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25B-NBOMe

25B-NBOMe, or 4-bromo-2,5-dimethoxy-N-(2-methoxybenzyl)phenethylamine, is a synthetic compound classified as a new psychoactive substance within the N-(2-methoxybenzyl) phenethylamine (NBOMe) series, structurally derived from the phenethylamine 2C-B by addition of an N-(2-methoxybenzyl) group that enhances its potency.^[1]^[2] It functions primarily as a highly selective and potent agonist at the serotonin 5-HT_2A receptor, mediating hallucinogenic effects at sub-milligram doses, with binding affinities in the picomolar to low nanomolar range.^[3] Despite its psychedelic properties, which include intense visual distortions, altered perception, and euphoria, 25B-NBOMe exhibits a narrow safety margin, frequently implicated in cases of acute toxicity characterized by agitation, tachycardia, seizures, vasoconstriction, and fatalities, often due to accidental overdose when misrepresented as LSD on blotter paper.^[5] First synthesized in academic research contexts around the early 2000s, it emerged recreationally circa 2012, prompting regulatory scheduling in multiple jurisdictions owing to its high abuse potential and public health risks.^[7] Preclinical studies reveal additional dopaminergic modulation contributing to reinforcing effects, alongside neurochemical disruptions in serotonin, dopamine, and glutamate systems that may underlie its hallucinogenic and toxic profile.^[1]

Chemistry

Molecular structure and properties

25B-NBOMe, chemically known as 2-(4-bromo-2,5-dimethoxyphenyl)-N-[(2-methoxyphenyl)methyl]ethanamine, features a core N-(2-methoxybenzyl)phenethylamine scaffold. This structure includes a phenethylamine backbone with methoxy substituents at the 2- and 5-positions and a bromine atom at the 4-position of the distal phenyl ring, distinguishing it within the NBOMe series.^[8]^[9] The molecular formula of 25B-NBOMe is C_{18}H_{22}BrNO_{3}, with a molar mass of 380.28 g/mol. Compared to its parent compound 2C-B (4-bromo-2,5-dimethoxyphenethylamine), which lacks the N-(2-methoxybenzyl) group, or mescaline (3,4,5-trimethoxyphenethylamine) with its different substitution pattern, the added N-substituent and halogenation define the NBOMe modifications that alter its chemical characteristics relative to unsubstituted phenethylamines.^[9] 25B-NBOMe is commonly utilized in its hydrochloride salt form to improve solubility in polar solvents and enhance chemical stability during storage and analysis. Analytical studies demonstrate stability in biological matrices such as dried blood spots when maintained at -20°C or 4°C for 180 days, with potential degradation observed at ambient temperatures over prolonged periods.^[10]

Synthesis and analogues

25B-NBOMe is synthesized through N-alkylation of the primary amine group in 2C-B (4-bromo-2,5-dimethoxyphenethylamine) with 2-methoxybenzyl chloride.^[9] This reductive amination or direct alkylation step typically employs a base such as triethylamine in solvents like ethanol or dimethylformamide, followed by acidification to form the hydrochloride salt.^[11] Overall yields for this and related NBOMe compounds range from 7% to 33%, depending on precursor purity and reaction conditions.^[12] The NBOMe series comprises structural analogues derived from various 2C-X phenethylamines, sharing the core N-(2-methoxybenzyl) substitution on the ethylamine nitrogen but differing at the 4-position of the phenyl ring.^[13] For instance, 25I-NBOMe features iodine, 25C-NBOMe chlorine, and 25B-NBOMe bromine at this position, with the halogen's size and electronegativity influencing receptor binding affinity and potency.^[9] These variants are produced via analogous alkylation of their respective 2C precursors, enabling rapid modification for research chemical applications.^[12] Clandestine synthesis of NBOMe compounds often yields impure products due to suboptimal reaction control and purification, with seized samples frequently containing unreacted phenethylamine precursors like 2C-B or related impurities from incomplete N-alkylation.^[13] Forensic analyses of blotter papers have detected varying concentrations of the target NBOMe alongside synthesis byproducts, compromising product purity and contributing to inconsistent dosing.^[14] Such challenges arise from the use of non-pharmaceutical grade reagents and lack of chromatographic purification in illicit settings.^[15]

