante; Peitl, Vjekoslav; Vlahović, Darko; Vojnović, Daniela; Karlović, Dalibor (2022-10-23). "Acute Mescaline Intoxication Followed by Catatonia" (in en). Archives of Psychiatry Research : An International Journal of Psychiatry and Related Sciences 58 (2): 287–292. doi:10.20471/dec.2022.58.02.12. ISSN 2671-1079. https://hrcak.srce.hr/clanak/411875. 
  53. ↑ Fiorentini, Alessio; Sara Volonteri, Lucia; Dragogna, Filippo; Rovera, Chiara; Maffini, Michele; Carlo Mauri, Massimo; A. Altamura, Carlo (2011-12-01). "Substance-Induced Psychoses: A Critical Review of the Literature". Current Drug Abuse Reviews 4 (4): 228–240. https://www.ingentaconnect.com/content/ben/cdar/2011/00000004/00000004/art00004. 
  54. ↑ DiSclafani, Antonio; Hall, Richard C. W.; Gardner, Earl R. (1981-10-01). "Drug-induced psychosis: Emergency diagnosis and management". Psychosomatics 22 (10): 845–855. doi:10.1016/S0033-3182(81)73092-5. ISSN 0033-3182. https://www.sciencedirect.com/science/article/pii/S0033318281730925. 
  55. ↑ Murrie, Benjamin; Lappin, Julia; Large, Matthew; Sara, Grant (2020-05-01). "Transition of Substance-Induced, Brief, and Atypical Psychoses to Schizophrenia: A Systematic Review and Meta-analysis". Schizophrenia Bulletin 46 (3): 505–516. doi:10.1093/schbul/sbz102. ISSN 0586-7614. PMID 31618428. PMC 7147575. https://doi.org/10.1093/schbul/sbz102. 
  56. ↑ 56.0 56.1 "Toxicology and Pharmacological Interactions of Classic Psychedelics". Psychedelic Harm Reduction. Current Topics in Behavioral Neurosciences. 77. Berlin, Heidelberg: Springer Berlin Heidelberg. 2024. pp. 43–62. doi:10.1007/7854_2024_508. ISBN 978-3-032-21106-4. 
  57. ↑ 57.0 57.1 "Comparison of acute lethal toxicity of commonly abused psychoactive substances". Addiction (Abingdon, England) 99 (6): 686–696. June 2004. doi:10.1111/j.1360-0443.2004.00744.x. PMID 15139867. 
  58. ↑ 58.0 58.1 Medical Toxicology (3 ed.). Lippincott Williams & Wilkins. 2004. p. 1706. ISBN 978-0-7817-2845-4. https://books.google.com/books?id=BfdighlyGiwC&pg=PA1706. "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." 
  59. ↑ 59.0 59.1 59.2 "Fatal peyote ingestion associated with Mallory-Weiss lacerations". The Western Journal of Medicine 170 (6): 328. June 1999. PMID 10443159. PMC 1305682. https://pmc.ncbi.nlm.nih.gov/articles/PMC1305682/pdf/westjmed00321-0010.pdf. 
  60. ↑ "A mescaline associated fatality". J Anal Toxicol 9 (4): 183–184. 1985. doi:10.1093/jat/9.4.183. PMID 4033076. 
  61. ↑ "Peyote". Proceedings of the Thirtieth International Congress of Americanists, Held in Cambridge, 18-23 August 1952. London: Royal Anthropological Institute. 1952. pp. 143–148. https://books.google.com/books?id=t4sTAAAAIAAJ&q=%22underhill%22+%22peyote%22. "[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." 
  62. ↑ "Religion Among American Indians". The Annals of the American Academy of Political and Social Science 311 (1): 127–136. 1 May 1957. 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.". 
  63. ↑ "Mescaline". Dictionary of Natural Products: 254–260. 2014. 
  64. ↑ "Mescaline". Encyclopedia of Toxicology (3rd ed.). Academic Press. 2014. pp. 221–222. doi:10.1016/B978-0-12-386454-3.00747-8. ISBN 978-0-12-386455-0. "There have been no reported deaths due to the physiological effects of peyote/mescaline. Traumatic deaths have occurred secondary to hallucinations." 
  65. ↑ "The Appeal of Peyote (Lophophora Williamsii) as a Medicine". American Anthropologist 40 (4): 698–715. 1938. 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.". 
  66. ↑ "The Mescal Plant and Ceremony". Therapeutic Gazette 12 (1): 7–11. 15 January 1896. https://scholar.google.com/scholar?cluster=14937694006741592826. "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.". 
  67. ↑ "Supplementum 276: Abstracts of the 8th Annual Spring Congress of the Swiss Society of General Internal Medicine: P162. Acute subjective effects and pharmacokinetics of different doses of mescaline". Swiss Medical Weekly 154 (5): 126S. 21 May 2024. doi:10.57187/s.3896. ISSN 1424-3997. PMID 38771022. 
  68. ↑ "Studies on mescaline. VI. Therapeutic aspects of the mescaline-chlorpromazine combination". The Journal of Nervous and Mental Disease 122 (5): 463–469. November 1955. doi:10.1097/00005053-195511000-00008. PMID 13320144. "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.". 
