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| Formula | C18H22ClNO3 |
| Molar mass | 335.83 g·mol−1 |
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25C-NBOMe (NBOMe-2C-C,2C-C-NBOMe,Cimbi-82) is apsychedelic drug and derivative of the psychedelicphenethylamine2C-C. 25C-NBOMe appeared on online vendor sites in 2010 but was not reported in the literature until 2011.[3] It acts as a potentagonist of the5-HT2Areceptor,[4] and has been studied in its11Cradiolabelled form as a potential ligand for mapping the distribution of 5-HT2A receptors in the brain, usingpositron emission tomography (PET).[3][5] Multiple deaths have occurred from usage of 25C-NBOMe due to the ease of accidental overdose. The long-term toxic effects of the drug have not been researched.
25C-NBOMe is derived from the psychedelic phenethylamine2C-C by substitution on the amine with a 2-methoxybenzyl group. 25C-NBOMe is a clumpy white powder with a notably bitter and metallic taste. 25C-NBOMe has been found on blotter mimics sold as LSD.[6]
25C-NBOMe is extremely potent and the effects of the drug increase greatly within a small window of dosage adjustment. Overdose may occur at as little as double an average dose. With inaccurate dosing of streetblotter paper, when mistaken for LSD, or when taken as a powder or liquid, this has resulted in multiple accidental deaths.[7]
One study has shown that 25C-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.[8] Sublingually, the threshold for the onset of hallucinogenic effects reportedly is about 100–250 μg, with mild effects at 250–450, strong effects at 450–800, and very strong effects over 800 μg.[9]
NBOMe-substituted compounds have a diminished absorption rate passing through mucous membranes, but generally remain inactive when taken orally.Buccal,sublingual orinsufflated routes of administration are all viable options. Absorption ratebuccally andsublingually can be increased when complexed withHPBCD complexing sugar, however the most efficient isnasal administration, which shortens the duration while increasing intensity, but has been attributed to several overdoses and deaths.[10]
Desired[edit]
| Neutral[edit]
| Undesired[edit](Includes negative side effects arising from overdose; likelihood of negative side effects increases with dose)
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NBOMe compounds are often associated with life-threatening toxicity and death.[12][13] Studies on NBOMe family of compounds demonstrated that the substance exhibit neurotoxic and cardiotoxic activity.[14] Reports ofautonomic dysfunction remains prevalent with NBOMe compounds, with most individuals experiencingsympathomimetic toxicity such asvasoconstriction,hypertension andtachycardia in addition to hallucinations.[15][16][17][18][19] Other symptoms oftoxidrome include agitation oraggression,seizure,hyperthermia,diaphoresis,hypertonia,rhabdomyolysis, and death.[15][19][13] Researchers report that NBOMe intoxication frequently display signs ofserotonin syndrome.[20] The likelihood of seizure is higher in NBOMes compared to other psychedelics.[14]
NBOMe and NBOHs are regularly sold as LSD in blotter papers,[13][21] which have a bitter taste and different safety profiles.[15][12] Despite high potency, recreational doses of LSD have only produced low incidents of acute toxicity.[12] Fatalities involved in NBOMe intoxication suggest that a significant number of individuals ingested the substance which they believed was LSD,[17] and researchers report that "users familiar with LSD may have a false sense of security when ingesting NBOMe inadvertently".[15] While most fatalities are due to the physical effects of the drug, there have also been reports of death due toself-harm and suicide under the influence of the substance.[22][23][15]
Given limited documentation of NBOMe consumption, the long-term effects of the substance remain unknown.[15] NBOMe compounds are not active orally,[a] and are usually taken sublingually.[25]: 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.[26][27][28]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.[13][18] 5-HT2B receptors have been strongly implicated in causing drug-inducedvalvular heart disease.[29][30][31] The high affinity of NBOMe compounds foradrenergic α1 receptor has been reported to contribute to the stimulant-type cardiovascular effects.[18]
In vitro studies, 25C-NBOMe has been shown to exhibitcytotoxicity on neuronal cell linesSH-SY5Y,PC12, and SN471, and the compound was more potent thanmethamphetamine at reducing the visibility of the respective cells; the neurotoxicity of the compound involves activation ofMAPK/ERK cascade and inhibition ofAkt/PKB signaling pathway.[14] 25C-NBOMe, including the other derivative25D-NBOMe, reduced the visibility ofcardiomyocytes H9c2 cells, and both substances downregulated expression level of p21 (CDC24/RAC)-activated kinase 1 (PAK1), an enzyme with documented cardiac protective effects.[14]
Preliminary studies on 25C-NBOMe have shown that the substance is toxic to development, heart health, and brain health inzebrafish, rats, andArtemia 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.[32][33]As of October 31, 2016; 25C-NBOMe is a controlled substance (Schedule III) in Canada.[34]
The NBOMe series of psychoactives became controlled in Israel in May, 2013.[35][36]
25C-NBOMe was sold as adesigner drug in New Zealand in early 2012, but was withdrawn from sale after a statement by Associate Health Minister Peter Dunne that 25C-NBOMe would be considered to be substantially similar in chemical structure to the illegal hallucinogenDOB, and was therefore a Class C controlled drug analogue.[37]
Russia became the first country to regulate the NBOME class. The entire NBOMe series of psychoactives became controlled in the Russian Federation starting October, 2011.[35][38]
Sveriges riksdag added 25C-NBOMe to schedule I ("substances, plant materials and fungi which normally do not have medical use") as narcotics in Sweden as of Aug 1, 2013, published byMedical Products Agency in their regulationLVFS 2013:15 listed as25C-NBOMe 2-(4-kloro-2,5-dimetoxifenyl)-N-(2-metoxibensyl)etanamin.[39]
This substance is aClass A drug in the United Kingdom as a result of theN-benzylphenethylamine catch-all clause in theMisuse of Drugs Act 1971.[40]
Several NBOMe series compounds will be temporarily scheduled in the United States for 2 years. The temporary scheduling applies to 25C-NBOMe, 25B-NBOMe, and 25I-NBOMe.[41] In November 2015, the temporary scheduling was extended for another year.[42]
As of October 2015 25C-NBOMe is a controlled substance in China.[43]
25C-NBOMe is banned in the Czech Republic.[44]
Analogues and derivatives of2C-C:
25C-NB*:
Recently, a new class of psychedelic compounds named NBOMe (or 25X-NBOMe) has appeared on the illegal drug market. NBOMes are analogs of the 2C family of phenethylamine drugs, originally synthesized by Alexander Shulgin, that contain a N-(2-methoxy)benzyl substituent. The most frequently reported drugs from this group are 25I-NBOMe, 25B-NBOMe, and 25C-NBOMe. NBOMe compounds are ultrapotent and highly efficacious agonists of serotonin 5-HT2A and 5-HT2C receptors (Ki values in low nanomolar range) with more than 1000-fold selectivity for 5-HT2A compared with 5-HT1A. They display higher affinity for 5-HT2A receptors than their 2C counterparts and have markedly lower affinity, potency, and efficacy at the 5-HT2B receptor compared to 5-HT2A or 5-HT2C.
