STP is a street name for DOM (2,5-dimethoxy-4-methylamphetamine), a synthetic psychedelic that burst onto the San Francisco drug scene during the Summer of Love in 1967 and quickly became infamous for its overwhelming potency and punishingly long duration. Though it shares the hallucinogenic territory of LSD, mescaline, and psilocybin, DOM carved out a reputation all its own thanks to a slow, deceptive onset that led many users to take too much and endure trips lasting far longer than they bargained for. The drug faded from street popularity within a few years but never left the laboratory, where it remains a valuable research tool for understanding how psychedelics act on the brain.
Where STP Came From
DOM was first synthesized by the chemist Alexander Shulgin, who explored it as an experimental substance with potential use in psychotherapy. The drug found its way to the public largely through Owsley Stanley, the legendary underground chemist already known for manufacturing enormous quantities of LSD. In 1967, Stanley distributed DOM for free in San Francisco’s Haight-Ashbury neighborhood, and it spread rapidly under the nickname STP.1PubMed. The origin of 2,5-dimethoxy-4-methylamphetamine (DOM, STP) The resulting wave of emergency room visits and bad trips turned STP into a cautionary tale and a public health crisis almost overnight.
A key part of the story is how different groups tried to make sense of this new substance. Young doctors in the Haight-Ashbury Free Clinic, underground chemists, and the users themselves all developed their own understanding of what STP was and what it did. But media coverage at the time largely credited only the medical professionals, while the knowledge circulating among users and chemists went unreported.2History of Pharmacy and Pharmaceuticals. Learning about STP: A Forgotten Psychedelic from the Summer of Love The drug’s bad reputation cemented itself during these early months and never really recovered, even as scientific understanding of it grew considerably in the decades that followed.
What the Name Means
The origin of the nickname “STP” has been disputed and mythologized almost since the drug first appeared. The most popular interpretation ties it to the motor oil additive of the same name, playing on the idea that the drug would supercharge your mind the way the product supposedly supercharged an engine. Other users claimed it stood for “Serenity, Tranquility, Peace,” which is darkly ironic given the anxiety-drenched experiences many people had with it. A third interpretation, “Super Terrific Psychedelic,” also circulated. None of these was ever an official designation. The scientific name DOM, standing for 2,5-dimethoxy-4-methylamphetamine, is the term used in research and pharmacology.
Why the Slow Onset Caused So Many Problems
The central danger of STP in its street days was a pharmacological mismatch between what users expected and what actually happened. Most people who tried it were familiar with LSD, which kicks in within roughly 30 to 45 minutes. DOM, by contrast, absorbs through the gut more slowly, with a delayed onset sometimes exceeding an hour.3ScienceDirect. Synthetic amphetamine derivatives, benzofurans, and benzodifurans Animal studies confirmed this gap: in rats trained to distinguish between DOM and LSD, DOM’s characteristic effects took significantly longer to develop than those of LSD.4PubMed. The time-dependent stimulus effects of R(-)-2,5-dimethoxy-4-methamphetamine (DOM): implications for drug-induced stimulus control as a method for the study of hallucinogenic agents
This slow ramp-up was not just an inconvenience; it was a trap. Users who felt only mild effects after an hour often assumed they had taken a weak dose and swallowed more. By the time the full effects of the original dose hit, they were already committed to a second, stacking the experiences into something far more intense than intended. The tablets distributed in Haight-Ashbury were reportedly dosed at high levels to begin with, which compounded the problem.
Unlike a difficult LSD trip that might wind down after six or eight hours, an STP overdose could stretch the experience to an agonizing length. Some people who sought medical care showed symptoms comparable to amphetamine psychosis, with effects persisting for up to four days. In addition to the psychological distress, DOM produced worrisome physical effects not typically seen with LSD, including sweating, tremors, and large spikes in heart rate.5History of Pharmacy and Pharmaceuticals. Learning about STP: A Forgotten Psychedelic from the Summer of Love – Section: Adverse Reactions to DOM These physical symptoms brought the drug to the attention of health care providers who had to learn about it on the fly, with little existing medical literature to guide treatment.
What STP Actually Does at Different Doses
At low doses, DOM produces a mild sense of well-being without strong perceptual changes. Doses above about 3 milligrams, however, cross a threshold into pronounced hallucinogenic territory, with effects described as similar in character to those of LSD, mescaline, and psilocybin and lasting around eight hours at a standard dose.6PubMed. 2,5-dimethoxy-4-methyl-amphetamine (STP): a new hallucinogenic drug At higher doses, the duration stretches well beyond that, which is where the problems described above become acute.
