DMT research: top findings and the state of play

A synthesis of 34 recent papers on DMT and its close analogue 5-MeO-DMT, written for a non-specialist professional audience.

DMT is a small naturally occurring molecule, structurally similar to the neurotransmitter serotonin, that produces an intense but extremely short-lived psychedelic experience when smoked, vaporised or injected. Until a few years ago it was a fringe research topic — known mainly as the active ingredient of the Amazonian brew ayahuasca and as a recreational curiosity. The papers reviewed here, almost all published between 2019 and 2026, document a transformation: DMT is now a serious candidate medicine.

The field has moved through phase 1 safety trials and into phase 2a efficacy trials in treatment-resistant depression, with response rates that compare favourably to anything in the existing antidepressant armamentarium. In parallel, basic science has begun to explain why the drug might work — through structural neural plasticity, dramatic but brief disruption of large-scale brain network dynamics, and, intriguingly, through hippocampal neurogenesis. A second compound, 5-MeO-DMT, is following hard on its heels with a different therapeutic profile. There remain real open questions about blinding, expectancy, cardiovascular safety in older patients, and whether the subjective psychedelic experience is necessary for the therapeutic effect — but the trajectory of the field is unmistakably toward clinical adoption within the decade.

What DMT is, in plain terms

DMT (N,N-dimethyltryptamine) is a tryptamine — meaning it shares its core chemical scaffold with serotonin and with psilocybin, the active component of "magic mushrooms". Three properties make it unusual and clinically interesting.

First, it is endogenous. Several papers, notably Dean and colleagues' 2019 work, demonstrate that the enzymes needed to synthesise DMT are co-expressed in mammalian cerebral cortex, choroid plexus and pineal gland. Crucially, baseline extracellular DMT in rat cerebral cortex sits at concentrations comparable to dopamine or serotonin, and rises sharply during experimental cardiac arrest. We do not yet know what endogenous DMT does, but the data make it harder to dismiss as a metabolic curiosity.

Second, when taken by mouth DMT is destroyed by gut and liver enzymes. The traditional ayahuasca brew gets around this by combining DMT-containing plants with monoamine-oxidase-inhibiting plants, producing a four- to six-hour experience. Modern clinical research instead administers DMT intravenously or as a vapour inhaled like a steroid asthma puff — both routes bypass first-pass metabolism and give a 10–20 minute experience, far shorter than psilocybin (4–6 hours) or LSD (8–12 hours).

Third, DMT acts primarily as an agonist at the serotonin 5-HT2A receptor — the same receptor that mediates the effects of all classical psychedelics. But it also binds at 5-HT1A, 5-HT2C, sigma-1, trace amine-associated receptors, and even the cardiac 5-HT4 receptor. This polypharmacology is part of what makes its mechanism interesting and not yet fully solved.

Rapid, sustained antidepressant effects in treatment-resistant depression

This is the headline result of the past three years and the reason there is now a clinical industry around the molecule.

Three independent clinical trials, conducted in three different countries with three different formulations, all reach the same conclusion: a single dose of pure DMT, given alongside light psychological support, produces large reductions in depression scores within 24 hours, and these reductions persist for weeks to months in a majority of patients.

• D'Souza and colleagues at Yale (2022) ran the first dose-escalation study of intravenous DMT in major depressive disorder. Even in a small open-label sample, depression scores dropped the day after dosing and remained reduced at two weeks. The setting was deliberately stripped down — a standard hospital room, no music or "ceremonial" elements, no intensive psychotherapy. The result still held.
• Falchi-Carvalho and colleagues in Brazil (2025) published a phase 2a trial of vaporised DMT in 14 patients with treatment-resistant depression. By day 7, the average reduction on the Montgomery–Åsberg Depression Rating Scale was 21 points — a roughly two-thirds reduction in symptoms. Response rate was 86%, remission rate 57%, and effects were sustained at three months. Suicidal ideation dropped sharply and stayed down.
• A randomised placebo-controlled phase 2a published in Nature Medicine in early 2026 confirmed these effects with a single 21.5 mg intravenous infusion in patients with moderate-to-severe major depression.

For context: conventional antidepressants take three to six weeks to work, fail to remit roughly a third of all depressed patients, and produce remission rates closer to 30%. Ketamine, the closest existing rapid-acting comparator, costs more, lasts longer per session and requires repeat dosing.