Pharmacology

Pharmacodynamics

25B-NBOMe functions primarily as a potent agonist at serotonin 5-HT_2A receptors, exhibiting a binding affinity (K_i) of approximately 0.5 nM, which underlies its efficacy at microgram doses.^[8] It displays partial agonism at 5-HT_2C receptors with a K_i of about 6.2 nM, contributing to its overall serotonergic profile within the NBOMe series of phenethylamines.^[8] These affinities position 25B-NBOMe as more selective for 5-HT_2A over 5-HT_2C compared to endogenous serotonin, aligning with structure-activity relationships observed in NBOMe derivatives where N-2-methoxybenzyl substitution enhances receptor potency.^[16] Activation of 5-HT_2A receptors by 25B-NBOMe triggers G_q/11-protein coupling, stimulating phospholipase C to hydrolyze phosphatidylinositol 4,5-bisphosphate into inositol 1,4,5-trisphosphate and diacylglycerol.^[17] This cascade elevates intracellular calcium levels, activates protein kinase C, and promotes excitatory postsynaptic signaling in cortical pyramidal neurons, directly mediating the compound's hallucinogenic potency as evidenced by parallels with other 5-HT_2A agonists.^[1] The neural excitation arising from this pathway causally links receptor agonism to perceptual alterations, independent of pharmacokinetic factors. Beyond serotonergic sites, 25B-NBOMe interacts with adrenergic α₁ receptors (K_i < 300 nM across NBOMe analogs), potentially modulating sympathetic responses, though with lower affinity than at 5-HT_2A.^[16] It shows negligible direct binding to dopamine D_1-3 receptors, with any dopaminergic effects likely arising indirectly from enhanced neurotransmitter release rather than receptor agonism.^[16] These secondary interactions do not dominate the pharmacodynamic profile but may influence peripheral effects observed in vivo.^[1]

Pharmacokinetics and metabolism

25B-NBOMe is rapidly absorbed following sublingual or buccal administration, with its high lipophilicity enabling quick diffusion across mucous membranes and the blood-brain barrier.^[18] In positron emission tomography (PET) studies using tracer doses, the compound demonstrates fast plasma clearance, consistent with reported onset times of 15-120 minutes and peak effects within 1-2 hours for NBOMe derivatives in recreational contexts.^[19] Duration of effects typically spans 6-10 hours, reflecting efficient distribution to central nervous system sites followed by metabolic inactivation.^[18] The primary metabolic pathway involves hepatic O-demethylation at the 5' position of the N-2-methoxybenzyl moiety, producing hydroxylated phase I metabolites that undergo glucuronidation as phase II conjugates for elimination.^[18] This process occurs predominantly via cytochrome P450 enzymes, with CYP2D6 contributing approximately 69% to net hepatic clearance; additional isoforms including CYP1A2, CYP2B6, CYP2C19, and CYP3A4 participate to a lesser extent.^[20] In vitro studies using human and porcine liver microsomes confirm these routes, yielding metabolites such as demethylated products (m/z 366) and glucuronides (m/z 542).^[18] Polymorphisms in CYP2D6 can lead to interindividual variability in metabolism, with poor metabolizers exhibiting reduced clearance and potentially higher systemic exposure to the active parent compound.^[20] Elimination primarily involves renal excretion of glucuronidated metabolites, as evidenced by their accumulation in plasma and detection in urine following administration.^[18] The parent compound clears rapidly from plasma in tracer-dose PET imaging, though dose-dependent half-life estimates for recreational use remain approximately 1-2 hours based on effect profiles and analog data.^[19] Forensic analyses have identified 25B-NBOMe and metabolites in urine for up to several days post-exposure, influenced by factors such as dose and hydration status.^[13]

