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MY'STORY
The MOVE Fire
This is a personal recollection on the Move fire on May 13, 1985 Philadelphia police fired thousands of rounds at the MOVE house, city officials approved dropping an explosive device on the roof, the resulting fire was allowed to burn, 11 people—including five children—died, and 61 homes were destroyed. Philadelphia City Council later called it a “brutal attack carried out by the City of Philadelphia on its own citizens” and acknowledged that no individual faced criminal consequences for the bombing. One timeline correction worth preserving for the BHP record: the major previous MOVE-police confrontation was August 8, 1978, about seven years before the bombing, not a year or two earlier. Officer James Ramp was killed, other police and firefighters were wounded, nine MOVE members were later convicted, and television cameras recorded police beating Delbert Africa during his arrest. The 1985 MOVE Commission later specifically criticized city planners for failing to adequately use lessons from that 1978 confrontation. And that actually strengthens the point you’re making: 1985 did not happen without precedent or institutional memory. There had already been a deadly confrontation with MOVE, years of conflict, negotiations and police involvement before Osage Avenue.
In August 1908, a white mob attacked Springfield, Illinois’s Black community, destroying homes and businesses and lynching two Black men. National outrage over the violence helped spur the movement that created the NAACP the following year.
Reflects the personal views, recollections, and perspective of the author, Mike Davis.
The MOVE Fire
This is a personal recollection on the Move fire on May 13, 1985
Philadelphia police fired thousands of rounds at the MOVE house, city officials approved dropping an explosive device on the roof, the resulting fire was allowed to burn, 11 people—including five children—died, and 61 homes were destroyed. Philadelphia City Council later called it a “brutal attack carried out by the City of Philadelphia on its own citizens” and acknowledged that no individual faced criminal consequences for the bombing.
One timeline correction worth preserving for the BHP record: the major previous MOVE-police confrontation was August 8, 1978, about seven years before the bombing, not a year or two earlier. Officer James Ramp was killed, other police and firefighters were wounded, nine MOVE members were later convicted, and television cameras recorded police beating Delbert Africa during his arrest. The 1985 MOVE Commission later specifically criticized city planners for failing to adequately use lessons from that 1978 confrontation.
And that actually strengthens the point you’re making: 1985 did not happen without precedent or institutional memory. There had already been a deadly confrontation with MOVE, years of conflict, negotiations and police involvement before Osage Avenue.
BHP gathered finds from its connected research sources.
Showing the 4
strongest Black History matches.
DMT has a rapid onset, intense effects, and a relatively short duration of action. For those reasons, DMT was known as the "businessman's trip" during the 1960s in the United States, as a user could access the full depth of a psychedelic experience in considerably less time than with other substances such as LSD or psilocybin mushrooms.[15] DMT can be inhaled or injected and its effects depend on the dose, as well as the mode of administration. When inhaled or injected, the effects last about five to fifteen minutes. Effects can last three hours or more when orally ingested along with a monoamine oxidase inhibitor (MAOI), such as the ayahuasca brew of many native Amazonian tribes.[16] DMT induces intense, often indescribable subjective experiences involving vivid visual hallucinations, altered sensory perception, ego dissolution, and encounters with seemingly autonomous entities. DMT is generally considered non addictive with low dependence and having little to no tolerance build-up with short-acting routes, but it may cause acute psychological distress or cardiovascular effects, especially in predisposed individuals.
DMT exhibits broad and variable binding affinities across numerous receptors, showing its strongest interactions with serotonin receptors, especially 5-HT2A, 5-HT1A, and 5-HT2C, which are believed to mediate its psychedelic effects. Endogenous DMT, a psychedelic compound, is naturally produced in mammals, with evidence showing its synthesis and presence in brain and body tissues, though its exact roles and origins remain debated. DMT is internationally illegal without authorization, with most countries banning its possession and trade, though some allow religious use of ayahuasca, a DMT-containing decoction. Short-acting psychedelics like DMT are considered scalable alternatives to longer-acting drugs like psilocybin for potential clinical use.[18][19] DMT is currently undergoing clinical trials for treatment-resistant depression.[20]
In his book TiHKAL (Tryptamines I Have Known and Loved) and other publications, Alexander Shulgin lists DMT's dose as greater than 350mg orally, 60 to 100mg intramuscularly, subcutaneously, or via smoking, and 4 to 30mg by intravenous injection.[1][3] He also reported that doses of 150 to 350mg or even up to 1,000mg orally and a dose of 100mg buccally produced no effects, whereas doses of 20 to 80mg intramuscularly, 30 to 100mg smoked, and 15 to 30mg intravenously were all active in producing effects.[1][29][21][23] In terms of intramuscular injection, threshold effects occur at a dose of 30mg and full effects occur at a dose of 50 to 100mg by this route.[29][1] Similarly, the dose for full effects with subcutaneous injection is likewise 60 to 100mg.[29] With regard to intravenous injection, a dose of 4mg was indistinguishable from placebo, 8mg produced physical effects but no psychoactive effects, 15mg produced threshold psychedelic effects, and 30mg produced strong psychedelic effects.[1] Shulgin lists the duration of parenteral DMT alone as up to 1hour.[1]
In other more recent publications, different dose ranges of inhaled DMT of 2 to 100mg or 15 to 60mg have been described[30][31] and typical doses have been reported to be 40 to 50mg.[11] Concerning intravenous injection and based on contemporary clinical studies, 15mg has been described as a low dose, 25mg as an intermediate or "good effect" dose, and 30mg as a high or "ego-dissolution" dose.[32] There may be a ceiling in the intensity of DMT's effects however, with saturation reached at doses of 15 to 20mg.[7] For intramuscular injection, a range of 50 to 100mg with an estimated typical dose of 75mg has been noted.[33] The onset of DMT has been given as 10 to 15seconds smoked,[5][2][4] within 2 to 5minutes intravenously,[2] and within 2 to 5minutes intramuscularly.[3][4] In addition, its duration is given as 5 to 20minutes (average 12minutes) via inhalation,[3][4][31] less than 30minutes intravenously,[4][11] and 30 to 60minutes intramuscularly.[3][4]
DMT by continuous intravenous infusion (i.e., an intravenous "drip", also sometimes known as "DMTx") has additionally been developed recently and can extend the duration of intravenous DMT to hours.[32][34][35][36][37] The dose range for this route is 0.6 to 1.8mg per minute, with 0.6mg/minute being a low dose, 1.2mg/minute being an intermediate or "good effect" dose, and 1.8 to 2.4mg/minute being a high or "ego dissolution" dose.[32][34] In addition to continuous intravenous infusion, DMT vape pens have been developed and distributed as an alternative to smoking.[38][39][40]
Besides parenteral DMT alone, Shulgin also described the properties of oral DMT in combination with the MAOI and distinct ibogaine-like hallucinogen harmaline or in some cases Peganum harmala seeds in TiHKAL.[41] This combination is a form of pharmahuasca and is similar to ayahuasca.[41] Doses of 20 to 50mg harmaline with 55 to 60mg DMT both orally were associated with few to no effects.[41] At higher harmaline doses, including 80 to 150mg, combined with 35 to 120mg DMT, both orally, clear MAOI activity occurred and more significant effects became apparent.[41] More recent publications have defined the usually recommended doses as 50mg DMT and 100mg harmaline orally.[11] Besides DMT with harmaline, the properties and effects of oral DMT in combination with harmine have also been studied by Jonathan Ott.[42][43] He found that the threshold dose was 20 or 30mg DMT and 120mg harmine orally.[42][43] Shulgin also reported in TiHKAL that 35 to 40mg DMT and 140 to 190mg harmine were unmistakably active, whereas smaller doses of 30mg DMT and 120 to 140mg harmine orally were inactive.[44] In notable contrast to harmaline, harmine does not have its own psychoactive effects when used at doses of up to at least 300mg orally.[44][45] In pharmahuasca, the harmala alkaloid is usually taken first and then DMT is taken 15 to 20minutes later, although a shorter or longer interval may also be employed.[11][44] The onset of oral DMT with an MAOI is within 1hour[3][4] and its duration is 4 to 6hours.[3][4][5][27]
Subjective experiences of DMT indubitably includes profound time-dilatory, visual, auditory, tactile, and proprioceptive distortions and hallucinations, and other experiences that, by most firsthand accounts, defy verbal or visual description.[46] Examples include perceiving hyperbolic geometry or seeing Escher-like impossible objects.[47]
Several scientific experimental studies have tried to measure subjective experiences of altered states of consciousness induced by drugs under highly controlled and safe conditions.
