2,5-Dimethoxy-4-methylamphetamine; 4-Methyl-2,5-dimethoxyamphetamine; 2,5-Dimethoxy-4-methyl-α-methylphenethylamine; Des-oxy-methyl; DOM; DMMTA; α-Me-2C-D; STP; Serenity, Tranquility, and Peace; Super Terrific Psychedelic; Stop The Police; Too Stupid to Puke;[1] K-61,082[2]
In his bookPiHKAL (Phenethylamines I Have Known and Loved) and other publications,Alexander Shulgin lists DOM's dose as 3 to 10mgorally and itsduration as 14 to 24hours.[3][18][19] An estimated typical dose is about 6mg.[1][2] The (R)-enantiomer, (R)-DOM, was active at a dose of 0.5mg, whereas DOM itself produces threshold effects only at 1mg.[3][1] The (S)-enantiomer, (S)-DOM, showed nopsychoactive effects at doses of up to 2.6mg.[3] As such, the activity of DOM appears to reside in (R)-DOM, with this enantiomer appearing to be roughly twice aspotent asracemic DOM.[3] In a review byRichard Glennon and colleagues, the approximate hallucinogenic dose was listed as 2 to 5mg for racemic DOM, 1.0 to 2.5mg for (R)-DOM, and greater than 4mg for (S)-DOM, with no known active level of the latter enantiomer.[20] DOM is said by Shulgin to have a slow build-up, with anonset of 30 to 60minutes and a peak of 2 to 6hours.[3][4][1] It may also have a very long duration of up to 3 or 4days when taken in excessively high doses such as 14 to 30mg.[3][4][8][1][2] However, it is unclear the extent to which this is actually true or may just be exaggeration.[1][2] DOM is about 50- to 150-fold as potent asmescaline and around 30- to 60-fold less potent than LSD.[2][8][3][18][19]
The effects of DOM were formally assessed inclinical studies bySolomon H. Snyder andLeo Hollister and colleagues in the late 1960s and early 1970s.[2][1][11][8][21][22][23] At low doses, such as 1 to 4mg, DOM produced effects includingstimulation,euphoria, enhancedself-awareness, and milddose-dependentperceptual disturbances.[2][1][8] At higher doses, of above 5 to 7mg, DOM produces marked and full psychedelic effects.[2][1][8] Hallucinogenic effects were said to start at doses of more than 3 to 5mg.[8][1] Other effects of the drug were also described.[8] Although Shulgin described the effects of DOM as typically lasting 14 to 20hours, clinical studies with low doses reported a duration of only 5 to 8hours, but with a lack of an unexpectedly long duration even at doses of up to 14mg.[8][1][2] Another source listed the average duration as only 8 to 15hours at doses of 5 or 10mg.[2] The reasons for these discrepancies are unclear.[1][2][8] The onset was 0.5 to 1.5hours and peak effects occurred after 3 to 5hours.[2][8]
Repeated administration of DOM results in rapidtolerance development.[3][4][23][24] In one study, in which five people were given 6mg DOM for 3days, there were "extremely intense" effects the first day, but diminished effects on the third day, ranging from "moderately strong" to "felt absolutely nothing".[3][4][24] In another study, in which two people were given gradually increasing doses from 1 to 12mg over 8days, there was development of marked partial tolerance to the effects of DOM.[23] Tolerance developed to both thepsychoactive andphysiological effects of the drug.[23]
DOM was firstsynthesized and tested in 1963 byAlexander Shulgin, who was investigating the effect of 4-positionsubstitutions onpsychedelicamphetamines.[1][3] His 15-year-old son Theodore "Ted" Shulgin assisted in the synthesis of DOM by performing the first step of the synthesis atDow Chemical Company on June 22, 1963 during a brief period when he was interested inchemistry.[2] Later, Alexander Shulgin completed the synthesis on November 30, 1963.[2] He initially discovered the effects of DOM on January 4, 1964, when he ingested a 1mg doseorally.[2] Thehallucinogenic effects of DOM were discovered on February 3, 1964 by Shulgin's colleague Thornton W. Sargent when he ingested 2.3mg.[2] The first clearlypsychedelic experience occurred with a dose of 4.1mg on November 6, 1964.[2] Shulgin hoped that Dow Chemical Company would develop DOM for medical purposes.[2]
