25N-NBOMe

Last updated

25N-NBOMe
25N-NBOMe.svg
Clinical data
Other names2C-N-NBOMe; NBOMe-2C-N
Drug class Serotonin 5-HT2A receptor agonist; Serotonergic psychedelic; Hallucinogen
ATC code
  • None
Legal status
Legal status
Identifiers
  • 2-(2,5-dimethoxy-4-nitrophenyl)-N-[(2-methoxyphenyl)methyl]ethan-1-amine
CAS Number
PubChem CID
ChemSpider
UNII
CompTox Dashboard (EPA)
Chemical and physical data
Formula C18H22N2O5
Molar mass 346.383 g·mol−1
3D model (JSmol)
  • COC1=C(CCNCC2=C(OC)C=CC=C2)C=C(OC)C([N+]([O-])=O)=C1
  • InChI=1S/C18H22N2O5/c1-23-16-7-5-4-6-14(16)12-19-9-8-13-10-18(25-3)15(20(21)22)11-17(13)24-2/h4-7,10-11,19H,8-9,12H2,1-3H3
  • Key:TXCKTIBHURMASQ-UHFFFAOYSA-N

25N-NBOMe, also known as 2C-N-NBOMe or NBOMe-2C-N, is a derivative of the hallucinogen 2C-N. The pharmacological properties of 25N-NBOMe have not been described in the scientific literature, but it is believed to act in a similar manner to related compounds such as 25I-NBOMe and 25C-NBOMe, which are potent agonists at the 5HT2A receptor. [2] [3] 25N-NBOMe has been sold as a street drug and has only been described in the literature in terms of identification by forensic analysis. [4] [5]

Contents

Use and effects

The dose range of 25N-NBOMe has been given as 0.1 to 1.3 mg or more sublingually, with a typical dose estimate of 0.6 mg. [6] Whereas 2C-N is much less potent in terms of dose than other 2C drugs, 25N-NBOMe appears to have a similar dose range as other NBOMe drugs. [6]

Toxicity and harm potential

This section is an excerpt from 25-NB § Toxicity and harm potential.[ edit ]

NBOMe compounds are often associated with life-threatening toxicity and death. [7] [8] Studies on NBOMe family of compounds demonstrated that the substance exhibit neurotoxic and cardiotoxic activity. [9] Reports of autonomic dysfunction remains prevalent with NBOMe compounds, with most individuals experiencing sympathomimetic toxicity such as vasoconstriction, hypertension and tachycardia in addition to hallucinations. [10] [11] [12] [13] [14] Other symptoms of toxidrome include agitation or aggression, seizure, hyperthermia, diaphoresis, hypertonia, rhabdomyolysis, and death. [10] [14] [8] Researchers report that NBOMe intoxication frequently display signs of serotonin syndrome. [15] The likelihood of seizure is higher in NBOMes compared to other psychedelics. [9]

NBOMe and NBOHs are regularly sold as LSD in blotter papers, [8] [16] which have a bitter taste and different safety profiles. [10] [7] Despite high potency, recreational doses of LSD have only produced low incidents of acute toxicity. [7] Fatalities involved in NBOMe intoxication suggest that a significant number of individuals ingested the substance which they believed was LSD, [12] and researchers report that "users familiar with LSD may have a false sense of security when ingesting NBOMe inadvertently". [10] While most fatalities are due to the physical effects of the drug, there have also been reports of death due to self-harm and suicide under the influence of the substance. [17] [18] [10]

Given limited documentation of NBOMe consumption, the long-term effects of the substance remain unknown. [10] NBOMe compounds are not active orally, [a] and are usually taken sublingually. [20] : 3  When NBOMes are administered sublingually, numbness of the tongue and mouth followed by a metallic chemical taste was observed, and researchers describe this physical side effect as one of the main discriminants between NBOMe compounds and LSD. [21] [22] [23]

Neurotoxic and cardiotoxic actions

This section is an excerpt from 25-NB § Neurotoxic and cardiotoxic actions.[ edit ]

Many of the NBOMe compounds have high potency agonist activity at additional 5-HT receptors and prolonged activation of 5-HT2B can cause cardiac valvulopathy in high doses and chronic use. [8] [13] 5-HT2B receptors have been strongly implicated in causing drug-induced valvular heart disease. [24] [25] [26] The high affinity of NBOMe compounds for adrenergic α1 receptor has been reported to contribute to the stimulant-type cardiovascular effects. [13]

