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DOM (2,5-dimethoxy-4-methylamphetamine), historically distributed as STP, is a potent, long-acting psychedelic amphetamine of the DOx family carrying a methyl group at the 4 position. It acts chiefly as an agonist at serotonin 5-HT2A receptors, and its potency correlates with 5-HT2 binding affinity, a relationship established in the radioligand studies that helped implicate this receptor as the common site of action for phenylisopropylamine hallucinogens. Synthesized by Alexander Shulgin and later characterized extensively in rodent and primate drug-discrimination work, DOM became a widely used training drug for probing 5-HT2A-mediated interoceptive effects and for screening novel agonists and antagonists. It gained notoriety after high-dose tablets were distributed on the street in 1967, producing prolonged, difficult experiences and a wave of hospital presentations. The compound produces a long psychedelic state with a stimulant edge and pronounced body load.
- Long, visual psychedelic character
- High potency at low milligram amounts
- Prototype 5-HT2A agonist used to define drug discrimination
- Slow onset historically led to dangerous early redosing
- Vasoconstriction and body load
- Overheating and agitation at overdose
Mechanism
DOM is a 2,5-dimethoxy-4-methyl amphetamine. Its core action is agonism at the receptor, the receptor that drives the classic psychedelic state, with additional activity at 5-HT2C; it acts as a high-affinity partial at these sites. The amphetamine backbone slows metabolism and adds a stimulant component, which contributes to its long duration and body load.
receptor fingerprint
receptorpartial agonist
5-HT2C receptoragonist
Safetyrisks and cautions, not medical advice
DOM is potent and long-acting, and its slow onset historically led people to redose too soon, producing overwhelming, drawn-out experiences and a rash of hospitalizations when it appeared as STP. Like other DOx compounds it causes vasoconstriction and body load, and overdoses can bring agitation and hyperthermia (dangerous overheating). It should not be combined with MAOIs or other strongly serotonergic drugs because of serotonin toxicity. People with heart conditions or a history of psychosis should avoid it. Not medical advice.
Subjective profileweighing the evidence above
Respect this one or leave it alone. The slow onset is precisely what caused the hospitalisations when it circulated as STP; people redosed and locked themselves into a very long, very intense trip, with vasoconstriction and overheating on top. Gentler psychedelics with better margins exist.
Resources
This entry is here for reference.
Research
- 1986first citedPossible involvement of serotonin receptors in the facilitatory effect of a hallucinogenic phen…
- 2024most recentThe origin of 2,5-dimethoxy-4-methylamphetamine (DOM, STP)
- 1.Discriminative stimulus properties of hallucinogens and related designer drugs
- 2.The origin of 2,5-dimethoxy-4-methylamphetamine (DOM, STP)
- 3.Radioligand binding evidence implicates the brain 5-HT2 receptor as a site of action for LSD and phenylisopropylamine hallucinogens.
- 4.Hallucinogenic drug interactions at human brain 5-HT2 receptors: implications for treating LSD-induced hallucinogenesis.
- 5.Possible involvement of serotonin receptors in the facilitatory effect of a hallucinogenic phenethylamine on single facial motoneurons.
- 6.Intravenous self-administration of (-)-cathinone and 2-amino-1-(2,5-dimethoxy-4-methyl)phenylpropane in rhesus monkeys.
- 7.Discriminative stimulus effects of 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM), ketanserin, and (R)-(+)-{alpha}-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenyl)ethyl]-4-pipidinemethanol (MDL100907) in rats.
- 8.Pharmacological properties and discriminative stimulus effects of a novel and selective 5-HT2 receptor agonist AL-38022A [(S)-2-(8,9-dihydro-7H-pyrano[2,3-g]indazol-1-yl)-1-methylethylamine].
- 9.Nefazodone in the rat: mimicry and antagonism of [-]-DOM-induced stimulus control.
- 10.Behavioral and biochemical evidence for a nonessential 5-HT2A component of the ibogaine-induced discriminative stimulus.
- 11.Antagonism of 5-hydroxytryptamine2 receptor-mediated phosphatidylinositol turnover by d-lysergic acid diethylamide.
11 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
What was STP?
STP was a street name for DOM in the 1960s; high-dose tablets caused many long, difficult experiences and hospital visits.
How does it work?
Mainly through high-affinity partial agonism at the 5-HT2A serotonin receptor.
Why did people end up in trouble with it?
Its slow onset led users to assume it was weak and redose, producing overwhelming and very long experiences.
Adverse effects
- Slow onset historically led to dangerous early redosing
- Vasoconstriction and body load
- Overheating and agitation at overdose