Chemistry:5-MeO-DiPT

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5-MeO-DiPT, also known as 5-methoxy-N,N-diisopropyltryptamine and sometimes as foxy methoxy or simply foxy, is an atypical psychedelic drug of the tryptamine and 5-methoxytryptamine families.[1][2][3] It has unique and distinct effects from other serotonergic tryptamines, including some stimulant- and entactogen-like effects, robust tactile and sexual enhancement, and only light hallucinogenic effects.[1][4][3][5][6] The drug is usually taken orally, but may also be used by other routes.[1][4][2][5][7]

It acts as a non-selective serotonin receptor agonist, including of the serotonin 5-HT1A and 5-HT2A receptors among others.[8][9][10][11][12] Uniquely among most tryptamines, the drug has been found to produce serotonergic neurotoxicity and associated cognitive deficits in rodents reminiscent of but distinct from those observed with MDMA.[2][13][14] Various severe and/or fatal intoxications associated with 5-MeO-DiPT have been reported in humans.[2][11][12] It is the 5-methoxy derivative of diisopropyltryptamine (DiPT) and is an analogue of other psychedelic tryptamines like 4-HO-DiPT, 5-MeO-DMT, and 5-MeO-MiPT.[1]

5-MeO-DiPT was first described in the literature by Alexander Shulgin and colleagues in 1980.[3][15][1][4] Subsequently, Shulgin described 5-MeO-DiPT in further detail in his 1997 book TiHKAL (Tryptamines I Have Known and Loved).[1] The drug was first encountered as a novel designer drug in 1999.[2][5] It is used recreationally as a "party drug" and sexual enhancer, with notable use among gay men and transgender women as part of "chemsex", although its use in general has declined over time and is rare.[3][5][2][16] 5-MeO-DiPT became a controlled substance in the United States in 2003.[2][17][18] The closely related drug 5-MeO-MiPT (moxy) has similar effects as 5-MeO-DiPT, remains legal in the United States and many other countries, and is often used as a substitute for 5-MeO-DiPT.[3][1][19][20][21]

Use and effects

In his book TiHKAL (Tryptamines I Have Known and Loved) and other publications, Alexander Shulgin reported the dose of 5-MeO-DiPT to be 6 to 12 mg orally, its onset to be 20 to 30 minutes or within 1 hour, its time to peak effects to be 1 to 1.5 hours, and its duration to be 4 to 8 hours.[1][4][22][23][6][5] However, in other publications besides TiHKAL he gave a dose range of 6 to 10 mg[4][6] or a dose range of 8 to 12 mg.[22][23][6] According to Shulgin, testing of 5-MeO-DiPT started at a dose of 0.1 mg and gradually titrated up in 10 human volunteers, with threshold effects occurring at a dose of 4 mg orally and full effects occurring at doses of 6 mg or more.[4][6] The drug's has been described as "fast-acting" and its duration has also been reported to be "short-lived" and as brief as 3 to 6 hours.[1][4][3][6][5] In addition to oral administration, 5-MeO-DiPT has been reported to be used less commonly by smoking, insufflation, or intravenous injection.[5][2][7] Forms known to be used include powder, tablets, and capsules.[5]

The psychedelic or perceptual effects of 5-MeO-DiPT have been reported to include colors on edges of eyesight, color contrasts and sparkle, altered facial perception, sensory distortion, few if any visual enhancements, some closed-eye imagery but only at high doses, feelings of strangeness, objects having special significance, some musical sound distortions reminiscent of those of DiPT, music sounding strange and fake, time dilation, having only mild hallucinogenic effects, outgoing rather than inwardly reflective intellectual activation, lack of intuitive leaps, and a wave-like experience wherein the effects "waved in and out".[1][4][3][5][6] Affective and behavioral effects have included stimulation, some entactogen-like effects, talkativeness, disinhibition, emotional enhancement, opening of affect, easy emotional expression, easy communication with others, reduced guards and reservations, relaxation, feeling happy, mild euphoria, and mellowness.[1][4][3][5][6] In addition, the drug has been reported to produce tactile or sensual enhancement, one's body feeling alive and alert, feeling like waves are passing back and forth over one's body, awareness of vibrations, feeling sexually aroused, and "dramatic" erotic or sexual enhancement.[1][4][3][5][6]

Negative emotional and behavioral effects have included uncomfortableness, agitation, feeling unnerved, paranoia, and social avoidance, but no hangover.[1][4][6] 5-MeO-DiPT has been described as having minimal physical side effects and as being relatively free of autonomic side effects and indicators of toxicity.[1][4] Reported physical side effects have included body load and discomfort, slight pupil dilation, mild nausea, some muscular hyperreflexia, muscle contractions and spasms, gastrointestinal disturbances, hypertension, and little change in appetite or sleep disruption.[1][4][6] The effects of 5-MeO-DiPT have been described as either being "positive" or a "mixed bag".[1][4] User responses are said to vary dramatically, with some people finding it appealing, sexual, invigorating, interesting, and enjoyable, and others finding it nauseating, annoying, diarrhea-inducing, and generally unpleasant.[5]

5-MeO-DiPT has been described as LSD-like in some ways but as being quite different from other psychedelics.[1][4][3] Descriptions have included the drug never being psychedelic in the way of classical psychedelics like LSD and psilocybin, there being an absence of intense sensory disturbances or hallucinogenic effects as with other psychedelics like dimethyltryptamine (DMT) and psilocybin, never feeling as though one was having a psychedelic experience, and being able to function normally on a social level including at public events even at high doses.[1][4][3] However, one user who took a high dose described reaching a "plus-three" on the Shulgin Rating Scale in a very LSD-like manner but without the visuals.[1] Higher doses may produce more psychedelic effects, but the drug is still described as not that psychedelic even at such doses.[3] Despite its lack of robust hallucinogenic effects at typical doses, 5-MeO-DiPT is described as nonetheless producing quite profound emotional and intellectual modifications.[4]

