Mescaline

DEA Schedule I Controlled Substance -> Hallucinogenic substances

Pharmaceuticals -> Synthetic Cannabinoids or Psychoactive Compounds

Moderately soluble in water; soluble in chloroform, benzene. Practically insoluble in ether, petroleum ether.

Soluble in ethanol; slightly soluble in lignin

Needles, mp 181 °C. Soluble in water, alcohol /Hydrochloride/

Prisms, mp 183-186 °C. Soluble in hot water, methanol; sparingly soluble in cold water, ethanol. /Sodium dihydrate/

Crystals, mp 158 °C /Acid sulfate/

Needles from aqueous alcohol, mp 121 °C. Very soluble in alcohol, ether /N-Benzoylmescaline/

For more Other Experimental Properties (Complete) data for 3,4,5-TRIMETHOXYPHENETHYLAMINE (7 total), please visit the HSDB record page.

Warning

H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]

P264, P270, P301+P317, P330, and P501 (click each P-code to see the statement)

The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.

Schedule I shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. ... Hallucinogenic substances. Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation, which contains any quantity of the following hallucinogenic substances, or which contains any of its salts, isomers, and salts of isomers whenever the existence of such salts, isomers, and salts of isomers is possible within the specific chemical designation (for purposes of this paragraph only, the term "isomer" includes the optical, position and geometric isomers): Mescaline, DEA Code: 7381.

Mescaline (25 mg/kg; 66 muc/kg) was injected (ip) in mice 45 min before chlorpromazine (2.5, 5, 15 mg/kg), thioridazine (10, 30, 45 mg/kg), or chlorpromazine-sulfoxide (15 mg/kg). Excitement, agitation, slight increase in ventilation and occasional head-shaking were seen 30 min after mescaline and continued for 30-45 min thereafter; locomotor activity and the number of scratching events were significantly increased during this period. chlorpromazine (2.5, 5, 15 mg/kg) and thioridazine (10, 30, 45 mg/kg) partially or completely blocked mescaline-induced gross behavior; chlorpromazine-sulfoxide (15 mg/kg) was not effective. Increased scratching responses and locomotor activity induced by mescaline were antagonized by all doses of chlorpromazine and thioridazine; at higher doses, both chlorpromazine (7.5, 15 mg/kg) and thioridazine (45 mg/kg) induced cataleptic-like condition and marked hypothermia. Tissue levels of mescaline, examined 3 hr after its administration, were increased by all doses of chlorpromazine and a higher dose of thioridazine (45 mg/kg); chlorpromazine-sulfoxide and lower doses of thioridazine had no effect.

/HUMAN EXPOSURE STUDIES/ The psychological, neuropsychological, and neurometabolic effects of the hallucinogenic agent mescaline were investigated in 12 normal men who were volunteers. Mescaline produced an acute psychotic state 3 1/2-4 hr after drug intake, as measured by the Brief Psychiatric Rating Scale (BPRS) and Paranoid Depression Scale (PDS). The Assessment of Altered States of Consciousness (APZ) questionnaire revealed specific effects of mescaline in the visual system. Neuropsychological effects were studied with a face/nonface decision task with known right-hemisphere advantage, in which mescaline induced a decrease of functioning of the right hemisphere. In functional brain imaging using single photon emission computed tomography (SPECT), mescaline produced a "hyperfrontal" pattern with an emphasis on the right hemisphere, which was correlated with mescaline-induced psychotic psychopathology. These findings question the validity of the concept of hypofrontality as an explanation for schizophrenic symptomatology. The study of psychoactive substances under controlled laboratory conditions has the methodological advantage of intraindividual control, and hence, minimal variability of data.

/SIGNS AND SYMPTOMS/ Mescaline produces hallucinations and symptoms of CNS and sympathetic stimulation. Mild elevations in pulse, blood pressure, respiratory rate, and temperature may be noted. Nausea and vomiting commonly precede the hallucinogenic effects. The clinical presentation may mimic an anticholinergic syndrome. Mydriasis, salivation, and blurred vision are common. Palpitations may occur. Nausea and vomiting, abdominal cramps, and diarrhea are common. GI effects may persist for several days. Antidiuretic effects and polyuria have been noted. Headaches, dizziness, ataxia, tremors, weakness, hallucinations, and paresthesias have been noted. Anxiety auditory and visual hallucinations, emotional instability, paranoia, and flashbacks may occur. Piloerection, flushing, and diaphoresis can occur. Shivering, tremors, increased muscle tone, hyperreflexia, and weakness may occur.

