2,5-Dimethoxy-4-iodoamphetamine

Last updated

DOI
R-DOI chemical structure.png
(R)-DOI, the (R)-enantiomer of DOI
DOI ball-and-stick chemical structure.png
DOI ball-and-stick model
Clinical data
Other namesDOI; 2,5-Dimethoxy-4-iodoamphetamine; 4-Iodo-2,5-dimethoxyamphetamine
Routes of
administration 		Oral [1]
Drug class Serotonergic psychedelic; Hallucinogen; Serotonin 5-HT2 receptor agonist; Anti-inflammatory agent
ATC code
  • None
Legal status
Legal status
Pharmacokinetic data
Duration of action 16–30 hours [1]
Identifiers
  • 1-(4-iodo-2,5-dimethoxyphenyl)propan-2-amine
CAS Number
PubChem CID
IUPHAR/BPS
ChemSpider
UNII
ChEMBL
CompTox Dashboard (EPA)
Chemical and physical data
Formula C11H16INO2
Molar mass 321.158 g·mol−1
3D model (JSmol)
Melting point 201.5 °C (394.7 °F) (hydrochloride)
Solubility in water 10 mg/mL [3]
  • IC(C=C1OC)=C(OC)C=C1CC(C)N
  • InChI=1S/C11H16INO2/c1-7(13)4-8-5-11(15-3)9(12)6-10(8)14-2/h5-7H,4,13H2,1-3H3 Yes check.svgY
  • Key:BGMZUEKZENQUJY-UHFFFAOYSA-N Yes check.svgY
   (verify)

2,5-Dimethoxy-4-iodoamphetamine (DOI) is a psychedelic drug of the phenethylamine, amphetamine, and DOx families. [4] [1] [5] [6] It is little-used recreationally, but is widely used in scientific research in the study of psychedelics and serotonin receptors. [4] [5] [6] [7] The drug is taken orally. [1]

Contents

It acts as a potent serotonin 5-HT2 receptor agonist, including of the serotonin 5-HT2A and 5-HT2C receptors. [5] [6] Analogues of DOI include 2C-I, DOB, DOC, DOM, and 25I-NBOMe, among others. [1]

DOI was first described in the scientific literature by Ronald Coutts and Jerry Malicky in 1973. [5] [8] Subsequently, it was described in greater detail by Alexander Shulgin in his 1991 book PiHKAL (Phenethylamines I Have Known and Loved). [1] DOI has been encountered as a novel designer drug. [4] [7] [9] Owing to their very long and disagreeable durations however, DOI and other DOx drugs have seen very little recreational availability and use. [4] [7] [5] [10] [11] [12] [13] Unlike many other psychedelic drugs, DOI is not an explicitly controlled substance in the United States. [14] However, in 2023, the Drug Enforcement Administration (DEA) began taking steps to make DOI a controlled substance. [15] [16] [7] As of late 2025, DOI is poised to become a Schedule I controlled substance in the United States. [4] [7]

Use and effects

In his book PiHKAL (Phenethylamines I Have Known and Loved), Alexander Shulgin lists DOI's dose as 1.5 to 3 mg orally and its duration as 16 to 30 hours. [1] The effects of DOI have been reported to include feelings of unreality, strangeness, closed-eye imagery, time dilation, having none of LSD's sparkle, depression and sadness, enhanced eroticism, lightheadedness, and spaciness, among others. [1] It was said to have little or no body load. [1] The (R)-enantiomer, (R)-DOI, was active at doses of 1.0 to 2.3 mg orally, whereas the (S)-enantiomer, (S)-DOI, was active at a dose of 6.3 mg orally. [1]

Interactions

It is unclear whether DOI may interact with monoamine oxidase inhibitors (MAOIs). [17]