Effects and recreational use

Subjective psychological effects

25B-NBOMe induces subjective psychological effects primarily through its potent agonism at 5-HT_2A receptors, resulting in perceptual and cognitive alterations comparable to those of classic serotonergic hallucinogens such as LSD, though with elevated reports of dysphoric components.^[21] In a large international survey of NBOMe users (including those reporting 25B-NBOMe use), participants described effects peaking around two hours post-administration, encompassing visual and auditory distortions alongside altered thought patterns, but noted significantly higher "negative effects while high" relative to other psychedelics.^[21]^[22] Prominent perceptual changes include intense open- and closed-eye visual hallucinations, often featuring geometric fractals, enhanced colors, and environmental morphing, alongside synesthesia where sensory modalities blend, such as sounds manifesting as visual patterns.^[23]^[24] Altered time perception is frequently reported, with durations feeling profoundly extended, contributing to a sense of temporal distortion during the experience.^[24] Cognitive effects exhibit dose-dependent variability; lower doses (around 500 μg sublingual) may evoke LSD-like euphoria, introspection, and mild ego softening, while higher doses (exceeding 1000 μg) often precipitate delirium, profound ego dissolution, and overwhelming anxiety or paranoia, sometimes escalating to panic states or perceived loss of sanity.^[21]^[25] Mystical or transcendent experiences akin to those in psilocybin trials occur in some accounts but are commonly undermined by dysphoria, confusion, or intrusive negative ideation, differentiating 25B-NBOMe from more consistently insightful psychedelics.^[21]^[1] These patterns align with animal behavioral proxies like the head-twitch response, indicative of hallucinogenic activity across a broad dose range, though human reports underscore the compound's unpredictable psychological intensity.^[1]

Physiological effects

25B-NBOMe elicits sympathomimetic autonomic responses, manifesting as tachycardia with heart rates typically ranging from 100 to 175 beats per minute, hypertension with systolic blood pressures reaching up to 200 mmHg, and mydriasis featuring pupil dilation to 6-8 mm.^[26] These effects arise from 5-HT2A receptor agonism with downstream adrenergic activation, observable even at recreational doses.^[27] Additional physiological changes include mild hyperthermia, with core body temperatures elevated to as high as 38.5°C, accompanied by diaphoresis in multiple cases.^[26] Vasoconstriction, a hallmark of the NBOMe class, often results in cold extremities and is attributed to serotonergic vascular modulation.^[7] Nausea occurs commonly, linked to peripheral 5-HT receptor stimulation, while increased salivation or drooling has been noted in isolated instances.^[28]^[26]

Toxicity and health risks

Acute adverse effects

Acute adverse effects of 25B-NBOMe at typical recreational doses (500–1,000 μg sublingually) manifest primarily as sympathomimetic and serotonergic overstimulation, driven by its potent 5-HT_2A receptor agonism, which can overwhelm physiological homeostasis even without intentional overdose. Common presentations include tachycardia (observed in 85% of NBOMe intoxication cases, including 25B-NBOMe), hypertension (65%), and agitation (85%), often accompanied by mydriasis and diaphoresis.^[29] Seizures occur in approximately 40% of clinically reported NBOMe exposures, with mechanisms linked to excessive serotonergic excitation and potential GABAergic disruption.^[29] In a series of 10 analytically confirmed 25B-NBOMe cases, violent agitation and hallucinations predominated, alongside hyperthermia, rhabdomyolysis, and renal injury in severe instances, with 70% of patients requiring benzodiazepine sedation for behavioral control.^[23] Hyperthermia, reported in 25% of NBOMe cases, arises from disrupted thermoregulation via 5-HT_2A-mediated hypothalamic effects, compounded by physical agitation and environmental factors during use.^[29] These symptoms mimic aspects of serotonin syndrome—such as autonomic instability and neuromuscular excitation—but stem more directly from biased agonism at hallucinogenic receptors, distinguishing them from classic multisystem serotonin toxicity.^[29] Prevalence in clinical data likely overrepresents severe outcomes due to selection bias toward emergency presentations, whereas self-reported user experiences on platforms like Erowid describe frequent but milder issues like vasoconstriction-induced discomfort and acute anxiety in 20–30% of accounts, attributable to the drug's narrow therapeutic index and inconsistent dosing on blotter media often mistaken for LSD. Dose miscalculation risks are heightened by 25B-NBOMe's microgram-level potency and variable bioavailability, leading to unintended receptor overload in otherwise typical recreational scenarios.^[9]