In vitro studies, 25C-NBOMe has been shown to exhibit cytotoxicity on neuronal cell lines SH-SY5Y, PC12, and SN471, and the compound was more potent than methamphetamine at reducing the visibility of the respective cells; the neurotoxicity of the compound involves activation of MAPK/ERK cascade and inhibition of Akt/PKB signaling pathway. [9] 25C-NBOMe, including the other derivative 25D-NBOMe, reduced the visibility of cardiomyocytes H9c2 cells, and both substances downregulated expression level of p21 (CDC24/RAC)-activated kinase 1 (PAK1), an enzyme with documented cardiac protective effects. [9]

Preliminary studies on 25C-NBOMe have shown that the substance is toxic to development, heart health, and brain health in zebrafish, rats, and Artemia salina , a common organism for studying potential drug effects on humans, but more research is needed on the topic, the dosages, and if the toxicology results apply to humans. Researchers of the study also recommended further investigation of the drug's potential in damaging pregnant women and their fetus due to the substance's damaging effects to development. [27] [28]

Emergency treatment

This section is an excerpt from 25-NB § Emergency treatment.[ edit ]
At present, there are no specific antidotes for NBOMes, and all acute intoxication is managed by symptomatic treatments, such as administration of benzodiazepines, antipsychotic drugs, and antiarrhythmic agents, such as beta blockers; some emergency interventions are intended to specifically treat rhabdomyolysis, which may lead to critical complications such as metabolic acidosis and acute kidney injury. [9]

Interactions

Pharmacology

Pharmacodynamics

25N-NBOMe activities
Target Affinity (Ki, nM)
5-HT1A 1,860–4,200 (Ki)
4,800 (EC50 Tooltip half-maximal effective concentration)
36% (Emax Tooltip maximal efficacy)
5-HT1B >10,000
5-HT1D 5,620
5-HT1E >10,000
5-HT1F ND
5-HT2A 0.11–1.41 (Ki)
0.204–70 (EC50)
34–137% (Emax)
5-HT2B 4.47–8.7 (Ki)
2.34–70 (EC50)
<10–58% (Emax)
5-HT2C 1.06–21 (Ki)
0.457–1.32 (EC50)
99–102% (Emax)
5-HT3 >10,000
5-HT4 ND
5-HT5A >10,000
5-HT6 55
5-HT7 >10,000
α1A 850–>10,000
α1B, α1D >10,000
α2A 501–590
α2B 1,100
α2C 692
β1 >10,000
β1 7,080
β3 >10,000
D1 18,000
D2 2,400–6,760
D3 2,190–4,500
D4 >10,000
D5 >10,000
H1 91–210
H2 1,070
H3, H4 >10,000
M1–M5 >10,000
I1 ND
σ1 537
σ2 58
MOR >10,000
DOR >10,000
KOR 2,820
TAAR1 Tooltip Trace amine-associated receptor 1>20,000 (Ki) (mouse)
2,200 (Ki) (rat)
>30,000 (EC50) (mouse)
1,500 (EC50) (rat)
>10,000 (EC50) (human)
IA (Emax) (mouse)
34% (Emax) (rat)
SERT Tooltip Serotonin transporter1,410–5,810 (Ki)
5,790–20,000 (IC50 Tooltip half-maximal inhibitory concentration)
IA (EC50)
NET Tooltip Norepinephrine transporter7,200–11,300 (Ki)
15,000–33,000 (IC50)
IA (EC50)
DAT Tooltip Dopamine transporter13,000–37,900 (Ki)
245,000 (IC50)
IA (EC50)
Notes: The smaller the value, the more avidly the drug binds to the site. All proteins are human unless otherwise specified. Refs: [29] [30] [31] [32] [33] [34] [35]

25N-NBOMe is a selective and highly potent agonist of the serotonin 5-HT2 receptors. [36] Its affinities (Ki) are 0.144 nM at the serotonin 5-HT2A receptor, 8.7 nM at the serotonin 5-HT2B receptor, and 1.06 nM at the serotonin 5-HT2C receptor. [36] In terms of affinity, the drug has approximately 7.4-fold selectivity for the serotonin 5-HT2A receptor over the serotonin 5-HT2C receptor and 60-fold selectivity for the 5-HT2A receptor over the serotonin 5-HT2B receptor. [36]