In mid-1967, tablets containing 20mg and later 10mg of DOM were widely distributed in theHaight-Ashbury District ofSan Francisco under the name of STP, having been manufactured by underground chemistsOwsley Stanley andTim Scully.[1][2] This short-lived appearance of DOM on theblack market proved disastrous for several reasons.[1][2] First, the tablets contained an excessively high dose of the chemical.[1][2] This, combined with DOM's slowonset (which encouraged some users, familiar with drugs that have quicker onsets, such asLSD, to re-dose) and its remarkably longduration, caused many users topanic and sent some to theemergency room.[1][2] Second, treatment of suchoverdoses was complicated by the fact that no one at the time knew that the tablets called STP were, in fact, DOM, and there was no effectiveantidote.[1][2]
The nameDOM is an acronym of the code name "des-oxy-methyl" coined by the drug's inventorAlexander Shulgin.[1][2] The drug was also initially known by the code nameK-61,082 and is widely known by its nicknameSTP.[1][2] TheSTP name has been said to stand for various acronyms, includingSerenity, Tranquility, and Peace,Super Terrific Psychedelic,Stop The Police, andToo Stupid to Puke, among others.[2][1]
DOM is schedule 9 under the AustraliaPoisons standard.[56] A schedule 9 substance is a "Substances which may be abused or misused, the manufacture, possession, sale or use of which should be prohibited by law except when required for medical or scientific research, or for analytical, teaching or training purposes with approval of Commonwealth and/or State or Territory Health Authorities."[56]
DOM is Schedule I in the United States.[58] This means it is illegal to manufacture, buy, possess, or distribute (make, trade, own or give) without a DEA license.
DOM, along withDOET, was of interest in the potential treatment ofpsychiatric disorders such asdepression in the 1960s.[2] Subsequently, the related compoundAriadne (4C-D; BL-3912; Dimoxamine) was investigated in the 1970s, but was not marketed either.[2][53]
^abcdefgGlennon RA (April 2017). "The 2014 Philip S. Portoghese Medicinal Chemistry Lectureship: The "Phenylalkylaminome" with a Focus on Selected Drugs of Abuse".J Med Chem.60 (7):2605–2628.doi:10.1021/acs.jmedchem.7b00085.PMID28244748.However, there was some concern that 2-DM-DOM and 5-DM-DOM might undergo further O-demethylation in vivo to a hydroquinone. It had been shown years earlier that DOM can undergo metabolic bis-demethylation to a hydroquinone, and that the hydroquinone undergoes oxidation to a para-quinone (and/or a cyclic iminoquinone) that reacts irreversibly with various proteins.44 As a consequence, this approach was not pursued because of potential risks of neurotoxicity. [...] 44. Jacob P. 3rd; Kline, T., Castagnoli, N. Jr. Chemical and biological studies of 1-(2,5-dihydroxy-4- methylphenyl)-2-aminopropane, an analogue of 6-hydroxydopamine. J Med Chem. 1979; 22:662– 671. [PubMed: 458821]
^abcdeEckler JR, Chang-Fong J, Rabin RA, Smith C, Teitler M, Glennon RA, Winter JC (July 2003). "Behavioral characterization of 2-O-desmethyl and 5-O-desmethyl metabolites of the phenylethylamine hallucinogen DOM".Pharmacol Biochem Behav.75 (4):845–852.doi:10.1016/s0091-3057(03)00159-x.PMID12957227.
^abcWills B, Erickson T (9 March 2012). "Psychoactive Phenethylamine, Piperazine, and Pyrrolidinophenone Derivatives". In Barceloux DG (ed.).Medical Toxicology of Drug Abuse: Synthesized Chemicals and Psychoactive Plants. Wiley. pp. 156–192.doi:10.1002/9781118105955.ch10.ISBN978-0-471-72760-6.
^Glennon RA, Rosecrans JA (1982). "Indolealkylamine and phenalkylamine hallucinogens: a brief overview".Neurosci Biobehav Rev.6 (4):489–497.doi:10.1016/0149-7634(82)90030-6.PMID6757811.
^Snyder SH, Faillace LA, Weingartner H (September 1968). "DOM (STP), a new hallucinogenic drug, and DOET: effects in normal subjects".Am J Psychiatry.125 (3):113–120.doi:10.1176/ajp.125.3.357.PMID4385937.