Pharmacology

Pharmacodynamics

Actions

DOI activities
Target Affinity (Ki, nM)
5-HT1A 2,219–4,177
5-HT1B >10,000
5-HT1D 458
5-HT1E 1,013–2,970
5-HT1F 1,739–2,511
5-HT2A 0.46–165 (Ki)
0.42–57 (EC50 Tooltip half-maximal effective concentration)
46–111% (Emax Tooltip maximal efficacy)
5-HT2B 1.4–336 (Ki)
1.4–39 (EC50)
71–103% (Emax)
5-HT2C 1.8–48 (Ki)
0.14–178 (EC50)
90–114% (Emax)
5-HT3 >10,000
5-HT4 ND
5-HT5A >10,000
5-HT5B 1,000 (rat)
5-HT6 2,113
5-HT7 5,769
α1A >10,000
α1B >10,000
α1D ND
α2A 74
α2B 340
α2C 601
β1 591
β2 139
D1 9,688
D2–D5 >10,000
H1 1,757
H2–H4 >10,000
M1 2,720
M2 1,989
M3 1,428
M4 578
M5 2,208
TAAR1 >1,000
I1 >10,000
σ1 8,565
σ2 9,172
SERT Tooltip Serotonin transporter685 (Ki)
NET Tooltip Norepinephrine transporter>10,000 (Ki)
DAT Tooltip Dopamine transporter>10,000 (Ki)
MAO-A Tooltip Monoamine oxidase A37,000 (IC50)
MAO-B Tooltip Monoamine oxidase B>200,000 (IC50)
Notes: The smaller the value, the more avidly the drug binds to the site. All proteins are human unless otherwise specified. Refs: [18] [19] [20] [6] [21] [22]
[23] [24] [25] [26] [27]

DOI is a serotonin 5-HT2A, 5-HT2B and 5-HT2C receptor agonist. [18] [19] [20] [6] It is said to be approximately 5- to 12-fold selective for the serotonin 5-HT2A receptor over the serotonin 5-HT2C receptor. [28] The drug shows biased agonism at the serotonin 5-HT2C receptor. [29]

The drug is not a monoamine releasing agent of serotonin or dopamine. [23]

DOI is an agonist of the rat trace amine-associated receptor 1 (TAAR1). [30]

The compound has a stereocenter, and R-(−)-DOI is the more active stereoisomer. [1] [5] [125I]-R-(−)-DOI is used as a radioligand and indicator of the presence of serotonin 5-HT2A receptors in studies. [5]

Effects

(R)-DOI and several other serotonergic psychedelics, including TCB-2, LSD, and LA-SS-Az, have been found to show potent inhibition of tumor necrosis factor alpha (TNFα)-induced inflammation. [31] [32] [33] (R)-DOI was the most active of the assessed drugs and showed extremely high potency that was in the picomolar range and was an order of magnitude more potent than its action as a hallucinogen. TNFα may play a mediating role in the pathophysiology of degenerative inflammatory conditions like rheumatoid arthritis and Alzheimer's disease. (R)-DOI has also been found to block pulmonary inflammation, mucus hyperproduction, airway hyperresponsiveness, and to turn off key genes in pulmonary immune response, effects which block the development of allergic asthma in animal models. [34] These findings could make DOI and other serotonin 5-HT2A agonists novel treatments for inflammatory conditions. [35]

DOI has been shown to induce rapid growth and reorganization of dendritic spines and synaptic connections with other neurons, processes known to underlie neuroplasticity, and hence to be a psychoplastogen. [36]

DOI, along with other psychedelics, has been reported to produce serotonergic neurotoxicity in vitro and in rodents in vivo at high doses given repeatedly. [37] [38] [39] [40] [41] Serotonin 5-HT2A receptor antagonism or knockdown could partially but greatly block this neurotoxicity in vitro. [37] [38] [39] [41]

Chemistry

DOI, also known as 2,5-dimethoxy-4-iodoamphetamine or as 2,5-dimethoxy-4-iodo-α-methylphenethylamine, is a substituted phenethylamine and amphetamine derivative and a member of the DOx family of drugs. [1] It is structurally related to the naturally occurring phenethylamine psychedelic mescaline (3,4,5-trimethoxyphenethylamine). [1]

Synthesis

The chemical synthesis of DOI has been described. [1]

Analogues

Analogues of DOI include 2C-I, 4C-I, DOB, DOC, DOF, and DOM, among many others. [1] Other analogues include N-methyl-DOI, IDNNA (N,N-dimethyl-DOI), DOI-NBOMe, and 25I-NBOMe, among others. [1]