  69. ↑ "Studies on mescaline IV: Antagonism between mescaline and chlorpromazine". Psychopharmacology. Publication No. 42. Washington: American Association for the Advancement of Science. 1956. pp. 141–144. https://scholar.google.com/scholar?cluster=10420705778026562690. "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." 
  70. ↑ "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. June 1956. doi:10.1097/00005053-195606000-00005. PMID 13406579. 
  71. ↑ Cite error: Invalid <ref> tag; no text was provided for refs named Denber1958
  72. ↑ 72.0 72.1 72.2 72.3 72.4 72.5 72.6 "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. January 2026. doi:10.1007/s40263-025-01256-7. PMID 41546846. 
  73. ↑ 73.0 73.1 "Pharmahuasca: On Phenethylamines and Potentiation". MAPS Newsletter 6 (3): 32–35. https://maps.org/wp-content/uploads/1996/04/v06n3_34-37_pharmauhsca.pdf. "[...] 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)". 
  74. ↑ 74.0 74.1 74.2 74.3 "New developments in metabolism of mescaline and related amines". Annals of the New York Academy of Sciences 96: 5–13. January 1962. doi:10.1111/j.1749-6632.1962.tb50097.x. PMID 13895218. 
  75. ↑ "PDSP Database" (in zu). https://pdsp.unc.edu/databases/pdsp.php?testFreeRadio=testFreeRadio&testLigand=mescaline&kiAllRadio=all&doQuery=Submit+Query. 
  76. ↑ "BindingDB BDBM50059891 1-amino-2-(3,4,5-trimethoxyphenyl)ethane::2-(3,4,5-trimethoxyphenyl)ethanamine::3,4,5-trimethoxybenzeneethanamine::3,4,5-trimethoxyphenethylamine::3,4,5-trimethoxyphenylethylamine::CHEMBL26687::Mescalin::Meskalin::TMPEA::US20240166618, Compound Mescaline::mescalina::mescaline::mezcalina". https://www.bindingdb.org/rwd/bind/chemsearch/marvin/MolStructure.jsp?monomerid=50059891. 
  77. ↑ 77.0 77.1 "Psychedelics and the human receptorome". PLOS ONE 5 (2). February 2010. doi:10.1371/journal.pone.0009019. PMID 20126400. Bibcode: 2010PLoSO...5.9019R. 
  78. ↑ "Receptor interaction profiles of novel N-2-methoxybenzyl (NBOMe) derivatives of 2,5-dimethoxy-substituted phenethylamines (2C drugs)". Neuropharmacology 99: 546–553. December 2015. doi:10.1016/j.neuropharm.2015.08.034. PMID 26318099. http://edoc.unibas.ch/56163/1/20170921163006_59c3cceeb8e5d.pdf. 
  79. ↑ 79.0 79.1 "Receptor interaction profiles of novel psychoactive tryptamines compared with classic hallucinogens". European Neuropsychopharmacology 26 (8): 1327–1337. August 2016. doi:10.1016/j.euroneuro.2016.05.001. PMID 27216487. http://edoc.unibas.ch/53326/1/20170117174852_587e4af45b658.pdf. 
  80. ↑ "Identification of 5-HT2A receptor signaling pathways associated with psychedelic potential". Nature Communications 14 (1). December 2023. doi:10.1038/s41467-023-44016-1. PMID 38102107. Bibcode: 2023NatCo..14.8221W. 
  81. ↑ "Functional selectivity of hallucinogenic phenethylamine and phenylisopropylamine derivatives at human 5-hydroxytryptamine (5-HT)2A and 5-HT2C receptors". The Journal of Pharmacology and Experimental Therapeutics 321 (3): 1054–1061. June 2007. doi:10.1124/jpet.106.117507. PMID 17337633. https://repositorio.uchile.cl/bitstream/handle/2250/119461/Moya_Pablo_R.pdf. 
  82. ↑ "Trace Amines and Their Receptors". Pharmacological Reviews 70 (3): 549–620. July 2018. doi:10.1124/pr.117.015305. PMID 29941461. 
  83. ↑ "In Vitro Characterization of Psychoactive Substances at Rat, Mouse, and Human Trace Amine-Associated Receptor 1". The Journal of Pharmacology and Experimental Therapeutics 357 (1): 134–144. April 2016. doi:10.1124/jpet.115.229765. PMID 26791601. https://d1wqtxts1xzle7.cloudfront.net/74120533/eae6c6e62565b82d46b4d111bbea0f77b9c2-libre.pdf?1635931703=&response-content-disposition=inline%3B+filename%3DIn_Vitro_Characterization_of_Psychoactiv.pdf&Expires=1746838268&Signature=Sy4fJ90yUhxs68314NxYsW5PAaNrBGePRu35WRR4PIF-3YC7Z~sLdnCn5wfqqbLg9bDEGdt~oW55ugMP3D3jgA0BoRI~~GOb0NQOwrtfUEQK1PQs1uuN9qg5Y1ct8z5NsABm44RgtukkwRMdU6fO7OlfIsQ68hOiFk129Ll7UYqldxD2f1xhE2fTTfsxSpb8cMCJzHn7-ItqLdwnAUPFK7WggDIjmY1kCnaHLwIxMwdJCAq8L6DYzSTg7pZkbR8qlou~GXbTPQt~gYpyZTJp5hgW-7V6K5wLlQ7Z2xE7B0f9wEfuc1W1QNafg125Tr-vvAe4LEGKXV58bnn1bpfWKw__&Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA. 