^Weingartner H, Snyder SH, Faillace LA (1971). "DOM (STP), a new hallucinogenic drug: specific perceptual changes".J Clin Pharmacol New Drugs.11 (2):103–111.doi:10.1177/009127007101100205.PMID5206471.
^abcdHollister LE, Macnicol MF, Gillespie HK (1969). "An hallucinogenic amphetamine analog (DOM) in man".Psychopharmacologia.14 (1):62–73.doi:10.1007/BF00401535.PMID5351858.
^abAngrist B, Rotrosen J, Gershon S (April 1974). "Assessment of tolerance to the hallucinogenic effects of DOM".Psychopharmacologia.36 (3):203–207.doi:10.1007/BF00421802.PMID4844244.
^Fantegrossi WE, Murnane KS, Reissig CJ (January 2008)."The behavioral pharmacology of hallucinogens".Biochem Pharmacol.75 (1):17–33.doi:10.1016/j.bcp.2007.07.018.PMC2247373.PMID17977517.Despite the reasonably constant recreational use of hallucinogens since at least the early 1970s [44], the reinforcing effects of hallucinogens have not been widely investigated in laboratory animals. Indeed, one of the earliest studies on the reinforcing effects of drugs using the intravenous self-administration procedure in rhesus monkeys found that no animal initiated self-injection of mescaline either spontaneously or after one month of programmed administration [45]. Likewise, the phenethylamine hallucinogen 2,5-dimethoxy-4-methylamphetamine (DOM) was not effective in maintaining self-administration in rhesus monkeys [46]. Nevertheless, the hallucinogen-like phenethylamine 3,4-methylenedioxymethamphetamine (MDMA) has been shown to act as a reinforcer in intravenous self-administration paradigms in baboons [47], rhesus monkeys [48 – 50], rats [51] and mice [52].
^Canal CE, Murnane KS (January 2017)."The serotonin 5-HT2C receptor and the non-addictive nature of classic hallucinogens".J Psychopharmacol.31 (1):127–143.doi:10.1177/0269881116677104.PMC5445387.PMID27903793.One of the earliest studies on the reinforcing effects of drugs using the intravenous self-administration procedure in rhesus monkeys found that no animal initiated self-injection of mescaline either spontaneously or after one month of programmed administration, [...] (Deneau et al., 1969). The lack of mescaline self-administration stood in contrast to positive findings of self-administration of morphine, codeine, cocaine, amphetamine, pentobarbital, ethanol, and caffeine. A subsequent study with rhesus monkeys using 2,5-dimethoxy-4-methylamphetamine (DOM; Yanagita, 1986) provided similar results as the mescaline study. These findings have withstood the test of time, as the primary literature is virtually devoid of any accounts of self-administration of [classical hallucinogens (CH)], suggesting that there are very limited conditions under which laboratory animals voluntarily consume CH.
^Yanagita T (June 1986). "Intravenous self-administration of (−)-cathinone and 2-amino-1-(2,5-dimethoxy-4-methyl)phenylpropane in rhesus monkeys".Drug Alcohol Depend.17 (2–3):135–141.doi:10.1016/0376-8716(86)90004-9.PMID3743404.
^Cha HJ, Jeon SY, Jang HJ, Shin J, Kim YH, Suh SK (May 2018). "Rewarding and reinforcing effects of 4-chloro-2,5-dimethoxyamphetamine and AH-7921 in rodents".Neurosci Lett.676:66–70.doi:10.1016/j.neulet.2018.04.009.PMID29626650.
^Kim YJ, Ma SX, Hur KH, Lee Y, Ko YH, Lee BR, Kim SK, Sung SJ, Kim KM, Kim HC, Lee SY, Jang CG (April 2021). "New designer phenethylamines 2C-C and 2C-P have abuse potential and induce neurotoxicity in rodents".Arch Toxicol.95 (4):1413–1429.Bibcode:2021ArTox..95.1413K.doi:10.1007/s00204-021-02980-x.PMID33515270.
^Custodio RJ, Sayson LV, Botanas CJ, Abiero A, You KY, Kim M, Lee HJ, Yoo SY, Lee KW, Lee YS, Seo JW, Ryu IS, Kim HJ, Cheong JH (November 2020). "25B-NBOMe, a novel N-2-methoxybenzyl-phenethylamine (NBOMe) derivative, may induce rewarding and reinforcing effects via a dopaminergic mechanism: Evidence of abuse potential".Addict Biol.25 (6) e12850.doi:10.1111/adb.12850.PMID31749223.