Rick Strassman and his colleagues conducted a five-year-long DMT study at the University of New Mexico in the 1990s.[48] The results provided insight about the quality of subjective psychedelic experiences. In this study participants received the DMT dose via intravenous injection and the findings suggested that different psychedelic experiences can occur, depending on the dose. Lower doses (0.01 and 0.05 mg/kg) produced some aesthetic and emotional responses, but not hallucinogenic experiences (e.g., 0.05 mg/kg had mild mood elevating and calming properties).[48] In contrast, responses produced by higher doses (0.2 and 0.4 mg/kg) researchers labeled as "hallucinogenic" that elicited "intensely colored, rapidly moving display of visual images, formed, abstract or both". Comparing to other sensory modalities, the most affected was the visual. Participants reported visual hallucinations, fewer auditory hallucinations and specific physical sensations progressing to a sense of bodily dissociation, as well as experiences of euphoria, calm, fear, and anxiety.[48] These dose-dependent effects match well with anonymously posted "trip reports" online, where users report "breakthroughs" above certain doses.[49][additional citation(s) needed]
Strassman also highlighted the importance of the context where the drug has been taken. He claimed that DMT has no beneficial effects of itself, rather the context when and where people take it plays an important role.[50][48]
It appears that DMT can induce a state or feeling wherein the person believes they "communicate with other intelligent lifeforms" (see "Entity encounters" below). High doses of DMT produce a state that involves a sense of "another intelligence" that people sometimes describe as "super-intelligent", but "emotionally detached".[48]
A 1995 study by Adolf Dittrich and Daniel Lamparter found that the DMT-induced altered state of consciousness (ASC) is strongly influenced by habitual rather than situative factors. In the study, researchers used three dimensions of the APZ questionnaire to examine ASC. The first dimension, oceanic boundlessness (OB), refers to dissolution of ego boundaries and is mostly associated with positive emotions.[51] The second dimension, anxious ego-dissolution (AED), represents a disordering of thoughts and decreases in autonomy and self-control. Last, visionary restructuralization (VR) refers to auditory/visual illusions and hallucinations.[52] Results showed strong effects within the first and third dimensions for all conditions, especially with DMT, and suggested strong intrastability of elicited reactions independently of the condition for the OB and VR scales.[51]
In addition to parenteral DMT, Shulgin described the effects of oral DMT plus harmaline or in some cases Peganum harmala seeds in TiHKAL.[41] The effects were reported to include closed-eye imagery such as colors, infinitely repeated and wavy sheets of patterns, and kaleidoscopic images, visual changes like brighter colors and patterns and distortions, music enhancement, time distortion, clarity, insights, intoxication, emotional changes, feeling alive and excited, depression, despair, and feeling psychotic.[41] Other effects included difficulty focusing on thoughts, short-termmemory disruption, feeling cold, nausea, gait impairment or difficulty walking, and an afterglow.[41] The preceding effects are variably due to both DMT and harmaline, with harmaline also producing its own hallucinogenic effects at sufficiently doses, for instance 150mg or more.[41]
Entities perceived while under the effects of DMT have been represented in diverse forms of psychedelic art. The term machine elf was coined by ethnobotanist Terence McKenna for the entities he encountered in DMT "hyperspace", along with terms like fractal elves, or self-transforming machine elves.[53][54] McKenna first encountered the "machine elves" after smoking DMT in Berkeley in 1965. His subsequent speculations regarding the hyperdimensional space in which they were encountered have inspired a great many artists and musicians, and the meaning of DMT entities has been a subject of considerable debate among participants in a networked cultural underground, enthused by McKenna's effusive accounts of DMT hyperspace.[55]Cliff Pickover has also written about the "machine elf" experience, in the book Sex, Drugs, Einstein, & Elves.[16] Strassman noted similarities between self-reports of his DMT study participants' encounters with these "entities", and mythological descriptions of figures such as Ḥayyot haq-Qodesh in ancient religions, including both angels and demons.[56] Strassman also argues for a similarity in his study participants' descriptions of mechanized wheels, gears and machinery in these encounters, with those described in visions of encounters with the Living Creatures and Ophanim of the Hebrew Bible, noting they may stem from a common neuropsychopharmacological experience.[56]
Strassman argues that the more positive of the "external entities" encountered in DMT experiences should be understood as analogous to certain forms of angels:
The medieval Jewish philosophers whom I rely upon for understanding the Hebrew Bible text and its concept of prophecy portray angels as God's intermediaries. That is, they perform a certain function for God. Within the context of my DMT research, I believe that the beings that volunteers see could be conceived of as angelic – that is, previously invisible, incorporeal spiritual forces that are engarbed or enclothed in a particular form – determined by the psychological and spiritual development of the volunteers – bringing a particular message or experience to that volunteer.[57]
Strassman's experimental participants also note that some other entities can subjectively resemble creatures more like insects and aliens.[58] As a result, Strassman writes these experiences among his experimental participants "also left me feeling confused and concerned about where the spirit molecule was leading us. It was at this point that I began to wonder if I was getting in over my head with this research."[59]
Hallucinations of strange creatures had been reported by Stephen Szára in a 1958 study in psychotic patients, in which he described how one of his subjects under the influence of DMT had experienced "strange creatures, dwarves or something" at the beginning of a DMT trip.[60][61]
Other researchers of the entities seemingly encountered by DMT users describe them as "entities" or "beings" in humanoid as well as animal form, with descriptions of "little people" being common (non-human gnomes, elves, imps, etc.).[62] Strassman and others have speculated that this form of hallucination may be the cause of alien abduction and extraterrestrial encounter experiences, which may occur through endogenously-occurring DMT.[63][64]
Likening them to descriptions of rattling and chattering auditory phenomena described in encounters with the Hayyoth in the Book of Ezekiel, Rick Strassman notes that participants in his studies, when reporting encounters with the alleged entities, have also described loud auditory hallucinations, such as one subject reporting typically "the elves laughing or talking at high volume, chattering, twittering".[56]
A 2018 study found significant relationships between DMT experiences and near-death experiences (NDE).[71] A 2019 large-scale study pointed that ketamine, Salvia divinorum, and DMT (and other classical psychedelic substances) may be linked to NDEs due to the semantic similarity of reports associated with the use of psychoactive compounds and NDE narratives, but the study concluded that with the current data it is neither possible to corroborate nor refute the hypothesis that the release of an endogenous ketamine-like neuroprotective agent underlies NDE phenomenology.[72]
According to a dose-response study in human subjects, dimethyltryptamine administered intravenously slightly elevated blood pressure, heart rate, pupil diameter, and rectal temperature, in addition to elevating blood concentrations of beta-endorphin, corticotropin, cortisol, and prolactin; growth hormone blood levels rose equally in response to all doses of DMT, and melatonin levels were unaffected."[48]
In the 1950s, the endogenous production of psychoactive agents was considered to be a potential explanation for the hallucinatory symptoms of some psychiatric diseases; this is known as the transmethylation hypothesis.[73] Several speculative and yet untested hypotheses suggest that endogenous DMT is produced in the human brain and is involved in certain psychological and neurological states.[74] DMT is naturally occurring in small amounts in rat brains, human cerebrospinal fluid, and other tissues of humans and other mammals.[75][76][77][78] Further, mRNA for the enzyme necessary for the production of DMT, INMT, are expressed in the human cerebral cortex, choroid plexus, and pineal gland, suggesting an endogenous role in the human brain.[79] In 2011, Nicholas Cozzi of the University of Wisconsin School of Medicine and Public Health, and three other researchers, concluded that INMT, an enzyme that is associated with the biosynthesis of DMT and endogenous hallucinogens is present in the non-human primate (rhesus macaque) pineal gland, retinal ganglion neurons, and spinal cord.[80] Neurobiologist Andrew Gallimore suggested in 2013 that while DMT might not have a modern neural function, it may have been an ancestral neuromodulator once secreted in psychedelic concentrations during REM sleep, a function now lost.[62]
