DMT
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4 sources
Collated from PsychonautWiki, TripSit, Pharmacology, TiHKAL. Where sources differ (e.g. dosing), Compare shows them side by side.
Also known as DMT, N,N-DMT, Dmitry, The Glory, The Spirit Molecule, dimethyltryptamine, INDOLE, 3-[2-(DIMETHYLAMINO)ETHYL], N,N-DIMETHYLTRYPTAMINE, 3-[2-(DIMETHYLAMINO)ETHYL]INDOLE, DESOXYBUFOTENINE, NIGERINEPW
A popular and powerful psychedelic, typically used in two ways; either it is vapourised for a short 'breakthrough' experience, or it is taken in combination with an enzyme inhibitor for a long, intense trip (this is also known as ayahuasca or pharmahuasca).TS
Intravenous
Route dataPsychonautWiki
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 4 mg | 4–10 mg | 10–15 mg | 15–20 mg | 20 mg+ |
| Onset | 2–10 seconds |
|---|---|
| Come-up | 70–100 seconds |
| Peak | 2–5 minutes |
| Offset | 10–20 minutes |
| Total | 15–30 minutes |
Smoked
Route dataPsychonautWiki
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 2 mg | 10–20 mg | 20–40 mg | 40–60 mg | 60 mg+ |
| Onset | 20–40 seconds |
|---|---|
| Come-up | 1–3 minutes |
| Peak | 2–8 minutes |
| Offset | 1–6 minutes |
| Total | 5–20 minutes |
| After-effects | 10–60 minutes |
Insufflated
Route dataTripSit
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| — | 10–25 mg | 25–50 mg | 50–125 mg | —+ |
| After-effects | 15–60 minutes |
|---|
Vapourized
Route dataTripSit
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| 5 mg | 10–15 mg | 15–25 mg | 25–35 mg | 35 mg+ |
| After-effects | 15–60 minutes |
|---|
Oral
Route dataTiHKAL
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| — | — | 60–100 mg | — | —+ |
| Total | 1–1 hours |
|---|
Dangerous interactionsPWTS
Unsafe interactionsPWTS
Caution / uncertainPWTS
🧬 Receptor activityPH
| Target | Action | Affinity | Source | |
|---|---|---|---|---|
| Mu-type opioid receptor | — | Ki 0.092 nM | CHEMBL | TargetMu-type opioid receptor Action— AffinityKi 0.092 nM SourceCHEMBL |
| Delta-type opioid receptor | — | Ki 80.8 nM | CHEMBL | TargetDelta-type opioid receptor Action— AffinityKi 80.8 nM SourceCHEMBL |
| Kappa-type opioid receptor | — | Ki 998 nM | CHEMBL | TargetKappa-type opioid receptor Action— AffinityKi 998 nM SourceCHEMBL |
Mechanism of actionPH
DMT acts as a non-selective agonist at most or all of the serotonin receptors.
N,N-dimethyltryptamine (DMT) is a hallucinogen found endogenously in human brain that is commonly recognized to target the 5-hydroxytryptamine 2A receptor or the trace amine-associated receptor to exert its psychedelic effect. DMT has been recently shown to bind sigma-1 receptors, which are ligand-regulated molecular chaperones whose function includes inhibiting various voltage-sensitive ion channels. Thus, it is possible that the psychedelic action of DMT might be mediated in part through sigma-1 receptors. ...
The psychotomimetic agent dimethyltryptamine (DMT) has been identified as an endogenous compound in the central nervous system of rodents using a sensitive electron capture gas chromatographic technique. DMT along with its proposed precursor, tryptamine, were identified and quantitated as the heptafluorobutyryl derivatives. A specific high affinity binding site on synaptosomal membranes has been proposed for DMT. This proposal is based on equilibrium dialysis experiments which indicate that DMT at a concentration of 1X10-5M will displace d-LSD on isolated membranes but will not displace bound serotonin at the same concentration. When DMT interacts with the synaptosomal membranes at a concentration of 5X10-10M, the membrane-bound enzyme adenylate cyclase is stimulated such that adenosine3', 5'-monophosphate (cAMP) is produced at a rate of 100 pM/min/mg of protein (2.3 times the endogenous rate). It has also been shown that its presumed precursor, tryptamine, inhibits this process. ... From data obtained in this study it has been postulated that DMT may have in vivo activity similar to those proposed for neurotransmitters or other neuroregulatory agents. ...
The interactions of the indolealkylamine N,N-dimethyltryptamine (DMT) with 5-hydroxytryptamine1A (5-HT1A) and 5-HT2 receptors in rat brain were analyzed using radioligand binding techniques and biochemical functional assays. The affinity of DMT for 5-HT1A sites labeled by (3)H-8-hydroxy-2-(di-n-propylamino)tetralin (3)H-8-OH-DPAT) was decreased in the presence of 1X10-4 M GTP, suggesting agonist activity of DMT at this receptor. Adenylate cyclase studies in rat hippocampi showed that DMT inhibited forskolin-stimulated cyclase activity, a 5-HT1A agonist effect. DMT displayed full agonist activity with an EC50 of 4X10-6 M in the cyclase assay. In contrast to the agonist actions of DMT at 5-HT1A receptors, DMT appeared to have antagonistic properties at 5-HT2 receptors. The ability of DMT to compete for (3)H-ketanserin-labeled 5-HT2 receptors was not affected by the presence of 1X10-4 M GTP, suggesting antagonist activity of DMT at 5-HT2 receptors. In addition, DMT antagonized 5-HT2-receptor-mediated phosphatidylinositol (PI) turnover in rat cortex at concentrations above 1X10-7 M, with 70% of the 5-HT-induced PI response inhibited at 1X10-4 M DMT. Micromolar concentrations of DMT produced a slight PI stimulation that was not blocked by the 5-HT2 antagonist ketanserin. These studies suggest that DMT has opposing actions on 5-HT receptor subtypes, displaying agonist activity at 5-HT1A receptors and antagonist activity at 5-HT2 receptors.
