25N-NBOMe

25N-NBOMe
Names
	Preferred IUPAC name 2-(2,5-Dimethoxy-4-nitrophenyl)-N-[(2-methoxyphenyl)methyl]ethan-1-amine
	Other names 2C-N-NBOMe, NBOMe-2C-N
Identifiers
CAS Number	1354632-03-3;
3D model (JSmol)	Interactive image;
ChemSpider	52085577;
PubChem CID	118536028;
UNII	0G7SSW2N0S ;
CompTox Dashboard (EPA)	DTXSID501014186 ;
	InChI InChI=1S/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 Key: TXCKTIBHURMASQ-UHFFFAOYSA-N;
	SMILES COC1=C(CCNCC2=C(OC)C=CC=C2)C=C(OC)C([N+]([O-])=O)=C1;
Properties
Chemical formula	C18H22N2O5
Molar mass	346.383 g·mol−1
Pharmacology
Legal status	BR: Class F2 (Prohibited psychotropics); UK: Class A;
	Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa). Infobox references

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.^[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]

Toxicity and harm potential

NBOMe compounds are often associated with life-threatening toxicity and death.^[6]^[7] Studies on NBOMe family of compounds demonstrated that the substance exhibit neurotoxic and cardiotoxic activity.^[8] 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.^[9]^[10]^[11]^[12]^[13] Other symptoms of toxidrome of include agitation or aggression, seizure, hyperthermia, diaphoresis, hypertonia, rhabdomyolysis, and death.^[9]^[13]^[7] Researchers report that NBOMe intoxication frequently display signs of serotonin syndrome.^[14] The likelihood of seizure is higher in NBOMes compared to other psychedelics.^[8]

NBOMe and NBOHs are regularly sold as LSD in blotter papers,^[7]^[15] which have a bitter taste and different safety profiles.^[9]^[6] Despite high potency, recreational doses of LSD have only produced low incidents of acute toxicity.^[6] Fatalities involved in NBOMe intoxication suggest that a significant number of individuals ingested the substance which they believed was LSD,^[11] and researchers report that "users familiar with LSD may have a false sense of security when ingesting NBOMe inadvertently".^[9] 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.^[16]^[17]^[9]

Given limited documentation of NBOMe consumption, the long-term effects of the substance remain unknown.^[9] NBOMe compounds are not active orally,^[a] and are usually taken sublingually.^[19]^: 3 When NBOMes are administered sublingually, numbness of the tongue and mouth followed by a metallic chemical taste was observed, and researchers describe this physical side effect as one of the main discriminants between NBOMe compounds and LSD.^[20]^[21]^[22]

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.^[7]^[12] 5-HT_2B receptors have been strongly implicated in causing drug-induced valvular heart disease.^[23]^[24]^[25] The high affinity of NBOMe compounds for adrenergic α₁ receptor has been reported to contribute to the stimulant-type cardiovascular effects.^[12]

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.^[8] 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.^[8]

Preliminary studies on 25C-NBOMe have shown that the substance is toxic to development, heart health, and brain health in zebrafish, rats, and Artemia salina, a common organism for studying potential drug effects on humans, but more research is needed on the topic, the dosages, and if the toxicology results apply to humans. Researchers of the study also recommended further investigation of the drug's potential in damaging pregnant women and their fetus due to the substance's damaging effects to development.^[26]^[27]

Emergency treatment

At present, there are no specific antidotes for NBOMes, and all acute intoxication is managed by symptomatic treatments, such as administration of benzodiazepines, antipsychotic drugs, and antiarrhythmic agents, such as beta blockers; some emergency interventions are intended to specifically treat rhabdomyolysis, which may lead to critical complications such as metabolic acidosis and acute kidney injury.^[8]

Legality

United States

25N-NBOMe is illegal in Alabama.^[28]

Hungary

25N-NBOMe is illegal in Hungary.^[29]

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.^[30]

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.^[31]

Notes

^ The potency of N-benzylphenethylamines via buccal, sublingual, or nasal absorption is 50-100 greater (by weight) than oral route compared to the parent 2C-x compounds.^[18] Researchers hypothesize the low oral metabolic stability of N-benzylphenethylamines is likely causing the low bioavailability on the oral route, although the metabolic profile of this compounds remains unpredictable; therefore researchers state that the fatalities linked to these substances may partly be explained by differences in the metabolism between individuals.^[18]