DPT

DPT holds two places that no other substance in this wiki occupies. It has been taken as a sacrament by a Manhattan church, and it served as an adjunct to end-of-life psychotherapy conducted by Grof and Richards at Spring Grove hospital between 1977 and 1980. Its singularity therefore does not lie in its pharmacology, whose profile its own authors describe as similar to that of the other psychedelic tryptamines: it is a synthetic tryptamine with no known natural occurrence, an agonist at the 5-HT2A receptor, orally active without a monoamine oxidase inhibitor. Between these two human histories and what the literature says about it there is a void that must be stated at the outset: no one has ever measured the pharmacokinetics of DPT, in any species, and its entire published human toxicology comes down to two people.

Neurochemical action

The only point on which all the sources agree is 5-HT2A agonism. Two recent datasets on human receptors do not concur on the rest, and it is better to give both than to arbitrate between them: Kozell et al. 2023 measure at 5-HT2A a Ki of 374 ± 97 nM, an EC50 of 943 ± 88 nM and an efficacy of 85.2% ± 5.1%; Tyagi, Saraf and Canal 2023 find an EC50 of 451 nM and an Emax of 106% ± 1.13, that is, a full agonist.

One figure circulates that must not be repeated on its own: the 3 nM. It exists, it is in Tyagi, but it is the high-affinity component of a two-site fit whose low-affinity component is 739 nM, and the authors themselves conclude that this is an agonist of moderate potency. Publishing that 3 nM in isolation would give DPT a potency roughly a hundred times greater than anything the functional data support, which fall between 451 and 943 nM.

At 5-HT1A, the spread between sources covers nearly three orders of magnitude: 100 nM in Thiagaraj 2005, which is a displacement IC50 and not a Ki, 186 ± 31 nM in Kozell, 1641 nM in Tyagi, and functional inactivity up to 10,000 nM in Blough 2014. Tyagi acknowledges the discrepancy, attributes it to the radioligand used, and does not resolve it. This is the molecule's second target, and it is not known whether it is engaged at human doses.

The serotonin transporter is the contested point that matters for what follows. DPT binds there at concentrations of the same order as its receptor affinities, Ki 480 ± 34 nM and reuptake IC50 172 ± 35 nM in Kozell, 0.594 ± 0.12 µmol/L in Cozzi 2009. But the nature of that engagement is disputed. Cozzi concludes that it is a releasing substrate, by an indirect binding-to-uptake ratio method. Blough 2014, who measures release directly, finds none and writes that this ratio method proved inconsistent and has been superseded. Nagai 2007 likewise finds reuptake inhibition with little effect on release, and the Fantegrossi group independently classes DPT among the reuptake inhibitors. Two direct measurements against one indirect inference that its successors judge obsolete, but the question remains open, and the two hypotheses do not carry the same risk profile alongside an antidepressant.

At the sigma-1 receptor, no affinity value exists. And on pharmacokinetics there is nothing at all: no metabolic pathway, no metabolite, no enzyme, no half-life, no bioavailability. DPT has never been measured as a substrate of monoamine oxidase, in any species. It is reported to be orally active without an MAOI, which is compatible with resistance to that enzyme, but compatible is not measured, and to write that DPT would be protected from MAO would go beyond everything that exists.

What animal behaviour shows, and what the affinities do not

The common reputation makes DPT an orally active DMT, the same effects but longer. What really separates the two is not to be read in the affinity tables, where DPT's profile is explicitly described as similar to the other psychedelic tryptamines, but in a behavioural experiment. Li, Rice and France 2007 describe a remarkable sequence in the rat. DPT alone produces flat body posture but not lower lip retraction, and it even blocks the retraction induced by a 5-HT1A agonist, which looks like antagonism. But under a 5-HT2A antagonist, DPT itself produces that retraction, which is in turn attenuated by a 5-HT1A antagonist. In other words, DPT's 5-HT1A agonism is present throughout and masked by its 5-HT2A agonism; it appears when the mask is removed. Fantegrossi 2008 points the same way, with a biphasic head-twitch curve and a functionally insurmountable 5-HT2A antagonism where the 5-HT1A antagonism is surmountable. In the rhesus monkey, the only primate data in existence, a Schild analysis gives pA2 values of 8.50, 7.71 and 7.65 for three antagonists whose potency follows their 5-HT2A affinity and not their 5-HT2C or alpha-1 affinities.