DMT can rarely cause hallucinogen-induced psychotic disorder (HIPD).[83][84] HIPD is a type of substance-induced psychosis.[85] The symptoms of HIPD are psychosis with paranoia, delusions, hallucinations, disorganized thinking, or insomnia that persist beyond the initial effects of the drug.[86] HIPD due to psychedelics is most commonly associated with LSD, but may be caused by DMT as well.[84] Hallucinogen-induced psychotic disorder is a medical emergency. Without treatment, the psychosis can persist for weeks or months.[87][88] The treatment is an atypical antipsychotic medication such as aripiprazole, quetiapine, olanzapine, or risperidone.[89] People with a personal or family history of mental illness are at the highest risk for hallucinogen-induced psychotic disorder.[90] The condition occurs in fewer than 1% of people with psychedelics.[91]
DMT, like other serotonergic psychedelics, is considered to be non-addictive with low abuse potential.[46] A study examining substance use disorder for the DSM-IV reported that almost no hallucinogens produced dependence, unlike psychoactive drugs of other classes such as stimulants and depressants.[81][92] At present, there have been no studies that report drug withdrawal syndrome with termination of DMT, and dependence potential of DMT and the risk of sustained psychological disturbance may be minimal when used infrequently; however, the physiological dependence potential of DMT and ayahuasca has not yet been documented convincingly.[93]
Unlike with other classical psychedelics, tolerance does not seem to develop to the subjective effects of DMT.[3][94] Studies report that DMT did not exhibit tolerance upon repeated administration of twice a day sessions, separated by 5hours, for 5consecutive days; field reports suggests a refractory period of only 15 to 30minutes, while the plasma levels of DMT was nearly undetectable 30minutes after intravenous administration.[94][95] Another study of four closely spaced DMT infusion sessions with 30minute intervals also suggests no tolerance buildup to the psychological effects of the compound, while heart rate responses and neuroendocrine effects were diminished with repeated administration.[94][95] Similarly to DMT by itself, tolerance does not appear to develop to ayahuasca.[21][96] A fully hallucinogenic dose of DMT did not demonstrate cross-tolerance to human subjects who are highly tolerant to LSD;[97] hence, research suggests that DMT exhibits unique pharmacological properties compared to other classical psychedelics.[95] Contrary to earlier findings however, subsequent clinical studies employing DMT by continuous intravenous infusion (also known as DMTx) have found rapid and moderate acute tolerance development with DMT.[7][35][36][37]
There have been no serious adverse effects reported on long-term use of DMT, apart from acute cardiovascular events.[82] Repeated and one-time administration of DMT produces marked changes in the cardiovascular system,[82] with an increase in systolic and diastolic blood pressure; although the changes were not statistically significant, a robust trend towards significance[clarification needed] was observed for systolic blood pressure at high doses.[98]
There have been cases of death with DMT.[99] In terms of extrapolated human lethal dose based on animal studies and human case reports, the lethal dose of DMT relative to a typical recreational dose is estimated to be 50-fold in the case of oral DMT (as ayahuasca).[99]
Chronic use of SSRIs, TCAs, and MAOIs diminish subjective effects of psychedelics due to presumed serotonin 5-HT2A receptors downregulation and/or desensitization secondary to elevated serotonin levels.[101]: 145 However, a clinical study of people with depression found that SSRIs did not diminish the effects of DMT and instead resulted in greater mystical experience, emotional breakthrough, and ego dissolution scores with DMT than in people with depression not on antidepressants.[102] This was in contrast to previous research finding that SSRIs diminished the effects of serotonergic psychedelics.[103]
It has also been shown to possess affinity for the dopamineD1, α1-adrenergic, α2-adrenergic, imidazoline-1, and σ1receptors.[123][112][128] Converging lines of evidence established activation of the σ1 receptor at concentrations of 50–100 μmol/L.[129] Its efficacies at the other receptor binding sites are unclear. It has also been shown in vitro to be a substrate for the cell-surface serotonin transporter (SERT) expressed in human platelets, and the rat vesicular monoamine transporter 2 (VMAT2), which was transiently expressed in fall armyworm Sf9 cells. DMT inhibited SERT-mediated serotonin uptake into platelets at an average concentration of 4.00 ± 0.70 μmol/L and VMAT2-mediated serotonin uptake at an average concentration of 93 ± 6.8 μmol/L.[130] In addition, DMT is a potent serotonin releasing agent with an EC50Tooltip half-maximal effective concentration value of 81–114nM and an EmaxTooltip maximal efficacy of 78%.[116][113][119]
As with other so-called "classical hallucinogens",[131] a large part of DMT psychedelic effects can be attributed to a functionally selective activation of the 5-HT2A receptor.[48][121][132][133][134][135][136] DMT concentrations eliciting 50% of its maximal effect (half maximal effective concentration = EC50) at the human 5-HT2A receptor in vitro are in the 0.118–0.983 μmol/L range.[121][112][124][137] This range of values coincides well with the range of concentrations measured in blood and plasma after administration of a fully psychedelic dose.
DMT is one of the only psychedelics that isn't known to produce tolerance to its hallucinogenic effects.[94][138] The lack of tolerance with DMT may be related to the fact that, unlike other psychedelics such as LSD and DOI, DMT does not desensitize serotonin 5-HT2A receptors in vitro.[94][124] This may be due to the fact that DMT is a biased agonist of the serotonin 5-HT2A receptor.[138][113] More specifically, DMT activates the Gqsignaling pathway of the serotonin 5-HT2A receptor without significantly recruiting β-arrestin2.[138][113] Activation of β-arrestin2 is linked to receptor downregulation and tachyphylaxis.[138][139][140] Similarly to DMT, 5-MeO-DMT is a biased agonist of the serotonin 5-HT2A receptor, with minimal β-arrestin2 recruitment, and likewise has been associated with little tolerance to its hallucinogenic effects.[141][113] On the other hand, the lack of apparent tolerance of DMT and similar agents may simply be related to their very short durations.[142] In contrast to the preceding findings however, subsequent research has found that continuous intravenous infusion of DMT does produce moderate acute tolerance.[7][35][36][37]
As DMT has been shown to have slightly better potency (EC50) at the human serotonin 5-HT2C receptor than at the serotonin 5-HT2A receptor,[112][124] the serotonin 5-HT2C receptor is also implicated in DMT's effects.[133][143] The drug shows pronounced biased agonism at the serotonin 5-HT2C receptor.[144] Other receptors such as the serotonin 5-HT1A receptor[123][133][135] and the sigma σ1 receptor may also play a role.[129][145]
In 2009, it was hypothesized that DMT may be an endogenous ligand for the σ1 receptor.[129][145] The concentration of DMT needed for σ1 activation in vitro (50–100 μmol/L) is similar to the behaviorally active concentration measured in mouse brain of approximately 106 μmol/L[146] This is minimally 4 orders of magnitude higher than the average concentrations measured in rat brain tissue or human plasma under basal conditions (see Endogenous DMT), so σ1 receptors are likely to be activated only under conditions of high local DMT concentrations. If DMT is stored in synaptic vesicles,[130] such concentrations might occur during vesicular release. To illustrate, while the average concentration of serotonin in brain tissue is in the 1.5-4 μmol/L range,[147][148] the concentration of serotonin in synaptic vesicles was measured at 270 mM.[149] Following vesicular release, the resulting concentration of serotonin in the synaptic cleft, to which serotonin receptors are exposed, is estimated to be about 300 μmol/L. Thus, while in vitro receptor binding affinities, efficacies, and average concentrations in tissue or plasma are useful, they are not likely to predict DMT concentrations in the vesicles or at synaptic or intracellular receptors. Under these conditions, notions of receptor selectivity are moot, and it seems probable that most of the receptors identified as targets for DMT (see above) participate in producing its psychedelic effects.