The most striking practical feature is the duration of the dosing visit itself. A psilocybin therapy session occupies most of a working day. A DMT session — preparation, dosing, integration — can plausibly fit within a 90-minute outpatient appointment. If the antidepressant effect holds up in larger trials, this matters enormously for cost, scalability and integration into existing psychiatric practice.

An unusually clean pharmacokinetic profile

DMT now has the cleanest dose-response data of any classical psychedelic. The Basel group (Vogt, Erne, Liechti and colleagues) has run a programme of double-blind, placebo-controlled crossover studies in healthy volunteers. The 2026 Erne paper is the definitive dose-response study, testing 5, 10, 15 and 20 mg intravenous boluses in 20 participants under double-blind randomisation, and comparing this to an open-label dose-escalation design.

The key numbers: peak plasma concentration is reached in about 2 minutes, peak subjective effect occurs within 1–3 minutes, and the elimination half-life is roughly 6–7 minutes. Subjective effects subside completely within 12–30 minutes. There is a clear ceiling effect on subjective intensity at around 15 mg — pushing the dose to 20 mg or 25 mg adds anxiety and adverse subjective experience but not psychedelic depth.

A clinically important and somewhat surprising finding: the same dose produces a markedly less intense and more tolerable experience under open-label dose-escalation than under double-blind randomisation. In other words, expectancy and context are not minor modifiers of the DMT experience — they are major modifiers. This has obvious implications for trial design and for clinical practice.

A 2023 paper from the same group showed that infusions of DMT (as opposed to bolus injections) produce a slower, more sustained, more controllable experience with less anxiety. This matters because it means the duration and intensity of the experience can be tailored — you can give a 30-minute experience or a 90-minute one by adjusting the infusion. That degree of pharmacological control is not available with psilocybin or LSD.

A coherent picture of brain mechanism is emerging

This is where the basic neuroscience has matured most rapidly. Fifteen years ago, what DMT does to the brain was essentially unknown. Today there is a converging multi-modal picture.

Electrophysiology. Timmermann and colleagues' 2019 paper, repeatedly cited across the corpus, showed that intravenous DMT markedly reduces alpha and beta band oscillatory power and dramatically increases what neuroscientists call "signal diversity" — a measure of how unpredictable, information-rich and varied the brain's electrical activity is. Increased signal diversity is now considered a robust signature of the psychedelic state and correlates with subjective intensity in real time. Animal work shows that this brain state is genuinely a hybrid — combining waking arousal with EEG features that resemble sleep, particularly slow-wave activity. This "vigilance state dissociation" is being proposed as a fundamental property of the psychedelic state and possibly the substrate of plasticity-promoting effects.

Functional MRI. Several papers converge on the same picture: DMT causes a transient flattening of the brain's functional hierarchy. Networks that normally segregate from one another — the default-mode network, the visual networks, sensory and association cortices — become globally integrated. The brain enters a "destabilised" state from which it can flexibly reach a wider range of dynamical configurations. After the drug clears, the network re-stabilises, but the reorganisation may leave traces.

Receptor-level mechanism. A landmark 2025 structural pharmacology paper used X-ray crystallography on the 5-HT2A receptor to show that DMT, psilocin and serotonin all bind in the same orthosteric pocket but with subtly different geometries. This work, together with the halogenated DMT analogue paper from 2026, is laying the groundwork for designing next-generation molecules that retain the therapeutic effects while reducing the hallucinogenic effects.

Structural and functional neuroplasticity

The most plausible mechanism for sustained therapeutic effects after a single short dose is that the drug rewires the brain. The corpus contains strong evidence that this is, literally, what happens.

In the medial frontal cortex of mice, a single dose of 5-MeO-DMT produces a roughly 10–15% increase in dendritic spine density that emerges within one day and persists for at least one month (Jefferson and colleagues, 2023). This is the same magnitude and timecourse as has previously been shown for psilocybin and ketamine. Spine formation rate, not elimination rate, drives the effect — i.e. the drug causes neurons to grow new connections rather than preventing existing ones from being pruned.

A 2026 paper in the corpus extends this picture in a striking way: a single dose of pure DMT given to mice subjected to chronic mild stress reverses anhedonia, behavioural despair and cognitive deficits, and this behavioural recovery is accompanied by increased adult-born neurons in the hippocampal dentate gyrus and a normalisation of where those new neurons end up integrating. DMT performed at least as well as four weeks of fluoxetine. This is the first preclinical evidence that DMT is doing something specifically therapeutic — not merely producing a transient altered state — in a validated rodent model of depression.

