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N,N-Dimethyltryptamine

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N,N-Dimethyltryptamine
Clinical data
Routes of
administration		Oral (with an MAOI), insufflated, rectal, vaporized, IM, IV
ATC code
  • none
Legal status
Legal status
Identifiers
  • 2-(1H-Indol-3-yl)-N,N-dimethylethanamine
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.000.463 Edit this at Wikidata
Chemical and physical data
FormulaC12H16N2
Molar mass188.269 g/mol g·mol−1
3D model (JSmol)
Density1.099 g/cm3
Melting point40 °C (104 °F)
Boiling point160 °C (320 °F)
@ 0.6 Torr (80 Pa)[1]
also reported as
80–135 °C (176–275 °F)
@ 0.03 Torr (4.0 Pa)[2]
  • CN(CCC1=CNC2=C1C=CC=C2)C
  • InChI=1S/C12H16N2/c1-14(2)8-7-10-9-13-12-6-4-3-5-11(10)12/h3-6,9,13H,7-8H2,1-2H3 checkY
  • Key:DMULVCHRPCFFGV-UHFFFAOYSA-N checkY
  (verify)
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N,N-Dimethyltryptamine (DMT or N,N-DMT) is a tryptamine molecule found in plants and animals.[3] When consumed by humans, it is known to cause hallucinations. It is claimed that it has been used by various primitive cultures for ritual purposes.[4][5] In many countries, DMT is illegal due to its dangerous effects and classified as a narcotic.

DMT has a rapid onset, intense effects and a relatively short duration of action.[6] DMT effects depend on the dose. When inhaled or injected, the effects last a short period of time: about 5 to 15 minutes. Effects can last 3 hours or more when orally ingested along with an MAOI.[7] DMT can produce hallucinations, including dynamic hallucinations of geometric forms.[8]

DMT is a structural analog of serotonin and melatonin and a functional analog of other tryptamines such as 4-AcO-DMT, 5-MeO-DMT, 5-HO-DMT, psilocybin (4-PO-DMT), and psilocin (4-HO-DMT).

Usage

DMT is produced in many species of plants often in conjunction with its close chemical relatives 5-MeO-DMT and bufotenin (5-OH-DMT).[9][10][11] It occurs as the primary alkaloid in several plants.[9][12] Psilocin and its precursor psilocybin are structurally similar to DMT. The hallucinogenic effects of DMT were studied by scientists who performed research with volunteers in the mid-1950s.[13] DMT is generally not active orally.[4][8]

Effects

Physical

According to a dose-response study, "dimethyltryptamine does slightly elevate 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 rise equally in response to all doses of DMT, and melatonin levels were unaffected."[14]

Dependence liability

DMT is illegal in many countries.

History

DMT was first synthesized in 1931 by chemist Richard Helmuth Fredrick Manske.[15][16] In general, its discovery as a natural product is credited to Brazilian chemist and microbiologist Oswaldo Gonçalves de Lima.[17] Since 1955, DMT has been found in a host of organisms: in at least fifty plant species belonging to ten families,[18] and in at least four animal species, including one gorgonian[19] and three mammalian species.

International law

DMT is classified as a Schedule I drug under the United Nations 1971 Convention on Psychotropic Substances, meaning that international trade in DMT is supposed to be closely monitored; use of DMT is supposed to be restricted to scientific research and medical use.[20]

By country and continent

Asia

Israel – DMT is an illegal substance; production, trade and possession are prosecuted as crimes.[21]

Europe

North America

  • Canada – DMT is classified as a Schedule III drug under the Controlled Drugs and Substances Act.
United States

In December 2004, the Supreme Court lifted a stay, thereby allowing the Brazil-based União do Vegetal (UDV) church to use a decoction containing DMT in their Christmas services that year. In September 2008, the three Santo Daime churches filed suit in federal court to gain legal status to import DMT-containing tea. The case, Church of the Holy Light of the Queen v. Mukasey,[24] presided over by Judge Owen M. Panner, was ruled in favor of the Santo Daime church.[25]

