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 5HT<sub>2A</sub> receptor. 25N-NBOMe has been sold as a street drug and has only been described in the literature in terms of identification by forensic analysis.
The dose range of 25N-NBOMe has been given as 0.1 to 1.3mg or more sublingually, with a typical dose estimate of 0.6mg. 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.
25N-NBOMe is a selective and highly potent agonist of the serotonin 5-HT<sub>2</sub> receptors. Its affinities (K<sub>i</sub>) are 0.144nM at the serotonin 5-HT<sub>2A</sub> receptor, 8.7nM at the serotonin 5-HT<sub>2B</sub> receptor, and 1.06nM at the serotonin 5-HT<sub>2C</sub> receptor. In terms of affinity, the drug has approximately 7.4-fold selectivity for the serotonin 5-HT<sub>2A</sub> receptor over the serotonin 5-HT<sub>2C</sub> receptor and 60-fold selectivity for the 5-HT<sub>2A</sub> receptor over the serotonin 5-HT<sub>2B</sub> receptor.
The () values of 25N-NBOMe are 0.51nM (87.9%) at the serotonin 5-HT<sub>2A</sub> receptor, 47nM (57.6%) at the serotonin 5-HT<sub>2B</sub> receptor, and 1.32nM (99.4%) at the serotonin 5-HT<sub>2C</sub> receptor. Hence, 25N-NBOMe is a full agonist of the serotonin 5-HT<sub>2A</sub> and 5-HT<sub>2C</sub> receptors and a partial agonist of the serotonin 5-HT<sub>2B</sub> receptor. In terms of functional activity, 25N-NBOMe had 2.6-fold selectivity for the serotonin 5-HT<sub>2A</sub> receptor over the serotonin 5-HT<sub>2C</sub> receptor and 92-fold selectivity for the serotonin 5-HT<sub>2A</sub> receptor over the serotonin 5-HT<sub>2C</sub> receptor.
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. Radioligand binding assays showed high binding affinity for serotonin 5-HT<sub>2</sub> receptors, with pK<sub>i</sub> values of 9.26 ñ 0.15 at 5-HT<sub>2A</sub>, 8.35 ñ 0.08 at 5-HT<sub>2B</sub>, and 8.16 ñ 0.07 at 5-HT<sub>2C</sub>. The compound was also screened across more than 40 additional CNS targets and found to be highly selective for the 5-HT<sub>2</sub> receptor subfamily.
In calcium flux functional assays, 25N-NBOMe was a potent full agonist at 5-HT<sub>2A</sub> (pEC<sub>50</sub> = 9.50 ñ 0.03; E<sub>max</sub> = 94 ñ 1%) and 5-HT<sub>2C</sub> (pEC<sub>50</sub> = 9.07 ñ 0.03; E<sub>max</sub> = 102 ñ 1%) receptors, while showing negligible agonist activity at 5-HT<sub>2B</sub> (E<sub>max</sub> < 10%).
Bioluminescence resonance energy transfer (BRET) functional assays measuring Gq dissociation and ò-arrestin2 recruitment signaling indicated strong agonist activity at 5-HT<sub>2A</sub>, with Gq pEC<sub>50</sub> = 9.69 ñ 0.04 (E<sub>max</sub> = 95.2 ñ 1.2%) and ò-arrestin2 recruitment pEC<sub>50</sub> = 9.66 ñ 0.09 (E<sub>max</sub> = 136.5 ñ 3.6%). This illustrates that 25N-NBOMe is a balanced 5-HT<sub>2A</sub> agonist across these pathways, in contrast to analogs like 25N-N1-Nap and 25N-NBPh which displayed functional selectivity or signaling bias for ò-arrestin2 recruitment. For 5-HT<sub>2C</sub>, Gq pEC<sub>50</sub> was 9.34 ñ 0.08 (E<sub>max</sub> = 100.0 ñ 2.5%), while weak partial agonist activity was observed at 5-HT<sub>2B</sub> (pEC<sub>50</sub> = 8.63 ñ 0.14; E<sub>max</sub> = 54.1 ñ 2.5%).
In vivo, 25N-NBOMe induced a robust head-twitch response (HTR) in mice with an ED<sub>50</sub> of 0.11 mg/kg (0.29 ümol/kg). Notably 25N-NBOMe produced the highest HTR frequency (4.890 counts per minute) among a panel of structurally related 25N analogs.
Unlike many other serotonergic psychedelics, 25N-NBOMe has shown reinforcing effects in rodents, including in terms of conditioned place preference (CPP) and self-administration. 25N-NBOMe has been found to increase phosphorylation of the dopamine transporter (DAT) in the striatum similarly to methamphetamine in rodents. DAT phosphorylation is associated with dopamine reverse transport and efflux, which in turn increases extracellular dopamine levels.
25N-NBOMe was first described in the scientific literature by 2012.
25N-NBOMe is a controlled substance in Canada under phenethylamine blanket-ban language.
25N-NBOMe is illegal in Hungary.
The Riksdag added 25N-NBOMe to 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.
25N-NBOMe is not an explicitly controlled substance in the United States. However, it could be considered a controlled substance under the Federal Analogue Act if intended for human consumption.
25N-NBOMe is illegal in Alabama.