# 25N-NBOMe

25N-NBOMe (2C-N-NBOMe, 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$_{2A}$ 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.

## Pharmacology
### Pharmacodynamics

25N-NBOMe is a selective and highly potent agonist of the serotonin 5-HT$_2$ receptors. Its affinities (K$_i$) are 0.144 nM at the serotonin 5-HT$_{2A}$ receptor, 8.7 nM at the serotonin 5-HT$_{2B}$ receptor, and 1.06 nM at the serotonin 5-HT$_{2C}$ receptor. In terms of affinity, the drug has approximately 7.4-fold selectivity for the serotonin 5-HT$_{2A}$ receptor over the serotonin 5-HT$_{2C}$ receptor and 60-fold selectivity for the 5-HT$_{2A}$ receptor over the serotonin 5-HT$_{2B}$ receptor.
The EC$_{50}$Tooltip half-maximal effective concentration (E$_{max}$Tooltip maximal efficacy) values of 25N-NBOMe are 0.51 nM (87.9%) at the serotonin 5-HT$_{2A}$ receptor, 47 nM (57.6%) at the serotonin 5-HT$_{2B}$ receptor, and 1.32 nM (99.4%) at the serotonin 5-HT$_{2C}$ receptor. Hence, 25N-NBOMe is a full agonist of the serotonin 5-HT$_{2A}$ and 5-HT$_{2C}$ receptors and a partial agonist of the serotonin 5-HT$_{2B}$ receptor. In terms of functional activity, 25N-NBOMe had 2.6-fold selectivity for the serotonin 5-HT$_{2A}$ receptor over the serotonin 5-HT$_{2C}$ receptor and 92-fold selectivity for the serotonin 5-HT$_{2A}$ receptor over the serotonin 5-HT$_{2C}$ receptor.
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.

## Toxicity and harm potential

NBOMe compounds are often associated with life-threatening toxicity and death. Studies on NBOMe family of compounds demonstrated that the substance exhibit neurotoxic and cardiotoxic activity. 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. Other symptoms of toxidrome include agitation or aggression, seizure, hyperthermia, diaphoresis, hypertonia, rhabdomyolysis, and death. Researchers report that NBOMe intoxication frequently display signs of serotonin syndrome. The likelihood of seizure is higher in NBOMes compared to other psychedelics.
NBOMe and NBOHs are regularly sold as LSD in blotter papers, which have a bitter taste and different safety profiles. Despite high potency, recreational doses of LSD have only produced low incidents of acute toxicity. Fatalities involved in NBOMe intoxication suggest that a significant number of individuals ingested the substance which they believed was LSD, and researchers report that "users familiar with LSD may have a false sense of security when ingesting NBOMe inadvertently". 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.

### Neurotoxic and cardiotoxic actions

Many of the NBOMe compounds have high potency agonist activity at additional 5-HT receptors and prolonged activation of 5-HT$_{2B}$ can cause cardiac valvulopathy in high doses and chronic use. 5-HT$_{2B}$ receptors have been strongly implicated in causing drug-induced valvular heart disease. The high affinity of NBOMe compounds for adrenergic α$_1$ receptor has been reported to contribute to the stimulant-type cardiovascular effects.
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. 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.

### Emergency treatment
## Legality
### United States

25N-NBOMe is illegal in Alabama.

### Hungary

25N-NBOMe is illegal in Hungary.

### 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.

### 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.