/SIGNS AND SYMPTOMS/ The clinical effects usually occur approximately one hour following ingestions, and begin with a gastrointestinal phase, predominantly nausea and vomiting, and may be accompanied by diaphoresis, hypertension, mydriasis, and ataxia. This is followed by the psychoactive phase, which generally peaks at 4 to 6 hours and resembles LSD intoxication. This temporal pattern of transition from the gastrointestinal phase to the psychoactive phase is markedly uniform and is characteristic of mescaline intoxication. Symptoms usually resolve within 12 hours of ingestion. Deaths are rare, and are usually associated with accidents due to the user's altered perception.

/CASE REPORTS/ The death of an individual under the influence of mescaline is presented. Concentrations of the drug were 9.7, 70.8, and 1163 micrograms/mL or micrograms/g in blood, liver, and urine respectively.

For more Human Toxicity Excerpts (Complete) data for 3,4,5-TRIMETHOXYPHENETHYLAMINE (7 total), please visit the HSDB record page.

/LABORATORY ANIMALS: Acute Exposure/ The central effect of mescaline and of its derivative N-(3,4,5- trimethoxyphenylethyl)-aziridine after their stereotaxic administration into the lateral ventricle of the brain was studied in behavioral experiments on rats. The effect of the two substances was tested by a method studying memory elicitation in response to appetitive motivation in a multiple T-maze. The results show that both substances worsened the behavior in question. The negative effect of mescaline (lengthening of the time of passage through the maze) was manifested both immediately and several weeks after a single dose. N-(3,4,5- trimethoxyphenylethyl)-aziridine likewise worsened the test reaction, but its effect was less pronounced than that of mescaline.

/LABORATORY ANIMALS: Acute Exposure/ Motor impairment, especially ataxia, is often mentioned as a 'side effect' of doses of psychoactive drugs which depress animal behavior; it is difficult to determine it accurately from visual observation, but relatively few attempts have been made to measure it objectively and quantitatively. Mescaline, in moderate to large doses, can induce biphasic--depressant followed by stimulant--effects on learned and other performance of laboratory rodents. Motor impairment, using three doses, was accordingly measured during the depressant phase by two methods. An 'ataxia' test, involving analyses of footprints, showed few irregularities of gait splay due to mescaline, but the drug markedly reduced the length of steps ('stride') in a dose-related manner. In a 'tilt plane' test for general motor control, the animals' ability to cling to a tilted plane decreased with 25 mg/kg mescaline, at 30 and 40 minutes after administration. Deficits of this kind can be relevant to interpreting drug actions on forms of behavior which involve movements for responding, and they also have interesting potential in their own right.

/LABORATORY ANIMALS: Acute Exposure/ The authors/ evaluated the behavioral response of guinea pigs to hallucinogenic agents in order to characterize the response of this species to a variety of known hallucinogenic drugs. The systemic injection of LSD in the guinea pig elicited a "myoclonic-like" response the frequency of which was dose-dependent. This behavior exhibited rapid tolerance which was more prominent at higher doses. Subacute mescaline pretreatment reduced the myoclonic response to LSD suggesting cross-tolerance. Mescaline, DOM, TMA, DMA and 5 Me-ODMT also elicited myoclonus in a dose-dependent manner and in potency ratios which approximate the human experience for hallucinogenic activity. ...

/LABORATORY ANIMALS: Acute Exposure/ The modifications of behavior caused in the rat by a chronic oral administration of mescaline have been studied in three experimental situations. In the staircase maze mescaline accelerated the spontaneous decay on the conditioned reflex (memory decay) during the period without daily training. Only the results observed at 30 mg/kg/day of mescaline were statistically significant. In a T maze two lateral alleys closed by two swinging doors, 30 mg/kg/day of mescaline increased the time spent in opening the first door. When the two doors of the lateral alleys were closed with a latch, mescaline 30 mg/kg/day, caused an increase in the time spent by the rat in opening the doors. Mescaline caused an increase in food consumption. The increase at 30 mg/kg/day is statistically significant.