Oceania

Australia
  • DMT is listed as a Schedule 9 prohibited substance in Australia under the Poisons Standard (October 2015).[28] 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."[29]

Under the Misuse of Drugs act 1981, 6.0 g of DMT is considered enough to determine a court of trial and 2.0 g is considered intent to sell and supply.[30]

Chemistry

DMT crystals

The DMT molecule contains a terminal secondary amine, which acts as a weak base with a pKa of approximately 10.5. Depending on the synthetic route, or extraction procedure, it is possible to isolate the free base or various salts obtained by protonation of the secondary amine. Common salts insluce the sulfate, the hydrochloride, the fumarate, the oxalate and the picrate.[31] The free base and each salt has its own properties including CAS Number, stability, solubility, and melting point. Each salt will also have a different molecular weight, thus also changing the exact dosage as measured in weight. [31]

Biosynthesis

Biosynthetic pathway for N,N-dimethyltryptamine

Dimethyltryptamine is an indole alkaloid derived from the shikimate pathway. Its biosynthesis is relatively simple and summarized in the adjacent picture. In plants, the parent amino acid L-tryptophan is produced endogenously where in animals L-tryptophan is an essential amino acid coming from diet. No matter the source of L-tryptophan, the biosynthesis begins with its decarboxylation by an aromatic amino acid decarboxylase (AADC) enzyme (step 1). The resulting decarboxylated tryptophan analog is tryptamine. Tryptamine then undergoes a transmethylation (step 2): the enzyme indolethylamine-N-methyltransferase (INMT) catalyzes the transfer of a methyl group from cofactor S-adenosyl-methionine (SAM), via nucleophilic attack, to tryptamine. This reaction transforms SAM into S-adenosylhomocysteine (SAH), and gives the intermediate product N-methyltryptamine (NMT).[32][33] NMT is in turn transmethylated by the same process (step 3) to form the end product N,N-dimethyltryptamine. Tryptamine transmethylation is regulated by two products of the reaction: SAH,[34][35][36] and DMT[34][36] were shown ex vivo to be among the most potent inhibitors of rabbit INMT activity.

This transmethylation mechanism has been repeatedly and consistently proven by radiolabeling of SAM methyl group with carbon-14 (14C-CH3)SAM).[32][34][36][37][38]

Laboratory synthesis

DMT can be synthesized through several possible pathways from different starting materials. Following Shulgin's notes, the first synthesis starts with tryptamine followed by trimethylation using methyl iodide to obtain the trimethylammonium iodide salt. This is then demethylated using LiEt3BH to obtain DMT. The iodide salt of the trimethylammonium intermediate can be converted to the chloride salt followed by a different demethylation procedure. The second procedure avoids the over methylation of the amine and uses ethyl formate reacted with tryptamine for a double N-formylation. These are then reduced using lithium aluminum hydride to obtain the dimethyl amine product. The third synthesis starts from indole and oxalyl chloride which forms indol-3-ylglyoxyl chloride. This is then reacted with dimethylamine followed by reduction using lithium aluminum hydride to obtain DMT. Depending on the final work-up the free base or any of its various salts may be obtained as products. Shulgin gives a procedure for obtaining the hydrochloride salt by dissolving DMT in diethyl ether followed by sparging with HCl gas. He also mentions the picrate, oxalate and fumarate salts.[39]

Clandestine manufacture

DMT during various stages of purification

In a clandestine setting, DMT is not typically synthesized due to the lack of availability of the starting materials, namely tryptamine and oxalyl chloride. It is more often extracted from plant sources using a hydrocarbon solvent such as hexane due to the ease of availability of both the plant source and solvents, neither of which are controlled in most countries.

