Top Qs
Timeline
Chat
Perspective
Diethyltryptamine
Psychedelic drug From Wikipedia, the free encyclopedia
Remove ads
Diethyltryptamine (DET), also known as N,N-diethyltryptamine or T-9, is a psychedelic drug of the tryptamine family closely related to dimethyltryptamine (DMT).[1] It is taken orally, but can also be used by parenteral routes.[1]
The drug acts as a non-selective serotonin receptor agonist, including of the serotonin 5-HT2A receptor among others.[4][5] It has not been found to occur endogenously.[6] DMT is a close structural homologue of DMT and dipropyltryptamine (DPT).[1] Other analogues of DET include 4-HO-DET (ethocin), ethocybin (4-PO-DET), and 5-MeO-DET.[1]
DET was first synthesized in 1956 by Stephen Szára and subsequently described in material published in 1957.[7] More systematic studies were reported later by Szára and colleagues[2] and independently by Böszörményi and colleagues.[8]
Remove ads
Use and effects
Summarize
Perspective
According to Alexander Shulgin in his book TiHKAL (Tryptamines I Have Known and Loved), DET's dose range is 50 to 100 mg orally and its duration is 2 to 4 hours.[1][9] It was also assessed at oral doses of 44 to 400 mg, though 150 mg was described as "a little too much" and the 400 mg dose was simply described as "too high".[1] Its onset is 40 minutes to more than 1 hour and peak effects occurred at just over 1 hour.[1] In addition to oral administration, DET was assessed by smoking at doses of 40 to 90 mg, by subcutaneous injection at a dose of 40 mg, by intramuscular injection at a dose of 60 mg, and by intravenous injection at a dose of 60 mg.[1][10] By these routes, it has a faster onset than when taken orally.[1] The drug is said to taste terrible when smoked, like "burning plastic".[1] DET was initially assumed to be inactive orally similarly to dimethyltryptamine (DMT), but this proved to be incorrect.[1]
The effects of DET have been reported to include similar "illusions" and hallucinations" as DMT, a wave-like time course of effects, closed-eye visuals, open-eye visuals, auditory and olfactory hallucinations, synesthesia, feeling like in another world, cosmic thinking, mystical and philosophical feelings, dream-like mysteriousness of objects, greater emotional significance of objects, peoples' faces seeming "mask-like", enhanced appreciation of art, architecture, and music, feeling like a small child perceiving the world and discovering it anew, time dilation, enjoyment and euphoria, increased empathy, and emotional insights.[1][9][2] Additional effects included feeling stoned, alcohol-like intoxication, drifting of thoughts, and difficulty concentrating and cognitive impairment.[1][2] The effects of the drug were described as highly dependent on set and setting, with prominent negative reactions in unfavorable environments or with too high of doses, including unpleasantness, anxiety, paranoia, social withdrawal, and unwillingness to take the drug again, among others.[1][2] Physical effects of DET included DMT-like vegetative or autonomic symptoms, pupil dilation, sweating, slight burning and numbness of hands and feet, dizziness, vertigo, feeling sick, paleness, shakiness, muscle tremors, athetoid movements, vomiting, feeling of hollowness in the chest, pronounced tachycardia, pressor effects, and other somatic symptoms.[1][9][2] Subsequent-day effects included an afterglow, hangover, lassitude, and cognitive fuzziness.[1]
Remove ads
Interactions
Pharmacology
Summarize
Perspective
Pharmacodynamics
Similarly to other classic psychedelics, DET acts as a non-selective serotonin receptor agonist, including of the serotonin 5-HT2A, 5-HT2B, and 5-HT2C receptors.[4][5][11] The drug has been shown to activate Gq-mediated signaling at the serotonin 5-HT2A receptor with Emax higher than 70%[12] and to produce the head-twitch response in rodents which is a behavioral proxy of psychedelic-like effects.[10][12]
DET is a very weak reversible monoamine oxidase inhibitor (MAOI), with IC50 values of 59 μM for serotonin and 5,000 μM for tryptamine as substrates.[3] Injections of 30 mg/kg to rats resulted in 67% reduction of brain MAO-A activity 15 minutes after administration.[3] The substance may also act as a serotonin reuptake inhibitor, with low affinity but moderate potency.[5] It shows no activity as a norepinephrine or dopamine reuptake inhibitor.[5]
Pharmacokinetics
DET demonstrates significant resistance to metabolism by monoamine oxidase A (MAO-A) compared to DMT. This may be due to the increased steric bulk of the N-ethyl substituents relative to the respective methyl groups of DMT which results in metabolic stability sufficient for oral activity.[3][13] This is also true for many other tryptamines with larger nitrogen substituents.[1]
The drug similarly to DMT is rapidly absorbed from the intraperitoneal cavity and quickly distributed through plasma, liver and brain. Most of the substance had disappeared from the aforementioned tissues 30 minutes from administration, except in the brain, where it could still be detected at 60 minutes.[3]