History

DOI was first described in the scientific literature by Ronald Coutts and Jerry Malicky in 1973. [5] [8] Subsequently, it was described in greater detail by Alexander Shulgin in his 1991 book PiHKAL (Phenethylamines I Have Known and Loved). [1] The radioactive iodine-125 form of DOI for PET imaging was first developed in the lab of David E. Nichols.[ citation needed ]

In January 2007, British police reported that three young men had fallen ill, reportedly, after taking DOI at a rave in Biggleswade, near Milton Keynes, and warned others who had taken it to seek medical attention. [42] This would appear to be the first indication that DOI has found more widespread use as a recreational drug in the United Kingdom. [42]

South Australian man Cody Edwards who brutally murdered Synamin Bell controversially plead guilty to the lesser sentence of manslaughter after attesting that the drug DOI had induced paranoia, and that he had subsequently acted in 'self-defence' when he had beaten the mother-of-three to death with a dumbbell, resulting in over fifty wounds. [43]

As of late 2025, DOI is expected to become a Schedule I controlled substance in the United States. [4] [7]

Society and culture

Scientific research

DOI is widely used in scientific research to study serotonergic psychedelics and the serotonin 5-HT2 receptors. [4] [5] [6] [7] This is in part due to the fact that it is not a controlled substance in the United States. [4] [5] [7] However, DOI is poised to become a Schedule I controlled substance in this country in the near future, which will greatly restrict access to the drug. [4] [7] A number of alternatives to DOI have been suggested for use in research, including the non-selective serotonin 5-HT2A receptor agonist TCB-2 and the selective serotonin 5-HT2A receptor agonists 25CN-NBOH and LPH-5. [4] Another notable but much more recent compound is TGF-8027, which is a highly selective serotonin 5-HT2A receptor agonist and among the most selective such drugs currently known. [44]

Australia

The Standard for the Uniform Scheduling of Medicines and Poisons (SUSMP) of Australia does not list DOI as a prohibited substance. [45]

Canada

Listed as a Schedule 1 [46] as it is an analogue of amphetamine. [47] The CDSA was updated as a result of the Safe Streets and Communities Act, changing amphetamines from Schedule 3 to Schedule 1. [48]

Denmark

Illegal since 8 April 2007. [49]

Finland

DOI is classified as a psychoactive substance banned from the consumer market in Finland. [50]

Sweden

Sveriges riksdag added DOI to schedule I ("substances, plant materials and fungi which normally do not have medical use") as narcotics in Sweden as of August 30, 2007, published by Medical Products Agency in their regulation LVFS 2007:10 listed as DOI, 4-jod-2,5-dimetoxi-amfetamin. [51]

United States

As of 2023, DOI is not scheduled in the United States. [14] However, DOI may be considered an analog of other controlled DOx drugs like DOB, in which case, sales or possession could be prosecuted under the Federal Analogue Act. The drug's non-controlled status has made it usefully accessible for use in scientific research, which has contributed to its popularity for such uses. [5]

In December 2023, the United States Drug Enforcement Administration (DEA) issued a notice of proposed rulemaking that would classify both DOI and DOC as schedule I controlled substances. [15] However, in May 2024, it was reported that the DEA's June 10, 2024 hearing on scheduling of DOI and DOC had been postponed. [16] [52] This followed opposition to the proposal by psychedelic researchers. [16] DOI is frequently used in scientific research due in considerable part to its non-scheduled status, [5] [6] and DOI becoming a controlled substance would cause problems for scientists. [15] [16] In any case, an administrative judge recommended placement of DOI into Schedule I in June 2025, and it is likely that the drug will be scheduled. [4] [7]

DOI is a Schedule I controlled substance in the state of Florida. [53]