  84. ↑ "Hallucinogens". Pharmacology & Therapeutics 101 (2): 131–181. February 2004. doi:10.1016/j.pharmthera.2003.11.002. PMID 14761703. 
  85. ↑ "Dihydrobenzofuran analogues of hallucinogens. 4. Mescaline derivatives". Journal of Medicinal Chemistry 40 (19): 2997–3008. September 1997. doi:10.1021/jm970219x. PMID 9301661. 
  86. ↑ "Involvement of 5-HT receptor subtypes in the discriminative stimulus properties of mescaline". European Journal of Pharmacology 159 (1): 41–46. January 1989. doi:10.1016/0014-2999(89)90041-1. PMID 2707301. 
  87. ↑ "Mechanism of the 5-hydroxytryptamine 2A receptor-mediated facilitation of synaptic activity in prefrontal cortex". Proceedings of the National Academy of Sciences of the United States of America 104 (23): 9870–9875. June 2007. doi:10.1073/pnas.0700436104. PMID 17535909. Bibcode: 2007PNAS..104.9870B. 
  88. ↑ "Serotonin 5-HT2C Receptor Signaling Analysis Reveals Psychedelic Biased Agonism". ACS Chemical Neuroscience 16 (19): 3899–3914. October 2025. doi:10.1021/acschemneuro.5c00647. PMID 40944639. 
  89. ↑ "Psychotomimetic drugs and brain 5-hydroxytryptamine metabolism". Biochemical Pharmacology (Elsevier BV) 19: 1181–1188. 1970. doi:10.1016/0006-2952(70)90378-3. ISSN 0006-2952. 
  90. ↑ "Studies on the concurrent behavioral and neurochemical effects of psychoactive drugs using the push-pull cannula". The Journal of Pharmacology and Experimental Therapeutics 181 (3): 387–398. June 1972. doi:10.1016/S0022-3565(25)29220-5. PMID 5033008. https://jpet.aspetjournals.org/content/181/3/387.long. 
  91. ↑ "Mescaline elicits behavioral effects in cats by an action at both serotonin and dopamine receptors". European Journal of Pharmacology 96 (1–2): 151–154. December 1983. doi:10.1016/0014-2999(83)90544-7. PMID 6581976. 
  92. ↑ "Cardiac effects of ephedrine, norephedrine, mescaline, and 3,4-methylenedioxymethamphetamine (MDMA) in mouse and human atrial preparations". Naunyn-Schmiedeberg's Archives of Pharmacology 396 (2): 275–287. February 2023. doi:10.1007/s00210-022-02315-2. PMID 36319858. 
  93. ↑ 93.0 93.1 "The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain". European Journal of Pharmacology 559 (2–3): 132–137. March 2007. doi:10.1016/j.ejphar.2006.11.075. PMID 17223101. 
  94. ↑ "Behavioral and neurochemical pharmacology of six psychoactive substituted phenethylamines: mouse locomotion, rat drug discrimination and in vitro receptor and transporter binding and function". Psychopharmacology (Berl) 231 (5): 875–888. March 2014. doi:10.1007/s00213-013-3303-6. PMID 24142203. 
  95. ↑ 95.0 95.1 "Fluorine in psychedelic phenethylamines". Drug Testing and Analysis 4 (7–8): 577–590. 2012. doi:10.1002/dta.413. PMID 22374819. http://bitnest.ca/external.php?id=%257DbxUgXXCNAUj%257E%257E%2507. 
  96. ↑ "Scalines: novel mescaline analogues targeting 5-HT2A, 5-HT2B, 5-HT2C, and 5-HT1A receptors". Neuroscience Applied 5. 2026. doi:10.1016/j.nsa.2025.106565. 
  97. ↑ "#157 TMA - 3,4,5-TRIMETHOXYAMPHETAMINE". PiHKAL: A Chemical Love Story. Erowid.org. https://www.erowid.org/library/books_online/pihkal/pihkal157.shtml. 
  98. ↑ "Studies of the relationship between molecular structure and hallucinogenic activity". Pharmacology, Biochemistry, and Behavior 24 (2): 335–340. February 1986. doi:10.1016/0091-3057(86)90362-x. PMID 3952123. 
  99. ↑ "Anaesthetic implications of psilocybin and lysergic acid diethylamide: what is old is now new: A narrative review on psychedelics and anaesthesia". Eur J Anaesthesiol 42 (5): 430–434. May 2025. doi:10.1097/EJA.0000000000002138. PMID 39967455. "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". 
  100. ↑ "Psychedelic therapy and postpartum depression: priorities and prospects". Ther Adv Psychopharmacol 16. 2026. doi:10.1177/20451253251408280. PMID 41816502. "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.". 
  101. ↑ 101.00 101.01 101.02 101.03 101.04 101.05 101.06 101.07 101.08 101.09 101.10 101.11 101.12 "Pharmacokinetics, Pharmacodynamics, and Urinary Recovery of Oral Mescaline Hydrochloride in Healthy Participants". Clinical Pharmacokinetics 64 (10): 1495–1506. July 2025. doi:10.1007/s40262-025-01544-x. PMID 40658345. "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.". 
  102. ↑ "The structural diversity of psychedelic drug actions revealed". Nature Communications 16 (1). March 2025. doi:10.1038/s41467-025-57956-7. PMID 40108183. Bibcode: 2025NatCo..16.2734G. 
