2-OH-2C-B

2-OH-2C-B
Clinical data
Other names2-Hydroxy-2C-B; 2-O-Desmethyl-2C-B; 2-DM-2C-B; B-2-HMPEA; 2-Hydroxy-5-methoxy-4-bromophenethylamine; 4-Bromo-2-hydroxy-5-methoxyphenethylamine
Drug classSerotonin receptor modulator; Serotonin 5-HT2A receptor agonist
ATC code
  • None
Identifiers
  • 2-(2-aminoethyl)-5-bromo-4-methoxyphenol
PubChem CID
ChemSpider
Chemical and physical data
FormulaC9H12BrNO2
Molar mass246.104 g·mol−1
3D model (JSmol)
  • COC1=C(C=C(C(=C1)CCN)O)Br
  • InChI=1S/C9H12BrNO2/c1-13-9-4-6(2-3-11)8(12)5-7(9)10/h4-5,12H,2-3,11H2,1H3
  • Key:LTIUWTXENMGCDK-UHFFFAOYSA-N

2-OH-2C-B, also known as 2-O-desmethyl-2C-B (2-DM-2C-B) or as 4-bromo-2-hydroxy-5-methoxyphenethylamine (B-2-HMPEA), is a serotonin receptor modulator of the phenethylamine family related to the 2C psychedelic 2C-B (2,5-dimethoxy-4-bromophenethylamine).[1] It is the 2-O-demethylated analogue of 2C-B.[1] The drug is a potent agonist of the serotonin 5-HT2A receptor, with an affinity (Ki) of 0.92 nM, an EC50Tooltip half-maximal effective concentration of 4.3 nM, and an EmaxTooltip maximal efficacy of 93%.[1] For comparison, 2C-B had an affinity (Ki) of 0.64 nM, an EC50 of 3.3 nM, and an Emax of 76%.[1] 2-OH-2C-B is a known metabolite of 2C-B in rodents and humans.[2][3][4][5][6][7][8][9][10][11] The predicted log P of 2-OH-2C-B is 1.5[12] and of 2C-B is 2.1.[13] The drug was first described in the scientific literature by 2003[2] and its pharmacology was described by 2013.[1]

See also

References

  1. ^ a b c d e McCorvy JD (16 January 2013). Mapping the binding site of the 5-HT2A receptor using mutagenesis and ligand libraries: Insights into the molecular actions of psychedelics (Ph.D. thesis). Purdue University. Archived from the original on 15 May 2025. Retrieved 27 May 2025 – via Purdue e-Pubs.{{cite thesis}}: CS1 maint: bot: original URL status unknown (link)
  2. ^ a b Kanamori T, Tsujikawa K, Ohmae Y, Iwata Y, Inoue H, Inouye Y, et al. (2003). "Excretory Profile of 4-Bromo-2,5-dimethoxyphenethylamine (2C-B) in Rat". Journal of Health Science. 49 (2): 166–169. doi:10.1248/jhs.49.166. ISSN 1344-9702. Retrieved 2 February 2026.
  3. ^ Carmo H, de Boer D, Remião F, Carvalho F, dos Reys LA, de Lourdes Bastos M (November 2004). "Metabolism of the designer drug 4-bromo-2,5-dimethoxyphenethylamine (2C-B) in mice, after acute administration". Journal of Chromatography. B, Analytical Technologies in the Biomedical and Life Sciences. 811 (2): 143–152. doi:10.1016/j.jchromb.2004.08.026. PMID 15522713.
  4. ^ Kanamori T, Tsujikawa K, Ohmae Y, Iwata YT, Inoue H, Kishi T, et al. (March 2005). "A study of the metabolism of methamphetamine and 4-bromo-2,5-dimethoxyphenethylamine (2C-B) in isolated rat hepatocytes". Forensic Science International. 148 (2–3): 131–137. doi:10.1016/j.forsciint.2004.04.084. PMID 15639607.
  5. ^ Carmo H, Hengstler JG, de Boer D, Ringel M, Remião F, Carvalho F, et al. (January 2005). "Metabolic pathways of 4-bromo-2,5-dimethoxyphenethylamine (2C-B): analysis of phase I metabolism with hepatocytes of six species including human". Toxicology. 206 (1): 75–89. doi:10.1016/j.tox.2004.07.004. PMID 15590110.
  6. ^ Kanamori T, Kuwayama K, Tsujikawa K, Miyaguchi H, Togawa-Iwata Y, Inoue H (2011). "A model system for prediction of the in vivo metabolism of designer drugs using three-dimensional culture of rat and human hepatocytes". Forensic Toxicology. 29 (2): 142–151. doi:10.1007/s11419-011-0116-3. ISSN 1860-8965. Retrieved 2 February 2026.
  7. ^ Kanamori T, Nagasawa K, Kuwayama K, Tsujikawa K, Iwata YT, Inoue H (January 2013). "Analysis of 4-bromo-2,5-dimethoxyphenethylamine abuser's urine: identification and quantitation of urinary metabolites". Journal of Forensic Sciences. 58 (1): 279–287. doi:10.1111/j.1556-4029.2012.02289.x. PMID 23066942.
  8. ^ Thomann J, Rudin D, Kraus S, Arikci D, Holze F, Liechti ME, et al. (June 2025). "Liquid chromatography-tandem mass spectrometry-based pharmacokinetic and metabolic analysis of 4-bromo-2,5-dimethoxyphenethylamine and its metabolites in human plasma". Drug Metabolism and Disposition. 53 (6) 100086. doi:10.1016/j.dmd.2025.100086. PMID 40408905. In addition to the primary metabolic pathway involving MAO and aldehyde-oxidizing enzymes, CYP2D6 rapidly degraded 2C-B, suggesting its role in this metabolic pathway. However, neither BDMPAA nor B-2-HMPAA was detected, and the identities of the resulting metabolites remain unknown. In rats, cytochrome P450 enzymes have been implicated in a major demethylation pathway that converts 2C-B into 4-bromo-2-hydroxy-5-methoxyphenethylamine or 4-bromo-5-hydroxy-2-methoxyphenethylamine, a process that may also occur to a lesser extent in humans (Carmo et al, 2005; Kanamori et al, 2013)
  9. ^ Meyer MR, Maurer HH (June 2010). "Metabolism of designer drugs of abuse: an updated review". Current Drug Metabolism. 11 (5): 468–482. doi:10.2174/138920010791526042. PMID 20540700.
  10. ^ Meyer MR, Maurer HH (18 April 2012). "Drugs of Abuse (Including Designer Drugs)". Metabolism of Drugs and Other Xenobiotics. Wiley. pp. 429–463. doi:10.1002/9783527630905.ch16. ISBN 978-3-527-32903-8. Retrieved 2 February 2026.
  11. ^ Papaseit E, Pérez-Mañá C, González D, Fonseca F, Torrens M, Farré M (10 October 2018). "Clinical Effects of 2C-B Abuse". Handbook of Novel Psychoactive Substances. New York, NY: Routledge. pp. 291–303. doi:10.4324/9781315158082-16. ISBN 978-1-315-15808-2. Retrieved 2 February 2026.
  12. ^ "4-Bromo-2-hydroxy-5-methoxyphenethylamine". PubChem. Retrieved 2 February 2026.
  13. ^ "4-Bromo-2,5-Dimethoxyphenethylamine". PubChem. Retrieved 2 February 2026.
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