The EC50 Tooltip half-maximal effective concentration (Emax Tooltip maximal efficacy) values of 25N-NBOMe are 0.51 nM (87.9%) at the serotonin 5-HT2A receptor, 47 nM (57.6%) at the serotonin 5-HT2B receptor, and 1.32 nM (99.4%) at the serotonin 5-HT2C receptor. [36] Hence, 25N-NBOMe is a full agonist of the serotonin 5-HT2A and 5-HT2C receptors and a partial agonist of the serotonin 5-HT2B receptor. [36] In terms of functional activity, 25N-NBOMe had 2.6-fold selectivity for the serotonin 5-HT2A receptor over the serotonin 5-HT2C receptor and 92-fold selectivity for the serotonin 5-HT2A receptor over the serotonin 5-HT2C receptor. [36]

In a 2023 study, the pharmacological properties of 25N-NBOMe (also referred to as compound 4) were extensively characterized using both in vitro and in vivo models. [37] Radioligand binding assays showed high binding affinity for serotonin 5-HT2 receptors, with pKi values of 9.26 ± 0.15 at 5-HT2A, 8.35 ± 0.08 at 5-HT2B, and 8.16 ± 0.07 at 5-HT2C. The compound was also screened across more than 40 additional CNS targets and found to be highly selective for the 5-HT2 receptor subfamily. [37]

In calcium flux functional assays, 25N-NBOMe was a potent full agonist at 5-HT2A (pEC50 = 9.50 ± 0.03; Emax = 94 ± 1%) and 5-HT2C (pEC50 = 9.07 ± 0.03; Emax = 102 ± 1%) receptors, while showing negligible agonist activity at 5-HT2B (Emax < 10%). [37]

Bioluminescence resonance energy transfer (BRET) functional assays measuring Gq dissociation and β-arrestin2 recruitment signaling indicated strong agonist activity at 5-HT2A, with Gq pEC50 = 9.69 ± 0.04 (Emax = 95.2 ± 1.2%) and β-arrestin2 recruitment pEC50 = 9.66 ± 0.09 (Emax = 136.5 ± 3.6%). This illustrates that 25N-NBOMe is a balanced 5-HT2A agonist across these pathways, in contrast to analogs like 25N-N1-Nap and 25N-NBPh which displayed functional selectivity or signaling bias for β-arrestin2 recruitment. For 5-HT2C, Gq pEC50 was 9.34 ± 0.08 (Emax = 100.0 ± 2.5%), while weak partial agonist activity was observed at 5-HT2B (pEC50 = 8.63 ± 0.14; Emax = 54.1 ± 2.5%). [37]

In vivo, 25N-NBOMe induced a robust head-twitch response (HTR) in mice with an ED50 of 0.11 mg/kg (0.29 μmol/kg). Notably 25N-NBOMe produced the highest HTR frequency (4.890 counts per minute) among a panel of structurally related 25N analogs. [37]

Unlike many other serotonergic psychedelics, 25N-NBOMe has shown reinforcing effects in rodents, including in terms of conditioned place preference (CPP) and self-administration. [38] 25N-NBOMe has been found to increase phosphorylation of the dopamine transporter (DAT) in the striatum similarly to methamphetamine in rodents. [39] [38] DAT phosphorylation is associated with dopamine reverse transport and efflux, which in turn increases extracellular dopamine levels. [39] [38]

History

25N-NBOMe was first described in the scientific literature by 2012. [40]

Society and culture

Hungary

25N-NBOMe is illegal in Hungary. [41]

Sweden

The Riksdag added 25N-NBOMe to Narcotic Drugs Punishments Act under swedish schedule I ("substances, plant materials and fungi which normally do not have medical use") as of January 16, 2015, published by Medical Products Agency (MPA) in regulation LVFS 2014:11 listed as 25N-NBOMe, and 2-(2,5-dimetoxi-4-nitrofenyl)-N-(2-metoxibensyl)etanamin. [42]

United Kingdom

This substance is a Class A drug in the United Kingdom as a result of the N-benzylphenethylamine catch-all clause in the Misuse of Drugs Act 1971 . [43]

United States

25N-NBOMe is illegal in Alabama. [44]