A last result counts for what it does not say: in the mouse of a genetic model of fragile X syndrome, DPT at 10 mg/kg completely prevents audiogenic seizures, with no serotonergic or sigma-1 antagonist blocking that effect. The mechanism is unknown, and it is in no way a therapeutic promise. At the network level, the only existing work is in vitro on rat cortex, where DPT reversibly increases the entropy of spontaneous activity. There is no human brain imaging under DPT.

Two human histories, and what has not been read of them

In 1973, Soskin, Grof and Richards published in Archives of General Psychiatry the only placebo-controlled, double-blind human study this molecule carries: 18 alcoholic patients, 72 sessions under DPT and 64 under placebo, doses of 15 to 30 mg, two-hour interviews. The route of administration is not given by the source, and the two hours are the duration of the interviews, not a measured duration of action. The therapists' ratings give, under DPT, increased recall of memories, greater emotional expressiveness, deeper self-exploration and more psychodynamic resolution. The title of the article speaks of low doses.

The end-of-life corpus, between 1977 and 1980, is the second fact that makes DPT singular: brief psychedelic-assisted psychotherapy in cancer patients, authored by Richards, Rhead, Grof and their colleagues. None of these articles has been read. What circulates through secondary relays, and which must therefore not be taken as verified, turns on around thirty patients, a dozen hours of conventional interview over four weeks followed by a single session under DPT, a range of 60 to 105 mg by the intramuscular route, and one case at 90 mg in a man of 70. The oldest human study identified, Faillace, Vourlekis and Szara 1967, has no abstract available and has not been read either. A molecule administered to dying people in a clinical setting, and to humans under protocol at Spring Grove from 1973 to 1980, whose half-life is still unknown: that is a result in itself.

The Temple of the True Inner Light is a religious centre in New York's East Village whose doctrine is that entheogens are God, and whose eucharist is DPT, synthesised as small crystals, which new converts smoke wrapped in raspberry leaves. All the sources available here are tertiary, and one point that circulates falsely must be corrected: the Temple is not a branch of the Native American Church but a split from it, founded in 1980 by a former head of one of its New York branches, with a doctrine that is not the Church's. An independent and minuscule convergence: a peer-reviewed journal notes that DPT is also known as The Light, which matches the Temple's vocabulary without going through it.

Duration, dose and tolerance

This is the section that hurts. There is no pharmacokinetics, no human dose-response curve, no bioavailability data by route. Everything that follows comes from a clinical series of 1973, from never-replicated self-experiments relayed by a tertiary source, or from a community corpus of users. A single anchor passes through a peer-reviewed article independent of these relays: 30 to 70 mg by the intramuscular route, mean 50 mg, adopted by Halberstadt et al. 2020 from Faillace 1967. The most reported oral band is 100 to 250 mg for 2 to 4 hours, with an isolated occurrence at 500 mg described as exhausting and lasting twelve hours, which is not a range. By the intravenous route, 12 to 36 mg.

On the smoked route, two sources contradict each other flatly, and no editor should settle it in their place. One gives 100 mg as the smoked dose; the other places 100 mg at the threshold of its heavy range and puts the common dose between 20 and 50 mg, a gap of a factor of two to five depending on the point of comparison. On the insufflated route, the asymmetry is of another kind: the oldest source calls it effective but very painful and gives no quantity, the community corpus proposes 50 to 100 mg as a common dose, and it is the route of the only published death. The only onset marker for injections, 10 to 15 minutes, is a single tertiary record that does not distinguish intramuscular from intravenous. On duration, two descriptions coexist without contradicting each other: longer than DMT, short on the scale of the psychedelics, with an order of magnitude of difference according to route, from the half hour smoked to the four hours oral.

In the mouse, DPT does not develop tolerance to daily administration, unlike DOI and 2C-T-7, which are phenethylamines. Two precautions inseparable from this result: it bears on the head twitch in the rodent and not on a human subjective effect, and the same work shows an insurmountable incoming cross-tolerance, mice made tolerant to DOI being tolerant to DPT as well. A recently consumed phenethylamine can therefore blunt DPT. No human tolerance data exists.