This steep dose-response curve is part of what made street STP so unpredictable. The difference between a pleasant, manageable experience and a multi-day ordeal could come down to a few extra milligrams, and the tablets circulating in 1967 were not manufactured with pharmaceutical precision. Users had no reliable way to know what dose they were actually taking.
How It Works in the Brain
DOM belongs to a class of compounds sometimes called the “D series” of psychedelic amphetamines. These drugs produce their hallucinogenic effects primarily by activating serotonin receptors, specifically the 5-HT2A and 5-HT2C subtypes, where they act as full agonists rather than partial ones.7ScienceDirect. 2,5 Dimethoxy 4 Methylamphetamine This means DOM fully activates these receptors rather than just nudging them partway, which accounts for its strong psychedelic potency relative to its dose.
The 5-HT2A receptor is the key player. In mice genetically engineered to lack the 5-HT2A receptor, DOM fails to produce the head-twitch response that researchers use as a behavioral marker for hallucinogenic activity. Blocking the receptor with a selective antagonist called M100907 also completely shuts down the response at every dose tested.8PubMed. 5-hydroxytryptamine 2C/1A receptors modulate the biphasic dose response of the head twitch response and locomotor activity induced by DOM in mice DOM is also relatively selective for these serotonin receptors, showing much higher affinity for 5-HT2A and 5-HT2C than for the 5-HT1A subtype.9PubMed Central. Short- and Long-Acting Psychedelics: Structure–Activity Relationships, Pharmacology, and Implications for Neuropsychiatric Therapeutics
An interesting quirk of DOM’s dose-response relationship is that it follows an inverted U-shaped curve in animal models. At low to moderate doses, both the head-twitch response and locomotor activity increase as the dose goes up. But at very high doses, both begin to fall off again. Researchers believe this ceiling effect involves other serotonin receptor subtypes, particularly 5-HT2C and 5-HT1A, which appear to put a brake on the 5-HT2A-driven effects at higher doses.10PubMed. 5-hydroxytryptamine 2C/1A receptors modulate the biphasic dose response of the head twitch response and locomotor activity induced by DOM in mice Whether this translates cleanly to the human experience is uncertain, but it does suggest the drug’s effects on the brain are not a simple linear ramp.
How STP Compares to LSD
People who encountered STP in the 1960s naturally compared it to LSD, and the two drugs do share the same core mechanism: both produce hallucinations primarily through serotonin 2A receptor activation. In drug discrimination studies, animals trained to recognize LSD will respond to DOM as though it were LSD, and the cross-substitution is blocked by the same serotonin receptor antagonists.11PubMed Central. Short- and Long-Acting Psychedelics: Structure–Activity Relationships, Pharmacology, and Implications for Neuropsychiatric Therapeutics To the brain, the two drugs look similar at the receptor level.
The practical differences, though, are significant. LSD is active at microgram doses (a typical dose is measured in millionths of a gram), while DOM requires milligrams. LSD’s effects peak relatively quickly and typically resolve within about 12 hours even at high doses. DOM’s slower onset and longer tail make it a very different experience in practice, even if the qualitative character of the hallucinations overlaps. Research comparing the two drugs delivered directly into the brain found that DOM had a noticeably slower offset than LSD when behavioral effects were measured over time.12Pharmacology Biochemistry and Behavior. Behavioral effects of intracerebroventricular administration of LSD, DOM, mescaline or lisuride
There is also a structural difference worth noting. LSD is an ergoline, a rigid multi-ring molecule derived originally from ergot fungus. DOM is a phenylalkylamine, essentially a modified amphetamine backbone with methoxy groups attached. Despite these very different chemical scaffolds, both converge on the same receptor target to produce hallucinations, which is one reason pharmacologists find the comparison so instructive.
DOM as a Modern Research Tool
Although STP vanished from the street drug market decades ago, DOM never left the laboratory. Its clean receptor profile and robust, reproducible effects in animal models have made it one of the standard reference compounds in psychedelic pharmacology research. Scientists use it to probe questions that go well beyond one particular drug.