The mechanism appears to involve activation of intracellular 5-HT2A receptors, induction of brain-derived neurotrophic factor, and engagement of sigma-1 receptors — a multi-pronged neuroplastic stimulus that converges with what is known about ketamine.

Phenomenology: unusual, replicable, possibly therapeutically relevant

DMT produces an experience that even seasoned psychedelic users describe as categorically different from psilocybin or LSD. Two papers in the corpus characterise it in detail.

The Lawrence 2022 paper analysed 3,778 first-person accounts of inhaled DMT posted to Reddit over a decade. The most common features: vivid geometric and fractal visuals (32%), encounters with "entities" experienced as autonomous and conscious (45%), feelings of entering a structured "DMT world" with rooms and corridors (15%), and overlap with the phenomenology of near-death experiences. Entity encounters were predominantly perceived as benevolent, intelligent, communicative and pedagogical — encounters with "machine elves", feminine archetypes, deities or aliens. About 6% of accounts described the experience as the most personally meaningful or beautiful event of the person's life.

These themes are remarkably consistent across cultures and across decades, which has fuelled speculation that DMT may engage innate neurocognitive modules — agency detection, social-role inference, animacy attribution — that normally subserve our perception of other minds.

The Ermakova 2025 paper does the same job with phenomenological rigour for intranasal 5-MeO-DMT in 32 psychedelic-naïve healthy adults. The 5-MeO-DMT experience is shorter, less visual, more emotional and bodily, more often involves complete ego dissolution, and is more often associated with mystical-type experiences than DMT proper.

This matters clinically because mystical-type and "emotional breakthrough" experiences correlate with therapeutic outcomes in the broader psychedelic literature. There is an active ongoing debate in the field about whether the subjective psychedelic experience is necessary for the therapeutic effect, or whether the underlying neuroplasticity is what does the work. The non-hallucinogenic 5-Br-DMT analogue (Puigseslloses 2026) shows antidepressant-like effects in mice without the head-twitch response that proxies hallucination, suggesting the question is empirically tractable.

Cardiovascular safety needs careful screening

Across the human studies, DMT consistently produces transient increases in blood pressure and heart rate, typically peaking 5–15 minutes after dosing and resolving within 30 minutes. The magnitude is roughly comparable to moderate exercise in healthy adults.

A 2025 paper in the corpus adds a mechanistic wrinkle: DMT and especially 5-MeO-DMT activate cardiac 5-HT4 receptors and increase the force of cardiac contraction in isolated human atrial tissue. The effect is unlikely to matter at therapeutic concentrations in healthy people, but it identifies a specific pharmacological mechanism that could become relevant in patients with cardiovascular disease, in overdose situations, or during drug-drug interactions. Tropisetron — a 5-HT antagonist used for chemotherapy-induced nausea — reverses this cardiac effect, suggesting an antidote pathway.

In the Yale trial, one participant with previously undisclosed autonomic instability had a serious adverse event (transient bradycardia and hypotension) that resolved without sequelae. This single incident has shaped how subsequent trials screen patients, with stricter cardiovascular work-up and an upper age limit of 60 or 65 years until larger safety datasets accumulate.

The broader signal is reassuring: across hundreds of dosing sessions in the corpus, no deaths, no lasting psychiatric injuries, no severe psychotic episodes, and the most common adverse events are pharyngeal irritation from the inhaled vapour, mild headache, and acute anxiety during dose onset.

The 5-MeO-DMT branch

Several papers focus on 5-methoxy-DMT, a structurally related toad-derived molecule that is four to ten times more potent than DMT and has a higher affinity for the 5-HT1A receptor. It is being developed in parallel by a different set of companies, most prominently for treatment-resistant depression and for sub-psychedelic anxiolytic indications.

The 2025 sublingual microdose study tested 6, 9 and 12 mg of 5-MeO-DMT given weekly for four weeks in adults with moderate anxiety or depression but no formal diagnosis. Doses below 15 mg produced perceptible but sub-psychedelic effects with a clean safety profile, suggesting a possible "psychedelic-lite" outpatient model. Cardiac considerations are arguably more pertinent for 5-MeO-DMT because of its higher 5-HT4 potency, but no clinical signals of harm have emerged yet.