DMT produces the head-twitch response (HTR), a behavioral proxy of psychedelic-like effects, in rodents.[2][3][150][33] However, its effects in the HTR paradigm in mice that are highly strain-dependent, including producing an HTR comparable to other psychedelics, producing an HTR that is much weaker than that of other psychedelics, or producing no HTR at all.[2][3][150] These conflicting results may be due to rapid metabolism of DMT and/or other peculiarities of DMT in different species.[3] Besides the HTR, DMT also substitutes for LSD and DOM in rodent drug discrimination tests.[33]
DMT has been found to increase oxytocin levels in humans.[35]
It is thought that the rate at which DMT enters the brain, and hence its route of administration, may influence its effects, with more rapid routes like intravenous administration and inhalation potentiating serotonin 5-HT2A receptor activation and consequent hallucinogenic effects.[7] As an example, a bolus intravenous injection of 15mg DMT produces stronger peak effects than a continuous infusion of 1mg/minute given over 1.5hours in spite of the latter achieving higher peak DMT levels.[7]
In September 2020, an in vitro and in vivo study found that DMT present in the ayahuasca infusion promotes neurogenesis.[151] DMT has been found to be a psychoplastogen, a compound capable of promoting rapid and sustained neuroplasticity that may have wide-ranging therapeutic benefit.[152]
The cryo-EMstructures of the serotonin 5-HT2A receptor with DMT, as well as with various other psychedelics and serotonin 5-HT2A receptor agonists, have been solved and published by Bryan L. Roth and colleagues.[153][154]
DMT peak level concentrations (Cmax) measured in the blood after intramuscular (IM) injection (0.7mg/kg, n = 11)[155] and in plasma following intravenous administration (0.4mg/kg, n = 10)[48] of fully psychedelic doses are in the range of around 14 to 154μg/L and 32 to 204μg/L, respectively. The corresponding molar concentrations of DMT are therefore in the range of 0.074–0.818μmol/L in whole blood and 0.170–1.08μmol in plasma.
DMT easily crosses the blood–brain barrier.[5] Studies on the llipophilicity of DMT have been contradictory – most studies find DMT to be either lipophilic or slightly lipophilic, but a 2023 study found it to be lipophobic.[9]
Several studies have described active transport and accumulation of DMT into rat and dog brains following peripheral administration.[159][160][161][162][163] Similar active transport and accumulation processes likely occur in human brains and may concentrate DMT in brain by several-fold or more (relatively to blood), resulting in local concentrations in the micromolar or higher range. Such concentrations would be commensurate with serotonin brain tissue concentrations, which have been consistently determined to be in the 1.5–4 μmol/L range.[147][148]
DMT is commonly handled and stored as a hemifumarate,[1][166] as other DMT acid salts are extremely hygroscopic and will not readily crystallize. Its freebase form, although less stable than DMT hemifumarate, is favored by recreational users choosing to vaporize the chemical as it has a lower boiling point.[1]
The chemical synthesis of DMT has been described.[2][1] It can be synthesized through several possible pathways from different starting materials. The two most commonly encountered synthetic routes are through the reaction of indole with oxalyl chloride followed by reaction with dimethylamine and reduction of the carbonyl functionalities with lithium aluminium hydride to form DMT.[1] The second commonly encountered route is through the N,N-dimethylation of tryptamine using formaldehyde followed by reduction with sodium cyanoborohydride or sodium triacetoxyborohydride. Sodium borohydride can be used but requires a larger excess of reagents and lower temperatures due to it having a higher selectivity for carbonyl groups as opposed to imines.[167] Procedures using sodium cyanoborohydride and sodium triacetoxyborohydride (presumably created in situ from cyanoborohydride though this may not be the case due to the presence of water or methanol) also result in the creation of cyanated tryptamine and beta-carboline byproducts of unknown toxicity while using sodium borohydride in absence of acid does not.[168] Bufotenine, a plant extract, can also be synthesized into DMT.[169]
Alternatively, an excess of methyl iodide or methyl p-toluenesulfonate and sodium carbonate can be used to over-methylate tryptamine, resulting in the creation of a quaternary ammonium salt, which is then dequaternized (demethylated) in ethanolamine to yield DMT. The same two-step procedure is used to synthesize other N,N-dimethylated compounds, such as 5-MeO-DMT.[170]
In a clandestine setting, DMT is not typically synthesized due to the lack of availability of the starting materials, namely tryptamine and oxalyl chloride. Instead, it is more often extracted from plant-sources using a nonpolar hydrocarbon solvent such as naphtha or heptane, and a base such as sodium hydroxide.[citation needed]
The chemicals involved in the extraction are commonly available. The plant-material may be illegal to procure in some countries. The end-product (DMT) is illegal in most countries.
DMT may be measured in blood, plasma or urine using chromatographic techniques as a diagnostic tool in clinical poisoning situations or to aid in the medicolegal investigation of suspicious deaths. In general, blood or plasma DMT levels in recreational users of the drug are in the 10–30 μg/L range during the first several hours post-ingestion.[citation needed] Less than 0.1% of an oral dose is eliminated unchanged in the 24-hour urine of humans.[171][172][clarification needed]
Before techniques of molecular biology were used to localize indolethylamine N-methyltransferase (INMT),[173][174] characterization and localization went on a par: samples of the biological material where INMT is hypothesized to be active are subject to enzyme assay. Those enzyme assays are performed either with a radiolabeled methyl donor like (14C-CH3)SAM to which known amounts of unlabeled substrates like tryptamine are added[175] or with addition of a radiolabeled substrate like (14C)NMT to demonstrate in vivo formation.[176][177] As qualitative determination of the radioactively tagged product of the enzymatic reaction is sufficient to characterize INMT existence and activity (or lack of), analytical methods used in INMT assays are not required to be as sensitive as those needed to directly detect and quantify the minute amounts of endogenously formed DMT. The essentially qualitative method thin layer chromatography (TLC) was thus used in a vast majority of studies.[175] Also, robust evidence that INMT can catalyze transmethylation of tryptamine into NMT and DMT could be provided with reverse isotope dilution analysis coupled to mass spectrometry for rabbit[178][179] and human[180] lung during the early 1970s.