  103. ↑ "Structures of Hallucinogenic and Non-Hallucinogenic Analogues of the 5-HT2A Receptor Reveals Molecular Insights into Signaling Bias". University of North Carolina at Chapel Hill Department of Pharmacology Research Retreat September 16th, 2022 – William and Ida Friday Center. September 2022. https://www.med.unc.edu/pharm/wp-content/uploads/sites/930/2022/07/COMPLETE-PHARM-RETREAT-PROGRAM-2022-UPDATE.pdf#page=37. 
  104. ↑ 104.0 104.1 "A molecular analysis of substituted phenylethylamines as potential microtubule targeting agents through in silico methods and in vitro microtubule-polymerization activity". Sci Rep 13 (1): 14406. September 2023. doi:10.1038/s41598-023-41600-9. PMID 37658096. "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.". 
  105. ↑ "Mescaline as a mitotic spindle inhibitor". Nature 260 (5547): 138–139. March 1976. doi:10.1038/260138a0. PMID 1256554. 
  106. ↑ 106.0 106.1 Cite error: Invalid <ref> tag; no text was provided for refs named DrugBank
  107. ↑ Cite error: Invalid <ref> tag; no text was provided for refs named OhLeitchAxelrod1967
  108. ↑ "Mescaline effects on rat behavior and its time profile in serum and brain tissue after a single subcutaneous dose". Psychopharmacology (Berl) 196 (1): 51–62. January 2008. doi:10.1007/s00213-007-0926-5. PMID 17922234. 
  109. ↑ 109.0 109.1 109.2 "Alteration by pretreatment with iproniazid and an inactive mescaline analogue of a behaviour change induced by mescaline". Nature 216 (5111): 196–197. October 1967. doi:10.1038/216196a0. PMID 6057240. Bibcode: 1967Natur.216..196S. 
  110. ↑ "The metabolism of mescaline-14-C in rats". Biochemical Pharmacology 16 (6): 963–970. June 1967. doi:10.1016/0006-2952(67)90268-7. PMID 6040403. 
  111. ↑ "Human plasma monoamine oxidase. 1. Purification and identification". The Journal of Biological Chemistry 240 (5): 2003–2010. May 1965. doi:10.1016/S0021-9258(18)97417-X. PMID 5888801. 
  112. ↑ "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. June 2025. doi:10.1007/s00204-025-04010-6. PMID 40064698. "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.". 
  113. ↑ "Substrates and inhibitors of dopamine-beta-oxidase". Biochimica et Biophysica Acta 64: 125–134. October 1962. doi:10.1016/0006-3002(62)90765-5. PMID 14023834. 
  114. ↑ "Interactions of amphetamine analogs with human liver CYP2D6". Biochemical Pharmacology 53 (11): 1605–1612. June 1997. doi:10.1016/S0006-2952(97)00014-2. PMID 9264312. 
  115. ↑ 115.0 115.1 115.2 "Unraveling the In Vitro Toxicity Profile of Psychedelic 2C Phenethylamines and Their N-Benzylphenethylamine (NBOMe) Analogues". Pharmaceuticals (Basel, Switzerland) 16 (8): 1158. August 2023. doi:10.3390/ph16081158. PMID 37631071. 
  116. ↑ 116.0 116.1 116.2 116.3 116.4 "Structure-activity relationships of phenethylamine hallucinogens". Journal of Pharmaceutical Sciences 70 (8): 839–849. August 1981. doi:10.1002/jps.2600700802. PMID 7031221. Bibcode: 1981JPhmS..70..839N. https://bitnest.netfirms.com/external/10.1002/jps.2600700802. 
  117. ↑ 117.0 117.1 117.2 "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. May 1995. doi:10.1248/bpb.18.696. PMID 7492985. 
  118. ↑ 118.0 118.1 "Discriminative stimulus properties of mescaline: mescaline or metabolite?". Pharmacology, Biochemistry, and Behavior 3 (1): 109–114. 1975. doi:10.1016/0091-3057(75)90088-x. PMID 1129346. 
  119. ↑ Slotta, K. H., & Muller, J. (1936). On the catabolism of mescaline and mescaline-like substances in the organism. Hoppe-Seyler's Z., 238, 14–22. https://scholar.google.com/scholar?cluster=12893490063723146887 https://scholar.google.com/scholar?cluster=12713934913707858633
  120. ↑ 120.0 120.1 120.2 120.3 120.4 120.5 120.6 120.7 "Metabolic fate of mescaline in man". Psychopharmacologia 9 (1): 48–63. 1966. doi:10.1007/BF00427703. PMID 5989103. 
  121. ↑ "Correlating the metabolic stability of psychedelic 5-HT₂A agonists with anecdotal reports of human oral bioavailability". Neurochemical Research 39 (10): 2018–2023. October 2014. doi:10.1007/s11064-014-1253-y. PMID 24519542. "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].". 
  122. ↑ 122.0 122.1 122.2 PubChem. "Mescaline". https://pubchem.ncbi.nlm.nih.gov/compound/4076. 
  123. ↑ 123.0 123.1 "Über dieAnhalonium-Alkaloide I. Anhalin und Mezcalin" (in de). Monatshefte für Chemie und Verwandte Teile Anderer Wissenschaften 40 (2): 129–154. February 1919. doi:10.1007/BF01524590. ISSN 0343-7329. 