^Seo JY, Hur KH, Ko YH, Kim K, Lee BR, Kim YJ, Kim SK, Kim SE, Lee YS, Kim HC, Lee SY, Jang CG (October 2019). "A novel designer drug, 25N-NBOMe, exhibits abuse potential via the dopaminergic system in rodents".Brain Res Bull.152:19–26.doi:10.1016/j.brainresbull.2019.07.002.PMID31279579.
^Lee JG, Hur KH, Hwang SB, Lee S, Lee SY, Jang CG (August 2023). "Designer Drug, 25D-NBOMe, Has Reinforcing and Rewarding Effects through Change of a Dopaminergic Neurochemical System".ACS Chem Neurosci.14 (15):2658–2666.doi:10.1021/acschemneuro.3c00196.PMID37463338.
^Kim YJ, Kook WA, Ma SX, Lee BR, Ko YH, Kim SK, Lee Y, Lee JG, Lee S, Kim KM, Lee SY, Jang CG (April 2024). "The novel psychoactive substance 25E-NBOMe induces reward-related behaviors via dopamine D1 receptor signaling in male rodents".Arch Pharm Res.47 (4):360–376.doi:10.1007/s12272-024-01491-4.PMID38551761.
^Shulgin AT (1980)."Hallucinogens". In Burger A, Wolf ME (eds.).Burger's Medicinal Chemistry. Vol. 3 (4 ed.). New York: Wiley. pp. 1109–1137.ISBN978-0-471-01572-7.OCLC219960627.The third principal metabolic route common to the hallucinogenic drugs is oxidation. Benzylic oxidation had been reported with both DOM (60.22aa) and DOET (60.22bb) (61, 62). Of greater theoretical interest is oxidative cyclization to form an indole species, reminiscent of the conversion of epinephrine to adrenochrome. Many of the hallucinogens are in fact indoles, and since the phenethylamine chain has the exact atom composition of indole itself, there has been frequent speculation that there might be some metabolic conversion from one family to the other. It has been shown (63) that one of the metabolites of DOM (2,5-dihydroxy[-4-methyl]phenylisopropylamine, 60.17), which bears a close chemical and pharmacological resemblance to the potent neurodegenerative agent 6-hydroxydopamine (60.18) (64), can undergo a facile oxidative cyclization to form a 5-hydroxyindole. The intermediate iminoquinone is potentially very reactive with nucleophilic agents found in normal body chemistry, and may be important in any explanation of biological activity.
^Castagnoli, Neal (1978). "Drug Metabolism: Review of Principles and the Fate of One-Ring Psychotomimetics".Stimulants. Boston, MA: Springer US. p. 335–387.doi:10.1007/978-1-4757-0510-2_7.ISBN978-1-4757-0512-6. Retrieved3 February 2026.FIG. 9. Metabolic pathways for amine III (DOM). [...] The third general metabolic pathway for 111 is oxidative O-demethylation of the methyl phenyl ether groups. All three possible O-demethylated metabolites, compounds 118-120, have been characterized in rabbit liver homogenates (Zweig and Castagnoli, 1975, 1977). The p-hydroquinone 120 is an analog of the sympatholytic agent 6-hydroxydopamine (107) and has been shown to possess some of the neurodegenerative properties of 6-hydroxydopamine (Butcher, 1975). Similar to 6-hydroxydopamine (Blank et ai., 1972), hydroquinone 120 undergoes facile oxidation to form the quinone 129 (Fig. 10), which cyclizes to the iminoquinone 130 (Zweig and Castagnoli, 1974). In the absence of nucleophiles, 130 is relatively stable at pH 7.4. As the pH is raised, however, proton rearrangements take place, eventually leading to the indole 132 via the indolinine 131. In view of the ease with which the hydroquinone 120 undergoes oxidation at pH 7.4, it is somewhat surprising that this compound survives the one hour pH 7.4 incubation. This stabilization may be analogous to the inhibition by liver constituents of hydroxylamine auto-oxidation. It should prove of interest to determine the nature and significance of the protection of these substances from air oxidation. [...] FIG. 10. Oxidative cyclization of p-hydroquinone metabolite derived from DOM. [...]