Harm reduction

Only one death has been published, and he did not die of what one expects. A 20-year-old man, experienced with hallucinogens, insufflates an unknown quantity of DPT. At 10 to 15 minutes, visual hallucinations, then growing apathy. At two hours, abdominal pain, then collapse, a convulsive seizure and vomiting. Resuscitation on site, hospital at 2.5 hours, extracorporeal circulatory support, death 21 hours after the dose. The autopsy concludes deep aspiration of gastric contents and cerebral oedema from oxygen deprivation. The authors stress that, unlike the usual tryptamine overdoses, this case presented no agitation, no hyperthermia and no tachycardia, and that the death was an indirect consequence of the consumption.

Three consequences, and they are the most actionable points on this page.

• The lethal chain is mechanical, not toxic: vomiting, plus altered consciousness, plus a supine position, equals inhalation. What killed here therefore calls not for a drug but for a position, someone sober alongside and the body put on its side before the first vomiting arrives.
• The published order is not the one you would expect. The vomiting comes last, after the collapse and the seizure, so in a person already unconscious. Monitoring must not wait for the first vomiting to begin.
• The collapse occurred at two hours, after the expected phase of effects, that is, precisely at the moment when those around relax their attention.

The measured concentrations, about 210 ng/mL in serum at four hours, 110 ng/mL in cardiac blood and 180 ng/mL in urine, are the first published in a fatal case. These are not toxicity thresholds: n equals one, dose and purity unknown, and the mechanism of death was not the concentration.

The second human case, a 19-year-old woman admitted with tachycardia at 200 beats per minute and psychomotor agitation, sedated with 3 mg of lorazepam, has no analytical confirmation: the substance is presumed from a vial found at the scene. The only two human cases are therefore contradictory on the cardiovascular side, 0 versus 200 beats per minute. With n equals two, nothing is concluded, and above all, the absence of tachycardia and hyperthermia is not reassuring, since it was the fatal case that lacked them.

Seizures, the best-supported convergence. In the mouse, 20 mg/kg produces seizures in 90% of the animals, with zero lethality and complete recovery; a study in the rat, known only by citation, reports a proconvulsant effect at 30 mg/kg; and the only published human death includes a seizure. Between 10 and 20 mg/kg in the mouse, the molecule switches from antiepileptic to proconvulsant. This is not proof, and transposing a murine mg/kg to a human milligram is not valid, but it is what grounds the warning. Contraindication: personal or family history of seizures, or epilepsy. Also concerned are the agents that lower the seizure threshold, tramadol and bupropion, lithium, and above all withdrawal from benzodiazepines and from alcohol.

On this point, DPT occupies both ends of a fact that runs across the wiki. Of the fourteen substances in this corpus, ten carry a seizure signal, very unevenly supported from one page to the next, from the counted human case to the bare clinical mention; DPT brings to it the strongest animal signal of the set, 90% of mice, and one of the thinnest human bases, one seizure in a single case. What follows from all this therefore holds here as elsewhere: what holds for DPT holds for its neighbours, and two of them taken together do not merely add up, they lower the same threshold. Outside the set, tramadol and lithium are flagged in the same direction by several of these pages independently, and lithium is the only medicine to which a death in this corpus has been attributed.

Combinations, and what the other substances in this wiki do there.