  124. ↑ "Über β-Phenyl-äthylamine, I. Mitteil.: Mezcalin und mezcalin-ähnliche Substanzen". Berichte der Deutschen Chemischen Gesellschaft (A and B Series) 63 (11): 3029–3044. 1930. doi:10.1002/cber.19300631117. 
  125. ↑ "Preparation of Mescaline from Eucalypt Lignin". Australian Journal of Pharmacy 49: 529. 1964. https://www.erowid.org/archive/rhodium/chemistry/mescalyptus.html. 
  126. ↑ "Über neue und über verbesserte Wege zum Aufbau von pharmakologisch wichtigen Aminen VI. Über Synthesen des Meskalins". Archiv der Pharmazie 270 (7): 410–413. 1932. doi:10.1002/ardp.19322700709. 
  127. ↑ "An Improved Synthesis of Mescaline". Journal of the American Chemical Society 73 (3): 1353. 1951. doi:10.1021/ja01147a505. Bibcode: 1951JAChS..73Q1353B. 
  128. ↑ "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. 1938. doi:10.1002/cber.19380711022. 
  129. ↑ "Synthesis of Phenethylamine Derivatives as Hallucinogen". Japanese Journal of Toxicology and Environmental Health 38 (6): 571–580. 1992. doi:10.1248/jhs1956.38.571. https://nootropicsfrontline.com/wp-content/uploads/2021/07/wiki_ohshita1992.pdf. Retrieved 20 June 2014. 
  130. ↑ "Über die Reduktion von β-Nitrostyrolen mit Lithiumaluminiumhydrid". Helvetica Chimica Acta 33 (4): 912–916. 1950. doi:10.1002/hlca.19500330420. Bibcode: 1950HChAc..33..912E. 
  131. ↑ "Über β-Phenyl-äthylamine.III. Mitteilung: Neue Darstellung von Mescalin". Journal für Praktische Chemie 137 (9–12): 339–350. 1933. doi:10.1002/prac.19331370907. 
  132. ↑ "The Reduction of Phenolic β-Nitrostyrenes by Lithium Aluminum Hydride". Journal of the American Chemical Society 72 (6): 2781–2782. 1950. doi:10.1021/ja01162a521. Bibcode: 1950JAChS..72.2781R. 
  133. ↑ "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. 1934. doi:10.1002/cber.19340670430. 
  134. ↑ 134.0 134.1 "A New Synthesis of Mescaline". Journal of the American Chemical Society 71 (11): 5495–5496. 1951. doi:10.1021/ja01155a562. Bibcode: 1951JAChS..73.5495T. 
  135. ↑ "Über die Darstellung des Oxymezcalins und Mezcalins 2. Mitteilung". Archiv der Pharmazie 285 (7): 323–326. 1952. doi:10.1002/ardp.19522850704. 
  136. ↑ Natural Products: A Laboratory Guide 2nd Ed. San Diego: Academic Press, Inc.. 1991. pp. 232–235. ISBN 978-0-12-370551-8. https://books.google.com/books?id=B7P8HQimBAIC&pg=PA243. 
  137. ↑ "Notiz über eine neue Synthese von Mezcalin, N-Methyl- und N-Dimethylmezcalin". Helvetica Chimica Acta 35 (5): 1577–1581. 1952. doi:10.1002/hlca.19520350519. 
  138. ↑ 138.0 138.1 "Could Synthetic Mescaline Protect Declining Peyote Populations?" (in en-US). 2021-08-02. https://chacruna.net/synthetic_mescaline_protect_declining_peyote_populations/. 
  139. ↑ 139.0 139.1 139.2 139.3 139.4 139.5 "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. September 2010. doi:10.1016/j.jep.2010.07.021. PMID 20637277. 
  140. ↑ "Cardon Grande (Echinopsis terscheckii)". Desert-tropicals.com. http://www.desert-tropicals.com/Plants/Cactaceae/Echinopsis_terscheckii.html. 
  141. ↑ 141.0 141.1 "Partial List of Alkaloids in Trichocereus Cacti". Thennok.org. http://www.thenook.org/archives/tek/alklist.htm. 
  142. ↑ "Forbidden Fruit Archives". http://entheogen.netfirms.com/articles/articles/Narcotic_Cacti.html. 
  143. ↑ 143.0 143.1 Drug Identification Bible. Grand Junction, CO: Amera-Chem, Inc.. 2007. ISBN 978-0-9635626-9-2. 
  144. ↑ "Mescaline Concentrations in Three Principal Tissues of Lophophora williamsii (Cactaceae): Implications for Sustainable Harvesting Practices". Haseltonia (Elsevier BV) 131 (2): 34–42. 2015. doi:10.2985/026.020.0107. Bibcode: 2015Hasel..20...34K. 
  145. ↑ "Cactus alkaloids. XIX. Crystallization of mescaline HCl and 3-methoxytyramine HCl from Trichocereus pachanoi". Lloydia 36 (4): 416–418. December 1973. PMID 4773270. http://catbull.com/alamut/Bibliothek/1973_d.m._crosby_8158_1.pdf. Retrieved 13 December 2013. 
  146. ↑ "Mescaline in Trichocereus" (in en-AU). https://www.themescalinegarden.com/mescaline-in-trichocereus. 