Selectivity rather than sensitivity proved to be a challenge for some TLC methods with the discovery in 1974-1975 that incubating rat blood cells or brain tissue with (14C-CH3)SAM and NMT as a substrate mostly yields tetrahydro-β-carboline derivatives,[175][176][181] and negligible amounts of DMT in brain tissue.[175] It is indeed simultaneously realized that the TLC methods used thus far in almost all published studies on INMT and DMT biosynthesis are incapable to resolve DMT from those tetrahydro-β-carbolines.[175] These findings are a blow for all previous claims of evidence of INMT activity and DMT biosynthesis in avian[182] and mammalian brain,[183][184] including in vivo,[185][186] as they all relied upon use of the problematic TLC methods:[175] their validity is doubted in replication studies that make use of improved TLC methods, and fail to evidence DMT-producing INMT activity in rat and human brain tissues.[187][188] Published in 1978, the last study attempting to evidence in vivo INMT activity and DMT production in brain (rat) with TLC methods finds biotransformation of radiolabeled tryptamine into DMT to be real but "insignificant".[189] Capability of the method used in this latter study to resolve DMT from tetrahydro-β-carbolines is questioned later.[176]
To localize INMT, a qualitative leap is accomplished with use of modern techniques of molecular biology, and of immunohistochemistry. In humans, a gene encoding INMT is determined to be located on chromosome 7.[174]Northern blot analyses reveal INMT messenger RNA (mRNA) to be highly expressed in rabbit lung,[173] and in human thyroid, adrenal gland, and lung.[174][190] Intermediate levels of expression are found in human heart, skeletal muscle, trachea, stomach, small intestine, pancreas, testis, prostate, placenta, lymph node, and spinal cord.[174][190] Low to very low levels of expression are noted in rabbit brain,[174] and human thymus, liver, spleen, kidney, colon, ovary, and bone marrow.[174][190] INMT mRNA expression is absent in human peripheral blood leukocytes, whole brain, and in tissue from seven specific brain regions (thalamus, subthalamic nucleus, caudate nucleus, hippocampus, amygdala, substantia nigra, and corpus callosum).[174][190] Immunohistochemistry showed INMT to be present in large amounts in glandular epithelial cells of small and large intestines. In 2011, immunohistochemistry revealed the presence of INMT in primate nervous tissue including retina, spinal cord motor neurons, and pineal gland.[80] A 2020 study using in-situ hybridization, a far more accurate tool than the northern blot analysis, found mRNA coding for INMT expressed in the human cerebral cortex, choroid plexus, and pineal gland.[79]
Publishing in Science in 1961, Julius Axelrod found an N-methyltransferase enzyme capable of mediating biotransformation of tryptamine into DMT in a rabbit's lung.[208] This finding initiated a still ongoing scientific interest in endogenous DMT production in humans and other mammals.[175][75] From then on, two major complementary lines of evidence have been investigated: Localization and further characterization of the N-methyltransferase enzyme, and analytical studies looking for endogenously produced DMT in body fluids and tissues.[175]
A study published in 2014 reported the biosynthesis of N,N-dimethyltryptamine (DMT) in the human melanoma cell line SK-Mel-147 including details on its metabolism by peroxidases.[210]
It is assumed that more than half of the amount of DMT produced by the acidophilic cells of the pineal gland is secreted before and during death,[citation needed] the amount being 2.5–3.4 mg/kg. Contrarily, this claim by Strassman has been criticized by David Nichols who notes that DMT does not appear to be produced in any meaningful amount by the pineal gland. Removal or calcification of the pineal gland does not induce any of the symptoms caused by removal of DMT. The symptoms presented are consistent solely with reduction in melatonin, which is the pineal gland's known function. Nichols instead suggests that dynorphin and other endorphins are responsible for the reported euphoria experienced by patients during a near-death experience.[211]
In 2014, researchers demonstrated the immunomodulatory potential of DMT and 5-MeO-DMT through the Sigma-1 receptor of human immune cells. This immunomodulatory activity may contribute to significant anti-inflammatory effects and tissue regeneration.[212]
N,N-Dimethyltryptamine (DMT), a psychedelic compound identified endogenously in mammals, is biosynthesized by aromatic L-amino acid decarboxylase (AADC) and indolethylamine-N-methyltransferase (INMT). Studies have investigated brain expression of INMT transcript in rats and humans, coexpression of INMT and AADC mRNA in rat brain and periphery, and brain concentrations of DMT in rats. INMT transcripts were identified in the cerebral cortex, pineal gland, and choroid plexus of both rats and humans via in situ hybridization. Notably, INMT mRNA was colocalized with AADC transcript in rat brain tissues, in contrast to rat peripheral tissues where there existed little overlapping expression of INMT with AADC transcripts. Additionally, extracellular concentrations of DMT in the cerebral cortex of normal behaving rats, with or without the pineal gland, were similar to those of canonical monoamine neurotransmitters including serotonin. A significant increase of DMT levels in the rat visual cortex was observed following induction of experimental cardiac arrest, a finding independent of an intact pineal gland. These results show for the first time that the rat brain is capable of synthesizing and releasing DMT at concentrations comparable to known monoamine neurotransmitters and raise the possibility that this phenomenon may occur similarly in human brains.[79]
The first claimed detection of endogenous DMT in mammals was published in June 1965: German researchers F. Franzen and H. Gross report to have evidenced and quantified DMT, along with its structural analog bufotenin (5-HO-DMT), in human blood and urine.[213] In an article published four months later, the method used in their study was strongly criticized, and the credibility of their results challenged.[214]
Few of the analytical methods used prior to 2001 to measure levels of endogenously formed DMT had enough sensitivity and selectivity to produce reliable results.[215][216]Gas chromatography, preferably coupled to mass spectrometry (GC-MS), is considered a minimum requirement.[216] A study published in 2005[75] implements the most sensitive and selective method ever used to measure endogenous DMT:[217]liquid chromatography-tandem mass spectrometry with electrospray ionization (LC-ESI-MS/MS) allows for reaching limits of detection (LODs) 12 to 200 fold lower than those attained by the best methods employed in the 1970s. The data summarized in the table below are from studies conforming to the abovementioned requirements (abbreviations used: CSF = cerebrospinal fluid; LOD = limit of detection; n = number of samples; ng/L and ng/kg = nanograms (10−9 g) per litre, and nanograms per kilogram, respectively):
DMT in body fluids and tissues (NB: units have been harmonized)
A 2013 study found DMT in microdialysate obtained from a rat's pineal gland, providing evidence of endogenous DMT in the mammalian brain.[209] In 2019, experiments showed that the rat brain is capable of synthesizing and releasing DMT. These results raise the possibility that this phenomenon may occur similarly in human brains.[79]
Quantities of dimethyltryptamine and O-methylbufotenin were found present in the cerebrospinal fluid of humans in a 1978 psychiatric study.[221]
DMT was first synthesized in 1931 by Canadian chemist Richard Manske.[29][225][226] In general, its discovery as a natural product is credited to Brazilian chemist and microbiologistOswaldo Gonçalves de Lima, who isolated an alkaloid he named nigerina (nigerine) from the root bark of Mimosa tenuiflora in 1946.[226][50][227] However, in a careful review of the case Jonathan Ott shows that the empirical formula for nigerine determined by Gonçalves de Lima, which notably contains an atom of oxygen, can match only a partial, "impure" or "contaminated" form of DMT.[42] It was only in 1959, when Gonçalves de Lima provided American chemists a sample of Mimosa tenuiflora roots, that DMT was unequivocally identified in this plant material.[42][228] Less ambiguous is the case of isolation and formal identification of DMT in 1955 in seeds and pods of Anadenanthera peregrina by a team of American chemists led by Evan Horning (1916-1993).[42][229] Since 1955, DMT has been found in a number of organisms: in at least fifty plant species belonging to ten families,[230] and in at least four animal species, including one gorgonian[231] and three mammalian species (including humans).[citation needed]
In terms of a scientific understanding, the hallucinogenic effects of DMT were not uncovered until 1956 by Hungarianchemist and psychiatristStephen Szára.[29][232] Szára, who later worked for the United States National Institutes of Health, researched DMT after his order to acquire LSD from the Swiss company Sandoz Laboratories was rejected on the grounds that the powerful psychotropic could be dangerous in the hands of a communist country.[50] In his paper Dimethyltryptamin: Its Metabolism in Man; the Relation of its Psychotic Effect to the Serotonin Metabolism, Szara employed synthetic DMT, synthesized by the Speeter–Anthony route, which was then administered to 20volunteers by intramuscular injection. Urine samples were collected from these volunteers for the identification of DMT metabolites.[232] This is considered to be the link between the chemical structure of DMT and its cultural consumption as a psychoactive and religious sacrament.[233]
Another historical milestone was the discovery of DMT in plants frequently used by Amazonian natives as additive to the vine Banisteriopsis caapi to make ayahuasca decoctions. In 1957, American chemists Francis Hochstein and Anita Paradies identified DMT in an "aqueous extract" of leaves of a plant they named Prestonia amazonicum [sic] and described as "commonly mixed" with B. caapi.[234] The lack of a proper botanical identification of Prestonia amazonica in this study led American ethnobotanistRichard Evans Schultes (1915–2001) and other scientists to raise serious doubts about the claimed plant identity.[235][236] The mistake likely led the writer William Burroughs to regard the DMT he experimented with in Tangier in 1961 as "Prestonia".[237] Better evidence was produced in 1965 by French pharmacologist Jacques Poisson, who isolated DMT as a sole alkaloid from leaves, provided and used by Aguaruna Indians, identified as having come from the vine Diplopterys cabrerana (then known as Banisteriopsis rusbyana).[236] Published in 1970, the first identification of DMT in the plant Psychotria viridis,[227] another common additive of ayahuasca, was made by a team of American researchers led by pharmacologist Ara der Marderosian.[238] Not only did they detect DMT in leaves of P. viridis obtained from Kaxinawáindigenous people, but they were also the first to identify it in a sample of an ayahuasca decoction, prepared by the same indigenous people.[227]
In the 1960s, DMT was known as a "businessman's trip" in the United States because of its very rapid onset and short duration when smoked.[15] It was also referred to by Timothy Leary as the "nuclear bomb of the psychedelic family" in the Psychedelic Review in 1966.[239]
In the 2022 Australian film Everything in Between, the lead character smokes what is implied to be DMT in the opening sequence, which is followed by hallucination-like visual effects and an altered state of consciousness.[240]
A man named Chris Cantelmo attempted to create an online cult around DMT called "Cantelmoism" in the late 2010s.[241] He was a wealthy biochemist and Yale University graduate who had worked in the pharmaceutical industry for several decades, including running multiple high-performance liquid chromatography (HPLC) companies.[241] Cantelmo began his DMT cult endeavor on Reddit and other social mediawebsites after trying DMT in 2018.[241] He rapidly spent his wealth in a fervent attempt to promote DMT and get as many people to try it as possible, forming a cult in the process and becoming an online spectacle.[241] Among other claims, Cantelmo asserted that DMT cured his brain cancer and that it would cure all other diseases.[241] However, he later admitted that he had never had brain cancer and that it had really cured his "severe" lifelong atheism, which he likened to cancer.[241] Cantelmo suffered from mental health issues and died of suicide whilst under pressure of losing his home in November 2019.[241]
Internationally, DMT is illegal to possess without authorisation, exemption or license, but ayahuasca and DMT brews and preparations are lawful. DMT is controlled by the Convention on Psychotropic Substances at the international level. The Convention makes it illegal to possess, buy, purchase, sell, to retail and to dispense without a licence.