See also

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Shulgin A, Shulgin A (1990). "#67 DOI". PiHKAL: A Chemical Love Story. Transform Press. Archived from the original on 2014-10-27. Retrieved 2014-12-17.
  2. ↑ Anvisa (2023-07-24). "RDC Nº 804 - Listas de Substâncias Entorpecentes, Psicotrópicas, Precursoras e Outras sob Controle Especial" [Collegiate Board Resolution No. 804 - Lists of Narcotic, Psychotropic, Precursor, and Other Substances under Special Control] (in Brazilian Portuguese). Diário Oficial da União (published 2023-07-25). Archived from the original on 2023-08-27. Retrieved 2023-08-27.
  3. ↑ "D101 DOI hydrochloride ≥98% (HPLC), solid" . Retrieved 13 April 2008.
  4. 1 2 3 4 5 6 7 8 9 10 11 Cameron LP, Jaster AM, Ramos R, Ullman EZ (2025). "The Utility of DOI For the Study of Serotonin 2A and 2C Receptors". Molecular Pharmacology 100093. doi:10.1016/j.molpha.2025.100093.
  5. 1 2 3 4 5 6 7 8 9 10 11 12 Glennon RA, Dukat M (June 2024). "1-(2,5-Dimethoxy-4-iodophenyl)-2-aminopropane (DOI): From an Obscure to Pivotal Member of the DOX Family of Serotonergic Psychedelic Agents - A Review". ACS Pharmacology & Translational Science. 7 (6): 1722–1745. doi: 10.1021/acsptsci.4c00157 . PMC   11184610 . PMID   38898956.
  6. 1 2 3 4 5 6 7 Canal CE, Morgan D (2012). "Head-twitch response in rodents induced by the hallucinogen 2,5-dimethoxy-4-iodoamphetamine: a comprehensive history, a re-evaluation of mechanisms, and its utility as a model". Drug Testing and Analysis. 4 (7–8): 556–576. doi:10.1002/dta.1333. PMC   3722587 . PMID   22517680.
  7. 1 2 3 4 5 6 7 8 9 10 Palamar JJ, Fitzgerald ND (October 2025). "The Epidemiology of Recreational Use and Availability of DOC and DOI in the United States". Journal of Psychoactive Drugs: 1–10. doi:10.1080/02791072.2025.2570937. PMC   12645445 . PMID   41065346.
  8. 1 2 Coutts RT, Malicky JL (1 May 1973). "The Synthesis of Some Analogs of the Hallucinogen 1-(2,5-Dimethoxy-4-methylphenyl)-2-aminopropane (DOM)". Canadian Journal of Chemistry. 51 (9): 1402–1409. doi:10.1139/v73-210. ISSN   0008-4042 . Retrieved 27 November 2025.
  9. ↑ "LSD Blotter Acid Mimics (Actually containing 4-IODO-2,5-DIMETHOXYAMPHETAMINE (DOI) and 4-CHLORO-2,5-DIMETHOXYAMPHETAMINE (DOC)) in Lantana, Florida". DEA Microgram Bulletin. Washington, DC: Office of Forensic Sciences, Drug Enforcement Administration. June 2008. Archived from the original on 2009-02-04. Retrieved 12 February 2009.
  10. ↑ Nichols DE (April 2016). "Psychedelics". Pharmacological Reviews. 68 (2): 264–355. doi:10.1124/pr.115.011478. PMC   4813425 . PMID   26841800. Although studies have appeared that employed psilocybin or LSD or a select few other agents, probably the majority of animal experiments have used the "psychedelic" 5-HT2A agonist DOI. That is another unfortunate consequence of the current drug laws. DOI has never been popular as a recreational drug, nor has any clinical study been carried out to compare its effects with classic drugs such as LSD, mescaline, or psilocybin, and only anecdotal reports of its human psychopharmacology exist (e.g., Shulgin and Shulgin, 1991). Although DOI is quite potent, it likely never became popular as a street drug because of its very prolonged duration of action, so it had never been placed into Schedule I of the Controlled Substances Act (although as of November 2015, there are congressional moves afoot to change that). Therefore, DOI has been commercially available to qualified investigators and did not require a U.S. Drug Enforcement Administration license to work with it.