  147. ↑ "Validation and exploratory application of a simple, rapid and economical procedure (MESQ) for the quantification of mescaline in fresh cactus tissue and aqueous cactus extracts". PhytoChem & BioSub Journal. 2022-04-03. doi:10.5281/zenodo.6409376. https://zenodo.org/records/6409376. 
  148. ↑ 148.0 148.1 "The chemistry of peyote alkaloids". Lloydia 36 (1): 9–35. March 1973. PMID 4593882. https://bibliography.maps.org/resources/download/13922. 
  149. ↑ 149.0 149.1 149.2 149.3 "Early peyote research an interdisciplinary study". Economic Botany 28 (4): 353–390. 1973. doi:10.1007/BF02862854. ISSN 0013-0001. "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.". 
  150. ↑ 150.0 150.1 "Biosynthetic studies on mescaline and related cactus alkaloids". Acta Pharmaceutica Suecica 8 (3): 275–302. June 1971. PMID 5560272. 
  151. ↑ "Chemistry of Acacia's from South Texas". Texas A&M Agricultural Research & Extension Center at Uvalde. http://uvalde.tamu.edu/pdf/chemtdaf.pdf. 
  152. ↑ Keeper Trout (16 January 2015). "Acacia species with data conflicts". sacredcacti.com. https://sacredcacti.com/blog/acacia/. 
  153. ↑ 153.0 153.1 "Catecholamies are active compounds in plants". Plant Science 172 (3): 433–440. March 2007. doi:10.1016/j.plantsci.2006.10.013. Bibcode: 2007PlnSc.172..433K. 
  154. ↑ Medicinal Natural Products: A Biosynthetic Approach. United Kingdom: John Wiley & Sons. 2009. pp. 335–336. ISBN 978-0-471-49641-0. 
  155. ↑ "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. 1976. doi:10.1093/schbul/2.1.90. PMID 779022. 
  156. ↑ Treatise on the Heathen Superstitions that Today Live Among the Indians Native to this New Spain, 1629. University of Oklahoma Press. 1984. ISBN 978-0-8061-2031-7. 
  157. ↑ "Use of psychoactive and stimulant plants on the south coast of Peru from the Early Intermediate to Late Intermediate Period". Journal of Archaeological Science 148. 2022-12-01. doi:10.1016/j.jas.2022.105688. ISSN 0305-4403. Bibcode: 2022JArSc.14805688S. 
  158. ↑ "Traditional medicinal plant use in Northern Peru: tracking two thousand years of healing culture". Journal of Ethnobiology and Ethnomedicine 2. November 2006. doi:10.1186/1746-4269-2-47. PMID 17090303. 
  159. ↑ "Traditional medicine applied by the Saraguro yachakkuna: a preliminary approach to the use of sacred and psychoactive plant species in the southern region of Ecuador". Journal of Ethnobiology and Ethnomedicine 10. February 2014. doi:10.1186/1746-4269-10-26. PMID 24565054. 
  160. ↑ "The oldest archeological data evidencing the relationship of Homo sapiens with psychoactive plants: A worldwide overview". Journal of Psychedelic Studies 3 (2): 63–80. 2019-06-01. doi:10.1556/2054.2019.008. 
  161. ↑ "Prehistoric peyote use: alkaloid analysis and radiocarbon dating of archaeological specimens of Lophophora from Texas". Journal of Ethnopharmacology 101 (1–3): 238–242. October 2005. doi:10.1016/j.jep.2005.04.022. PMID 15990261. 
  162. ↑ 162.0 162.1 ""Muscale Buttons"—Physiological Effects—Personal Experience". The Medical Register 1: 267–268. 8 April 1887. https://bibliography.maps.org/resources/download/12878. 
  163. ↑ 163.0 163.1 163.2 163.3 Daniel M. Perrine (2001). "Visions of the Night Western Medicine Meets Peyote 1887-1899". The Heffter Review of Psychedelic Research 2: 6–52. https://www.heffter.org/wp-content/uploads/2020/04/chap2.pdf. 
  164. ↑ "Arthur Heffter". Character Vaults. Erowid.org. http://www.erowid.org/culture/characters/heffter_arthur/heffter_arthur.shtml. 
  165. ↑ 165.0 165.1 165.2 "[Chapter 14: A Brief History of Psychedelics"]. Food of the Gods: The Search for the Original Tree of Knowledge: a Radical History of Plants, Drugs and Human Evolution. Rider. 1999. pp. 223–245. ISBN 978-0-7126-7038-8. https://alquimiahealingarts.com/wp-content/uploads/2020/03/Food-Of-The-Gods-Terence-Mckenna.pdf#page=117. 
  166. ↑ "History of the administration of psychedelics in France". Frontiers in Psychology 14. 2023. doi:10.3389/fpsyg.2023.1131565. PMID 37744588. "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). [...]". 
  167. ↑ "Über die Verwendung von Rauschdrogen (Meskalin und Lysergsäurediaethylamid) in der Psychotherapie" (in de). Psyche (Stuttg) 7 (6): 342–364. September 1953. PMID 13112311. https://elibrary.utb.de/doi/10.5555/ps-7-6-342. 