See also

Notes

  1. ↑ The potency of N-benzylphenethylamines via buccal, sublingual, or nasal absorption is 50- to 100-fold greater (by weight) than oral route compared to the parent 2C-x compounds. [19] Researchers hypothesize the low oral metabolic stability of N-benzylphenethylamines is likely causing the low bioavailability on the oral route, although the metabolic profile of this compounds remains unpredictable; therefore researchers state that the fatalities linked to these substances may partly be explained by differences in the metabolism between individuals. [19]

References

  1. ↑ 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.
  2. ↑ Hansen M, Phonekeo K, Paine JS, Leth-Petersen S, Begtrup M, Bräuner-Osborne H, et al. (Mar 2014). "Synthesis and Structure-Activity Relationships of N-Benzyl Phenethylamines as 5-HT2A/2C Agonists". ACS Chemical Neuroscience. 5 (3): 243–249. doi:10.1021/cn400216u. PMC   3963123 . PMID   24397362.
  3. ↑ Hansen M (2010-12-16). Design and Synthesis of Selective Serotonin Receptor Agonists for Positron Emission Tomography Imaging of the Brain (Ph.D. thesis). University of Copenhagen. doi:10.13140/RG.2.2.33671.14245.
  4. ↑ Hays PA, Casale JF (2012). "Characterization of Eleven 2,5-Dimethoxy-N-(2-methoxybenzyl)phenethylamine (NBOMe) Derivatives and Differentiation from their 3- and 4-Methoxybenzyl Analogues - Part I" (PDF). Microgram Journal. 9 (2): 84–109. Retrieved 14 January 2014.
  5. ↑ Uchiyama N, Shimokawa Y, Matsuda S, Kawamura M, Kikura-Hanajiri R, Goda Y (2014). "Two new synthetic cannabinoids, AM-2201 benzimidazole analog (FUBIMINA) and (4-methylpiperazin-1-yl)(1-pentyl-1H-indol-3-yl)methanone (MEPIRAPIM), and three phenethylamine derivatives, 25H-NBOMe 3,4,5-trimethoxybenzyl analog, 25B-NBOMe, and 2C-N-NBOMe, identified in illegal products". Forensic Toxicology. 32 (1): 105–115. doi:10.1007/s11419-013-0217-2. S2CID   32599561.
  6. 1 2 Luethi D, Liechti ME (October 2018). "Monoamine Transporter and Receptor Interaction Profiles in Vitro Predict Reported Human Doses of Novel Psychoactive Stimulants and Psychedelics". Int J Neuropsychopharmacol. 21 (10): 926–931. doi:10.1093/ijnp/pyy047. PMC   6165951 . PMID   29850881. Supplementary Table S2. Dose estimates and data sources for psychedelics.
  7. 1 2 3 Sean I, Joe R, Jennifer S, and Shaun G (28 March 2022). "A cluster of 25B-NBOH poisonings following exposure to powder sold as lysergic acid diethylamide (LSD)" . Clinical Toxicology . 60 (8): 966–969. doi:10.1080/15563650.2022.2053150. PMID   35343858. S2CID   247764056.
  8. 1 2 3 4 Amy E, Katherine W, John R, Sonyoung K, Robert J, Aaron J (December 2018). "Neurochemical pharmacology of psychoactive substituted N-benzylphenethylamines: High potency agonists at 5-HT2A receptors". Biochemical Pharmacology. 158: 27–34. doi:10.1016/j.bcp.2018.09.024. PMC   6298744 . PMID   30261175.
  9. 1 2 3 4 5 Jolanta Z, Monika K, and Piotr A (26 February 2020). "NBOMes–Highly Potent and Toxic Alternatives of LSD". Frontiers in Neuroscience. 14 78. doi: 10.3389/fnins.2020.00078 . PMC   7054380 . PMID   32174803. Recently, a new class of psychedelic compounds named NBOMe (or 25X-NBOMe) has appeared on the illegal drug market. NBOMes are analogs of the 2C family of phenethylamine drugs, originally synthesized by Alexander Shulgin, that contain a N-(2-methoxy)benzyl substituent. The most frequently reported drugs from this group are 25I-NBOMe, 25B-NBOMe, and 25C-NBOMe. NBOMe compounds are ultrapotent and highly efficacious agonists of serotonin 5-HT2A and 5-HT2C receptors (Ki values in low nanomolar range) with more than 1000-fold selectivity for 5-HT2A compared with 5-HT1A. They display higher affinity for 5-HT2A receptors than their 2C counterparts and have markedly lower affinity, potency, and efficacy at the 5-HT2B receptor compared to 5-HT2A or 5-HT2C.
