25N-NBOMe
Width250px
ClassSerotonin 5-HT2A receptor agonist; Serotonergic psychedelic; Hallucinogen
Atc prefixNone
Legal brF2
Legal br comment[1]
Legal ukClass A
Cas number1354632-03-3
Pubchem118536028
Chemspiderid52085577
Unii0G7SSW2N0S
Synonyms2C-N-NBOMe; NBOMe-2C-N
Iupac name2-(2,5-dimethoxy-4-nitrophenyl)-N-[(2-methoxyphenyl)methyl]ethan-1-amine
C18
H22
N2
O5
SmilesCOC1=C(CCNCC2=C(OC)C=CC=C2)C=C(OC)C([N+]([O-])=O)=C1
Stdinchi1S/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
StdinchikeyTXCKTIBHURMASQ-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]

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]

Interactions

See also: Psychedelic drug#Interactions and Trip killer#Serotonergic psychedelic antidotes

Pharmacology

Pharmacodynamics

25N-NBOMe activities
TargetAffinity (Ki, nM)
5-HT1A1,860–4,200 (Ki)
4,800 (EC50)
36% (Emax)
5-HT1B>10,000
5-HT1D5,620
5-HT1E>10,000
5-HT1FND
5-HT2A0.11–1.41 (Ki)
0.204–70 (EC50)
34–173% (Emax)
5-HT2B4.47–8.7 (Ki)
2.34–70 (EC50)
<10–58% (Emax)
5-HT2C1.06–21 (Ki)
0.457–1.32 (EC50)
99–102% (Emax)
5-HT3>10,000
5-HT4ND
5-HT5A>10,000
5-HT655
5-HT7>10,000
α1A850–>10,000
α1B, α1D>10,000
α2A501–590
α2B1,100
α2C692
β1>10,000
β17,080
β3>10,000
D118,000
D22,400–6,760
D32,190–4,500
D4>10,000
D5>10,000
H191–210
H21,070
H3, H4>10,000
M1–M5>10,000
I1ND
σ1537
σ258
MOR>10,000
DOR>10,000
KOR2,820
TAAR1>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)
SERT1,410–5,810 (Ki)
5,790–20,000 (IC50)
IA (EC50)
NET7,200–11,300 (Ki)
15,000–33,000 (IC50)
IA (EC50)
DAT13,000–37,900 (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: [7][8][9][10][11][12][13][14]

25N-NBOMe is a selective and highly potent agonist of the serotonin 5-HT2 receptors.[15] 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.[15] 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.[15]

The EC50 (Emax) 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.[15] 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.[15] 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.[15]

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.[16] 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.[16]

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%).[16]

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%).[16]

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.[16]

Unlike many other serotonergic psychedelics, 25N-NBOMe has shown reinforcing effects in rodents, including in terms of conditioned place preference (CPP) and self-administration.[17] 25N-NBOMe has been found to increase phosphorylation of the dopamine transporter (DAT) in the striatum similarly to methamphetamine in rodents.[18][17] DAT phosphorylation is associated with dopamine reverse transport and efflux, which in turn increases extracellular dopamine levels.[18][17]

History

25N-NBOMe was first described in the scientific literature by 2012.[19]

Society and culture

Canada

25N-NBOMe is a controlled substance in Canada under phenethylamine blanket-ban language.[20]

Hungary

25N-NBOMe is illegal in Hungary.[21]

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.[22]

United States

25N-NBOMe is not an explicitly controlled substance in the United States.[23] However, it could be considered a controlled substance under the Federal Analogue Act if intended for human consumption.

25N-NBOMe is illegal in Alabama.[24]

See also

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. Archived 2023-08-27 at the Wayback Machine. Retrieved 2023-08-27.
  2. ^ Hansen M, Phonekeo K, Paine JS, Leth-Petersen S, Begtrup M, Bräuner-Osborne H, Kristensen JL (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.). 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". 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. ^ 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. ^ "Kᵢ Database". PDSP. 20 June 2025. Retrieved 20 June 2025.
  8. ^ 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)". Neuropharmacology. 99: 546–553. doi:10.1016/j.neuropharm.2015.08.034. PMID 26318099
  9. ^ 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
  10. ^ 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. doi:10.1016/j.forsciint.2020.110553. PMID 33160102
  11. ^ Pottie E, Poulie CB, Simon IA, Harpsøe K, D'Andrea L, Komarov IV, Gloriam DE, Jensen AA, Kristensen JL, Stove CP (August 2023). "Structure-Activity Assessment and In-Depth Analysis of Biased Agonism in a Set of Phenylalkylamine 5-HT2A Receptor Agonists". ACS Chem Neurosci. 14 (15): 2727–2742. doi:10.1021/acschemneuro.3c00267. PMID 37474114
  12. ^ "Selective, partial, and arrestin-biased 5-ht2a agonists with utility in various disorders". Google Patents. 11 May 2022. Retrieved 20 June 2025.
  13. ^ Wallach J, Cao AB, Calkins MM, Heim AJ, Lanham JK, Bonniwell EM, Hennessey JJ, Bock HA, Anderson EI, Sherwood AM, Morris H, de Klein R, Klein AK, Cuccurazzu B, Gamrat J, Fannana T, Zauhar R, Halberstadt AL, McCorvy JD (December 2023). "Identification of 5-HT2A receptor signaling pathways associated with psychedelic potential". Nat Commun. 14 (1). Bibcode:2023NatCo..14.8221W. doi:10.1038/s41467-023-44016-1. PMC 10724237. PMID 38102107
  14. ^ 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". J Pharmacol Exp Ther. 357 (1): 134–144. doi:10.1124/jpet.115.229765. PMID 26791601. Archived from the original on 2025-05-09.
  15. ^ 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
  16. ^ Wallach J, Cao AB, Calkins MM, Heim AJ, Lanham JK, Bonniwell EM, Hennessey JJ, Bock HA, Anderson EI, Sherwood AM, Morris H, de Klein R, Klein AK, Cuccurazzu B, Gamrat J, Fannana T, Zauhar RJ, Halberstadt AL, McCorvy JD (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
  17. ^ Seo JY, Hur KH, Ko YH, Kim K, Lee BR, Kim YJ, Kim SK, Kim SE, Lee YS, Kim HC, Lee SY, Jang CG (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
  18. ^ Kim YJ, Ma SX, Hur KH, Lee Y, Ko YH, Lee BR, Kim SK, Sung SJ, Kim KM, Kim HC, Lee SY, Jang CG (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.
  19. ^ 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
  20. ^ "Controlled Drugs and Substances Act". Department of Justice Canada. Retrieved 19 January 2026.
  21. ^ 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
  22. ^ "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] (in Swedish). Archived from the original on 2015-03-16. Retrieved 2017-04-21.
  23. ^ "Orange Book: List of Controlled Substances and Regulated Chemicals (January 2026)", United States: U.S. Department of Justice: Drug Enforcement Administration (DEA): Diversion Control Division, January 2026
  24. ^ Alabama Senate Bill SB 333: Controlled Substances