  168. ↑ "Intoxicant drugs (mescaline and lysergic acid diethylamide) in psychotherapy". The Journal of Nervous and Mental Disease 121 (3): 262–266. March 1955. doi:10.1097/00005053-195503000-00010. PMID 14381913. 
  169. ↑ "History of Psychedelics: An Overview". South Atlantic Quarterly 124 (2): 295–305. 1 April 2025. doi:10.1215/00382876-11626609. ISSN 0038-2876. 
  170. ↑ 170.0 170.1 "Introduction to the chemistry and pharmacology of psychedelic drugs". Australian Journal of Chemistry 76 (5): 236–257. 17 July 2023. doi:10.1071/CH23050. ISSN 0004-9425. "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]". 
  171. ↑ 171.0 171.1 "The History Hour, Why a British MP was filmed taking mescaline". 15 May 2021. https://www.bbc.co.uk/programmes/w3ct1z6v. 
  172. ↑ 172.0 172.1 "Panorama: The Mescaline Experiment". February 2005. http://sotcaa.net/hiddenarchive/mayhew01.html. 
  173. ↑ "The Fascinating History of Mescaline, the OG Psychedelic". VICE. 15 May 2019. https://www.vice.com/en/article/history-of-mescaline-mike-jay/. 
  174. ↑ 174.0 174.1 174.2 174.3 "Anthropology of Psychedelics". Anthropology of Consciousness 36 (2). 2025. doi:10.1111/anoc.70002. ISSN 1053-4202. 
  175. ↑ 175.0 175.1 "Ueber Pellote: Beiträge zur chemischen und pharmakologischen Kenntniss der Cacteen Zweite Mittheilung" (in de). Archiv für Experimentelle Pathologie und Pharmakologie 40 (5–6): 385–429. 1898. doi:10.1007/BF01825267. ISSN 0028-1298. 
  176. ↑ "The experimentation of S. Weir Mitchell with mescal". Neurology 39 (2 Pt 1): 303–304. February 1989. doi:10.1212/wnl.39.2.303. PMID 2644583. 
  177. ↑ "Remarks on the Effects of Anhelonium Lewinii (the Mescal Button)". British Medical Journal 2 (1875): 1625–1629. December 1896. doi:10.1136/bmj.2.1875.1625. PMID 20756623. 
  178. ↑ "Mescal: A New Artificial Paradise". The Contemporary Review. LXXIII. 1898. https://archive.org/stream/contemporaryrev23unkngoog#page/n142/mode/2up. 
  179. ↑ Rudgley R (1993). "VI". The Alchemy of Culture: Intoxicants in Society. British Museum Press. ISBN 978-0-7141-1736-2. 
  180. ↑ Drugs of Abuse (Second ed.). Los Angeles: Practice Management Information Corp. 1997. ISBN 978-1-57066-053-5. 
  181. ↑ 181.0 181.1 181.2 181.3 "A Divine Intoxicant". 1 November 1929. https://www.theatlantic.com/magazine/archive/1929/11/a-divine-intoxicant/650792/. 
  182. ↑ 182.0 182.1 182.2 182.3 "James's Encounter with Mescal, Mescaline, and Peyote". William James Studies (William James Society) 18 (2): 85–90. 2023. ISSN 19338295. 
  183. ↑ 183.0 183.1 183.2 "Sartre's Bad Trip by Mike Jay". 2019-08-21. https://www.theparisreview.org/blog/2019/08/21/sartres-bad-trip/. 
  184. ↑ 184.0 184.1 184.2 "Mescaline left Jean Paul Sartre in the grip of lobster madness". The Sunday Times. 22 November 2009. https://www.thetimes.com/comment/register/article/mescaline-left-jean-paul-sartre-in-the-grip-of-lobster-madness-mkgqxxcln2k. 
  185. ↑ "Patti Smith Channels French Poet Antonin Artaud on Peyote" (in en-US). Rolling Stone. 2019-05-20. https://www.rollingstone.com/music/music-news/watch-patti-smith-channel-french-poet-antonin-artaud-on-peyote-837533/. Retrieved 2022-04-03. 
  186. ↑ Jane Kramer (1968-08-10). "The Father of Flower Power" (in en-US). The New Yorker. http://www.newyorker.com/magazine/1968/08/17/paterfamilias-i. Retrieved 2022-04-03. 
  187. ↑ Nikotyna, alkohol, kokaina, peyotl, morfina, eter+ appendix.. Warsaw: Drukarnia Towarzystwa Polskiej Macierzy Szkolnej. 1932. https://pl.wikisource.org/wiki/Nikotyna_Alkohol_Kokaina_Peyotl_Morfina_Eter_%2B_Appendix. 
  188. ↑ "Alexander Shulgin: why I discover psychedelic substances". Mexico. 1996. https://www.youtube.com/watch?v=QD260LPqHKA&t=3m18s. 
  189. ↑ "Acute Pharmacological Effects of 2C-B in Humans: An Observational Study" (in English). Frontiers in Pharmacology 9. 2018. doi:10.3389/fphar.2018.00206. PMID 29593537. 
  190. ↑ "Mescaline" (in en-US). Psychedelic Science Review. 2019-12-02. https://psychedelicreview.com/compound/mescaline/. 
  191. ↑ 100 Ideas that Changed Art.. London: Laurence King Publishing. 2012. 