Evidence in mammals

Published in Science in 1961, Julius Axelrod found an N-methyltransferase enzyme capable of mediating biotransformation of tryptamine into DMT in a rabbit's lung.[32] This finding initiated a still ongoing scientific interest in endogenous DMT production in humans and other mammals.[33][40] 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.[33]

In 2013 researchers first reported DMT in the pineal gland microdialysate of rodents.[41]

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.[42]

In a 2014 paper a group first 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.[43]

Endogenous DMT

The first claimed detection of mammalian endogenous DMT 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.[44] In an article published four months later, the method used in their study was strongly criticized, and the credibility of their results challenged.[45]

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.[46][47] Gas chromatography, preferably coupled to mass spectrometry (GC-MS), is considered a minimum requirement.[47] A study published in 2005[40] implements the most sensitive and selective method ever used to measure endogenous DMT:[48] 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)
Species Sample Results
Human Blood serum < LOD (n = 66)[40]
Blood plasma < LOD (n = 71)[40]  ♦  < LOD (n = 38); 1,000 & 10,600 ng/L (n = 2)[49]
Whole blood < LOD (n = 20); 50–790 ng/L (n = 20)[50]
Urine < 100 ng/L (n = 9)[40]  ♦  < LOD (n = 60); 160–540 ng/L (n = 5)[47]  ♦  Detected in n = 10 by GC-MS[51]
Feces < 50 ng/kg (n = 12); 130 ng/kg (n = 1)[40]
Kidney 15 ng/kg (n = 1)[40]
Lung 14 ng/kg (n = 1)[40]
Lumbar CSF 100,370 ng/L (n = 1); 2,330–7,210 ng/L (n = 3); 350 & 850 ng/L (n = 2)[52]
Rat Kidney 12 &16 ng/kg (n = 2)[40]
Lung 22 & 12 ng/kg (n = 2)[40]
Liver 6 & 10 ng/kg (n = 2)[40]
Brain 10 &15 ng/kg (n = 2)[40]  ♦  Measured in synaptic vesicular fraction[53]
Rabbit Liver < 10 ng/kg (n = 1)[40]

A 2013 study found DMT in microdialysate obtained from a rat's pineal gland, providing evidence of endogenous DMT in the mammalian brain.[41]

Detection in body fluids

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.[54][55][clarification needed]

INMT

Before techniques of molecular biology were used to localize indolethylamine N-methyltransferase (INMT),[36][38] 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[33] or with addition of a radiolabeled substrate like (14C)NMT to demonstrate in vivo formation.[34][37] 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 (see DMT subsection below). The essentially qualitative method thin layer chromatography (TLC) was thus used in a vast majority of studies.[33] 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[56][57] and human[58] lung during the early 1970s.

Selectivity rather than sensitivity proved to be an Achilles’ heel 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 substrate mostly yields tetrahydro-β-carboline derivatives,[33][34][59] and negligible amounts of DMT in brain tissue.[33] 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.[33] These findings are a blow for all previous claims of evidence of INMT activity and DMT biosynthesis in avian[60] and mammalian brain,[61][62] including in vivo,[63][64] as they all relied upon use of the problematic TLC methods:[33] 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.[65][66] 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".[67] Capability of the method used in this latter study to resolve DMT from tetrahydro-β-carbolines is questioned later.[34]
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.[38] Northern blot analyses reveal INMT messenger RNA (mRNA) to be highly expressed in rabbit lung,[36] and in human thyroid, adrenal gland, and lung.[38][68] Intermediate levels of expression are found in human heart, skeletal muscle, trachea, stomach, small intestine, pancreas, testis, prostate, placenta, lymph node, and spinal cord.[38][68] Low to very low levels of expression are noted in rabbit brain,[38] and human thymus, liver, spleen, kidney, colon, ovary, and bone marrow.[38][68] INMT mRNA expression is absent in human peripheral blood leukocytes, whole brain, and in tissue from 7 specific brain regions (thalamus, subthalamic nucleus, caudate nucleus, hippocampus, amygdala, substantia nigra, and corpus callosum).[38][68] 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.[69]

Pharmacology

Pharmacokinetics

DMT peak level concentrations (Cmax) measured in whole blood after intramuscular (IM) injection (0.7 mg/kg, n = 11)[70] and in plasma following intravenous (IV) administration (0.4 mg/kg, n = 10)[14] of dangerous doses are in the range of ≈14 to 154 μg/L and 32 to 204 μg/L, respectively. The corresponding molar concentrations of DMT are therefore in the range of 0.074–0.818 µM in whole blood and 0.170–1.08 µM in plasma. However, several studies have described active transport and accumulation of DMT into rat and dog brain following peripheral administration.[71][72][73][74][75] Similar active transport, and accumulation processes likely occur in human brain 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 μM range.[76][77]

