5-DM-25B-NBOMe

Last updated

5-DM-25B-NBOMe
Clinical data
Other names5-O-Desmethyl-25B-NBOMe; 5-OH-25B-NBOMe; N-(2-Methoxybenzyl)-4-bromo-5-hydroxy-2-methoxyphenethylamine
Drug class Serotonin receptor modulator; 5-HT2A receptor agonist; 5-HT2C receptor agonist
ATC code
  • None
Identifiers
  • 2-bromo-4-methoxy-5-(2-{[(2-methoxyphenyl)methyl]amino}ethyl)phenol
Chemical and physical data
Formula C17H20BrNO3
Molar mass 366.255 g·mol−1
3D model (JSmol)
  • COC1=C(CCN([H])CC2=C(OC)C=CC=C2)C=C(O[H])C(Br)=C1
  • InChI=1S/C17H20BrNO3/c1-21-16-6-4-3-5-13(16)11-19-8-7-12-9-15(20)14(18)10-17(12)22-2/h3-6,9-10,19-20H,7-8,11H2,1-2H3
  • Key:IVVHUBRWCYPDHE-UHFFFAOYSA-N

5-DM-25B-NBOMe, also known as 5-O-desmethyl-25B-NBOMe, is a serotonin receptor modulator of the phenethylamine family related to the NBOMe psychedelic 25B-NBOMe. [1] [2] [3] It is the 5-O-desmethyl analogue of 25B-NBOMe. [1] [2] The drug is a potent agonist of the serotonin 5-HT2A and 5-HT2C receptors. [2] Its affinity (Ki), EC50 Tooltip half-maximal effective concentration, and Emax Tooltip maximal efficacy values at the serotonin 5-HT2A receptor were 2.24 nM, 1.20 nM, and 61%, respectively, whereas its values at the serotonin 5-HT2C receptor were 10.5 nM, 0.617 nM, and 73%, respectively. [2] At the serotonin 5-HT2A receptor, the drug showed 11-fold lower affinity, 1.3-fold lower activational potency, and a numerical efficacy decrease of 22% compared to 25B-NBOMe. [2] It is a major metabolite of 25B-NBOMe and is formed by cytochrome P450 enzymes. [4] [5] [6] [7] 5-DM-25B-NBOMe was first described in the scientific literature by 2016. [2] [6] [7]

Contents

See also

References

  1. 1 2 Duan W, Cao D, Wang S, Cheng J (January 2024). "Serotonin 2A Receptor (5-HT2AR) Agonists: Psychedelics and Non-Hallucinogenic Analogues as Emerging Antidepressants". Chemical Reviews. 124 (1): 124–163. doi:10.1021/acs.chemrev.3c00375. PMID   38033123. In order to increase the metabolic stability of NBOMes, compounds such as 115−122 were reported in 2016.181 [...]
  2. 1 2 3 4 5 6 Leth-Petersen S, Petersen IN, Jensen AA, Bundgaard C, Bæk M, Kehler J, et al. (November 2016). "5-HT2A/5-HT2C Receptor Pharmacology and Intrinsic Clearance of N-Benzylphenethylamines Modified at the Primary Site of Metabolism". ACS Chemical Neuroscience. 7 (11): 1614–1619. doi:10.1021/acschemneuro.6b00265. PMID   27564969.
  3. ↑ Marcher-Rørsted E, Halberstadt AL, Klein AK, Chatha M, Jademyr S, Jensen AA, et al. (May 2020). "Investigation of the 2,5-Dimethoxy Motif in Phenethylamine Serotonin 2A Receptor Agonists". ACS Chemical Neuroscience. 11 (9): 1238–1244. doi:10.1021/acschemneuro.0c00129. PMID   32212672. To our surprise, removal of the 5-methoxy group from the NBOMescaffold resulted in only a 10-fold decrease in 5-HT2AR binding affinity compared to the parent compound 20 (pKi = 9.68 and 8.68, respectively), whereas the effect on agonist potency and agonist efficacy was even smaller (20: pEC50 = 9.04, Rmax = 83%; 22: pEC50 = 8.87, Rmax = 70%).
  4. ↑ 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. In a follow-up study, five phase I metabolites of 25B-NBOMe were identified. All three O-demethylated metabolites (4−6) were found in approximately the same abundancies, as were the hydroxylated metabolites (7−8), albeit with relatively lower abundancy. 2CB, the N-debenzylated metabolite, was also detected, but it also had lower abundancy.107 [...] Scheme 3. Putative Phase I Metabolic Pathways for 25BNBOMe in Humans [...]
  5. ↑ Halberstadt AL (2017). "Pharmacology and Toxicology of N-Benzylphenethylamine ("NBOMe") Hallucinogens". Current Topics in Behavioral Neurosciences. 32: 283–311. doi:10.1007/7854_2016_64. ISBN   978-3-319-52442-9. PMID   28097528. NBOMes are extensively metabolized. Caspar et al. tentatively identified 37 phase I and 31 phase II metabolites of 25I-NBOMe in rat and human urine [125]. The primary metabolites of 25I-NBOMe are 2-O-desmethyl-25I-NBOMe, 5-O-desmethyl-25INBOMe, 25I-NBOH, and their glucuronic acid conjugates [125–128]. Similar findings have been reported for 25B-NBOMe and 25C-NBOMe [128–130]. CYP3A4 is the major cytochrome P450 isoenzyme responsible for the biotransformation of 25INBOMe, with CYP2C9 and CYP2C19 potentially also contributing [125, 126].
  6. 1 2 Leth-Petersen S, Gabel-Jensen C, Gillings N, Lehel S, Hansen HD, Knudsen GM, et al. (January 2016). "Metabolic Fate of Hallucinogenic NBOMes". Chemical Research in Toxicology. 29 (1): 96–100. doi:10.1021/acs.chemrestox.5b00450. PMID   26669514.
  7. 1 2 Boumrah Y, Humbert L, Phanithavong M, Khimeche K, Dahmani A, Allorge D (February 2016). "In vitro characterization of potential CYP- and UGT-derived metabolites of the psychoactive drug 25B-NBOMe using LC-high resolution MS". Drug Testing and Analysis. 8 (2): 248–256. doi:10.1002/dta.1865. PMID   26382567.
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