  192. ↑ "George Carlin's Last Interview". Psychology Today. 23 June 2008. http://www.psychologytoday.com/blog/brainstorm/200806/george-carlins-last-interview?page=4. 
  193. ↑ "Dazed and Confused: 10 Classic Drugged-Out Shows". Rolling Stone. 1989. https://www.rollingstone.com/music/pictures/10-classic-drugged-out-performances-from-santana-to-green-day-20130606/1-santana-at-woodstock-1969-mescaline-0973315. "Santana at Woodstock, 1969 - Mescaline". 
  194. ↑ "Ward Kimball's Final Farewell". cartoonician.com. 4 March 2016. http://cartoonician.com/ward-kimballs-final-farewell/. 
  195. ↑ "Michael Cera Took Drugs On-Camera". Huffington Post. 10 July 2013. http://www.huffingtonpost.com/2013/07/10/michael-cera-drugs-mescaline-crystal-fairy_n_3575056.html. 
  196. ↑ "FLOW MY Tears". www.philipkdickfans.com. http://www.philipkdickfans.com/mirror/websites/pkdweb/FLOW%20MY%20TEARS.HTM. 
  197. ↑ 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
  198. ↑ "The Matrix Quotes". https://www.imdb.com/title/tt0133093/quotes/?item=qt0324290. "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." 
  199. ↑ United States Department of Justice (2026-07-01). "Drug Scheduling". http://www.usdoj.gov/dea/pubs/scheduling.html. 
  200. ↑ "List of psychotropic substances under international control". International Narcotics Control Board. http://www.incb.org/pdf/e/list/green.pdf. 
  201. ↑ "City of Boerne v. Flores". Federal Judicial Center. https://www.fjc.gov/history/cases/cases-that-shaped-the-federal-courts/city-boerne-v-flores. 
  202. ↑ "State v. Mooney". utcourts.gov. http://www.utcourts.gov/opinions/supopin/mooney062204.htm. 
  203. ↑ "Colorado Proposition 122, Decriminalization and Regulated Access Program for Certain Psychedelic Plants and Fungi Initiative (2022)". https://ballotpedia.org/Colorado_Proposition_122,_Decriminalization_and_Regulated_Access_Program_for_Certain_Psychedelic_Plants_and_Fungi_Initiative_(2022). 
  204. ↑ Veterinary Toxicology: Basic and Clinical Principles (Third ed.). Academic Press. 2018. pp. 363–390. ISBN 978-0-12-370467-2. 
  205. ↑ "2007 U.K. Trichocereus Cacti Legal Case Regina v. Saul Sette". Erowid.org. June 2007. http://www.erowid.org/plants/cacti/cacti_law2.shtml. 
  206. ↑ 206.0 206.1 Poisons Standard February 2020. comlaw.gov.au
  207. ↑ "Justice Laws Search". laws-lois.justice.gc.ca. http://laws-lois.justice.gc.ca/Search/Search.aspx?txtS3archA11=mescaline&txtT1tl3=%22Controlled+Drugs+and+Substances+Act%22&h1ts0n1y=0&ddC0nt3ntTyp3=Acts.. 
  208. ↑ "Постановление Правительства РФ от 30.06.1998 N 681 "Об утверждении перечня наркотических средств, психотропных веществ и их прекурсоров, подлежащих контролю в Российской Федерации" (с изменениями и дополнениями) - ГАРАНТ". http://base.garant.ru/12112176/. 
  209. ↑ 209.0 209.1 "Naturalistic Use of Mescaline Is Associated with Self-Reported Psychiatric Improvements and Enduring Positive Life Changes". ACS Pharmacology & Translational Science 4 (2): 543–552. April 2021. doi:10.1021/acsptsci.1c00018. PMID 33860184. 
  210. ↑ "Could LSD treat alcoholism?". ABC News. 9 March 2012. https://abcnews.go.com/blogs/health/2012/03/09/could-lsd-treat-alcoholism/. 
  211. ↑ "The Ethnopharmacological Use of Mescaline for Psychiatric Disorders: A Systematic Review". International Journal of Molecular Sciences 27 (7): 3081. March 2026. doi:10.3390/ijms27073081. PMID 41977267. 
  212. ↑ "Mescaline is Resurgent (Yet Again) As a Potential Medicine" (in en-US). 2021-07-08. https://www.lucid.news/mescaline-is-resurgent-yet-again-as-a-potential-medicine/. 
  213. ↑ "Psychedelic Drug Development Tracker". Psychedelic Alpha. https://psychedelicalpha.com/resources/psychedelic-drug-development-tracker/. 
  214. ↑ "Hitting the Reset Button: Ceremonial Use of Peyote and Experiences of Personal Change". Journal of Drug Issues 56 (1): 150–170. 2026. doi:10.1177/00220426241274737. ISSN 0022-0426. 
  215. ↑ "Mescaline HCl". 2 August 2022. https://adisinsight.springer.com/drugs/800069596. 
  216. ↑ "BMND 06". 28 April 2025. https://adisinsight.springer.com/drugs/800067963. 
  217. ↑ "Biomind Labs". 28 September 2025. https://adisinsight.springer.com/drugs/800064976. 
  218. ↑ "Journey Colab Looks to Mescaline for Treating Alcohol Use Disorder". 17 May 2022. https://www.lucid.news/journey-colab-looks-to-mescaline-for-treating-alcohol-use-disorder/. 



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