The state of play, summarised

Five years ago, most of the human DMT literature consisted of Strassman's pioneering 1990s studies and a handful of ayahuasca trials. Today, the field has the following structure:

• Clinical pipeline. Multiple companies have DMT or 5-MeO-DMT formulations in phase 1, 2a or 2b trials, principally for treatment-resistant depression. A vaporised DMT and an intravenous DMT infusion have both completed phase 2a with positive results.
• Mechanistic understanding. The 5-HT2A receptor agonism that drives the acute experience is now structurally characterised. The downstream consequences — increased cortical signal diversity, transient breakdown of network segregation, dendritic spine formation, hippocampal neurogenesis, BDNF induction — are converging into a coherent story. Whether the subjective experience is necessary, useful, or incidental remains contested.
• Safety. Acute safety in screened, healthy or moderately ill adults is well-characterised and reassuring. Long-term safety, repeat dosing, drug-drug interactions and cardiovascular safety in higher-risk groups are the areas where data are still thin.
• Methodological challenge. Blinding is essentially impossible — the subjective experience is unmistakable and develops within seconds. Expectancy clearly modifies effects. The field is converging on active comparators, dose-finding designs and naturalistic comparator studies to triangulate the placebo problem.

Open questions and outlook

For a professional in another field, the most important things to take away are these.

First, the basic claim that a single short dose of an old controlled substance can produce sustained relief from severe treatment-resistant depression has now been reproduced enough times, in enough places, that it is unlikely to be a chance result or a pure placebo effect — though some of the effect is undoubtedly placebo, set, setting and expectancy.

Second, the practical advantages of DMT specifically — short duration, intravenous or vaporised dosing, well-characterised pharmacokinetics — make it a more plausible candidate for routine clinical use than its psychedelic relatives.

Third, the mechanism is most likely a transient, dramatic disruption of large-scale brain dynamics that opens a window of plasticity, during which the brain regrows synaptic connections. The conscious experience may be epiphenomenal to this, partially necessary, or wholly necessary — and that question is the central scientific battleground of the next five years.

The unresolved concerns are not trivial. Long-term effects of repeated dosing are unknown. Effects in patients with bipolar disorder, psychotic vulnerability, severe cardiovascular disease, or older age are largely uncharacterised. The intense subjective experience — including encounters with seemingly autonomous "entities" and brief but profound ego dissolution — presents real psychological risks for vulnerable patients and real conceptual challenges for clinicians, regulators and insurers used to treating drugs as inert chemical interventions.

But the direction of travel is clear. Within a decade, vaporised or infused DMT is likely to be a regulated medicine for treatment-resistant depression in at least some jurisdictions, alongside psilocybin. The deeper scientific questions DMT raises — about endogenous psychedelics, about the nature of consciousness, about what the brain looks like when it is briefly knocked out of its usual dynamical attractors — are likely to outlive the immediate clinical application and reshape how psychiatry thinks about the brain for a generation.

References

The following studies were reviewed in preparing this synthesis. They are grouped thematically rather than alphabetically, to make the underlying literature easier to navigate.

Clinical trials and human dosing studies

1. D'Souza DC, Syed SA, Flynn LT, Safi-Aghdam H, Cozzi NV, Ranganathan M. Exploratory study of the dose-related safety, tolerability, and efficacy of dimethyltryptamine (DMT) in healthy volunteers and major depressive disorder. Neuropsychopharmacology. 2022;47:1854–1862. doi:10.1038/s41386-022-01344-y

2. Falchi-Carvalho M, Palhano-Fontes F, Wießner I, Barros H, Bolcont R, Laborde S, et al. Rapid and sustained antidepressant effects of vaporized N,N-dimethyltryptamine: a phase 2a clinical trial in treatment-resistant depression. Neuropsychopharmacology. 2025;50:895–903. doi:10.1038/s41386-025-02091-6

3. A short-acting psychedelic intervention for major depressive disorder: a phase IIa randomized placebo-controlled trial (SPL026 trial). Nature Medicine. 2026;32:591–598. doi:10.1038/s41591-025-04154-z

4. Vogt SB, Ley L, Erne L, Straumann I, Becker AM, Klaiber A, et al. Acute effects of intravenous DMT in a randomized placebo-controlled study in healthy participants. Translational Psychiatry. 2023;13:172. doi:10.1038/s41398-023-02477-4

5. Erne L, Mueller L, Straumann I, Ademaj B, Eckert A, Vukalovic I, et al. Dose-dependent pharmacokinetics and acute effects of intravenous bolus N,N-dimethyltryptamine: double-blind, randomized versus open-label dose-escalation administration study in healthy participants. Translational Psychiatry. 2026;16:213. doi:10.1038/s41398-026-03987-7