• 2C-T-7 is the only partner in this wiki with which an interaction has been measured. In the rat and in the monkey, DPT and 2C-T-7 additively potentiate the discriminative stimulus of DOM. This is animal discrimination data and not a quantified risk, but it goes in the general direction of that work: in animals, adding a second 5-HT2A agonist to DPT adds up.
• Syrian rue and MAOIs in general: an evidential void in both directions. DPT combined with an MAO inhibitor has never been studied, in any species. Since DPT is orally active without an MAOI, adding one brings no clear pharmacological benefit and adds the serotonergic load of the MAOI. The argument rests on the absence of benefit, not on a measured mechanism, since no one has measured DPT as a substrate of MAO. Treating the combination as contraindicated by default is a deliberate choice of caution, to be presented as such. Targeted here are the pharmaceutical MAOIs, moclobemide, phenelzine, tranylcypromine, selegiline, rasagiline, linezolid and methylene blue, and the plant MAOIs, Syrian rue and Banisteriopsis caapi. The same absence-of-benefit reasoning would hold for AMT, which with Syrian rue is one of the only two established MAO inhibitors in this corpus, but that is an extension nothing has ever tested, neither in a case report nor in a study.
• The class has deaths in this configuration, and they do not concern DPT. The death published after ingestion of an extract containing beta-carbolines and tryptamines concerns 5-MeO-DMT, with no anatomical cause found at autopsy and with a manner of death classed as undetermined. Class evidence, never a DPT case.
• Serotonergic antidepressants: the uncertainty is not reassuring. If DPT is a releasing substrate at SERT, combining it with an SSRI falls under the classic pattern of serotonergic toxicity; if it is a pure reuptake inhibitor, it falls rather under competition and attenuation. No case of serotonin syndrome involving DPT has been found. As long as the mechanism is not settled, the combination is treated as a risk.
• Sedatives and depressants. DPT is the substance in this corpus whose only published death is an aspiration. Anything that adds sedation or blunts the airway protection reflexes therefore aggravates precisely the chain that killed: DXM, diphenhydramine, nitrous oxide, alcohol, benzodiazepines. No case documents these combinations with DPT, and the reasoning is about the mechanics of aspiration, not about a pharmacology.

No one will be identified in the emergency department. There is no immunoassay screen for the tryptamine derivatives, and they do not figure in routine analyses: a department will not find DPT if it does not look for it specifically, and a negative screen rules nothing out. Saying what was taken and keeping the bag materially changes the care given. Street reagents are no more help: DPT turns Ehrlich purple and Marquis yellow, according to a source we have not read, but these reagents distinguish it neither from 5-MeO-DPT, nor from 4-HO-DPT, nor from 4-AcO-DPT, which circulate with very different potencies. Worse, AMT and 5-MeO-DiPT are also indoles and also react to Ehrlich: this reagent separates no tryptamine in this wiki from the others. A positive test says there is an indole in the bag, nothing more.

On the other populations, the material is thin and it can be said in three lines. On pregnancy, nothing exists for DPT; a teratogenicity result in the female rat concerns N-methyltryptamine, another molecule, not to be transferred and from which no safety can be inferred either. On psychotic vulnerability, the caution is a class caution, psychosis figuring among the negative effects relayed by user reports, which is not a case report. On cardiovascular vulnerability, the data are contradictory with n equals two.

Legal status. Our search has not established the status of DPT in France: it appears neither in the ANSM decision of May 2026, which covers seven other tryptamine derivatives, nor in the recorded entries of the 1990 order, but this reading may have been incomplete and the consolidated list has not been opened. Nothing must be published either way before human verification.