One active line of research involves understanding what separates a hallucinogenic drug from a non-hallucinogenic one at the molecular level. Both types can activate the 5-HT2A receptor, so receptor binding alone does not explain why some drugs cause hallucinations and others do not. Recent work has pointed to differences in the signaling pathways triggered downstream. When DOM activates the 5-HT2A receptor, it engages both the Gq and the Gs protein signaling cascades. Non-hallucinogenic drugs that hit the same receptor tend to activate only the Gq pathway. Experiments showed that boosting Gs-related signaling increased the head-twitch response in mice, while blocking it reduced the response, suggesting that the Gs pathway is a critical piece of the hallucinogenic puzzle.13PubMed. G(s) signaling pathway distinguishes hallucinogenic and nonhallucinogenic 5-HT(2A)R agonists induced head twitch response in mice
This finding matters because the psychedelic therapy field is deeply interested in whether it is possible to separate a drug’s therapeutic effects from its hallucinogenic ones. If the Gs pathway is specifically responsible for hallucinations, it might be possible to design compounds that activate the therapeutic arm of the receptor without flipping on the perceptual fireworks. DOM, because it reliably produces both effects in predictable doses, serves as the benchmark hallucinogen against which non-hallucinogenic candidates are compared.
Another area where DOM has proven useful involves the glutamate system. Researchers have shown that activating a different receptor type called mGluR2 can dampen DOM’s hallucinogenic effects in a dose-dependent way, while blocking mGluR2 enhances them.14PubMed. Modulation of DOM-Induced Head-Twitch Response by mGluR2 Agonist/Inverse Agonist is Associated with 5-HT(2A)R-Mediated G(s) Signaling Pathway This cross-talk between the serotonin and glutamate systems has implications for understanding not just psychedelic drugs but also conditions like schizophrenia, where similar receptor interactions appear to play a role.
Tolerance and Receptor Changes
Like other psychedelics, DOM produces tolerance with repeated use. When rats were given DOM daily for a week, the drug’s ability to produce its characteristic stimulus effects decreased. Interestingly, the way tolerance developed at the receptor level was more nuanced than a simple across-the-board reduction. Chronic DOM treatment led to a decrease in 5-HT2A receptor levels, but only in a specific brain region (the olfactory nucleus), rather than the widespread receptor downregulation seen with the antipsychotic clozapine.15ScienceDirect. Effects of clozapine and 2,5-dimethoxy-4-methylamphetamine [DOM] on 5-HT2A receptor expression in discrete brain areas
This finding is a reminder that psychedelic tolerance is not just about having fewer receptors available. The brain’s response is region-specific and involves complex regulatory changes that scientists are still mapping out. For the practical user, the takeaway is straightforward: taking DOM on consecutive days diminishes its effects, and attempting to overcome that tolerance by increasing the dose is a recipe for the kind of dangerously prolonged experience that gave STP its grim reputation in 1967.
Why STP Disappeared From the Street
STP’s street career was remarkably brief. Within a year or two of its 1967 debut, it had largely vanished from the drug market. Several factors contributed. The drug’s reputation for causing frighteningly long, physically unpleasant trips made it unpopular with users who had access to LSD, which offered a more controllable experience. Word spread through the counterculture press and through the Haight-Ashbury Free Clinic that STP was something to avoid. Authorities also moved quickly to schedule the drug, making it illegal to manufacture or possess.
The combination of user self-selection and legal restriction was effective. Unlike LSD, which maintained a persistent underground market for decades, DOM essentially dropped out of recreational circulation. Occasional seizures by law enforcement and sporadic reports in drug-checking services suggest it still appears in small quantities, sometimes as an adulterant in tablets sold as other substances, but it is nowhere near as available as it was during those few chaotic months in San Francisco.
Abuse Liability and Opioid Interactions
One finding from animal research that may surprise people familiar with the amphetamine side of DOM’s chemical heritage is that the drug does not appear to carry the same reinforcement profile as stimulants or opioids. In rhesus monkeys trained to self-administer the opioid fentanyl, DOM did not increase the monkeys’ tendency to press the lever for more fentanyl, suggesting it lacks the kind of cross-reinforcement that would make it a driver of compulsive use alongside opioids.16PubMed Central. Short- and Long-Acting Psychedelics: Structure–Activity Relationships, Pharmacology, and Implications for Neuropsychiatric Therapeutics This is consistent with the broader pattern seen across classical psychedelics, which generally do not produce the compulsive-redosing behavior characteristic of addictive substances. The main danger with DOM was never addiction in the traditional sense; it was the acute harm that came from taking too much of an extremely long-lasting, potent hallucinogen without understanding what it was.
Despite its amphetamine-derived structure, DOM behaves pharmacologically much more like a psychedelic than a stimulant. It does not produce the dopamine-driven euphoria and craving cycle associated with methamphetamine or cocaine. Its effects are serotonergic, and while those effects can be profoundly disorienting and physically taxing at high doses, they do not create the pull toward repeated use that defines substances with high abuse potential. The physical symptoms that alarmed emergency physicians in 1967, like elevated heart rate and tremors, were real and concerning, but they were consequences of acute serotonergic overstimulation rather than signs of the cardiovascular toxicity pattern seen with stimulant abuse.