5-MeO-DiPT is reported to differ in its subjective effects from the structurally related DiPT in most respects but to share some auditory effects with this drug.[4][1] In terms of these effects, whereas DiPT caused harmonic distortion of heard sounds, 5-MeO-DiPT caused changes in musical character and interpretation without apparent changes in harmonic structure.[1] As such, while both produced auditory effects, DiPT and 5-MeO-DiPT caused different distortions of musical interpretation.[1] 5-MeO-DiPT has been described as a "psychedelic stimulant" and has a reputation as a "sexual enhancer" or "aphrodisiac".[3][5] Among its effects, the pro-sexual effects of 5-MeO-DiPT have been especially highlighted, with these effects being present at low doses.[1] Users have remarked that it took them to a "marvelous sexy place", that "everything [was] shaded with eroticism", that the "erotic world was fantastic, explosive, almost scary", and that the drug may vie with 2C-B as a sexual enhancer or that it left 2C-B "in the dust" in this regard.[1][3]

5-MeO-DiPT has been described as having effects similar to those of 5-MeO-MiPT and these drugs as having unique and distinct effects from those of other psychedelic tryptamines.[3][21] They are reported to be very pro-sexual, much more stimulant, and more like party drugs than other tryptamines.[3][2][21] While 5-MeO-DiPT and 5-MeO-MiPT are described as pro-sexual, they may not be innately aphrodisiac but instead may produce tactile enhancement in a way that lends itself to sex.[3] The tactile enhancement and "body high" with 5-MeO-DiPT and 5-MeO-MiPT may in part be why they have been compared to entactogens like MDMA.[3] 5-MeO-DiPT has been described as being closer to MDMA in its effects than to psychedelic tryptamines and that the effects are a "body high kind of thing".[3] The drug is also known to be combined with other drugs such as MDMA.[24]

Side effects

Flashbacks have been reported with 5-MeO-DiPT.[25][26] There is a report of a prolonged delusional state associated with 5-MeO-DiPT.[27]

Overdose

Excessive doses or overdose have caused clinical intoxication, characterized by nausea, vomiting, agitation, hypotension, mydriasis, tachycardia, and hallucinations, in a number of young adults. A number of these overdoses are attributed to the drug's delayed onset of action, where first time users, who were unfamiliar with the drug, administered a second dose after initially feeling no effects. Rhabdomyolysis and renal failure occurred in one young man and another one died 3 to 4 hours after an apparent rectal overdose.[28] There have been a number of published cases of severe and/or fatal intoxication with 5-MeO-DiPT.[2][11][12][6][29][30][31][32][33]

Interactions

The effects of 5-MeO-DiPT may be potentiated when used in combination with cannabis.[6][1]

Pharmacology

Pharmacodynamics

5-MeO-DiPT activities
Target Affinity (Ki, nM)
5-HT1A 16–170 (Ki)
34–>10,000 (EC50)
44–114% (Emax)
5-HT1B 5,137–>10,000 (Ki)
85–170 (EC50)
100–134% (Emax)
5-HT1D 293–1,718 (Ki)
41–126 (EC50)
92–104% (Emax)
5-HT1E >10,000 (Ki)
407–2,190 (EC50)
67–86% (Emax)
5-HT1F ND (Ki)
871–3,240 (EC50)
53–83% (Emax)
5-HT2A 162–>10,000 (Ki)
6.2–946 (EC50)
99–124% (Emax)
5-HT2B 35–163 (Ki)
13–56 (EC50)
80–110% (Emax)
5-HT2C 1,740–>10,000 (Ki)
30–1,789 (EC50)
71–101% (Emax)
5-HT3 >10,000
5-HT4 ND
5-HT5A >10,000 (Ki)
>10,000 (EC50)
ND (Emax)
5-HT6 2,190–>10,000 (Ki)
324 (EC50)
87% (Emax)
5-HT7 1,231–>10,000 (Ki)
>10,000 (EC50)
ND (Emax)
α1A, α1B >10,000
α1D ND
α2A >10,000
α2B 5,293–>10,000
α2C 2,865–3,081
β1, β2 >10,000
β3 ND
D1–D5 >10,000
H1–H4 >10,000
M1–M5 >10,000
I1 760
σ1 9,443–>10,000
σ2 291–3,002
TAAR1 ND
SERT 874–>10,000 (Ki)
239–24,215 (IC50)
>100,000 (EC50) (rat)
NET >10,000 (Ki)
8,200–>10,000 (IC50)
>100,000 (EC50) (rat)
DAT >10,000 (Ki)
65,000 (IC50)
>100,000 (EC50) (rat)
Notes: The smaller the value, the more avidly the drug interacts with the site. All proteins are human unless otherwise specified. Refs: [34][35][8][9][36][37]
[10][38][11][12][39]

5-MeO-DiPT acts as a non-selective serotonin receptor agonist, including of the serotonin 5-HT1A, 5-HT1B, 5-HT1D, 5-HT2A, 5-HT2B, and 5-HT2C receptors, among others.[35][8][9][10][11][12] It has shown variably strong preference for the serotonin 5-HT1A receptor in terms of binding affinity, with 2-fold, 25-fold, >76-fold, and 161-fold higher for this receptor over the serotonin 5-HT2A receptor in different studies.[35][8][12][36][37][25][2] However, in terms of receptor activation, 5-MeO-DiPT showed similar potency at the serotonin 5-HT1A receptor and the serotonin 5-HT2A receptor and had several-fold preference for these receptors over the serotonin 5-HT2C receptor.[11]

In addition to its direct serotonin receptor interactions, 5-MeO-DiPT is a serotonin reuptake inhibitor with potency ranging from similar to its serotonin 5-HT2A receptor agonism to very low in different studies.[11][40][41][12] Conversely, it does not significantly affect dopamine or norepinephrine reuptake and shows no activity as a monoamine releasing agent.[10][12][42][38][41] The drug can block the serotonin release induced by methamphetamine in vitro.[42][41] 5-MeO-DiPT can elevate brain serotonin levels in rodents, presumably via its serotonin reuptake inhibition.[24][43] The elevations in serotonin levels caused by 5-MeO-DiPT may be limited by its concomitant serotonin 5-HT1A receptor agonism, as serotonin 5-HT1A receptors serve as inhibitory autoreceptors that limit serotonin release.[40] By an unknown mechanism, but possibly serotonin 5-HT2A receptor agonism, 5-MeO-DiPT may also elevate brain dopamine levels in rodents, including in the prefrontal cortex, striatum, and/or nucleus accumbens, although findings are mixed.[24][40][43] The mechanism of action of the psychedelic effects of 5-MeO-DiPT is thought to be serotonin 5-HT2A receptor agonism, but its full mechanism of action is unclear and additional mechanisms may also be involved.[42][36][38]