  10. 1 2 3 4 5 6 Lipow M, Kaleem SZ, Espiridion E (30 March 2022). "NBOMe Toxicity and Fatalities: A Review of the Literature". Transformative Medicine. 1 (1): 12–18. doi: 10.54299/tmed/msot8578 . ISSN   2831-8978. S2CID   247888583.
  11. ↑ Tirri M, Bilel S, Arfè R, Corli G, Marchetti B, Bernardi T, et al. (2022). "Effect of -NBOMe Compounds on Sensorimotor, Motor, and Prepulse Inhibition Responses in Mice in Comparison With the 2C Analogs and Lysergic Acid Diethylamide: From Preclinical Evidence to Forensic Implication in Driving Under the Influence of Drugs". Front Psychiatry. 13 875722. doi: 10.3389/fpsyt.2022.875722 . PMC   9069068 . PMID   35530025.
  12. 1 2 Cristina M, Matteo M, Nicholas P, Maria C, Micaela T, Raffaella A, et al. (12 December 2019). "Neurochemical and Behavioral Profiling in Male and Female Rats of the Psychedelic Agent 25I-NBOMe". Frontiers in Pharmacology. 10 1406. doi: 10.3389/fphar.2019.01406 . PMC   6921684 . PMID   31915427.
  13. 1 2 3 Anna R, Dino L, Julia R, Daniele B, Marius H, Matthias L (December 2015). "Receptor interaction profiles of novel N-2-methoxybenzyl (NBOMe) derivatives of 2,5-dimethoxy-substituted phenethylamines (2C drugs)" . Neuropharmacology. 99: 546–553. doi:10.1016/j.neuropharm.2015.08.034. ISSN   1873-7064. PMID   26318099. S2CID   10382311.
  14. 1 2 David W, Roumen S, Andrew C, Paul D (6 February 2015). "Prevalence of use and acute toxicity associated with the use of NBOMe drugs" . Clinical Toxicology. 53 (2): 85–92. doi:10.3109/15563650.2015.1004179. PMID   25658166. S2CID   25752763.
  15. ↑ Humston C, Miketic R, Moon K, Ma P, Tobias J (2017-06-05). "Toxic Leukoencephalopathy in a Teenager Caused by the Recreational Ingestion of 25I-NBOMe: A Case Report and Review of Literature". Journal of Medical Cases. 8 (6): 174–179. doi: 10.14740/jmc2811w . ISSN   1923-4163.
  16. ↑ Justin P, Stephen R, Kylin A, Alphonse P, Michelle P (2015). "Analysis of 25I-NBOMe, 25B-NBOMe, 25C-NBOMe and Other Dimethoxyphenyl-N-[(2-Methoxyphenyl) Methyl]Ethanamine Derivatives on Blotter Paper". Journal of Analytical Toxicology. 39 (8): 617–623. doi:10.1093/jat/bkv073. PMC   4570937 . PMID   26378135.
  17. ↑ Morini L, Bernini M, Vezzoli S, Restori M, Moretti M, Crenna S, et al. (October 2017). "Death after 25C-NBOMe and 25H-NBOMe consumption" . Forensic Science International. 279: e1 –e6. doi:10.1016/j.forsciint.2017.08.028. PMID   28893436.
  18. ↑ Byard RW, Cox M, Stockham P (November 2016). "Blunt Craniofacial Trauma as a Manifestation of Excited Delirium Caused by New Psychoactive Substances" . Journal of Forensic Sciences. 61 (6): 1546–1548. doi:10.1111/1556-4029.13212. PMID   27723094. S2CID   4734566.
  19. 1 2 Sabastian LP, Christoffer B, Martin H, Martin AC, Jan K, Jesper LK (14 February 2014). "Correlating the Metabolic Stability of Psychedelic 5-HT2A Agonists with Anecdotal Reports of Human Oral Bioavailability" . Neurochemical Research. 39 (10): 2018–2023. doi:10.1007/s11064-014-1253-y. PMID   24519542. S2CID   254857910.