^Jacob P, Kline T, Castagnoli N (June 1979). "Chemical and biological studies of 1-(2,5-dihydroxy-4-methylphenyl)-2-aminopropane, an analogue of 6-hydroxydopamine".J Med Chem.22 (6):662–671.doi:10.1021/jm00192a011.PMID458821.
^Butcher LL (1975). "Degenerative processes after punctate intracerebral administration of 6-hydroxydopamine".J Neural Transm.37 (3):189–203.doi:10.1007/BF01670128.PMID1185165.Similarly, 1-(2,5-dihydroxy-4-methylphenyl)-2-aminopropane was not a more potent cytotoxin than 6-OHDA even though this new neurotoxin has a propane side chain which renders it immune to monoamine oxidase. [...] The neurotoxin 1-(2,5-dihydroxy-4-methylphenyl)-2-aminopropane-HC1 (DIMPAP) was synthesized by Dr. Nell Castagnoli, University of California Medical Center, San Francisco, CA, U.S.A. [...] Fig. 28. Chemical structure of 1-(2, 5-dihydroxy-4-methylphenyl)-2-aminopropaneHC1 (DIMPAP) [...] The extent of zone-3 damage: after intrastriatal infusion of various doses of DIMPAP is depicted in figures 29–33. No significant difference exists between the non-selective damage produced by DIMPAP and similar doses of 6-OHDA (e.g., compare Figs. 29–33 with Figs. 25–30 in Butcher et al., 1974). Furthermore, nialamide pre-treatment does not alter the destructive potency of either 6-OHDA or DIMPAP (compare Figs. 34–38 with Figs. 39–43 and Figs. 44–47).
^Hassan Z, Bosch OG, Singh D, Narayanan S, Kasinather BV, Seifritz E, Kornhuber J, Quednow BB, Müller CP (2017)."Novel Psychoactive Substances-Recent Progress on Neuropharmacological Mechanisms of Action for Selected Drugs".Front Psychiatry.8 152.doi:10.3389/fpsyt.2017.00152.PMC5563308.PMID28868040.The next, even though less accidental, producer of NPS hallucinogens was Alexander T. Shulgin, who synthesized hundreds of novel hallucinogenic tryptamines and phenylethylamines in his home laboratory. He described the synthesis of these compounds and also their psychotomimetic effects experienced in self-experiments in detail in his books PIHKAL and TIHKAL (199, 200). He created several dimethoxy-substituted phenylethylamines, such as DOM, 2,5-dimethoxy-4-bromoamphetamine (DOB), 2,5-dimethoxy-4-iodoamphetamine (DOI), and 2,5-dimethoxy-4-ethylamphetamine (DOET), which all display strong hallucinogenic properties. These drugs usually have much longer durations of action (12–30 h) and are much more potent agonists at 5-HT2A-Rs (50- to 175-fold) compared to their related phenylethylamine derivative mescaline (duration of action: 4–8 h) (189, 199, 200).
^Markert, John (23 May 2013).Hooked in Film: Substance Abuse on the Big Screen. Bloomsbury Publishing USA. pp. 224–.ISBN979-8-216-22555-3. Retrieved12 February 2026.Psych-Out (1968) is thematically similar to The Trip, but with a more evolved storyline. Its primary "educational" value was to warn the viewer that while LSD is fine, one should at all costs avoid STP: "Don't get near that stuff. [You] don't know what's in it. They say it's LSD, cocaine, and methadrine." Another character chimes in: "It's like driving a Ferrari with the gas pedal strapped to the floor. It's nothing to play with." To drive home the admonition, Strasberg's character shortly thereafter is given some STP and freaks out: she sees fireballs in her mind's eye and attempts to flee them by running across a San Francisco bridge while cars careen around her. This was a critical warning to audiences when the film was released. In 1967, tablets containing DOM (2.5-Dimethoxy-4-methylamphetamine) were widely distributed in the Haight-Ashbury district of San Francisco under the name STP, which stood for Serenity-Tranquility-Peace. The short-lived appearance of DOM proved disastrous for several reasons. [...]
Notes: (1) TAAR1 activity of ligands varies significantly between species. Some agents that are TAAR1 ligands in some species are not in other species. This navbox includes all TAAR1 ligands regardless of species. (2) See the individual pages for references, as well as theList of trace amines,TAAR, andTAAR1 pages. See also:Receptor/signaling modulators
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