5-MeO-DiPT produces the head-twitch response, a behavioral proxy of psychedelic-like effects, in rodents.[44][25][2][45][12][46][36] As with many other psychedelics, this follows an inverted U-shaped dose–response curve.[45][36] The head-twitch response induced by 5-MeO-DiPT is blocked by serotonin 5-HT2A receptor antagonists such as volinanserin.[45][36] 5-MeO-DiPT's head-twitch response is described as robust but also weak and much lower in magnitude than that produced by other serotonergic psychedelics such as 5-MeO-DMT or DOM.[37][36][12] The serotonin 5-HT1A receptor agonism of 5-MeO-DiPT may inhibit its serotonin 5-HT2A receptor-mediated head-twitch response.[36] 5-MeO-DiPT partially substitutes for LSD in rodent drug discrimination tests, with 52% responding at 1 mg/kg, 75% responding at 3 mg/kg, and behavioral disruption at higher doses.[36] In addition, it substitutes for DOM in rodent drug discrimination tests.[36][47] The stimulus properties of 5-MeO-DiPT in LSD substitution tests are completely and insurmountably blocked by the serotonin 5-HT2A receptor antagonist volinanserin.[37][36] Conversely, they are partially and surmountably blocked by the serotonin 5-HT1A receptor antagonist WAY-100635.[37][36] Besides psychedelic-like effects, 5-MeO-DiPT also produces hypolocomotion and hypothermia in rodents and potentiates the forepaw treading induced by the serotonin 5-HT1A receptor agonist 8-OH-DPAT.[12][46][48][24]

Neurotoxicity

5-MeO-DiPT has been reported to produce neurotoxicity in rodents.[49][42][24][50][2] Administration of 5-MeO-DiPT to adolescent rodents produced marked decreases in spatial navigation performance in adulthood that were suggestive of deficits in cognitive flexibility, attention, and/or perseveration as well as other cognitive deficits.[2][51][13][52] This was associated with serotonergic neurotoxicity and substantial 26 to 49% reductions in cortical and hippocampal serotonin levels that were analogous to those occurring with MDMA.[2][13] However, the neurotoxic effects of 5-MeO-DiPT are described as less severe than and distinct from those of MDMA.[13][14] The drug has also been reported to produce cytotoxicity as well as neurotoxic effects on serotonergic neurons ex vivo.[42][50] The mechanisms underlying the serotonergic neurotoxicity of 5-MeO-DiPT are unknown.[42][13] The drug might also produce prolonged dopaminergic adaptations or dopaminergic neurotoxicity in rodents as evidenced by long-lasting decreases in dopamine levels.[24][50] In addition, it has been associated with marked genotoxicity or oxidative DNA damage, which has also been seen with MDMA and methamphetamine.[24][50] It has been said to be the first known tryptamine to be associated with such toxicity.[24] However, various other psychedelics have also been found to produce neurotoxicity in preclinical research, with this including serotonergic neurotoxicity.[53][54][55][56]

Pharmacokinetics

The pharmacokinetics and metabolism of 5-MeO-DiPT have been studied.[57][2][58][59][60]

Chemistry

Properties

The log P of 5-MeO-DiPT is 3.68.[12]

Synthesis

The chemical synthesis of 5-MeO-DiPT has been described.[1]

Analogues

Analogues of 5-MeO-DiPT include diisopropyltryptamine (DiPT), 4-HO-DiPT (iprocin), 4-AcO-DiPT (ipracetin), 4-MeO-DiPT, 5-HO-DiPT, 5-MeO-DMT, 5-MeO-DET, 5-MeO-DPT, 5-MeO-DALT, 5-MeO-MiPT, 5-MeO-MsBT, 5-MeO-EiPT, 5-MeO-PiPT, 5-MeO-iPALT (ASR-3001), and 5-MeO-DiBF (1-oxa-5-MeO-DiPT), among others.[1]

Positional isomers

4-MeO-DiPT, 6-MeO-DiPT, and 7-MeO-DiPT are known positional isomers of 5-MeO-DiPT.[1][23] 6-MeO-DiPT and 7-MeO-DiPT have been described by Alexander Shulgin as being inactive at doses of up to 50 mg and 70 mg orally, respectively, whereas 4-MeO-DiPT was not assessed.[1][23]

History

5-MeO-DiPT was discovered in the 1970s and was first described by Alexander Shulgin and Michael Carter in 1980.[3][15][1][4] Shulgin tested it and discovered its effects starting in 1975.[61] The drug started to be encountered as a novel recreational and designer drug in 1999.[2][5] 5-MeO-DiPT became a temporarily controlled substance in the United States in 2003 and a permanently controlled substance in 2004.[2][17][18] The recreational use of 5-MeO-DiPT appears to have declined over time and its use is described as being not very prevalent.[5][3][2]

Society and culture

Recreational use

5-MeO-DiPT tablets seized from Salem, Oregon.