Neurotoxic and cardiotoxic mechanisms

25B-NBOMe exerts neurotoxic effects primarily through oxidative stress and excitotoxic mechanisms mediated by its potent agonism at 5-HT_2A receptors. In vivo rodent studies demonstrate that acute administration of low doses (0.3 mg/kg intraperitoneally) induces significant DNA damage in the rat frontal cortex, a marker of oxidative stress resulting from reactive oxygen species (ROS) generation.^[30] In vitro assays further confirm elevated ROS levels, with 25B-NBOMe causing approximately a twofold increase in cellular oxidative burden, leading to genotoxic damage and compromised neuronal integrity.^[31] Concurrently, 25B-NBOMe elevates extracellular glutamate levels across multiple brain regions in rats, promoting excitotoxicity via overactivation of glutamatergic pathways downstream of 5-HT_2A stimulation.^[1] These pathways culminate in neuronal apoptosis, as evidenced by increased caspase-3 activation and apoptotic markers in human lymphoblastoid cell lines exposed to 25B-NBOMe concentrations mimicking recreational exposure.^[32] Rodent hippocampal slice cultures treated with related NBOMe analogs exhibit similar programmed cell death, underscoring a conserved mechanism of 5-HT_2A-driven neurotoxicity independent of acute hallucinogenic effects.^[33] Claims minimizing long-term neurotoxic potential are contradicted by these findings, particularly developmental toxicity data from zebrafish embryos, where NBOMe exposure disrupts morphogenesis and induces teratogenic abnormalities at sublethal concentrations, paralleling rat models of cortical damage.^[34]^[35] Cardiotoxicity arises from blockade of the hERG (K_v11.1) potassium channel, which prolongs cardiac action potential duration and predisposes to torsades de pointes arrhythmias. For 25B-NBOMe, the IC₅₀ for hERG inhibition is 2.4 μM, a potency level where recreational doses (typically 0.5–2 mg) can yield plasma concentrations sufficient to impair repolarization, especially under conditions of repeated dosing or metabolic variability.^[36] This mechanism aligns with observations in NBOMe class compounds, where hERG blockade correlates with QT interval prolongation in preclinical cardiac models, amplifying arrhythmia risk beyond acute sympathomimetic effects.^[7]

Long-term and chronic risks

Limited empirical data exist on the long-term risks of repeated 25B-NBOMe exposure, as its high acute toxicity discourages chronic use and few longitudinal studies have been conducted; most insights derive from case reports, animal models, and pharmacological analogies to other 5-HT_2A agonists.^[37] ^[30] Persistent psychotic symptoms have been documented following NBOMe series exposure, potentially linked to serotonin receptor dysregulation or neurotoxic excitotoxicity from prolonged 5-HT_2A overstimulation, though causality remains inferential absent controlled trials. A case report described chronic psychosis in a 30-year-old male emerging five months after a single 25I-NBOMe dose, manifesting as self-referential delusions and auditory hallucinations unresponsive to antipsychotics, highlighting risks of enduring hallucinogen-induced perceptual alterations akin to hallucinogen persisting perception disorder (HPPD).^[38] ^[39] Similar long-lasting visual disturbances suggestive of HPPD have been reported with 25I-NBOMe, implying comparable vulnerabilities for 25B-NBOMe due to shared pharmacodynamics.^[40] Chronic cardiovascular strain may accumulate from recurrent vasoconstriction, tachycardia, and hypertension observed in acute exposures, potentially exacerbating endothelial damage or arrhythmogenic substrates over time, though direct evidence from repeated dosing is absent. Rodent studies indicate repeated 25B-NBOMe administration (1 mg/kg for 7 days) elevates dopamine in nucleus accumbens tissue, which could indirectly contribute to sustained sympathomimetic stress on cardiac tissue.^[41] ^[29] While 25B-NBOMe exhibits low dependence potential typical of serotonergic hallucinogens, preclinical data reveal dopaminergic reinforcement mechanisms that confer some abuse liability, raising risks of escalating use patterns in vulnerable individuals despite absent withdrawal syndromes.^[8] ^[42] Chronic risks are further compounded by frequent adulteration in recreational batches, where impurities from synthesis or mislabeling as LSD could introduce cumulative toxicities unrelated to the parent compound.^[37]