... The sigma-1 receptor pharmacophore includes an alkylamine core, also found in the endogenous compound N,N-dimethyltryptamine (DMT). DMT acts as a hallucinogen, but its receptor target has been unclear. DMT bound to sigma-1 receptors and inhibited voltage-gated sodium ion (Na+) channels in both native cardiac myocytes and heterologous cells that express sigma-1 receptors. ... DMT induced hypermobility in wild-type mice but not in sigma-1 receptor knockout mice. These biochemical, physiological, and behavioral experiments indicate that DMT is an endogenous agonist for the sigma-1 receptor.
For more Mechanism of Action (Complete) data for N,N-Dimethyltryptamine (7 total), please visit the HSDB record page.
Pharmacokinetics
AbsorptionPH
(14)C-DMT accumulates in rat brain cortical slices incubated at 37 °C. ... Most of the accumulated (14)C-DMT was associated with the cytoplasmic fraction. Of the portion associated with the crude mitochondrial fraction, 54.4% was associated with nerve-ending fraction.
The hallucinogenic substance N',N'-dimethyltryptamine and its precursor N-methyltryptamine were found in 24-hr specimens of urine from 19 normal human subjects; the mean excretion rates were 386 ng 24 hr(-1) and 856 ng 24 hr(-1) respectively. The urinary excretion of both compounds was unrelated to age, sex, urinary volume, or creatinine, nor was any consistent diurnal pattern observed. Rates for the mono and dimethylated compounds were not correlated. Diet and the intestinal flora were excluded as a source of urinary dimethyltryptamine. Administration to 4 subjects of sufficient ammonium chloride to /decrease/ the /pH/ of the urine caused a transient increase in dimethyltryptamine excretion but no consistent increase in the rate for N-methyltryptamine. Acidification of the urine did not appear to be the determining factor in this result since in one subject the same drop in urinary pH was achieved by feeding methionine without any increase in dimethyltryptamine excretion.
... Eighteen volunteers with prior experience in the use of psychedelics received single oral doses of encapsulated freeze-dried ayahuasca (0.6 and 0.85 mg of DMT/kg of body weight) and placebo. Ayahuasca produced significant subjective effects, peaking between 1.5 and 2 hr, involving perceptual modifications and increases in ratings of positive mood and activation. ...Cmax values for DMT after the low and high ayahuasca doses were 12.14 ng/mL and 17.44 ng/mL, respectively. Tmax (median) was observed at 1.5 hr after both doses. The Tmax for DMT coincided with the peak of subjective effects. ...
The endogenous hallucinogen, N,N-dimethyltryptamine (DMT), was labeled with (11)C and its regional distribution in rat brain studied. (11)C-DMT showed higher accumulation in the cerebral cortex, caudate putamen, and amygdaloid nuclei. Studies of the subcellular distribution of (11)C-DMT revealed the specific localization in the fractions enriched with serotonin receptors only when a very low dose was injected into rats. ...
For more Absorption, Distribution and Excretion (Complete) data for N,N-Dimethyltryptamine (8 total), please visit the HSDB record page.
MetabolismPH
Following intraperitoneal administration, 5-methoxy-N,N-dimethyltryptamine and N,N-dimethyltryptamine are subject to both a very rapid uptake into, and clearance from, all tissues examined. The current studies in vivo confirm previous in vitro observations that the routes involved in the metabolism of these compounds include oxidative deamination, N-demethylation, O-demethylation, and N-oxidation. The analysis of metabolic profiles in various tissues led to the identification of the N-oxides as major metabolites...
... /From/ ... urine samples collected from three individuals that were administered ayahuasca ... /authors/ show that the major metabolite of the hallucinogenic component of ayahuasca, N,N-dimethyltryptamine (DMT), is the corresponding N-oxide... Further, very little DMT was detected in urine, despite the inhibition of monoamine oxidase afforded by the presence of the harmala alkaloids in ayahuasca. ...
Behavioral aspects and metabolic fate of N,N-dimethyltryptamine (DMT) were studied in mice pretreated with beta-diethylaminoethyl-diphenylpropylacetate (SKF 525-A), iproniazid or chlorpromazine (CPZ.). ... Dose-dependent increases with rapid uptake and disappearance in the brain, plasma and hepatic levels of DMT were measured with doses of 10 and 25 mg/kg DMT. ... It is concluded that DMT is metabolized chiefly by monoamine oxidase rather than by drug-metabolizing hepatic microsomal enzymes and that DMT-induced behavioral effects are due to the parent compound rather than its metabolite.
Studies were conducted using tritiated DMT and DMT-N-oxide (DMT-NO), and metabolites were identified and quantified using thin-layer chromatography and liquid scintillation counting techniques. Metabolite confirmation was obtained by incubation of alpha,alpha,beta,beta-tetradeutero-DMT (DDMT) with whole brain homogenate followed by combined gas chromatographic/mass spectrometric analyses. The metabolites of DMT were identified as indoleacetic acid (IAA), DMT-NO, N-methyltryptamine (NMT), 2-methyl-1,2,3,4-tetrahydro-beta-carboline (2-MTHBC), tryptamine (TA) and 1,2,3,4- tetrahydro-beta-carboline (THBC). DMT-NO was metabolized to give DMT, NMT, IAA and 2-MTHBC. Formation of these metabolites from DMT-NO was stimulated by anaerobic incubation. ...
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