Use of 5-MeO-DiPT has been found to be particularly prevalent among gay men who use drugs as part of chemsex.[2][62][63] It is also seen in transgender women.[16][64] The drug is described as a stimulant, sexual enhancer, party drug, and light psychedelic.[3] 5-MeO-DiPT has been associated with increased risk of HIV diagnosis in multiple studies in Asia, perhaps due to risky sexual behavior involving the drug.[3][63][65][16]

Canada

5-MeO-DiPT is not an explicitly nor implicitly controlled substance in Canada as of 2025.[66]

China

As of October 2015, 5-MeO-DiPT is a controlled substance in China.[67]

Denmark

Germany

Greece

Japan

Illegal since April 2005.[2]

Singapore

Sweden

Sveriges riksdags health ministry Statens folkhälsoinstitut classified 5-MeO-DiPT as "health hazard" under the act Lagen om förbud mot vissa hälsofarliga varor (translated Act on the Prohibition of Certain Goods Dangerous to Health) as of Oct 1, 2004, in their regulation SFS 2004:696 listed as 5-metoxi-N,N-diisopropyltryptamin (5-MeO-DIPT), making it illegal to sell or possess.[68]

United States

On April 4, 2003, the United States DEA added both 5-MeO-DiPT and α-methyltryptamine (AMT) to Schedule I of the Controlled Substances Act under "emergency scheduling" procedures.[2] The drugs were officially placed into Schedule I on September 29, 2004.[2] Prior to its prohibition in the U.S., 5-MeO-DiPT was sold online alongside psychoactive analogues such as diisopropyltryptamine (DiPT), and dipropyltryptamine (DPT), neither of which have yet been expressly outlawed.

