25I-NBOMe

25I-NBOMe (2C-I-NBOMe, Cimbi-5, Smiles and also shortened to "25I") is a novel synthetic psychoactive substance with strong hallucinogenic properties, synthesized in 2003 for research purposes. Since 2010, it has circulated in the recreational drug scene, often misrepresented as LSD. The recreational usage of 25I is associated with severe intoxication and deaths in humans.[3]

25I-NBOMe
Clinical data
Routes of
administration		Buccal (sublabial), sublingual, insufflated, inhalation, intravenous, intramuscular, rectal
ATC code
  • none
Legal status
Legal status
Identifiers
  • 2-(4-iodo-2,5-dimethoxyphenyl)-N-[(2-methoxyphenyl)methyl]ethanamine
CAS Number
PubChem CID
ChemSpider
UNII
ChEMBL
CompTox Dashboard (EPA)
Chemical and physical data
FormulaC18H22INO3
Molar mass427.282 g·mol−1
3D model (JSmol)
  • COC1=CC=CC=C1CNCCC2=CC(=C(C=C2OC)I)OC
  • InChI=1S/C18H22INO3/c1-21-16-7-5-4-6-14(16)12-20-9-8-13-10-18(23-3)15(19)11-17(13)22-2/h4-7,10-11,20H,8-9,12H2,1-3H3 checkY
  • Key:ZFUOLNAKPBFDIJ-UHFFFAOYSA-N checkY
 ☒NcheckY (what is this?)  (verify)
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25I was synthesized for biochemistry research to map the brain's usage of the type 2A serotonin receptor. A derivative of the substituted phenethylamine 2C-I family, it is the most well-known member of the 25-NB family. It was discovered in 2003 by chemist Ralf Heim at the Free University of Berlin, who published his findings in his PhD dissertation.[4] The compound was subsequently investigated by a team at Purdue University led by David Nichols.[5]

The carbon-11 labelled version of 25I-NBOMe, [11C]Cimbi-5, was synthesized and validated as a radiotracer for positron emission tomography (PET) in Copenhagen.[6][7] Being the first 5-HT2A receptor full agonist PET radioligand, [11C]-CIMBI-5 shows promise as a more functional marker of these receptors, particularly in their high affinity states.[6]

Street and media nicknames for this drug are: "N-Bomb", "Solaris", "Smiles", and "Wizard", although the drug is frequently fraudulently sold as LSD.[8][9][10]

Due to its physical effects and risk of overdose, there have been multiple deaths attributed to the drug. Its long term toxicity is unknown due to lack of existing research.

Recreational use

Although 25I-NBOMe was discovered in 2003, it did not emerge as a common recreational drug until 2010, when it was first sold by vendors specializing in the supply of designer drugs.[11] In a slang context, the name of the compound is often shortened to "25I" or is simply called "N-Bomb".[12] According to a 2014 survey, 25I-NBOMe was the most frequently used of the NBOMe series.[13] By 2013, case reports of 25I-NBOMe intoxication, with and without analytic confirmation of the drug in the body, were becoming increasingly common in the medical literature.[14]

25I-NBOMe is widely rumored to be orally inactive; however, apparent overdoses have occurred via oral administration. Common routes of administration include sublingual, buccal, and intranasal.[13] For sublingual and buccal administration, 25I-NBOMe is often applied to sheets of blotter paper of which small portions (tabs) are held in the mouth to allow absorption through the oral mucosa.[15][16] There are reports of intravenous injection of 25I-NBOMe solution and smoking the drug in powdered form.[17][18]

Due to its potency and much lower cost than so-called classical or traditional psychedelics, 25I-NBOMe blotters are frequently misrepresented as, or mistaken for, LSD blotters.[19] Even small quantities of 25I-NBOMe can produce a large number of blotters. Vendors would import 25I-NBOMe in bulk (e.g. 1 kg containers) and resell individual doses for a considerable profit.[16]

Dosage

25I-NBOMe is potent, being active in sub-milligram doses. A common dose of the hydrochloride salt is 600–1,200 μg. The UK Advisory Council on the Misuse of Drugs states that a common dose is between 50 and 100 μg,[16] although other sources indicate that these figures are incorrect; Erowid tentatively suggests that the threshold dosage for humans is 50–250 μg, with a light dose between 200–600 μg, a common dose at 500–800 μg, and a strong dose at 700–1500 μg.[20]

At this level of potency, it is not possible to accurately measure a single dose of 25I-NBOMe powder without an analytical balance, and attempting to do so may put the user at significant risk of overdose.[16] There is a high risk of overdose due to the small margin between a high-dose and an over-dose, which is not a risk with the similar drug LSD. One study has shown that 25I-NBOMe blotters have 'hotspots' of the drug and the dosage is not evenly applied over the surface of the paper, which could lead to overdose.[21]

Effects

25I-NBOMe effects usually last 6–10 hours if taken sublingually, or buccally (between gum and cheek).[18] When it is insufflated (snorted), effects usually last 4–6 hours.[18]