  11. ↑ Today P (21 January 2025). "Is the DEA Sabotaging Psychedelic Research? Inside the Push to Schedule DOI and DOC". Psychedelics Today. Retrieved 6 June 2025.
  12. ↑ Baggott MJ (1 October 2023). "Learning about STP: A Forgotten Psychedelic from the Summer of Love" (PDF). History of Pharmacy and Pharmaceuticals. 65 (1): 93–116. doi: 10.3368/hopp.65.1.93 . ISSN   2694-3034 . Retrieved 27 January 2025.
  13. ↑ Trout K, Daley PF (December 2024). "The origin of 2,5-dimethoxy-4-methylamphetamine (DOM, STP)". Drug Testing and Analysis. 16 (12): 1496–1508. doi:10.1002/dta.3667. PMID   38419183.
  14. 1 2 "PART 1308 - Section 1308.11 Schedule I". www.deadiversion.usdoj.gov. Archived from the original on 2009-08-27. Retrieved 2014-12-17.
  15. 1 2 3 "Schedules of Controlled Substances: Placement of 2,5-dimethoxy-4-iodoamphetamine (DOI) and 2,5-dimethoxy-4-chloroamphetamine (DOC) in Schedule I". www.regulations.gov.
  16. 1 2 3 4 Hu JC (17 May 2024), "Revisions made to report critical of Lykos's research on MDMA-assisted therapy; Lawsuit postpones hearing for contentious DEA proposal; and former MAPS employees make troubling allegations", The Microdose, U.C. Berkeley Center for the Science of Psychedelics, retrieved 6 February 2025
  17. ↑ Rached G, Campana A, Fiani D, Nguyen C, Van den Eynde V, Gillman PK, et al. (January 2026). "Safety and Efficacy of Monoamine Oxidase Inhibitors in Patients Who Use Psychoactive Substances: Potential Drug Interactions and Substance Use Disorder Treatment Data". CNS Drugs. doi:10.1007/s40263-025-01256-7. PMID   41546846.
  18. 1 2 "PDSP Database". UNC (in Zulu). Retrieved 4 February 2025.
  19. 1 2 Liu T. "BindingDB BDBM28582 1-(4-iodo-2,5-dimethoxyphenyl)propan-2-amine::CHEMBL6616::DOI::DOI,(+)::DOI,(-)::US20240166618, Compound DOI::[125I]2,5-dimethoxy-4-iodoamphetamine::[125I]4-iodo-2,5-dimethoxyphenylisopropylamine::[125I]DOI". BindingDB. Retrieved 4 February 2025.
  20. 1 2 Ray TS (February 2010). "Psychedelics and the human receptorome". PLOS ONE. 5 (2) e9019. Bibcode:2010PLoSO...5.9019R. doi: 10.1371/journal.pone.0009019 . PMC   2814854 . PMID   20126400.
  21. ↑ van Wijngaarden I, Soudijn W (1997). "5-HT2A, 5-HT2B and 5-HT2C receptor ligands". Pharmacochemistry Library. Vol. 27. Elsevier. pp. 161–197. doi:10.1016/s0165-7208(97)80013-x. ISBN   978-0-444-82041-9.
  22. ↑ Reyes-Parada M, Iturriaga-Vasquez P, Cassels BK (2019). "Amphetamine Derivatives as Monoamine Oxidase Inhibitors". Frontiers in Pharmacology. 10 1590. doi: 10.3389/fphar.2019.01590 . PMC   6989591 . PMID   32038257.
  23. 1 2 Matsumoto T, Maeno Y, Kato H, Seko-Nakamura Y, Monma-Ohtaki J, Ishiba A, et al. (August 2014). "5-hydroxytryptamine- and dopamine-releasing effects of ring-substituted amphetamines on rat brain: a comparative study using in vivo microdialysis". European Neuropsychopharmacology. 24 (8): 1362–1370. doi:10.1016/j.euroneuro.2014.04.009. PMID   24862256.
  24. ↑ Rudin D, Luethi D, Hoener MC, Liechti ME (2022). "Structure-activity Relation of Halogenated 2,5-Dimethoxyamphetamines Compared to their α‑Desmethyl (2C) Analogues". The FASEB Journal. 36 (S1) fasebj.2022.36.S1.R2121. doi: 10.1096/fasebj.2022.36.S1.R2121 . ISSN   0892-6638.