  20. ↑ Adam H (18 January 2017). "Pharmacology and Toxicology of N-Benzylphenethylamine ("NBOMe") Hallucinogens". Neuropharmacology of New Psychoactive Substances. Current Topics in Behavioral Neurosciences. Vol. 32. Springer. pp. 283–311. doi:10.1007/7854_2016_64. ISBN   978-3-319-52444-3. PMID   28097528.
  21. ↑ Boris D, Cristian C, Marcelo K, Edwar F, Bruce KC (August 2016). "Analysis of 25 C NBOMe in Seized Blotters by HPTLC and GC–MS". Journal of Chromatographic Science. 54 (7): 1153–1158. doi:10.1093/chromsci/bmw095. PMC   4941995 . PMID   27406128.
  22. ↑ Francesco SB, Ornella C, Gabriella A, Giuseppe V, Rita S, Flaminia BP, et al. (3 July 2014). "25C-NBOMe: preliminary data on pharmacology, psychoactive effects, and toxicity of a new potent and dangerous hallucinogenic drug". BioMed Research International. 2014: 734749. doi: 10.1155/2014/734749 . PMC   4106087 . PMID   25105138.{{cite journal}}: CS1 maint: article number as page number (link)
  23. ↑ Adam JP, Simon HT, Simon LH (September 2021). "Pharmacology and toxicology of N-Benzyl-phenylethylamines (25X-NBOMe) hallucinogens". Novel Psychoactive Substances: Classification, Pharmacology and Toxicology (2 ed.). Academic Press. pp. 279–300. doi:10.1016/B978-0-12-818788-3.00008-5. ISBN   978-0-12-818788-3. S2CID   240583877.
  24. ↑ Rothman RB, Baumann MH, Savage JE, Rauser L, McBride A, Hufeisen SJ, et al. (Dec 2000). "Evidence for possible involvement of 5-HT(2B) receptors in the cardiac valvulopathy associated with fenfluramine and other serotonergic medications". Circulation. 102 (23): 2836–41. doi: 10.1161/01.CIR.102.23.2836 . PMID   11104741.
  25. ↑ Fitzgerald LW, Burn TC, Brown BS, Patterson JP, Corjay MH, Valentine PA, et al. (Jan 2000). "Possible role of valvular serotonin 5-HT(2B) receptors in the cardiopathy associated with fenfluramine". Molecular Pharmacology. 57 (1): 75–81. doi:10.1016/S0026-895X(24)26444-0. PMID   10617681.
  26. ↑ Roth BL (Jan 2007). "Drugs and valvular heart disease" . The New England Journal of Medicine. 356 (1): 6–9. doi:10.1056/NEJMp068265. PMID   17202450.
  27. ↑ Xu P, Qiu Q, Li H, Yan S, Yang M, Naman CB, et al. (26 February 2019). "25C-NBOMe, a Novel Designer Psychedelic, Induces Neurotoxicity 50 Times More Potent Than Methamphetamine In Vitro" . Neurotoxicity Research. 35 (4): 993–998. doi:10.1007/s12640-019-0012-x. PMID   30806983. S2CID   255763701.
  28. ↑ Álvarez-Alarcón N, Osorio-Méndez JJ, Ayala-Fajardo A, Garzón-Méndez WF, Garavito-Aguilar ZV (2021). "Zebrafish and Artemia salina in vivo evaluation of the recreational 25C-NBOMe drug demonstrates its high toxicity". Toxicology Reports. 8: 315–323. Bibcode:2021ToxR....8..315A. doi:10.1016/j.toxrep.2021.01.010. ISSN   2214-7500. PMC   7868744 . PMID   33598409.
  29. ↑ "Kᵢ Database". PDSP. 20 June 2025. Retrieved 20 June 2025.
  30. ↑ Rickli A, Luethi D, Reinisch J, Buchy D, Hoener MC, Liechti ME (December 2015). "Receptor interaction profiles of novel N-2-methoxybenzyl (NBOMe) derivatives of 2,5-dimethoxy-substituted phenethylamines (2C drugs)" (PDF). Neuropharmacology. 99: 546–553. doi:10.1016/j.neuropharm.2015.08.034. PMID   26318099.
  31. ↑ Eshleman AJ, Wolfrum KM, Reed JF, Kim SO, Johnson RA, Janowsky A (December 2018). "Neurochemical pharmacology of psychoactive substituted N-benzylphenethylamines: High potency agonists at 5-HT2A receptors". Biochem Pharmacol. 158: 27–34. doi:10.1016/j.bcp.2018.09.024. PMC   6298744 . PMID   30261175.