25I-NBOMe has similar effects to LSD, though users report more negative effects while under the influence and more risk of harm following use as compared to the classical psychedelics.[13]

Case reports of seven British males who presented to an emergency room following analytically confirmed 25I-NBOMe intoxication suggest the following potential adverse effects: "tachycardia (n = 7), hypertension (4), agitation (6), aggression, visual and auditory hallucinations (6), seizures (3), hyperpyrexia (3), clonus (2), elevated white blood cell count (2), elevated creatine kinase (7), metabolic acidosis (3), and acute kidney injury (1)."[17]

25I-NBOMe can be consumed in liquid, powder or paper form and can be snorted, injected, mixed with food, or smoked, but sublingual administration is most common.[22]

Toxicity and harm potential
This section is an excerpt from 25-NB § Toxicity and harm potential.[edit]

NBOMe compounds are often associated with life-threatening toxicity and death.[23][24] Studies on NBOMe family of compounds demonstrated that the substance exhibit neurotoxic and cardiotoxic activity.[25] 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.[26][27][28][29][30] Other symptoms of toxidrome of include agitation or aggression, seizure, hyperthermia, diaphoresis, hypertonia, rhabdomyolysis, and death.[26][30][24] Researchers report that NBOMe intoxication frequently display signs of serotonin syndrome.[31] The likelihood of seizure is higher in NBOMes compared to other psychedelics.[25]

NBOMe and NBOHs are regularly sold as LSD in blotter papers,[24][32] which have a bitter taste and different safety profiles.[26][23] Despite high potency, recreational doses of LSD have only produced low incidents of acute toxicity.[23] Fatalities involved in NBOMe intoxication suggest that a significant number of individuals ingested the substance which they believed was LSD,[28] and researchers report that "users familiar with LSD may have a false sense of security when ingesting NBOMe inadvertently".[26] 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.[33][34][26]

Given limited documentation of NBOMe consumption, the long-term effects of the substance remain unknown.[26] NBOMe compounds are not active orally,[lower-alpha 1] and are usually taken sublingually.[36]: 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.[37][38][39]

Neurotoxic and cardiotoxic actions
This section is an excerpt from 25-NB § Neurotoxic and cardiotoxic actions.[edit]

Many of the NBOMe compounds have high potency agonist activity at additional 5-HT receptors and prolonged activation of 5-HT2B can cause cardiac valvulopathy in high doses and chronic use.[24][29] 5-HT2B receptors have been strongly implicated in causing drug-induced valvular heart disease.[40][41][42] The high affinity of NBOMe compounds for adrenergic α1 receptor has been reported to contribute to the stimulant-type cardiovascular effects.[29]

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.[25] 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.[25]

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.[43][44]

Emergency treatment
This section is an excerpt from 25-NB § Emergency treatment.[edit]
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.[25]

Attributed deaths

Reports of deaths and significant injuries have been attributed to the use of 25I-NBOMe, prompting some governments to control its possession, production, and sale. The website Erowid states that 25I-NBOMe is extremely potent and should not be snorted, and that the drug "appears to have led to several deaths in the past year."[19] Several non-fatal overdoses requiring prolonged hospitalization have also been reported.[16][14][17]

As of August 2015, 25I-NBOMe has reportedly led to at least 19 overdose deaths in the United States.[12][45] In June 2012, two teens in Grand Forks, North Dakota and East Grand Forks, Minnesota fatally overdosed on a substance that was allegedly 25I-NBOMe, resulting in lengthy sentences for two of the parties involved and a Federal indictment against the Texas-based online vendor.[46] A 21-year-old man from Little Rock, Arkansas died in October 2012 after taking a liquid drop of the drug nasally at a music festival. He was reported to have consumed caffeinated alcoholic beverages for "several hours" beforehand. It is unclear what other drugs he may have consumed, as autopsies generally do not test for the presence of research chemicals.[47] In January 2013, an 18-year-old in Scottsdale, Arizona, died after consuming 25I-NBOMe sold as LSD; a toxicology screening found no other drugs in the person's system. The drug is the suspected cause of death in another Scottsdale, Arizona, incident in April 2013.[16] It is also cited in the death of a 21-year-old woman in August 2013[48] and the death of a 17-year-old in Minnesota in January 2014,[49] as well as the death of a 15-year old in Washington in September 2014.[50] In October 2015, a 20-year-old UCSB student from Isla Vista, California died of "acute hallucinogenic polysubstance intoxication" with an additional significant cause of death being "sharp force trauma of the upper extremity", according to a statement from Santa Barbara County Sheriff's office; the autopsy determined Sanchez was under the influence of two hallucinogenic drugs at the time of his death: ketamine and 25I-NBOMe. The noted sharp force trauma refers to a deep cut on Sanchez's right forearm, which was caused when he punched and broke a large residential window while suffering hallucinations.[51]

25I-NBOMe has been implicated in multiple deaths in Australia. In March 2012, a man in Australia died from injuries sustained by running into trees and power poles while intoxicated by 25I-NBOMe.[52] A Sydney teenager jumped off a balcony to his death on June 5, 2013, while on 25I-NBOMe.[53]