  25. ↑ Acuña-Castillo C, Villalobos C, Moya PR, Sáez P, Cassels BK, Huidobro-Toro JP (June 2002). "Differences in potency and efficacy of a series of phenylisopropylamine/phenylethylamine pairs at 5-HT(2A) and 5-HT(2C) receptors". British Journal of Pharmacology. 136 (4): 510–519. doi:10.1038/sj.bjp.0704747. PMC   1573376 . PMID   12055129.
  26. ↑ Hemanth P, Nistala P, Nguyen VT, Eltit JM, Glennon RA, Dukat M (2023). "Binding and functional structure-activity similarities of 4-substituted 2,5-dimethoxyphenyl isopropylamine analogues at 5-HT2A and 5-HT2B serotonin receptors". Frontiers in Pharmacology. 14 1101290. doi: 10.3389/fphar.2023.1101290 . PMC   9902381 . PMID   36762110.
  27. ↑ Wallach J, Cao AB, Calkins MM, Heim AJ, Lanham JK, Bonniwell EM, et al. (December 2023). "Identification of 5-HT2A receptor signaling pathways associated with psychedelic potential". Nature Communications. 14 (1) 8221. Bibcode:2023NatCo..14.8221W. doi:10.1038/s41467-023-44016-1. PMC   10724237 . PMID   38102107.
  28. ↑ Poulie CB, Jensen AA, Halberstadt AL, Kristensen JL (December 2020). "DARK Classics in Chemical Neuroscience: NBOMes". ACS Chemical Neuroscience. 11 (23): 3860–3869. doi:10.1021/acschemneuro.9b00528. PMC   9191638 . PMID   31657895. The psychedelic phenethylamines typically exhibit less than 5–10-fold selectivity for 5-HT2A over 5-HT2C receptors.53,54 [...] The reported selectivity of 25CN-NBOH for 5-HT2A over 5-HT2C varies depending on the experimental conditions,49,59,60 but 25CN-NBOH is clearly more selective than DOI, which is only ~5-fold and 12-fold selective for 5-HT2A over 5-HT2C at the human and murine receptors, respectively.93–95 [...]
  29. ↑ Bonniwell EM, Alabdali R, Hennessey JJ, McKee JL, Cavalco NG, Lammers JC, et al. (October 2025). "Serotonin 5-HT2C Receptor Signaling Analysis Reveals Psychedelic Biased Agonism". ACS Chemical Neuroscience. 16 (19): 3899–3914. doi:10.1021/acschemneuro.5c00647. PMC   12629614 . PMID   40944639.
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  32. ↑ Yu B, Becnel J, Zerfaoui M, Rohatgi R, Boulares AH, Nichols CD (November 2008). "Serotonin 5-hydroxytryptamine(2A) receptor activation suppresses tumor necrosis factor-alpha-induced inflammation with extraordinary potency". The Journal of Pharmacology and Experimental Therapeutics. 327 (2): 316–323. doi:10.1124/jpet.108.143461. PMID   18708586. S2CID   25374241.
  33. ↑ Pelletier M, Siegel RM (December 2009). "Wishing away inflammation? New links between serotonin and TNF signaling". Molecular Interventions. 9 (6): 299–301. doi:10.1124/mi.9.6.5. PMC   2861806 . PMID   20048135.
  34. ↑ "LSU Health New Orleans research finds psychedelic drug prevents asthma development in mice". EurekAlert!.
  35. ↑ Yu B, Becnel J, Zerfaoui M, Rohatgi R, Boulares AH, Nichols CD (November 2008). "Serotonin 5-hydroxytryptamine(2A) receptor activation suppresses tumor necrosis factor-alpha-induced inflammation with extraordinary potency". The Journal of Pharmacology and Experimental Therapeutics. 327 (2): 316–323. doi:10.1124/jpet.108.143461. PMID   18708586. S2CID   25374241.