See also

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 1.20 1.21 1.22 1.23 1.24 1.25 1.26 1.27 1.28 1.29 Shulgin, Alexander; Shulgin, Ann (September 1997). TiHKAL: The Continuation. Berkeley, California: Transform Press. ISBN 0-9630096-9-9. OCLC 38503252. http://www.erowid.org/library/books_online/tihkal/tihkal.shtml. 
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 "The hallucinogenic world of tryptamines: an updated review". Arch Toxicol 89 (8): 1151–1173. August 2015. doi:10.1007/s00204-015-1513-x. PMID 25877327. Bibcode: 2015ArTox..89.1151A. https://psilosybiini.info/paperit/The%20hallucinogenic%20world%20of%20tryptamines,%20an%20updated%20review%20(Ara%FAjo%20et%20al.,%202015).pdf. 
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 3.21 3.22 "A qualitative descriptive analysis of effects of psychedelic phenethylamines and tryptamines". Hum Psychopharmacol 35 (1). January 2020. doi:10.1002/hup.2719. PMID 31909513. "Other 5-MeO compounds 5-MeO compounds were less prevalent in this sample of experienced tryptamine users. We received few comments about the effects of individual compounds in this subclass, and these compounds tended to be described as being more sexual than other compounds. One participant also pointed out that 5-Meo-DIPT (“Foxy Methoxy” or “Foxy”) gained notoriety in the United States as a sexual enhancement drug. 5-Meo-DIPT, Foxy, or Moxy (5-Meo-MIPT) are tryptamines that are distinct. A lot of people I know that like them think they're very aphrodisiac and much more stimulant and a party drug. My opinion on 5-MeO-MIPT is that it was a very sexual chemical … it feels good to touch things, and that sort of sensation certainly lends itself to sex but I wouldn't call it innately an aphrodisiac. These increased sensations of touch are likely why some users compared the “body high” with the high associated with MDMA use. The effects of 5-MeO compounds were also described as being shorter lasting than other tryptamines. I would actually say that it is closer to MDMA in its effects. The whole series of 5-MeO and 4-MeO … they're both very closely related in their effects so it tends to be a body high kind of thing. At higher doses it can get more psychedelic, but it's not that psychedelic. [...] first discovered or first synthesized as early as [...] in the 1970s (e.g., 4-HO-MET and 5-MeO-DIPT). However, use does not appear to be very prevalent (Palamar & Le, 2019; Palamar, Martins, Su, & Ompad, 2015), and most of these compounds do not have much of a presence in the published literature. [...] Finally, 5-MeO-DIPT (“Foxy”) was also used by a few of our participants, and they noted sexual effects of the drug. Although sometimes described as a sex drug on the internet, academic literature does not seem to describe sexual effects of the drug. However, multiple studies in Asia have linked use of 5-MeO-DIPT to increased risk for HIV diagnosis, likely due to risky sexual behavior involving the drug (Hayashi, Wakabayashi, Ikushima, & Tarui, 2017; Kuwahara et al., 2008; Shan et al., 2018).". 
  4. ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 4.15 4.16 4.17 4.18 "N, N-Diisopropyltryptamine (DIPT) and 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT). Two orally active tryptamine analogs with CNS activity". Commun Psychopharmacol 4 (5): 363–369. 1980. PMID 6949674. https://bitnest.netfirms.com/external/Commun.Psychopharmacol/4.5.363. 
  5. ↑ 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 5.10 5.11 5.12 5.13 5.14 "5-MeO-DiPT" (in ru). https://aipsin.com/newsubstance/799/. 
  6. ↑ 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 6.11 6.12 "Foxy, a designer tryptamine hallucinogen". J Anal Toxicol 27 (5): 313–317. 2003. doi:10.1093/jat/27.5.313. PMID 12908946. "Foxy is slang for 5-methoxy-N,N-diisopropyltryptamine. It has hallucinogenic properties, similar to other tryptamine compounds, and is mildly euphoric. [...] This case report describes a 21-year-old Caucasian man who ingested a pill called Foxy containing an unknown amount of drug. He was observed in hospital for 2 h, during which time he had mild hallucinations and could not move his limbs. [...] Clinically, the drug promotes emotional expression, a talkative uninhibited state (7), and visual and auditory sensory distortions (8). No other clinical studies appear in the medical literature. There are no reported pharmacological studies in humans. Some of the drug's physiological properties are also common to the recreational drug methylenedioxymethamphetamine (Ecstasy). Not surprisingly, 5-MeO-DIPT is a club drug (2) and has been substituted for Ecstasy on the street (3). [...] In 1980, Shulgin and Carter (7) described the administration of 5-MeO-DIPT to 10 human subjects. Each person received a 0.1mg oral dose which was then increased in increments of 30 to 50% in subsequent drug administrations. Threshold subjective effects were observed with a 4-mg dose. Effective doses were between 6 and 10 mg. The peak drug effect occurred at 1 to 1.5 h after ingestion, and recovery was observed after 3 h with no residual symptoms at 6 h. Subjects reported a relaxed feeling associated with emotional enhancement. They were frequently talkative and felt their conversations to be expressive and stimulating. Shulgin and Shulgin (8) later summarized the responses from an additional 10 human subjects upon administration of 6 to 12 mg of 5-MeO-DIPT. Most subjects reported auditory and visual distortions. Two indicated aphrodisiac tendencies; one experienced gastrointestinal emptying, muscle spasms, and agitation; and one indicated a synergistic effect with marijuana. [...] In our patient, the drug lasted 3.5 h. He said he felt "weird" (apprehensive) and saw symbols (visual hallucination) as opposed to being talkative or expressive of his emotions.". 
  7. ↑ 7.0 7.1 "Toxicology and Analysis of Psychoactive Tryptamines". Int J Mol Sci 21 (23): 9279. December 2020. doi:10.3390/ijms21239279. PMID 33291798. 