For more Non-Human Toxicity Excerpts (Complete) data for 3,4,5-TRIMETHOXYPHENETHYLAMINE (7 total), please visit the HSDB record page.

For patient with a "bad trip" or panic reaction, provide gentle reassurance and relaxation techniques in a quiet environment. Treat agitation or severe anxiety states with diazepam or midazolam. Butyrophenones such as haloperidol are useful despite a small theoretic risk of lowering seizure threshold. Treat seizures, hyperthermia, rhabdomyolysis, hypertension, and cardiac arrhythmias if they occur. /LSD and other hallucinogens/

Specific Drugs and Antidotes: There are no specific antidote. Sedating doses of diazepam may alleviate anxiety, and hypnotic doses can induce sleep for the duration of the "trip". /LSD and other hallucinogens/

Decontamination: Most of these drugs are taken orally in small doses, and decontamination procedures are relatively ineffective and likely to aggravate psychological distress. Consider the use of activated charcoal ... only after recent (within 30-60 minutes) large ingestions. /LSD and other hallucinogens/

Enhanced Elimination: These procedures are not useful. Although urinary acidification may increase the urine concentrations of some agents, it does not significantly enhance total-body elimination and may aggravate myoglobinuric renal failure. /LSD and other hallucinogens/

Schedule I shall consist of the drugs and other substances, by whatever official name, common or usual name, chemical name, or brand name designated, listed in this section. ... Hallucinogenic substances. Unless specifically excepted or unless listed in another schedule, any material, compound, mixture, or preparation, which contains any quantity of the following hallucinogenic substances, or which contains any of its salts, isomers, and salts of isomers whenever the existence of such salts, isomers, and salts of isomers is possible within the specific chemical designation (for purposes of this paragraph only, the term "isomer" includes the optical, position and geometric isomers): Mescaline, DEA Code: 7381.

Hallucinogens, including mescaline, psilocybin, and lysergic acid diethylamide (LSD), profoundly affect perception, cognition, and mood. All known drugs of this class are 5-HT(2A) receptor (2AR) agonists, yet closely related 2AR agonists such as lisuride lack comparable psychoactive properties. Why only certain 2AR agonists are hallucinogens and which neural circuits mediate their effects are poorly understood. By genetically expressing 2AR only in cortex, we show that 2AR-regulated pathways on cortical neurons are sufficient to mediate the signaling pattern and behavioral response to hallucinogens. Hallucinogenic and nonhallucinogenic 2AR agonists both regulate signaling in the same 2AR-expressing cortical neurons. However, the signaling and behavioral responses to the hallucinogens are distinct. While lisuride and LSD both act at 2AR expressed by cortex neurons to regulate phospholipase C, LSD responses also involve pertussis toxin-sensitive heterotrimeric G(i/o) proteins and Src. These studies identify the long-elusive neural and signaling mechanisms responsible for the unique effects of hallucinogens.

The mechanism of action of mescaline is unknown. Hallucinogenic effects are believed to be due to stimulation of serotonin and dopamine receptors in the CNS.

Mescaline (3,4,5-trimethoxyphenylethylamine; MES) and its analogs, anhalinine (ANH) and methylenemescaline trimer (MMT) were investigated, using sciatic-sartorius preparations of the frog and cortical tissue from the rat. The effects of MES and its analogs were examined with respect to muscle twitch, resting membrane potential and nicotinic receptor binding. Mescaline and its analogs (10-100 microM) blocked both directly and neurally evoked twitches but their effects on neurally evoked twitches were greater than those on directly evoked twitches. Mescaline, ANH and MMT decreased amplitude of the miniature endplate and endplate potentials, decreased acetylcholine (ACh) quantal content, hyperpolarized the resting membrane potential and prolonged duration of the action potential. They did not significantly displace the binding of [125I]-alpha-bungarotoxin (alpha-BTX) to nicotinic receptors, at concentrations which blocked neuromuscular transmission. These Mescaline (3,4,5-trimethoxyphenylethylamine; MES) and its analogs, anhalinine (ANH) and methylenemescaline trimer (MMT) were investigated, using sciatic-sartorius preparations of the frog and cortical tissue from the rat. The effects of MES and its analogs were examined with respect to muscle twitch, resting membrane potential and nicotinic receptor binding. Mescaline and its analogs (10-100 microM) blocked both directly and neurally evoked twitches but their effects on neurally evoked twitches were greater than those on directly evoked twitches. Mescaline, ANH and MMT decreased amplitude of the miniature endplate and endplate potentials, decreased acetylcholine (ACh) quantal content, hyperpolarized the resting membrane potential and prolonged duration of the action potential. They did not significantly displace the binding of [125I]-alpha-bungarotoxin (alpha-BTX) to nicotinic receptors, at concentrations which blocked neuromuscular transmission. These results suggest that MES and its analogs inhibit cholinergic neuromuscular transmission by blocking release of ACh; they also affect K+ conductance.