  32. ↑ Åstrand A, Guerrieri D, Vikingsson S, Kronstrand R, Green H (December 2020). "In vitro characterization of new psychoactive substances at the μ-opioid, CB1, 5HT1A, and 5-HT2A receptors-On-target receptor potency and efficacy, and off-target effects". Forensic Sci Int. 317 110553. doi:10.1016/j.forsciint.2020.110553. PMID   33160102.
  33. ↑ "Selective, partial, and arrestin-biased 5-ht2a agonists with utility in various disorders". Google Patents. 11 May 2022. Retrieved 20 June 2025.
  34. ↑ 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". Nat Commun. 14 (1) 8221. Bibcode:2023NatCo..14.8221W. doi:10.1038/s41467-023-44016-1. PMC   10724237 . PMID   38102107.
  35. ↑ Simmler LD, Buchy D, Chaboz S, Hoener MC, Liechti ME (April 2016). "In Vitro Characterization of Psychoactive Substances at Rat, Mouse, and Human Trace Amine-Associated Receptor 1" (PDF). J Pharmacol Exp Ther. 357 (1): 134–144. doi:10.1124/jpet.115.229765. PMID   26791601. Archived from the original (PDF) on 2025-05-09.
  36. 1 2 3 4 5 6 Eshleman AJ, Wolfrum KM, Reed JF, Kim SO, Johnson RA, Janowsky A (December 2018). "Neurochemical pharmacology of psychoactive substituted N-benzylphenethylamines: High potency agonists at 5-HT2A receptors". Biochemical Pharmacology. 158: 27–34. doi:10.1016/j.bcp.2018.09.024. PMC   6298744 . PMID   30261175.
  37. 1 2 3 4 5 Wallach J, Cao AB, Calkins MM, Heim AJ, Lanham JK, Bonniwell EM, et al. (2023). "Identification of 5-HT2A receptor signaling pathways associated with psychedelic potential". Nature Communications. 14 (1): 8221. doi: 10.1186/s12969-023-00927-3 . PMC   10694965 . PMID   38001451.
  38. 1 2 3 Seo JY, Hur KH, Ko YH, Kim K, Lee BR, Kim YJ, et al. (October 2019). "A novel designer drug, 25N-NBOMe, exhibits abuse potential via the dopaminergic system in rodents". Brain Research Bulletin. 152: 19–26. doi:10.1016/j.brainresbull.2019.07.002. PMID   31279579.
  39. 1 2 Kim YJ, Ma SX, Hur KH, Lee Y, Ko YH, Lee BR, et al. (April 2021). "New designer phenethylamines 2C-C and 2C-P have abuse potential and induce neurotoxicity in rodents". Archives of Toxicology. 95 (4): 1413–1429. Bibcode:2021ArTox..95.1413K. doi:10.1007/s00204-021-02980-x. PMID   33515270. 25N-NBOMe and other 2C drug derivatives similarly increased p-DAT levels in the NAc and striatum of mice (Seo et al. 2019). [...] increased p-DAT levels lead to an increase in dopamine release, which contribute to elevated dopamine levels.
  40. ↑ Casale, J. F., & Hays, P. A. (2012). Characterization of eleven 2, 5-dimethoxy-N-(2-methoxybenzyl) phenethylamine (NBOMe) derivatives and differentiation from their 3-and 4-methoxybenzyl analogues—part I. Microgram Journal, 9(2), 84–109. https://www.dea.gov/sites/default/files/pr/microgram-journals/2012/mj9_84-109.pdf
  41. ↑ A Daath.hu kiegészítése a BSZKI "designer jogi listáján" nem szereplő, de az UP jegyzék 1.-4. szerkezeti leírásainak megfelelő, illetve az 5. felsorolásában szereplő néhány anyagról
  42. ↑ "Föreskrifter om ändring i Läkemedelsverkets föreskrifter (LVFS 2011:10) om förteckningar över narkotika" [Regulations amending the Medical Products Agency's regulations (LVFS 2011:10) on lists of narcotics](PDF) (in Swedish). Archived from the original (PDF) on 2015-03-16. Retrieved 2017-04-21.
  43. ↑ "The Misuse of Drugs Act 1971 (Ketamine etc.) (Amendment) Order 2014". UK Statutory Instruments 2014 No. 1106. www.legislation.gov.uk.
  44. ↑ Alabama Senate Bill SB 333: Controlled Substances
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