6. Timmermann C, Zeifman RJ, Erritzoe D, Nutt DJ, Carhart-Harris RL. Effects of DMT on mental health outcomes in healthy volunteers. Scientific Reports. 2024;14:3097. doi:10.1038/s41598-024-53363-y

7. Perkins D, Halman A, Urokohara A, Palumbo J, Low M, Ruffell S, et al. Acute experiences and persisting psychological effects associated with an encapsulated DMT-harmala alkaloid combination: results of a phase 1 study. Scientific Reports. 2025;15:41152. doi:10.1038/s41598-025-25767-x

8. Bistue Millón MB, et al. Safety and tolerability of multiple sublingual microdoses of 5-MeO-DMT. Neuropsychopharmacology. 2025;50:1715–1723.

9. Ermakova AO, Dunbar F, Seynaeve M, Millière R. Mapping the phenomenology of intranasal 5-MeO-DMT in psychedelic-naïve healthy adults. Scientific Reports. 2025;15:38874. doi:10.1038/s41598-025-22620-z

Phenomenology and naturalistic use

10. Lawrence DW, Carhart-Harris R, Griffiths R, Timmermann C. Phenomenology and content of the inhaled N,N-dimethyltryptamine (N,N-DMT) experience. Scientific Reports. 2022;12:8562. doi:10.1038/s41598-022-11999-8

11. Véliz-García O, Domic-Siede M. Latin American adults who regularly use macrodoses of psychedelics: a cross-sectional study. Scientific Reports. 2024;14.

12. Schlomberg JTT, Meling D, Grylka R, Vasella EA, Augustinovic D, Scheidegger M. Mixed-methods analysis on psychedelic-augmented meditation experiences from a randomized controlled mindfulness retreat. Scientific Reports. 2026;16:14236. doi:10.1038/s41598-026-39261-5

Brain mechanism (human neuroimaging and electrophysiology)

13. Timmermann C, Roseman L, Schartner M, Millière R, Williams LTJ, Erritzoe D, et al. Neural correlates of the DMT experience assessed with multivariate EEG. Scientific Reports. 2019;9:16324. doi:10.1038/s41598-019-51974-4

14. Vohryzek J, Luppi AI, Atasoy S, Deco G, Carhart-Harris RL, Timmermann C, Kringelbach ML. N,N-dimethyltryptamine effects on connectome harmonics, subjective experience and comparative psychedelic experiences. Neuropsychopharmacology. 2025;50:1768–1776. doi:10.1038/s41386-025-02190-4

15. Singleton SP, Timmermann C, Luppi AI, Eckernäs E, Roseman L, Carhart-Harris RL, Kuceyeski A. Network control energy reductions under DMT relate to serotonin receptors, signal diversity, and subjective experience. Communications Biology. 2025;8:631. doi:10.1038/s42003-025-08078-9

16. Piccinini JI, Sanz Perl Y, Pallavicini C, Deco G, Kringelbach M, Nutt D, et al. Transient destabilization of whole brain dynamics induced by N,N-Dimethyltryptamine (DMT). Communications Biology. 2025;8:409. doi:10.1038/s42003-025-07576-0

17. Lima G, Soares C, Teixeira M, Pais M, Cabral C, Rijo P, Castelo-Branco M. Inhaled N,N-dimethyltryptamine diminishes connectivity between the ventral tegmental area and the nucleus accumbens: relevance to pathologies of mesolimbic and mesocortical pathways. Scientific Reports. 2026;16:1744. doi:10.1038/s41598-025-31431-1

18. Girn M, Doss MK, Roseman L, Preller KH, Palhano-Fontes F, Pasquini L, et al. An international mega-analysis of psychedelic drug effects on brain circuit function. Nature Medicine. 2026;32:1543–1554. doi:10.1038/s41591-026-04287-9

Preclinical neuroscience (rodents and non-human primates)

19. Jefferson SJ, Gregg I, Dibbs M, Liao C, Wu H, Davoudian PA, et al. 5-MeO-DMT modifies innate behaviors and promotes structural neural plasticity in mice. Neuropsychopharmacology. 2023;48:1257–1266.