  8. ↑ 8.0 8.1 8.2 8.3 "Psychedelics and the human receptorome". PLOS ONE 5 (2). February 2010. doi:10.1371/journal.pone.0009019. PMID 20126400. Bibcode: 2010PLoSO...5.9019R. 
  9. ↑ 9.0 9.1 9.2 "Receptor interaction profiles of novel psychoactive tryptamines compared with classic hallucinogens". European Neuropsychopharmacology 26 (8): 1327–1237. August 2016. doi:10.1016/j.euroneuro.2016.05.001. PMID 27216487. https://psilosybiini.info/paperit/Receptor%20interaction%20profiles%20of%20novel%20psychoactive%20tryptamines%20compared%20with%20classic%20hallucinogens%20(Rickli%20et%20al.,%202016).pdf. 
  10. ↑ 10.0 10.1 10.2 10.3 "Interaction of psychoactive tryptamines with biogenic amine transporters and serotonin receptor subtypes". Psychopharmacology (Berl) 231 (21): 4135–4144. October 2014. doi:10.1007/s00213-014-3557-7. PMID 24800892. PMC 4194234. https://psilosybiini.info/paperit/Interaction%20of%20psychoactive%20tryptamines%20with%20biogenic%20amine%20transporters%20and%20serotonin%20receptor%20subtypes%20(Blough%20et%20al.,%202014).pdf. 
  11. ↑ 11.0 11.1 11.2 11.3 11.4 11.5 11.6 "Pharmacologic Activity of Substituted Tryptamines at 5-Hydroxytryptamine (5-HT)2A Receptor (5-HT2AR), 5-HT2CR, 5-HT1AR, and Serotonin Transporter". J Pharmacol Exp Ther 385 (1): 62–75. April 2023. doi:10.1124/jpet.122.001454. PMID 36669875. 
  12. ↑ 12.00 12.01 12.02 12.03 12.04 12.05 12.06 12.07 12.08 12.09 12.10 12.11 "Structure-activity relationships of serotonergic 5-MeO-DMT derivatives: insights into psychoactive and thermoregulatory properties". Mol Psychiatry 29 (8): 2346–2358. August 2024. doi:10.1038/s41380-024-02506-8. PMID 38486047. PMC 11412900. https://www.nature.com/articles/s41380-024-02506-8.pdf. 
  13. ↑ 13.0 13.1 13.2 13.3 13.4 "5-methoxy-N,N-di(iso)propyltryptamine hydrochloride (Foxy)-induced cognitive deficits in rat after exposure in adolescence". Physiol Behav 103 (2): 203–209. May 2011. doi:10.1016/j.physbeh.2011.01.021. PMID 21295050. 
  14. ↑ 14.0 14.1 "Comparison of the developmental effects of 5-methoxy-N,N-diisopropyltryptamine (Foxy) to (+/-)-3,4-methylenedioxymethamphetamine (ecstasy) in rats". Psychopharmacology (Berl) 204 (2): 287–297. June 2009. doi:10.1007/s00213-009-1459-x. PMID 19198809. 
  15. ↑ 15.0 15.1 "The Varieties of the Psychedelic Experience: A Preliminary Study of the Association Between the Reported Subjective Effects and the Binding Affinity Profiles of Substituted Phenethylamines and Tryptamines". Front Integr Neurosci 12. 2018. doi:10.3389/fnint.2018.00054. PMID 30467466. "5-MeO-DiPT (5-Methoxy-N,N-diisopropyltryptamine): substituted tryptamine, first synthesized and tested by Shulgin and Carter (1979).". 
  16. ↑ 16.0 16.1 16.2 "Correlates of HIV infection among transgender women in two Chinese cities". Infect Dis Poverty 7 (1). December 2018. doi:10.1186/s40249-018-0508-2. PMID 30509315. 
  17. ↑ 17.0 17.1 Drug Enforcement Administration (Dea), Department of Justice (April 2003). "Schedules of controlled substances: temporary placement of alpha-methyltryptamine and 5-methoxy-N,N-diisopropyltryptamine into Schedule I. Final rule". Fed Regist 68 (65): 16427–16430. PMID 12678045. 
  18. ↑ 18.0 18.1 Drug Enforcement Administration (Dea), Department of Justice (September 2004). "Schedules of controlled substances: placement of alpha-methyltryptamine and 5-methoxy-N,N-diisopropyltryptamine into schedule I of the Controlled Substances Act. Final rule". Fed Regist 69 (188): 58950–58953. PMID 15455477. 
  19. ↑ "DEA Proposes Adding Five Psychedelic Compounds to Schedule 1" (in en-US). 2022-01-25. https://www.lucid.news/dea-proposes-five-psychedelic-compounds-schedule-1/. 
  20. ↑ Aragón, Matthew (9 January 2024). "Meet Moxy: The Novel Psychedelic the DEA Tried To Ban". https://doubleblindmag.com/what-is-moxy/. 
  21. ↑ 21.0 21.1 21.2 "5-MeO-MiPT" (in ru). https://aipsin.com/newsubstance/1109/. 
  22. ↑ 22.0 22.1 "Basic Pharmacology and Effects". Hallucinogens: A Forensic Drug Handbook. Forensic Drug Handbook Series. Elsevier Science. 2003. pp. 67–137. ISBN 978-0-12-433951-4. https://citeseerx.ist.psu.edu/document?repid=rep1&type=pdf&doi=6bb3a7499da8e9852b39cd4db16891147c83f5c6. Retrieved 1 February 2025. 
  23. ↑ 23.0 23.1 23.2 23.3 "Structure-activity relationships of the classic hallucinogens and their analogs". NIDA Res Monogr 146: 74–91. 1994. PMID 8742795. https://archives.nida.nih.gov/sites/default/files/monograph146.pdf#page=79. 
  24. ↑ 24.0 24.1 24.2 24.3 24.4 24.5 24.6 24.7 "Neurotoxic Effects of 5-MeO-DIPT: A Psychoactive Tryptamine Derivative in Rats". Neurotox Res 30 (4): 606–619. November 2016. doi:10.1007/s12640-016-9654-0. PMID 27461536. 
  25. ↑ 25.0 25.1 25.2 "Psychedelics". Pharmacol Rev 68 (2): 264–355. April 2016. doi:10.1124/pr.115.011478. PMID 26841800. PMC 4813425. https://psilosybiini.info/paperit/Psychedelics%20(Nichols,%202016).pdf. "Ikeda et al. (2005) reported flashbacks after use of 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT) by a 35-year-old man without a previous psychiatric history. He had used the substance six or seven times over 5 months but discontinued it after he had a bad trip, with anxiety, palpitations, auditory oversensitiveness, and visual distortions. Treatment with oral risperidone ameliorated his symptoms. [...] Fantegrossi et al. (2006) demonstrated that 5-MeODIPT induced the head twitch in mice, and the effect was antagonized by pretreatment with the 5-HT2A– selective antagonist M100907. The affinity of 5-MeO-DIPT was measured at rat 5-HT1A, 5-HT2A, and 5-HT2C receptors using antagonist radioligands, with Ki values determined to be 35 nM, 5620 nM, and 1700 nM, respectively. Thus, despite the higher affinity for 5-MeO-DIPT at the 5-HT1A receptor, the head twitch was mediated through the 5-HT2A receptor.". 
  26. ↑ "5-methoxy-N,N-diisopropyltryptamine-induced flashbacks". Am J Psychiatry 162 (4): 815. April 2005. doi:10.1176/appi.ajp.162.4.815. PMID 15800171. 
