Diethyltryptamine

Clinical data
Other names	DET;N,N-Diethyltryptamine;N,N-DET; T-9; T9
Routes of administration	Oral,inhalation (smoking),intramuscular,intravenous,subcutaneous[1]
Drug class	Non-selectiveserotonin receptor agonist;Serotonin5-HT2A receptoragonist;Serotonergic psychedelic;Hallucinogen
ATC code	None
Legal status
Legal status	BR: Class F2 (Prohibited psychotropics) CA: Schedule III DE: Anlage I (Authorized scientific use only) UK: Class A US: Schedule I UN: Psychotropic Schedule I
Pharmacokinetic data
Metabolism	Oxidative deamination (MAO-ATooltip Monoamine oxidase A),N-oxidation,N-dealkylation[1][2][3]
Metabolites	Indole-3-acetic acid (12–17% inurine)[2] 6-HO-DET (3–4% in urine)[2]
Onset of action	Oral: 40–60 min[1] Intramuscular: 15 min[1]
Duration of action	2–4 hours[1]
Excretion	urine[2]
Identifiers
IUPAC name N,N-diethyl-2-(1H-indol-3-yl)ethan-2-amine
CAS Number	61-51-8 Y
PubChemCID	6090
DrugBank	DB01460 Y
ChemSpider	5865 Y
UNII	916E8V4S2V
KEGG	C22726
ChEBI	CHEBI:184081
ChEMBL	ChEMBL142936 Y
CompTox Dashboard(EPA)	DTXSID9052763
Chemical and physical data
Formula	C14H20N2
Molar mass	216.328 g·mol−1
3D model (JSmol)	Interactive image
Melting point	169 to 171 °C (336 to 340 °F)
SMILES CCN(CC)CCC1=CNC2=C1C=CC=C2
InChI InChI=1S/C14H20N2/c1-3-16(4-2)10-9-12-11-15-14-8-6-5-7-13(12)14/h5-8,11,15H,3-4,9-10H2,1-2H3 Y Key:LSSUMOWDTKZHHT-UHFFFAOYSA-N Y
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Diethyltryptamine (DET), also known asN,N-diethyltryptamine orT-9, is apsychedelic drug of thetryptamine family closely related todimethyltryptamine (DMT).^[1] It is takenorally, but can also be used byparenteralroutes.^[1]

The drug acts as anon-selectiveserotonin receptor agonist, including of theserotonin5-HT_2A receptor among others.^[4][5] It has not been found to occurendogenously.^[6] DMT is a close structuralhomologue of DMT anddipropyltryptamine (DPT).^[1] Otheranalogues of DET include4-HO-DET (ethocin),ethocybin (4-PO-DET), and5-MeO-DET.^[1]

DET was firstsynthesized in 1956 byStephen 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]

According toAlexander Shulgin in his bookTiHKAL (Tryptamines I Have Known and Loved), DET's dose range is 50 to 100 mgorally and itsduration 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] Itsonset 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 bysmoking at doses of 40 to 90 mg, bysubcutaneous injection at a dose of 40 mg, byintramuscular injection at a dose of 60 mg, and byintravenous 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 todimethyltryptamine (DMT), but this proved to be incorrect.^[1]

The effects of DET have been reported to include similar "illusions" andhallucinations" as DMT, a wave-like time course of effects,closed-eye visuals,open-eye visuals,auditory andolfactoryhallucinations,synesthesia,feeling like in another world, cosmic thinking,mystical andphilosophical feelings,dream-like mysteriousness of objects, greater emotional significance of objects, peoples' faces seeming "mask-like", enhanced appreciation ofart,architecture, andmusic, feeling like a small child perceiving the world and discovering it anew,time dilation,enjoyment andeuphoria, increasedempathy, andemotionalinsights.^[1][9][2] Additional effects includedfeeling stoned,alcohol-likeintoxication, drifting of thoughts, and difficulty concentrating and cognitive impairment.^[1][2] The effects of the drug were described as highly dependent onset and setting, with prominent negative reactions in unfavorable environments or with too high of doses, includingunpleasantness,anxiety,paranoia,social withdrawal, and unwillingness to take the drug again, among others.^[1][2] Physical effects of DET included DMT-likevegetative or autonomic symptoms,pupil dilation,sweating, slightburning andnumbness of hands and feet,dizziness,vertigo,feeling sick,paleness,shakiness,muscle tremors, athetoid movements,vomiting,feeling of hollowness in the chest, pronouncedtachycardia,pressor effects, and other somatic symptoms.^[1][9][2] Subsequent-day effects included anafterglow,hangover,lassitude, andcognitive fuzziness.^[1]