In some countries, ayahuasca is a forbidden or controlled or regulated substance, while in other countries it is not a controlled substance or its production, consumption, and sale, is allowed to various degrees.
Belgium - DMT cannot be possessed, sold, purchased or imported. Usage is not specifically prohibited, but since usage implies possession one could be prosecuted that way.[245]
France - DMT, along with most of its plant-sources, is classified as a stupéfiant (narcotic).
Germany - DMT is prohibited as a class I drug.[246]
Ireland - DMT is an illegal Schedule 1 drug under the Misuse of Drugs Acts.[247] An attempt in 2014 by a member of the Santo Daime church to gain a religious exemption to import the drug failed.[248]
Netherlands - The drug is banned as it is classified as a List 1 Drug per the Opium Law. Production, trade and possession of DMT are prohibited.
Serbia - DMT, along with stereoisomers and salts is classified as List 4 (Psychotropic substances) substance according to Act on Control of Psychoactive Substances.
Sweden - DMT is considered a Schedule 1 drug. The Swedish supreme court concluded in 2018 that possession of processed plant material containing a significant amount of DMT is illegal. However, possession of unprocessed such plant material was ruled legal.[251][252]
Canada - DMT is classified as a Schedule III drug under the Controlled Drugs and Substances Act, but is legal for religious groups to use.[253] In 2017 the Santo Daime Church Céu do Montréal received religious exemption to use ayahuasca as a sacrament in their rituals.[254]
Australia - DMT is listed as a Schedule 9 prohibited substance in Australia under the Poisons Standard (October 2015).[259] A Schedule 9 drug is outlined in the Poisons Act 1964 as "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 the CEO".[260] Between 2011 and 2012, the Australian federal government was considering changes to the Australian Criminal Code that would classify any plants containing any amount of DMT as "controlled plants".[261] DMT itself was already controlled under current laws. The proposed changes included other similar blanket bans for other substances, such as a ban on any and all plants containing mescaline or ephedrine. The proposal was not pursued after political embarrassment on realisation that this would make the official floral emblem of Australia, Acacia pycnantha (golden wattle), illegal.[citation needed] The Therapeutic Goods Administration and federal authority had considered a motion to ban the same, but this was withdrawn in May 2012 (as DMT may still hold potential entheogenic value to native and/or religious people).[262] Under the Misuse of Drugs Act 1981 6.0g (3/16oz) of DMT is considered enough to determine a court of trial and 2.0g (1/16oz) is considered intent to sell and supply.[263]
In December 2004, the U.S. Supreme Court lifted a stay allowing the Brazil-based União do Vegetal church to use a decoction containing DMT in their Christmas services that year. This decoction is a tea made from boiled leaves and vines, known as hoasca within the UDV, and ayahuasca in different cultures. In Gonzales v. O Centro Espírita Beneficente União do Vegetal, the Supreme Court heard arguments on November 1, 2005, and unanimously ruled in February 2006 that the U.S. federal government must allow the UDV to import and consume the tea for religious ceremonies under the 1993 Religious Freedom Restoration Act.
Also suing under the Religious Freedom Restoration Act, three Santo Daime churches filed suit in federal court to gain legal status to import DMT-containing ayahuasca tea in 2008. The U.S. District Court in Oregon ruled in Church of the Holy Light of the Queen v. Mukasey (615 F.Supp.2d 1210) ruled that the religious group could import, distribute, and brew ayahuasca. A matter of religious freedom protected by the religious freedom law, the court issued a permanent injunction barring the government from prohibiting or penalizing the sacramental use of the religious drink.
Short-acting psychedelics like DMT and 5-MeO-DMT show rapid and sustained antidepressant effects in treatment-resistant depression, potentially offering a more scalable alternative to psilocybin, though larger controlled trials are needed to confirm efficacy.[18][19]
A recent Phase 1/2 clinical trial evaluated the safety, tolerability, pharmacokinetics, and antidepressant effects of SPL026, an intravenous formulation of DMT fumarate, in both healthy volunteers and patients with moderate-to-severe major depressive disorder, using randomized, placebo-controlled and open-label dosing protocols.[264] It found that inhaled 5-MeO-DMT (GH001) was well tolerated and produced rapid antidepressant effects in treatment-resistant depression, with individualized dosing showing the highest remission rates.[265]
A Phase 1 open-label study assessed the safety, tolerability, pharmacokinetics, and preliminary efficacy of intravenous SPL026 alone or combined with SSRIs in patients with major depressive disorder whose symptoms were not fully relieved by SSRIs.[266]
In a Phase 2a open-label trial, inhaled DMT produced rapid, well-tolerated, and sustained antidepressant effects in patients with treatment-resistant depression, showing high response and remission rates within 7 days and lasting up to 3 months.[267]
A single-day, open-label trial found that vaporized DMT produced rapid and sustained antidepressant effects in treatment-resistant depression, with up to 50% of participants maintaining remission one month post-dose.[268]
There are completed and ongoing trials of VLS-01, a buccal film formulation of DMT, in treating patients with treatment-resistant depression. In a completed Phase 1 trial, this formulation was found to be well tolerated, with adverse effects being mild or moderate.[269] As of April 2026, there are phase 2 trials ongoing in the United States and Australia.[270][271][272]
DMT exists naturally in humans and other animals; it may play significant roles in mammalian physiology—potentially as a neurotransmitter, hormone, and immunomodulator—despite longstanding skepticism based on outdated or flawed evidence.[138]
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^ abCozzi NV, Gopalakrishnan A, Anderson LL, Feih JT, Shulgin AT, Daley PF, et al. (December 2009). "Dimethyltryptamine and other hallucinogenic tryptamines exhibit substrate behavior at the serotonin uptake transporter and the vesicle monoamine transporter". Journal of Neural Transmission. 116 (12): 1591–1599. doi:10.1007/s00702-009-0308-8. PMID19756361.