  27. ↑ "Prolonged delusional state triggered by repeated ingestion of aromatic liquid in a past 5-methoxy-N, N-diisopropyltryptamine abuser". Addict Sci Clin Pract 8 (1). April 2013. doi:10.1186/1940-0640-8-9. PMID 23577618. 
  28. ↑ Disposition of Toxic Drugs and Chemicals in Man (8th ed.). Foster City, CA: Biomedical Publications. 2008. pp. 975–976. 
  29. ↑ "A foxy intoxication". Forensic Sci Int 148 (1): 31–36. February 2005. doi:10.1016/j.forsciint.2004.04.017. PMID 15607587. 
  30. ↑ "Foxy methoxy: a new drug of abuse". J Med Toxicol 1 (1): 22–25. December 2005. doi:10.1007/BF03160901. PMID 18072099. 
  31. ↑ "A fatal poisoning with 5-methoxy-N,N-diisopropyltryptamine, Foxy". Forensic Science International 163 (1–2): 152–154. November 2006. doi:10.1016/j.forsciint.2005.11.026. PMID 16406422. 
  32. ↑ "Rhabdomyolysis after ingestion of "foxy," a hallucinogenic tryptamine derivative". Mayo Clin Proc 81 (4): 550–551. April 2006. doi:10.4065/81.4.550. PMID 16610577. 
  33. ↑ "Acute confusional state after designer tryptamine abuse". Psychiatry Clin Neurosci 61 (2): 196–199. April 2007. doi:10.1111/j.1440-1819.2007.01638.x. PMID 17362440. 
  34. ↑ "Kᵢ Database". 26 March 2025. https://pdsp.unc.edu/kidb2/kidb/web/kis-results/index?KisResultsSearch%5Binput_receptors%5D=&KisResultsSearch%5Binput_sources%5D=&KisResultsSearch%5Binput_species%5D=&KisResultsSearch%5Binput_hot_ligands%5D=&KisResultsSearch%5Binput_test_ligands%5D=&KisResultsSearch%5Binput_test_ligands%5D%5B%5D=12949&KisResultsSearch%5Binput_citations%5D=&KisResultsSearch%5BsearchType%5D=&KisResultsSearch%5Bki_val_from%5D=&KisResultsSearch%5Bki_val_to%5D=&KisResultsSearch%5Bcustom_ki_val%5D=. 
  35. ↑ 35.0 35.1 35.2 "The polypharmacology of psychedelics reveals multiple targets for potential therapeutics". Neuron 113 (19): 3129–3142.e9. July 2025. doi:10.1016/j.neuron.2025.06.012. PMID 40683247. https://www.cell.com/cms/10.1016/j.neuron.2025.06.012/attachment/7d8365fe-51f3-4a28-bf40-9999bec837f6/mmc11.pdf. 
  36. ↑ 36.00 36.01 36.02 36.03 36.04 36.05 36.06 36.07 36.08 36.09 36.10 36.11 "Hallucinogen-like actions of 5-methoxy-N,N-diisopropyltryptamine in mice and rats". Pharmacol Biochem Behav 83 (1): 122–129. January 2006. doi:10.1016/j.pbb.2005.12.015. PMID 16460788. 
  37. ↑ 37.0 37.1 37.2 37.3 37.4 "The behavioral pharmacology of hallucinogens". Biochem Pharmacol 75 (1): 17–33. January 2008. doi:10.1016/j.bcp.2007.07.018. PMID 17977517. 
  38. ↑ 38.0 38.1 38.2 "The effects of non-medically used psychoactive drugs on monoamine neurotransmission in rat brain". Eur J Pharmacol 559 (2–3): 132–137. March 2007. doi:10.1016/j.ejphar.2006.11.075. PMID 17223101. https://citeseerx.ist.psu.edu/document?repid=rep1&type=pdf&doi=00665d67c36dcf1777989b70cc901c654420a0c7. 
  39. ↑ "In Vitro Characterization of Psychoactive Substances at Rat, Mouse, and Human Trace Amine-Associated Receptor 1". J Pharmacol Exp Ther 357 (1): 134–144. April 2016. doi:10.1124/jpet.115.229765. PMID 26791601. https://d1wqtxts1xzle7.cloudfront.net/74120533/eae6c6e62565b82d46b4d111bbea0f77b9c2-libre.pdf?1635931703=&response-content-disposition=inline%3B+filename%3DIn_Vitro_Characterization_of_Psychoactiv.pdf&Expires=1746838268&Signature=Sy4fJ90yUhxs68314NxYsW5PAaNrBGePRu35WRR4PIF-3YC7Z~sLdnCn5wfqqbLg9bDEGdt~oW55ugMP3D3jgA0BoRI~~GOb0NQOwrtfUEQK1PQs1uuN9qg5Y1ct8z5NsABm44RgtukkwRMdU6fO7OlfIsQ68hOiFk129Ll7UYqldxD2f1xhE2fTTfsxSpb8cMCJzHn7-ItqLdwnAUPFK7WggDIjmY1kCnaHLwIxMwdJCAq8L6DYzSTg7pZkbR8qlou~GXbTPQt~gYpyZTJp5hgW-7V6K5wLlQ7Z2xE7B0f9wEfuc1W1QNafg125Tr-vvAe4LEGKXV58bnn1bpfWKw__&Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA. 
  40. ↑ 40.0 40.1 40.2 "Dual actions of 5-MeO-DIPT at the serotonin transporter and serotonin 5-HT1A receptor in the mouse striatum and prefrontal cortex". Neuropsychopharmacol Rep 41 (1): 91–101. March 2021. doi:10.1002/npr2.12161. PMID 33547882. 
  41. ↑ 41.0 41.1 41.2 "5-Methoxy-N,N-diisopropyltryptamine (Foxy), a selective and high affinity inhibitor of serotonin transporter". Toxicol Lett 170 (1): 75–82. April 2007. doi:10.1016/j.toxlet.2007.02.007. PMID 17382495. Bibcode: 2007ToxL..170...75S. 
  42. ↑ 42.0 42.1 42.2 42.3 42.4 42.5 "Neuropsychotoxicity of abused drugs: molecular and neural mechanisms of neuropsychotoxicity induced by methamphetamine, 3,4-methylenedioxymethamphetamine (ecstasy), and 5-methoxy-N,N-diisopropyltryptamine (foxy)". J Pharmacol Sci 106 (1): 2–8. January 2008. doi:10.1254/jphs.fm0070141. PMID 18198474. 
  43. ↑ 43.0 43.1 "A systematic study of changes in monoamine neurotransmitters in the rat brain following acute administration of alpha-methyltryptamine (AMT), 5-methoxy-alpha-methyltryptamine (5-MeO-AMT) and 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DiPT)". Neurosci Res 216. July 2025. doi:10.1016/j.neures.2025.04.006. PMID 40288614. 
  44. ↑ "Effect of Hallucinogens on Unconditioned Behavior". Behavioral Neurobiology of Psychedelic Drugs: Effect of Hallucinogens on Unconditioned Behavior. Current Topics in Behavioral Neurosciences. 36. 2018. 159–199. doi:10.1007/7854_2016_466. ISBN 978-3-662-55878-2. http://www.ouramazingworld.org/uploads/4/3/8/6/43860587/halberstadt2016.pdf. Retrieved 2025-03-26. "Likewise, the HTR is induced by ring-substituted tryptamines, including psilocin, psilocybin, 5-MeO-DMT, and 5-MeO-DIPT (Corne and Pickering 1967; Bedard and Pycock 1977; Fantegrossi et al. 2006; González-Maeso et al. 2007; Halberstadt et al. 2011)." 
  45. ↑ 45.0 45.1 45.2 "Multiple receptors contribute to the behavioral effects of indoleamine hallucinogens". Neuropharmacology 61 (3): 364–381. September 2011. doi:10.1016/j.neuropharm.2011.01.017. PMID 21256140. "Certain indolealkylamines, including DMT, N,N-dipropyltryptamine (DPT), 5-MeO-DMT, and 5-methoxy-N,Ndiisopropyltryptamine (5-MeO-DIPT) block 5-HT uptake at micromolar concentrations (Nagai et al., 2007; Sogawa et al., 2007; Cozzi et al., 2009) and serve as substrates for the 5-HT transporter (Cozzi et al., 2009). [...] Likewise, HTR induced by DPT, 5-MeO-DIPT, and TCB-2 in mice is blocked by M100,907 and MDL 11,939 (Fantegrossi et al., 2006, 2008; Fox et al., 2009). [...] Fantegrossi and colleagues have reported that the HTR induced by DOI, 2C-T-7, DPT, and 5-MeO-DIPT in NIH Swiss and Swiss-Webster mice typically follows an inverted U-shaped dose–response function (Fantegrossi et al., 2005, 2006, 2008, 2010).". 