Likewise to DMT the substance is metabolized through 6-hydroxylation and N-dealkylation to form the corresponding intermediates.[14] These metabolites were found to be excreted in urine of about 20% of the administered dose as the glucoronide conjugate, of which the parent compound can be detected by chromatographic analysis at low concentrations (3–5%). Hepatic 6-hydroxylation of the indole ring, yields a minor, psychoactively inactive metabolite 6-hydroxy-DET (6-HO-DET) in similar concentration, with additional hydroxylation possible at alternative positions. Repeated administration of DET, or second exposure one to two weeks after the first, resulted in significant metabolic changes. The unchanged drug excreted after a later exposure was significantly lower, while the excretion of the metabolites which were measured in this case were higher than at the first exposure to DET.[2][14]
Remove ads
Chemistry
DET, also known as N,N-diethyltryptamine, is a synthetic compound in the tryptamine class, structurally related to the endogenous neurotransmitter serotonin and the naturally occurring psychedelic compounds dimethyltryptamine (DMT) and dipropyltryptamine (DPT). It is the ethyl analogue of DMT.[9]
Synthesis
The chemical synthesis of DET has been described.[1][15][16]
Analogues
Analogues of DET include dimethyltryptamine (DMT), dipropyltryptamine (DPT), methylethyltryptamine (MET), methylpropyltryptamine (MPT), ethylpropyltryptamine (EPT), 4-HO-DET, 5-HO-DET, 6-HO-DET, 4-AcO-DET, ethocybin (4-PO-DET or CEY-19), 6F-DET, and 2-Me-DET.[1]
Remove ads
History
Summarize
Perspective
DET was first synthesized and administered intramuscularly in a 60 mg dose by Stephen Szára in 1956. It was subsequently described in his material published in 1957.[7] More systematic studies were reported later by Szara and colleagues and independently by Böszörményi and colleagues.[8][2] Early research began as a search for “psychosis mimics” in psychiatry, then expanded into broader psychedelic and structure–activity studies. Selection of study subjects for some of these studies was criticized by Alexander Shulgin in his 1997 book TiHKAL (Tryptamines I Have Known and Loved) for its "oppressive research environment".[1] For many years, based on early clinical reports and private communications, Shulgin maintained that DET exhibited psychoactive effects only when administered via parenteral routes. He eventually revised his view, ultimately acknowledging that the substance is also orally active.[1]
Initially, DET was not classified as a controlled substance, and some early clinical and experimental psychopharmacological research used it without scheduling restrictions. By the late 1960s and early 1970s, however, increasing regulatory attention led to tighter controls and this led to DET getting placed in Schedule I internationally by the Convention on Psychotropic Substances.[17]
Modern research on DET remains limited compared to dimethyltryptamine (DMT), due to its status as a controlled substance and the predominance of focus on other tryptamines with greater prevalence in traditional or clinical contexts. Most recent studies and reviews refer to DET primarily in comparative molecular pharmacology, assessing its receptor binding and signaling at serotonin receptors.[4][5]
Remove ads
Society and culture
Summarize
Perspective
Legal status
International
DET is listed under Schedule I of the United Nations 1971 Convention on Psychotropic Substances, placing it under international control.[17] This means that countries that are parties to the Convention are required to regulate DET production, distribution, and use, restricting it to scientific and very limited medical purposes. Possession and trade of DET without appropriate authorization is prohibited under international law.
Australia
DET is considered a Schedule 9 prohibited substance in Australia under the Poisons Standard (October 2015).[18] A Schedule 9 substance is a substance 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 Commonwealth and/or State or Territory Health Authorities.
Germany
DET is controlled under Anlage I BtMG (Narcotics Act, Schedule I).[19] as of January 24, 1974.[20] It is illegal to manufacture, possess, import, export, buy, sell, procure or dispense it without a license.[21]
Italy
DET is a Schedule I controlled substance.[22]
New Zealand
DET is a Class A controlled substance in New Zealand.[23]
Switzerland
DET is a controlled substance specifically named under Verzeichnis D.[24]
United Kingdom
DET is a Class A controlled substance.[25]
United States
DET is a Schedule I controlled substance.[26]
Remove ads
Research
Psychosis model
Early studies of DET as well as other psychedelics were focused on their presumed psychotomimetic properties.[27] Researchers theorized that abnormal metabolites of endogenous chemicals such as tryptamine, serotonin, and tryptophan could be the explanation for mental disorders such as schizophrenia, or psychosis.[28] DET, along with other synthetic psychedelics, was administered to both patients and healthy volunteers to understand its effects and as a possible biological model for psychosis. With the progression of science and pharmacological understanding, this belief has been dismissed by most researchers.[29][30]
Mushroom production
Although DET is a synthetic compound with no known natural sources, it has been used in conjunction with the mycelium of Psilocybe cubensis to biosynthetically produce the chemicals ethocybin (4-PO-DET) and ethocin (4-HO-DET). Isolation of the alkaloids resulted in 3.3% ethocybin and 0.01-0.8% ethocin.[6]
Remove ads
See also
References
External links
Wikiwand - on
Seamless Wikipedia browsing. On steroids.
Remove ads