^Glennon RA (1994). "Classical hallucinogens: an introductory overview". In Lin GC, Glennon RA (eds.). Hallucinogens: An Update(PDF). NIDA Research Monograph Series. Vol. 146. Rockville, MD: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Institute on Drug Abuse. pp. 4–32. OCLC461332776. Archived from the original on 2004-10-21. Retrieved 2026-09-12.{{cite book}}: CS1 maint: bot: original URL status unknown (link)
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^ abcdeJiménez JH, Bouso JC (August 2022). "Significance of mammalian N, N-dimethyltryptamine (DMT): A 60-year-old debate". Journal of Psychopharmacology. 36 (8): 905–919. doi:10.1177/02698811221104054. PMID35695604.
^Martin WR, Sloan JW (1977). "Pharmacology and Classification of LSD-like Hallucinogens". Drug Addiction II: Amphetamine, Psychotogen, and Marihuana Dependence. Berlin, Heidelberg: Springer Berlin Heidelberg. pp. 305–368. doi:10.1007/978-3-642-66709-1_3. ISBN978-3-642-66711-4. The observation that tolerance to LSD does not confer cross tolerance to several of DMT's autonomic effects suggests that these N-disubstituted compounds may differ in some respects from LSD. The duration of action of DMT is less than that of LSD. Further, we have not been able to demonstrate tachyphylaxis to the actions of tryptamine in the dog (MARTIN and EADES, 1972). Tryptamine's duration of action is less than that of DMT. It is possible that a long duration of action is a necessary attribute of LSD-like hallucinogens for them to effectively induce tolerance (see Subsect. E.III).
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^Eckernäs E, Macan-Schönleben A, Andresen-Bergström M, Birgersson S, Hoffmann KJ, Ashton M (December 2023). "N, N-dimethyltryptamine forms oxygenated metabolites via CYP2D6 - an in vitro investigation". Xenobiotica; the Fate of Foreign Compounds in Biological Systems. 53 (8–9): 515–522. doi:10.1080/00498254.2023.2278488. hdl:10067/2011610151162165141. PMID37916667.
^Riba J, McIlhenny EH, Bouso JC, Barker SA (May 2015). "Metabolism and urinary disposition of N,N-dimethyltryptamine after oral and smoked administration: a comparative study". Drug Testing and Analysis. 7 (5): 401–406. doi:10.1002/dta.1685. PMID25069786.
^Cozzi NV, Daley PF (October 2020). "Synthesis and characterization of high-purity N,N-dimethyltryptamine hemifumarate for human clinical trials". Drug Testing and Analysis. 12 (10): 1483–1493. doi:10.1002/dta.2889. PMID32608093.
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^Baselt R (2011). Disposition of Toxic Drugs and Chemicals in Man (9th ed.). Seal Beach, CA: Biomedical Publications. pp. 525–526. ISBN978-0-9626523-8-7.
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^Mandel LR, Rosenzweig S, Kuehl FA (March 1971). "Purification and substrate specificity of indoleamine-N-methyl transferase". Biochemical Pharmacology. 20 (3): 712–716. doi:10.1016/0006-2952(71)90158-4. PMID5150167.
^Lin R, Narasimhachari N (June 1975). "N-Methylation of 1-methyltryptamines by indolethylamine N-methyltransferase". Biochemical Pharmacology. 24 (11–12): 1239–1240. doi:10.1016/0006-2952(75)90071-4. PMID1056183.
^Mandel LR, Ahn HS, VandenHeuvel WJ (April 1972). "Indoleamine-N-methyl transferase in human lung". Biochemical Pharmacology. 21 (8): 1197–1200. doi:10.1016/0006-2952(72)90113-X. PMID5034200.
^Rosengarten H, Meller E, Freidhoff AJ (1976). "Possible source of error in studies of enzymatic formation of dimethyltryptamine". Journal of Psychiatric Research. 13 (1): 23–30. doi:10.1016/0022-3956(76)90006-6. PMID1067427.
^Mandell AJ, Morgan M (March 1971). "Indole(ethyl)amine N-methyltransferase in human brain". Nature. 230 (11): 85–87. doi:10.1038/newbio230085a0. PMID5279043.
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^Wu PH, Boulton AA (July 1973). "Distribution and metabolism of tryptamine in rat brain". Canadian Journal of Biochemistry. 51 (7): 1104–1112. doi:10.1139/o73-144. PMID4725358.
^Boarder MR, Rodnight R (September 1976). "Tryptamine-N-methyltransferase activity in brain tissue: a re-examination". Brain Research. 114 (2): 359–364. doi:10.1016/0006-8993(76)90680-6. PMID963555.
^Gomes UR, Neethling AC, Shanley BC (September 1976). "Enzymatic N-methylation of indoleamines by mammalian brain: fact or artefact?". Journal of Neurochemistry. 27 (3): 701–705. doi:10.1111/j.1471-4159.1976.tb10397.x. PMID823298.
^Stramentinoli G, Baldessarini RJ (October 1978). "Lack of enhancement of dimethyltryptamine formation in rat brain and rabbit lung in vivo by methionine or S-adenosylmethionine". Journal of Neurochemistry. 31 (4): 1015–1020. doi:10.1111/j.1471-4159.1978.tb00141.x. PMID279646.
^Tekes K, Szegi P, Hashemi F, Laufer R, Kalász H, Siddiq A, et al. (2013). "Medicinal chemistry of antimigraine drugs". Current Medicinal Chemistry. 20 (26): 3300–3316. doi:10.2174/0929867311320260012. PMID23746273.
^Allen AK (10 November 2025). "Psychedelics potential set to extend beyond mental health". Pharmaceutical Technology. Retrieved 13 November 2025. "When you look at molecules like psilocybin, lysergic acid diethylamide (LSD) or dimethyltryptamine (DMT), they are all almost identical to approved headache medications in terms of their chemical structure and pharmacological profile," Schindler states.
^Nichols DE, Glennon RA (1984). "Medicinal Chemistry and Structure-Activity Relationships of Hallucinogens". In Jacobs BL (ed.). Hallucinogens: Neurochemical, Behavioral, and Clinical Perspectives. New York: Raven Press. pp. 95–142. ISBN978-0-89004-990-7. OCLC10324237. Lengthening of the side chain of DMT by a single methylene group produces N,N-dimethylhomotryptamine (DMHT; 76, R = H, n = 3). which produced hyperthermia when administered to rabbits (7,232) but was found to be inactive in man (235). Intravenous administration of 5 and 10 mg and intramuscular injection of 20 to 70 mg DMHT was without psychologic effect in 10 human subjects (235). Additional studies on DMHT homologs (i.e., 76, n = 4–10) did not show any interesting activity (7,232).
^Beaton JM, Barker SA, Liu WF (May 1982). "A comparison of the behavioral effects of proteo-and deutero-N, N-dimethyltryptamine". Pharmacology, Biochemistry, and Behavior. 16 (5): 811–814. doi:10.1016/0091-3057(82)90240-4. PMID6806829.
^Barker SA, Beaton JM, Christian ST, Monti JA, Morris PE (May 1984). "In vivo metabolism of alpha,alpha,beta,beta-tetradeutero-N, N-dimethyltryptamine in rodent brain". Biochemical Pharmacology. 33 (9): 1395–1400. doi:10.1016/0006-2952(84)90404-0. PMID6587850.