Closely coextending with dangerous effects, mean time to reach peak concentrations (Tmax) was determined to be 10–15 minutes in whole blood after IM injection,[70] and 2 minutes in plasma after IV administration.[14] When taken orally mixed in an ayahuasca decoction, and in freeze-dried ayahuasca gel caps, DMT Tmax is considerably delayed: 107.59 ± 32.5 minutes,[78] and 90–120 minutes,[79] respectively. The pharmacokinetics for vaporizing DMT have not been studied or reported.

Pharmacodynamics

DMT binds non-selectively with affinities < 0.6 μM to the following serotonin receptors: 5-HT1A,[80][81][82] 5-HT1B,[80][83] 5-HT1D,[80][82][83] 5-HT2A,[80][82][83][84] 5-HT2B,[80][83] 5-HT2C,[80][83][84] 5-HT6,[80][83] and 5-HT7.[80][83] An agonist action has been determined at 5-HT1A,[81] 5-HT2A and 5-HT2C.[80][83][84] Its efficacies at other serotonin receptors remain to be determined. Of special interest will be the determination of its efficacy at human 5-HT2B receptor as two in vitro assays evidenced DMT's high affinity for this receptor: 0.108 μM[83] and 0.184 μM.[80] This may be of importance because chronic or frequent uses of serotonergic drugs showing preferential high affinity and clear agonism at 5-HT2B receptor have been causally linked to valvular heart disease.[85][86][87]

It has also been shown to possess affinity for the dopamine D1, α1-adrenergic, α2-adrenergic, imidazoline-1, and σ1 receptors.[82][83][88] Converging lines of evidence established activation of the σ1 receptor at concentrations of 50–100 μM.[89] 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) and the intracellular vesicular monoamine transporter 2 (VMAT2), inhibiting SERT-mediated serotonin uptake in human platelets at an average concentration of 4.00 ± 0.70 μM and VMAT2-mediated serotonin uptake in vesicles (of army worm Sf9 cells) expressing rat VMAT2 at an average concentration of 93 ± 6.8 μM.[90]

As with other so-called "classical hallucinogens",[91] a large part of DMT dangerous effects can be attributed to a functionally selective activation of the 5-HT2A receptor.[14][80][92][93][94][95][96] DMT concentrations eliciting 50% of its maximal effect (half maximal effective concentration = EC50 or Kact) at the human 5-HT2A receptor in vitro are in the 0.118–0.983 μM range.[80][83][84][97] This range of values coincides well with the range of concentrations measured in blood and plasma after administration of a dangerous dose (see Pharmacokinetics).

As DMT has been shown to have slightly better efficacy (EC50) at human serotonin 2C receptor than at the 2A receptor,[83][84] 5-HT2C is also likely implicated in DMT's overall effects.[93][98] Other receptors, such as 5-HT1A[82][93][95] σ1,[89][99] may also play a role.

In 2009, it was hypothesized that DMT may be an endogenous ligand for the σ1 receptor.[89][99] The concentration of DMT needed for σ1 activation in vitro (50–100 μM) is similar to the behaviorally active concentration measured in mouse brain of approximately 106 μM[100] 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,[90] such concentrations might occur during vesicular release. To illustrate, while the average concentration of serotonin in brain tissue is in the 1.5-4 μM range,[76][77] the concentration of serotonin in synaptic vesicles was measured at 270 mM.[101] Following vesicular release, the resulting concentration of serotonin in the synaptic cleft, to which serotonin receptors are exposed, is estimated to be about 300 μM. 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.

Binding Sites Binding Affinity Ki (µM)[102]
5-HT1A 0.075
5-HT2A 0.237
5-HT2C 0.424
D1 6
D2 3
D3 6.3
α1A 1.3
α2A 2.1
TAAR1 2.2
H1 0.22
SERT 6
DAT 22
NET 6.5

See also

References

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