  36. ↑ Jones KA, Srivastava DP, Allen JA, Strachan RT, Roth BL, Penzes P (November 2009). "Rapid modulation of spine morphology by the 5-HT2A serotonin receptor through kalirin-7 signaling". Proceedings of the National Academy of Sciences of the United States of America. 106 (46): 19575–19580. Bibcode:2009PNAS..10619575J. doi: 10.1073/pnas.0905884106 . PMC   2780750 . PMID   19889983.
  37. 1 2 Rudin D, Liechti ME, Luethi D (September 2021). "Molecular and clinical aspects of potential neurotoxicity induced by new psychoactive stimulants and psychedelics". Exp Neurol. 343 113778. doi: 10.1016/j.expneurol.2021.113778 . PMID   34090893.
  38. 1 2 Capela JP, Carmo H, Remião F, Bastos ML, Meisel A, Carvalho F (June 2009). "Molecular and cellular mechanisms of ecstasy-induced neurotoxicity: an overview". Mol Neurobiol. 39 (3): 210–271. 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].
  39. 1 2 Capela JP, Ruscher K, Lautenschlager M, Freyer D, Dirnagl U, Gaio AR, et al. (2006). "Ecstasy-induced cell death in cortical neuronal cultures is serotonin 2A-receptor-dependent and potentiated under hyperthermia". Neuroscience. 139 (3): 1069–1081. doi:10.1016/j.neuroscience.2006.01.007. PMID   16504407.
  40. ↑ Custodio RJ, Ortiz DM, Lee HJ, Sayson LV, Kim M, Lee YS, et al. (July 2025). "Serotonin 2C receptors are also important in head-twitch responses in male mice". Psychopharmacology (Berl). 242 (7): 1585–1605. doi:10.1007/s00213-023-06482-9. PMID   37882810.
  41. 1 2 Capela JP, da Costa Araújo S, Costa VM, Ruscher K, Fernandes E, Bastos Mde L, et al. (January 2013). "The neurotoxicity of hallucinogenic amphetamines in primary cultures of hippocampal neurons". Neurotoxicology. 34: 254–263. doi:10.1016/j.neuro.2012.09.005. PMID   22983118.
  42. 1 2 "New drug alert as three taken ill". BBC News . 29 January 2007.
  43. ↑ "Man sentenced to prison for manslaughter of partner, as government moves to close 'defence loophole' - ABC News". amp.abc.net.au. 6 September 2024. Retrieved 2024-09-06.
  44. ↑ Fenske TG, McKee JL, Cavalco NG, Schalk SS, Bonniwell EM, Lammers JC, et al. (September 2025). "Discovery of Highly Selective 5-HT2A Agonists Using Structure-Guided Design". J Med Chem acs.jmedchem.5c01855. doi:10.1021/acs.jmedchem.5c01855. PMID   40997862.
  45. ↑ Gill A (22 July 2013). "POISONS STANDARD 2013" (PDF). Therapeutic Goods Administration. Australian Government Department of Health and Ageing. Retrieved 4 March 2014.
  46. ↑ "Controlled Drugs and Substances Act: Legislative history · Schedule I · Section 19: Tramadol [Proposed]; Amphetamines". isomerdesign.com. Archived from the original on 2022-03-31. Retrieved 2012-11-27.
  47. ↑ "Controlled Drugs and Substances Act: Definitions and Interpretations". isomerdesign.com. Archived from the original on 2013-11-10. Retrieved 2012-11-27.
  48. ↑ "Backgrounder: The Safe Streets and Communities Act Four Components Coming Into Force". Department of Justice. Government of Canada. Archived from the original on 18 October 2012.
  49. ↑ "FINLEX ® - Ajantasainen lainsäädäntö: Valtioneuvoston asetus kuluttajamarkkinoilta… 1130/2014".
  50. ↑ "Läkemedelsverkets föreskrifter - LVFS och HSLF-FS | Läkemedelsverket" (PDF).
  51. ↑ "Judge Halts DEA's Hearing On Proposed Psychedelics Ban". Law360. 9 May 2024. Retrieved 6 February 2025.
  52. ↑ "Statutes & Constitution :View Statutes: Online Sunshine". leg.state.fl.us.
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