^Kargbo RB (April 2023). "Orally Active Forms of DMT, 5-MeO-DMT, and Long-Acting MDMA for the Treatment of Neuropsychiatric Disorders". ACS Medicinal Chemistry Letters. 14 (4): 367–368. doi:10.1021/acsmedchemlett.3c00077. PMC10108390. PMID37077395. Parent DMT and 5-MeO−DMT suffer from inherent pharmacokinetic limitations: DMT has an ultrashort half-life (t1/2 = 8−13 min in mice) and is orally inactive without MAOI coadministration, while 5-MeO−DMT also requires MAOI to achieve meaningful oral exposure. To overcome these barriers, Terran Biosciences has developed proprietary prodrugs designed for single oral dosing that bypass first-pass metabolism and subsequently potentially improve CNS delivery after bioconversion (WO2023283364A2).50 Preclinical data demonstrate the success of this approach: oral administration of a DMT prodrug (compound Exp. 2−17, 10 mg/kg) in rats achieved a t1/2 of 1.24 h [10.3 h] for DMT, whereas parent DMT given orally is essentially inactive without MAOI coadministration. Similarly, a 5-MeO−DMT prodrug (Exp. 2− 19, 10 mg/kg) yielded a Cmax of 106 ng/mL, and a t1/2 of 2.02 h for 5-MeO−DMT.50
^Palfreyman MG, Varty GB, Stang E, Boltaev U, Avery K, Nivorozhkin A (December 2025). "Modification of natural tryptamines for the treatment of neuropsychiatric diseases". Journal of Psychopharmacology. 39 (12): 1338–1350. doi:10.1177/02698811251368362. PMID41045211. In addition to psilocin, DMT and 5-MeO-DMT have been made into prodrugs despite lacking the 4-hydroxyl group attachment point. [...] In another approach, the dimethylamino group of DMT or 5-MeO-DMT has been used to generate betaine-like prodrugs of these classic psychedelics (e.g., see N-phosphonooxymethyl prodrugs of DMT and 5-MeO-DMT in Table 3 (Khan et al., 2024)).
^ abBarker SA, Borjigin J, Lomnicka I, Strassman R (December 2013). "LC/MS/MS analysis of the endogenous dimethyltryptamine hallucinogens, their precursors, and major metabolites in rat pineal gland microdialysate". Biomedical Chromatography. 27 (12): 1690–1700. doi:10.1002/bmc.2981. hdl:2027.42/101767. PMID23881860.
^Siegel M (October 1965). "A sensitive method for the detection of N,N-dimethylserotonin (bufotenin) in urine; failure to demonstrate its presence in the urine of schizophrenic and normal subjects". Journal of Psychiatric Research. 3 (3): 205–211. doi:10.1016/0022-3956(65)90030-0. PMID5860629.
^Barker SA, Littlefield-Chabaud MA, David C (February 2001). "Distribution of the hallucinogens N,N-dimethyltryptamine and 5-methoxy-N,N-dimethyltryptamine in rat brain following intraperitoneal injection: application of a new solid-phase extraction LC-APcI-MS-MS-isotope dilution method". Journal of Chromatography. B, Biomedical Sciences and Applications. 751 (1): 37–47. doi:10.1016/S0378-4347(00)00442-4. PMID11232854.
^ abcForsström T, Tuominen J, Karkkäinen J (2001). "Determination of potentially hallucinogenic N-dimethylated indoleamines in human urine by HPLC/ESI-MS-MS". Scandinavian Journal of Clinical and Laboratory Investigation. 61 (7): 547–556. doi:10.1080/003655101753218319. PMID11763413.
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^Oon MC, Rodnight R (December 1977). "A gas chromatographic procedure for determining N, N-dimethyltryptamine and N-monomethyltryptamine in urine using a nitrogen detector". Biochemical Medicine. 18 (3): 410–419. doi:10.1016/0006-2944(77)90077-1. PMID271509.
^Corbett L, Christian ST, Morin RD, Benington F, Smythies JR (February 1978). "Hallucinogenic N-methylated indolealkylamines in the cerebrospinal fluid of psychiatric and control populations". The British Journal of Psychiatry. 132 (2): 139–144. doi:10.1192/bjp.132.2.139. PMID272218.
^Lin RL, Narasimhachari N, Himwich HE (September 1973). "Inhibition of indolethylamine-N-methyltransferase by S-adenosylhomocysteine". Biochemical and Biophysical Research Communications. 54 (2): 751–759. Bibcode:1973BBRC...54..751L. doi:10.1016/0006-291X(73)91487-3. PMID4756800.
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^Pachter IJ, Zacharias DE, Ribeiro O (September 1959). "Indole alkaloids of Acer saccharinum (the silver maple), Dictyoloma incanescens, Piptadenia colubrina, and Mimosa hostilis". Journal of Organic Chemistry. 24 (9): 1285–1287. Bibcode:1959JOrgC..24.1285P. doi:10.1021/jo01091a032.
^Fish MS, Johnson NM, Horning EC (November 1955). "Piptadenia alkaloids. Indole bases of P. peregrina (L.) Benth. and related species". Journal of the American Chemical Society. 72 (22): 5892–5895. Bibcode:1955JAChS..77.5892F. doi:10.1021/ja01627a034.
^Cimino G, De Stefano S (1978). "Chemistry of Mediterranean gorgonians: simple indole derivatives from Paramuricea chamaeleon". Comparative Biochemistry and Physiology C. 61 (2): 361–362. doi:10.1016/0306-4492(78)90070-9.
^ abSzara S (November 1956). "Dimethyltryptamin: its metabolism in man; the relation to its psychotic effect to the serotonin metabolism". Experientia. 12 (11): 441–442. doi:10.1007/bf02157378. PMID13384414.
^McKenna DJ, Callaway JC, Grob CS (1998). "The scientific investigation of Ayahuasca: a review of past and current research". The Heffter Review of Psychedelic Research. 1 (65–77): 195–223.
^Hochstein FA, Paradies AM (1957). "Alkaloids of Banisteria caapi and Prestonia amazonicum". Journal of the American Chemical Society. 79 (21): 5735–5736. Bibcode:1957JAChS..79.5735H. doi:10.1021/ja01578a041.
^ abPoisson J (April 1965). "Note on "Natem", A Toxic Peruvian Beverage, and ITS Alkaloids" [Note on "Natem", a toxic Peruvian beverage, and its alkaloids]. Annales Pharmaceutiques Françaises (in French). 23: 241–244. PMID14337385.
^Leary T (November 1966). "Programmed Communication During Experiences with DMT (Dimethyltryptamine)"(PDF). Psychedelic Review. 1 (8): 83–95. During the first two years of the Harvard Psychedelic Research Project rumors circulated about a "powerful" psychedelic agent called dimethyltryptamine: DMT. The effect of this substance was supposed to last for less than an hour and to produce shattering, terrorizing effects. It was alleged to be the nuclear bomb of the psychedelic family.
^Health, Disability and Ageing (30 September 2015). "Poisons Standard October 2015". comlaw.gov.au. Office Parliamentary Counsel. Archived from the original on 2016-01-19. Retrieved 2016-01-06.
^Clinical trial number NCT04673383 for "A Double-blind, Randomised, Placebo-controlled Study of Intravenous Doses of SPL026 (DMT Fumarate), a Serotonergic Psychedelic, in Healthy Subjects (Part A) and Patients With Major Depressive Disorder (Part B) " at ClinicalTrials.gov
^Clinical trial number NCT05553691 for "An Open-Label Study Investigating the Safety, Tolerability, Pharmacokinetics, Pharmacodynamics & Exploratory Efficacy of Intravenous SPL026 Drug Product (DMT Fumarate) Alone or in Combination With SSRIs in Patients With Major Depressive Disorder" at ClinicalTrials.gov
^Clinical trial number NCT06524830 for "A Phase 2, Multicenter, Double-blind, Randomized, Placebo-controlled Trial to Assess the Efficacy, Safety, and Tolerability of Repeated Doses of VLS-01 Buccal Film in Participants With Treatment Resistant Depression" at ClinicalTrials.gov
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Madam C.J. Walker
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A thriving Black political and business community in Wilmington, North Carolina was attacked as white supremacists seized control of local government. Black citizens were killed and expelled, and elected leadership was overthrown. The event reshaped the city and suppressed Black political power for generations.