20. Lima da Cruz RV, de Miranda Costa RBG, de Queiroz GM, Stojanovic T, Moulin TC, Leão RN. Single-dose DMT reverses anhedonia and cognitive deficits via restoration of neurogenesis in a stress-induced depression model. Translational Psychiatry. 2026;16:101. doi:10.1038/s41398-026-03852-7

21. Nogueira M, Ferreira Golbert DC, Menezes R, de Almeida RN, Galvão-Coelho NL, Siroky AN, et al. Serotonergic psychedelic 5-MeO-DMT alters plasticity-related gene expression and generates anxiolytic effects in stressed mice. Molecular Psychiatry. 2025;30:50–60. doi:10.1038/s41380-024-02655-w

22. Souza AC, Souza BC, França A, Moradi M, Souza NC, Leão KE, et al. 5-MeO-DMT induces sleep-like LFP spectral signatures in the hippocampus and prefrontal cortex of awake rats. Scientific Reports. 2024;14:11281. doi:10.1038/s41598-024-61474-9

23. Bréant BJB, Prius Mengual J, Andrews A, Hoerder-Suabedissen A, Patel J, Bannerman DM, Sharp T, Vyazovskiy VV. Vigilance state dissociation induced by 5-MeO-DMT in mice. Communications Biology. 2026;9:163. doi:10.1038/s42003-025-09412-x

24. Morales-Garcia JA, Calleja-Conde J, Lopez-Moreno JA, Alonso-Gil S, Sanz-SanCristobal M, Riba J, Perez-Castillo A. N,N-dimethyltryptamine compound found in the hallucinogenic tea ayahuasca regulates adult neurogenesis in vitro and in vivo. Translational Psychiatry. 2020;10:331.

25. Masthay JC, Kwan AC, Chang SWC. Psychedelic studies in nonhuman primates: past and future. Molecular Psychiatry. 2026;31:514–525. doi:10.1038/s41380-025-03240-5

Receptor-level pharmacology and structural biology

26. Gumpper RH, Jain MK, Kim K, Sun R, Sun N, Xu Z, et al. The structural diversity of psychedelic drug actions revealed. Nature Communications. 2025;16:2734. doi:10.1038/s41467-025-57956-7

27. Warren AL, Lankri D, Cunningham MJ, Serrano IC, Parise LF, Kruegel AC, et al. Structural pharmacology and therapeutic potential of 5-methoxytryptamines. Nature. 2024;630:237–246. doi:10.1038/s41586-024-07403-2

28. Puigseslloses P, Nadal-Gratacós N, Ketsela G, Weiss N, Berzosa X, Estrada-Tejedor R, et al. Structure-activity relationships of serotonergic 5-MeO-DMT derivatives: insights into psychoactive and thermoregulatory properties. Molecular Psychiatry. 2024;29:2346–2358. doi:10.1038/s41380-024-02506-8

29. Puigseslloses P, et al. Neuropharmacology of halogenated DMT analogs: psychoplastogenic and antidepressant pro-psychedelic. Molecular Psychiatry. 2026;31:1733–1745.

30. Neumann J, Dietrich T, Azatsian K, Hofmann B, Gergs U. Cardiac effects of two hallucinogenic natural products, N,N-dimethyl-tryptamine and 5-methoxy-N,N-dimethyl-tryptamine. Scientific Reports. 2025;15:6715. doi:10.1038/s41598-025-91400-6

Endogenous DMT biology

31. Dean JG, Liu T, Huff S, Sheler B, Barker SA, Strassman RJ, Wang MM, Borjigin J. Biosynthesis and extracellular concentrations of N,N-dimethyltryptamine (DMT) in mammalian brain. Scientific Reports. 2019;9:9333. doi:10.1038/s41598-019-45812-w

Forensic detection and computational chemistry

32. Alharby TN, Alanazi M, Alanazi J. Doped C₂₀ fullerenes as a new generation of efficient nanosorbents and nanosensors for rapid detection of dimethyltryptamine in drug detection. Scientific Reports. 2026;16:1228. doi:10.1038/s41598-025-30816-6

33. Alshahrani SM. Computational evaluation of aluminum and zinc doped C₂₀ fullerenes as advanced sensors for the detection of the narcotic dimethyltryptamine. Scientific Reports. 2026;16:12688. doi:10.1038/s41598-026-41537-9

Notes on the source set

The set comprises 33 distinct studies on N,N-dimethyltryptamine and its close analogue 5-methoxy-N,N-dimethyltryptamine. Two additional files in the source folder are worth flagging: the D'Souza 2022 exploratory study above (reference 1) was supplied as two separate PDFs that turned out to contain the same paper, and a 2016 paper on a bacterial drug/metabolite transporter superfamily protein (Tsuchiya et al., Nature 2016;534:417–420) shares the "DMT" acronym but is unrelated to the psychedelic molecule and was excluded from the synthesis.