25I-NBOMe has been linked to a major case on January 20, 2016, in Cork, Republic of Ireland, which left six teenagers hospitalized, one of whom later died. At least one of the teenagers suffered a cardiac arrest, according to reports, along with extreme internal bleeding.[54]

At least one suicide, and two attempted suicides leading to hospitalisation, have occurred while under the effects of 25I-NBOMe.[55]

Pharmacology
25I-NBOMe[56][57]
ReceptorKd (nM)±
5-HT2A 0.044
5-HT2B 23173
5-HT2C 2
5-HT6 7312
μ-opioid 8214
κ-opioid 28850
H1 18935

25I-NBOMe acts as a highly potent full agonist for the human 5-HT2A receptor,[56][58] with a dissociation constant (Kd) of 0.044 nM, making it some sixteen times the potency of 2C-I itself at this receptor. A radiolabelled form of 25I-NBOMe can be used for mapping the distribution of 5-HT2A receptors in the brain.[57]

25I-NBOMe induces a head-twitch response in mice which is blocked completely by a selective 5-HT2A antagonist, suggesting its psychedelic effects are mediated by 5-HT2A. This study suggested that 25I-NBOMe is approximately 14-fold more potent than 2C-I in-vivo.[59]

While in-vitro studies showed that N-benzyl derivatives of 2C-I were significantly increased in potency compared to 2C-I, the N-benzyl derivatives of the related compound DOI were inactive.[60]

25I-NBOMe also has weaker interactions with multiple other receptors. Kd values for interaction with the following targets were greater than 500 nM: 5-HT1A, D3, H2, 5-HT1D, α1A adrenergic, δ opioid, serotonin uptake transporter, 5-HT5A, 5-HT1B, D2, 5-HT7, D1, 5-HT3, 5-HT1E, D5, muscarinic M1-M5, H3, and the dopamine uptake transporter.[57]

Chemistry

Like other 2C-X-NBOMe molecules, 25I-NBOMe is a derivative of the 2C family of phenethylamines described by chemist Alexander Shulgin in his book PiHKAL.[16][14] Specifically, 25I-NBOMe is an N-benzyl derivative of the phenethylamine molecule 2C-I, formed by adding a 2-methoxybenzyl (BnOMe) onto the nitrogen (N) of the phenethylamine backbone. This substitution significantly increases the potency of the molecule.[16]

Analogues

Analogues and derivatives of 2C-I:

25I-NB*:

N-(2C)-fentanyl:

  • N-(2C-I) fentanyl[61]

Synthesis

25I-NBOMe is usually synthesised from 2C-I and 2-methoxybenzaldehyde, via reductive alkylation. It can be done stepwise by first making the imine and then reducing the formed imine with sodium borohydride, or by direct reaction with sodium triacetoxyborohydride.[4]

Society and culture

Australia

25I-NBOMe was explicitly scheduled in Queensland drug law in April 2012, and in New South Wales in October 2013, as were some related compounds such as 25B-NBOMe. The Australian federal government has no specific legislation concerning any of the N-benzyl phenethylamines.[62]

Canada

As of October 31, 2016; 25I-NBOMe is a controlled substance (Schedule III) in Canada.[63]

China

As of October 2015 25I-NBOMe is a controlled substance in China.[64]

European Union

In September 2014 the European Union implemented a ban of 25I-NBOMe in all its member states.[65]

Israel

Israel banned 25I-NBOMe in 2013.[66]

Russia

Russia was the first country to pass specific regulations on the NBOMe series. All drugs in the NBOMe series, including 25I-NBOMe, became illegal in Russia in October 2011.[66]

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.[67]

United States

On Nov 15, 2013, the DEA added 25I-NBOMe (and 25C-, and 25B-NBOMe) to Schedule I using their emergency scheduling powers, making those NBOMe compounds "temporarily" in Schedule I for 2 years.[45] In November 2015, the temporary scheduling was extended for an additional year[68] while permanent scheduling was arranged.[69] 25I-NBOMe, 25B-NBOMe and 25C-NBOMe are currently Schedule 1 Substances according to 21 CFR 1308.11(d).[70]

Romania

In 2011, Romania banned all psychoactive substances.[71]

Serbia

25I-NBOMe was put on the list of prohibited substances in March 2015.[72]

Sweden

The Riksdag added 25I-NBOMe to Narcotic Drugs Punishments Act under Swedish schedule I ("substances, plant materials and fungi which normally do not have medical use") as of August 1, 2013, published by Medical Products Agency (MPA) in regulation LVFS 2013:15 listed as 25I-NBOMe, and 2-(4-jodo-2,5-dimetoxifenyl)-N-(2-metoxibensyl)etanamin.[73]

Taiwan

Following the European rule from 2014, 25I-NBOMe was put in class 4 of prohibited substances.[74]

Brazil

All drugs in the NBOMe family, including 25I-NBOMe, are illegal.

Notes
  1. 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.[35] 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.[35]

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