Similarly to otherclassic psychedelics, DET acts as anon-selectiveserotonin receptor agonist, including of theserotonin5-HT_2A,5-HT_2B, and5-HT_2C receptors.^[4][5][11] The drug has been shown to activateG_q-mediated signaling at the serotonin 5-HT_2A receptor withE_maxhigher than 70%[12] and to produce thehead-twitch response in rodents which is a behavioral proxy ofpsychedelic-like effects.^[10][12]

DET is a very weakreversiblemonoamine oxidase inhibitor (MAOI), withIC₅₀Tooltip half-maximal inhibitory concentration values of 59 μM for serotonin and 5,000 μM fortryptamine assubstrates.^[3] Injections of 30 mg/kg torats resulted in 67% reduction of brainMAO-A activity 15 minutes after administration.^[3] The substance may also act as aserotonin reuptake inhibitor, with lowaffinity but moderate potency.^[5] It shows no activity as anorepinephrine ordopamine reuptake inhibitor.^[5]

DET demonstrates significant resistance tometabolism bymonoamine oxidase A (MAO-A) compared toDMT. This may be due to the increasedsteric bulk of theN-ethylsubstituents relative to the respectivemethyl groups of DMT which results in metabolic stability sufficient fororal activity.^[3][13] This is also true for many othertryptamines with largernitrogen substituents.^[1]

The drug similarly to DMT is rapidlyabsorbed from theintraperitoneal cavity and quicklydistributed throughplasma,liver andbrain. 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 andN-dealkylation to form the correspondingintermediates.^[14] These metabolites were found to beexcreted inurine of about 20% of the administered dose as theglucoronide conjugate, of which the parent compound can be detected bychromatographic analysis at lowconcentrations (3–5%). Hepatic 6-hydroxylation of theindole ring, yields a minor,psychoactively inactivemetabolite6-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]

DET, also known asN,N-diethyltryptamine, is asynthetic compound in thetryptamine class,structurally related to theendogenousneurotransmitterserotonin and the naturally occurringpsychedelic compoundsdimethyltryptamine (DMT) anddipropyltryptamine (DPT). It is theethyl analogue of DMT.^[9]

Thechemical synthesis of DET has been described.^[1][15][16]

Analogues of DET includedimethyltryptamine (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, and2-Me-DET.^[1]

DET was firstsynthesized and administeredintramuscularly in a 60 mg dose byStephen 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 broaderpsychedelic andstructure–activity studies. Selection of study subjects for some of these studies was criticized byAlexander Shulgin in his 1997 bookTiHKAL (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 viaparenteral routes. He eventually revised his view, ultimately acknowledging that the substance is alsoorally active.^[1]

Initially, DET was not classified as acontrolled 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 theConvention on Psychotropic Substances.^[17]

Modern research on DET remains limited compared todimethyltryptamine (DMT), due to its status as acontrolled substance and the predominance of focus on othertryptamines with greater prevalence in traditional or clinical contexts. Most recent studies and reviews refer to DET primarily in comparative molecularpharmacology, assessing itsreceptor binding andsignaling atserotoninreceptors.^[4][5]

DET is listed under Schedule I of theUnited Nations 1971Convention 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.

DET is considered a Schedule 9 prohibited substance inAustralia under thePoisons 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.

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]

DET is a Schedule I controlled substance.^[22]

DET is a Class A controlled substance in New Zealand.^[23]

DET is a controlled substance specifically named under Verzeichnis D.^[24]

DET is a Class A controlled substance.^[25]

DET is a Schedule I controlled substance.^[26]

Early studies of DET as well as otherpsychedelics were focused on their presumedpsychotomimetic properties.^[27] Researchers theorized that abnormalmetabolites of endogenous chemicals such astryptamine,serotonin, andtryptophan could be the explanation formental disorders such asschizophrenia, orpsychosis.^[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 andpharmacological understanding, this belief has been dismissed by most researchers.^[29][30]

Although DET is asynthetic compound with no knownnatural sources, it has been used in conjunction with themycelium ofPsilocybe cubensis tobiosynthetically produce the chemicalsethocybin (4-PO-DET) andethocin (4-HO-DET). Isolation of thealkaloids resulted in 3.3% ethocybin and 0.01-0.8% ethocin.^[6]

• Substituted tryptamine

• DET - Isomer Design
• DET - PsychonautWiki
• DET - Erowid
• DET - TiHKAL - Erowid
• DET - TiHKAL - Isomer Design
• The Modest & Dandy DET thread - Bluelight

• Drugs not assigned an ATC code
• 5-HT1A agonists
• 5-HT2A agonists
• 5-HT2C agonists
• Designer drugs
• N,N-Dialkyltryptamines
• Diethylamino compounds
• Psychedelic tryptamines
• Serotonin receptor agonists
• Serotonin reuptake inhibitors
• TiHKAL

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