Sources

• L.B. Kozell et al. (2023), pharmacological activity of substituted tryptamines at 5-HT2A, 5-HT2C, 5-HT1A and SERT, J Pharmacol Exp Ther (full text read; complete DPT table).
• R. Tyagi, T.S. Saraf, C.E. Canal (2023), DPT prevents seizures in a mouse model of fragile X through a mechanism independent of serotonin and sigma-1, ACS Pharmacol Transl Sci (full text read; seizures at 20 mg/kg, absence of any pharmacokinetics).
• B.E. Blough et al. (2014), interaction of psychoactive tryptamines with biogenic amine transporters, Psychopharmacology (full text read; direct measurement of release, named criticism of the Cozzi method).
• N.V. Cozzi et al. (2009), substrate behaviour of hallucinogenic tryptamines at SERT and VMAT2, J Neural Transm (abstract read; substrate hypothesis).
• F. Nagai, R. Nonaka, K. Satoh Kamimura (2007), effects of non-medical psychoactive drugs on monoaminergic neurotransmission, Eur J Pharmacol (abstract read).
• H.V. Thiagaraj et al. (2005), binding properties of DPT at the human 5-HT1A, Pharmacology (abstract read; full text not read).
• J.X. Li, K.C. Rice, C.P. France (2007), behavioural effects of DPT in the rat, Behav Pharmacol (abstract read; 5-HT1A unmasking sequence).
• W.E. Fantegrossi et al. (2008), hallucinogenic effects of DPT in the rodent, Pharmacol Biochem Behav (abstract read; full text not read).
• J.X. Li, K.C. Rice, C.P. France (2008), pA2 analysis in the rhesus monkey, J Pharmacol Exp Ther (abstract read; only primate data).
• J.X. Li, W. Koek, K.C. Rice, C.P. France (2010), 5-HT1A agonists and the discriminative stimulus of DOM in the rat and the monkey, J Pharmacol Exp Ther (abstract read; additivity of DPT and 2C-T-7).
• D.A. Smith et al. (2014), tolerance and cross-tolerance in the head twitch, J Pharmacol Exp Ther (abstract read).
• A.L. Halberstadt et al. (2020), correlation between head-twitch potency and subjective effects, Neuropharmacology (full text read; ED50 1.90 mg/kg, 95% CI 1.14 to 3.19, and human dose 30 to 70 mg IM, table 3).
• T.F. Varley et al. (2024), DPT alters the information-processing dynamics of cortical circuits in vitro, Netw Neurosci (abstract read; full text not read).
• M.A. Neukamm et al. (2024), fatal aspiration case after DPT consumption, J Pharm Biomed Anal (abstract read, it carries all the figures used here; full text not read).
• S. Malaca et al. (2020), toxicology and analysis of psychoactive tryptamines, Int J Mol Sci (full text read; absence of an immunoassay).
• J. Sklerov et al. (2005), fatal intoxication following ingestion of 5-MeO-DMT in an ayahuasca preparation, J Anal Toxicol (abstract read; concerns 5-MeO-DMT, not DPT).
• R.A. Soskin, S. Grof, W.A. Richards (1973), low doses of dipropyltryptamine in psychotherapy, Arch Gen Psychiatry (abstract only read, full text not read; the route of administration does not appear in it).
• W.A. Richards, J.C. Rhead, F.B. DiLeo, R. Yensen, A.A. Kurland (1977), Journal of Psychedelic Drugs 9(1), 1-10, and W.A. Richards et al. (1980), OMEGA 10(1), 9-26, on DPT in the psychotherapy of cancer patients. Texts not read, existence and references confirmed. Everything that circulates about the doses in these works comes from secondary relays.
• S. Grof, R.A. Soskin, W.A. Richards, A.A. Kurland (1973), Int Pharmacopsychiatry 8(1), 104-115, pilot study on 51 alcoholic patients. Not read, no abstract available.
• L.A. Faillace, A. Vourlekis, S. Szara (1967), J Nerv Ment Dis 145(4), 306-313. Not read, no abstract. Probably the oldest human series on DPT; it is from this one that Halberstadt draws the intramuscular range.
• A. Halman, G. Kong, J. Sarris, D. Perkins (2024), drug interactions of the classic psychedelics, systematic review, J Psychopharmacol (full text read). ⚠️ Does not cover DPT: its search did not include this molecule. Never to be cited on the subject.
• Erowid, DPT Vault and TiHKAL entry no. 9. Not read, HTTP 403 to any automated access. Corpus of user reports, to be read on site; its licence forbids reproduction. All the dose ranges attributed here to TiHKAL pass through a tertiary relay and require a human reading of the source before publication.
• PsychonautWiki, DPT (read; community corpus not sourced to primary literature, source of the alternative smoked, oral and insufflated ranges, and of the tramadol, lithium and stimulant combinations).
• T. Spratley (2004), analytical profiles of five synthetic tryptamines, Microgram Journal 3(1-2). Not read; it is the source for the Ehrlich and Marquis reagents, known by relay.
• CFSRE / NPS Discovery, N,N-Dipropyltryptamine monograph. Not read: page returning a 403 and document in PDF only.
• ANSM, decision of 12 May 2026 classifying seven tryptamine derivatives (read; DPT does not appear in it). The consolidated list of narcotics exists only as a PDF and has not been opened: the French status remains undetermined.