It is metabolized in the liver by mescaline oxidase into numerous inactive metabolites. These include 3,4,5-trimethoxyphenylacetic acid; 3,4,5-trimethoxybenzoic acid; 3,4-dihydroxy-5-methoxy-phenyl-lacetyl glutamine; 3-hydroxy-4,5-dimethoxyphenylethylamine; N-acetylmescaline; and N-acetyl-3,4-dimethoxy-5-hydroxyphenylethylamine.

Metabolism of mescaline by several rabbit tissues was examined in vitro. Mescaline-oxidizing activity (micromoles/ per milligram of protein/15 min) of lung homogenates was 4 times greater than that of either liver or kidney. Brain and plasma each had comparatively little capacity to metabolize mescaline. Mescaline metabolism in vitro was sensitive to inhibition by semicarbazide. Removal of mescaline from the medium perfusing the isolated rabbit lung was explained by intrapulmonary metabolism. Semicarbazide (10(-3) M pargyline. Semicarbazide-treated lungs accumulated more mescaline than did untreated lungs. Mescaline efflux from lung was slower than that of its metabolite. These results indicate that the intact lung removes perfused mescaline and may be important in the disposition of circulating mescaline in vivo.

Drugs capable of inducing illusions, hallucinations, delusions, paranoid ideations, and other alterations of mood and thinking. Despite the name, the feature that distinguishes these agents from other classes of drugs is their capacity to induce states of altered perception, thought, and feeling that are not experienced otherwise.

Endogenous compounds and drugs that bind to and activate SEROTONIN RECEPTORS. Many serotonin receptor agonists are used as ANTIDEPRESSANTS; ANXIOLYTICS; and in the treatment of MIGRAINE DISORDERS.

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.

Sixty percent of mescaline is excreted unchanged in a 24 hour urine, and the rest is excreted as metabolites.

Peyote is rapidly absorbed after ingestion. The onset of action is between 30 minutes and 2 hours, and peak blood levels occur 2 hours after ingestion. The duration of the effect usually ranges from 6 to 12 hours but may last up to 14 hours. /Peyote/

Rats of 1, 4, 8, 12, 20, and 60 days postnatal age were injected ip with (14)C-mescaline (50 nCi/g). The levels of mescaline and its deaminated metabolite, 3,4,5-trimethoxyphenylacetic acid, were examined in the brain, liver, heart, spleen, lung, and kidney at 30, 60, 90, and 120 min. Mescaline was rapidly taken up by all the organs examined. In general, the organs of younger rats accumulated much larger amounts than those of adult animals. Brain concentrated the lowest amounts in comparison with other tissues. In the brain, the uptake was the highest in 1-day-old rats and decreased with age. The disappearance of mescaline in various organs was comparatively slower in younger animals than in 20-day or older rats. Rats immediately after birth and uptake was the highest in 1-day-old rats and decreased with age. The disappearance of mescaline in various organs was comparatively slower in younger animals than in 20-day or older rats. Rats immediately after birth and up to 20 days of age metabolized mescaline less efficiently than adults. From the data, it appears that the blood-brain barrier for mescaline develops gradually with age but is not completely impermeable in adults.

Therapeutic use: Experimental psychotomimetic.

Biochemical and medical research, hallucinogenic drug

The legal use of peyote and mescaline in the United States today is limited to Indian tribes in the Native American Church who use the peyote as part of their religious ceremony.