  46. ↑ 46.0 46.1 "Effects of three tryptamines: alpha-methyltryptamine, 5-methoxy-alpha-methyltryptamine, and 5-methoxy- N , N -diisopropyltryptamine on acute toxicity, locomotor activity, and hallucinogenic behavior in mice". Behav Pharmacol 36 (6): 429–437. September 2025. doi:10.1097/FBP.0000000000000841. PMID 40622300. 
  47. ↑ "DOM-stimulus generalization to LSD and other hallucinogenic indolealkylamines". Eur J Pharmacol 86 (3–4): 453–459. January 1983. doi:10.1016/0014-2999(83)90196-6. PMID 6572591. 
  48. ↑ "Alterations in body temperature, corticosterone, and behavior following the administration of 5-methoxy-diisopropyltryptamine ('foxy') to adult rats: a new drug of abuse". Neuropsychopharmacology 32 (6): 1404–1420. June 2007. doi:10.1038/sj.npp.1301232. PMID 17047665. 
  49. ↑ Gołembiowska, Krystyna (2022). "Pharmacology and Neurotoxicity of 5-MeO-DIPT". Handbook of Neurotoxicity. Cham: Springer International Publishing. pp. 1403–1414. doi:10.1007/978-3-031-15080-7_207. ISBN 978-3-031-15079-1. 
  50. ↑ 50.0 50.1 50.2 50.3 "Effects of exposure to 5-MeO-DIPT during adolescence on brain neurotransmission and neurotoxicity in adult rats". Forensic Toxicol 37 (1): 45–58. 2019. doi:10.1007/s11419-018-0433-x. PMID 30636982. 
  51. ↑ "An examination of the effects of 5-Methoxy-n, n-di(ISO)propyltryptamine hydrochloride (Foxy) on cognitive development in rats". Psychol Rep 98 (3): 651–661. June 2006. doi:10.2466/pr0.98.3.651-661. PMID 16933659. 
  52. ↑ "The effect of repeated-intermittent exposure to 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT) during adolescence on learning and memory in adult rats". Pharmacol Rep 70 (5): 890–895. October 2018. doi:10.1016/j.pharep.2018.04.001. PMID 30096487. 
  53. ↑ "Molecular and clinical aspects of potential neurotoxicity induced by new psychoactive stimulants and psychedelics". Exp Neurol 343. September 2021. doi:10.1016/j.expneurol.2021.113778. PMID 34090893. 
  54. ↑ "Serotonin 2C receptors are also important in head-twitch responses in male mice". Psychopharmacology (Berl) 242 (7): 1585–1605. July 2025. doi:10.1007/s00213-023-06482-9. PMID 37882810. 
  55. ↑ "Ecstasy-induced cell death in cortical neuronal cultures is serotonin 2A-receptor-dependent and potentiated under hyperthermia". Neuroscience 139 (3): 1069–1081. 2006. doi:10.1016/j.neuroscience.2006.01.007. PMID 16504407. 
  56. ↑ "Molecular and cellular mechanisms of ecstasy-induced neurotoxicity: an overview". Mol Neurobiol 39 (3): 210–271. June 2009. doi:10.1007/s12035-009-8064-1. PMID 19373443. "To further corroborate the fact that MDMA agonistic properties at the 5-HT2A receptor could produce neuronal death, DOI, a prototypical agonist of that receptor was added to cortical neurons [289]. DOI (10 to 100 μM for 24 or 48 h) also induced a dose- and time-dependent apoptotic cortical neuronal apoptosis, which was attenuated by ketanserin and R-96544 [289]. Ketanserin and R-96544 are competitive selective 5-HT2A receptor antagonists and only attenuated MDMA-induced cortical neurodegeneration. However, an antibody raised against the 5-HT2A-receptor, an “irreversible” non-competitive 5-HT2A receptor blocker, prevented almost completely MDMA- and DOI-induced cortical neurotoxicity [289, 290]. Neuronal apoptosis mediated by MDMA is accompanied by activation of caspase 3, which could be blocked by the antibody raised against the 5-HT2A receptor [290]. Therefore, it is likely that DOI- and MDMA-induced neuronal apoptosis arises from direct stimulation of the 5-HT2A receptor [289, 290].". 
  57. ↑ "Metabolism of designer drugs of abuse: an updated review". Curr Drug Metab 11 (5): 468–482. June 2010. doi:10.2174/138920010791526042. PMID 20540700. 
  58. ↑ "Indolealkylamines: biotransformations and potential drug-drug interactions". AAPS J 10 (2): 242–253. June 2008. doi:10.1208/s12248-008-9028-5. PMID 18454322. 
  59. ↑ "Metabolism of the psychotomimetic tryptamine derivative 5-methoxy-N,N-diisopropyltryptamine in humans: identification and quantification of its urinary metabolites". Drug Metab Dispos 34 (2): 281–287. February 2006. doi:10.1124/dmd.105.005835. PMID 16280455. 
  60. ↑ "Oxidative metabolism of 5-methoxy-N,N-diisopropyltryptamine (Foxy) by human liver microsomes and recombinant cytochrome P450 enzymes". Biochem Pharmacol 71 (9): 1377–1385. April 2006. doi:10.1016/j.bcp.2006.01.015. PMID 16510126. 
  61. ↑ "5-OCH3-DIPT timeline". https://isomerdesign.com/pihkal/notebooks/transcripts/p1/p1.176.pdf. 
  62. ↑ "Substance use and sexual behaviours of Japanese men who have sex with men: a nationwide internet survey conducted in Japan". BMC Public Health 6. September 2006. doi:10.1186/1471-2458-6-239. PMID 17002800. 
  63. ↑ 63.0 63.1 "Problems in three Japanese drug users with Human Immunodeficiency Virus infection". J Med Invest 55 (1–2): 156–160. February 2008. doi:10.2152/jmi.55.156. PMID 18319560. 
  64. ↑ "Perceived Stress Predicts Drug Use in Transgender Women: The Mediating Role of Loneliness". Transgend Health 9 (5): 421–426. October 2024. doi:10.1089/trgh.2022.0121. PMID 39449793. 
  65. ↑ "Recreational drug use and related social factors among HIV-positive men in Japan". AIDS Care 28 (7): 932–940. July 2016. doi:10.1080/09540121.2016.1140888. PMID 26887351. 
  66. ↑ "Controlled Drugs and Substances Act". 5 December 2025. https://laws-lois.justice.gc.ca/eng/acts/c-38.8/FullText.html. 
  67. ↑ "关于印发《非药用类麻醉药品和精神药品列管办法》的通知" (in zh). China Food and Drug Administration. 27 September 2015. http://www.sfda.gov.cn/WS01/CL0056/130753.html. 
  68. ↑ "notisum.se". http://www.notisum.se/rnp/sls/sfs/20040696.pdf. 

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