Fatalities and epidemiological data

Fatalities directly attributed to 25B-NBOMe intoxication have been documented in forensic case reports, with at least two confirmed cases of pure or primary toxicity, including postmortem blood concentrations of 19.8 ng/mL in one instance. In a comprehensive literature review of 42 NBOMe intoxication cases (encompassing analogs like 25B-NBOMe), 9 resulted in death (21% fatality rate), with 6 attributed to direct NBOMe toxicity rather than complicating factors such as trauma or polydrug effects.^[22] For 25B-NBOMe specifically, 18 acute toxicity cases have been reported, including these fatalities, often involving young males (average age ~21 years) who mistook the substance for LSD, leading to inadvertent overdose.^[9] Epidemiological patterns indicate underreporting due to the drug's emergence as a novel psychoactive substance around 2012, but available toxicology data highlight a narrow safety margin: lethal blood concentrations range from 0.18 ng/mL in serum to 3.14–19.8 ng/mL in postmortem samples, far lower than recreational thresholds.^[29]^[43] Polydrug use (e.g., with ethanol or stimulants) complicates many cases, yet direct causation is evident in mono-intoxications via mechanisms like serotonin syndrome or cardiac arrest, as seen in a cluster of New Zealand exposures with no deaths but severe outcomes at similar doses.^[44] In contrast to LSD, which has no recorded pure-overdose fatalities owing to its high LD50 (>1000 times active dose), 25B-NBOMe's full agonism at 5-HT2A receptors induces toxicity at doses as low as 1–2 mg, amplifying risks when misrepresented as a safer hallucinogen.^[29]^[9] This underscores causal differences in potency and end-organ effects, with NBOMe series linked to dozens of global fatalities since 2010, though precise counts remain elusive absent centralized surveillance.^[22]

Overdose and clinical management

Symptoms of overdose

Overdose of 25B-NBOMe, a highly potent 5-HT_2A receptor agonist, elicits a rapid progression of symptoms that intensify beyond typical recreational effects, often due to its narrow safety margin where active doses range from 0.5-1 mg sublingually while toxicity emerges at 2 mg or higher. Initial manifestations mimic amplified psychedelic experiences with overwhelming visual and auditory hallucinations, but quickly evolve into severe psychological distress including intense confusion, panic, and agitated delirium, distinguishing overdose from dose-dependent tolerance via the compound's steep dose-response curve that lacks a plateau before critical thresholds.^[7]^[29] Physiological hallmarks include sympathomimetic toxidrome features such as tachycardia (heart rates >140 bpm in over 80% of cases), hypertension (systolic pressures frequently >160 mmHg, with severe instances exceeding 200 mmHg), and hyperthermia (core temperatures up to >40°C), accompanied by mydriasis, diaphoresis, nausea, vomiting, and clonus. Seizures occur in approximately 40% of intoxications, often generalized and refractory, while autonomic instability may precipitate rhabdomyolysis, acute kidney injury, and metabolic acidosis.^[29]^[44]^[22] In terminal progression, symptoms advance to coma, respiratory failure, bradycardia, and hypotension as compensatory mechanisms fail, with reported blood concentrations in fatalities ranging from 0.5-10 ng/mL postmortem, underscoring the risk of supratherapeutic exposure even from minor dosing errors. This toxidrome's severity correlates with plasma levels, where small increments above 1-2 mg trigger disproportionate adrenergic and serotonergic overload, absent in subthreshold use.^[7]^[29]

Emergency treatment protocols

Emergency treatment for 25B-NBOMe intoxication focuses on supportive measures, as no specific antidote exists. Initial management prioritizes airway protection, oxygenation, and hemodynamic stabilization, with intubation and mechanical ventilation indicated for severe respiratory depression or agitation unresponsive to sedation.^[45] ^[7] Benzodiazepines, such as lorazepam or midazolam, are the first-line agents for controlling seizures, severe agitation, and hallucinations, often requiring high doses due to the drug's potent serotonergic effects.^[44] ^[45] Aggressive intravenous fluid resuscitation addresses dehydration, tachycardia, and hypotension, while active cooling measures (e.g., ice packs, evaporative cooling) are essential for hyperthermia exceeding 40°C to prevent complications like rhabdomyolysis.^[44] ^[7] Continuous monitoring of creatine kinase levels, electrolytes, renal function, and electrocardiography is recommended to detect rhabdomyolysis, acidosis, or arrhythmias.^[7] Stimulants should be avoided to prevent exacerbation of sympathomimetic toxicity, and antipsychotics used cautiously owing to risks of QT prolongation and torsades de pointes associated with NBOMe compounds.^[22] ^[7] In reported case series of 25B-NBOMe overdoses, approximately 20-30% of patients required intensive care unit admission for advanced monitoring or ventilation, but mortality remains low with prompt intervention, with most patients recovering within 24-72 hours following supportive care.^[44] ^[22] Activated charcoal may be considered if ingestion occurred within 1-2 hours, though its efficacy is limited by the drug's rapid onset and low oral bioavailability.^[45] Consultation with a regional poison control center is advised for tailored guidance.^[45]

Drug interactions

Pharmacological interactions

25B-NBOMe, functioning primarily as a potent 5-HT_2A receptor agonist, carries a risk of potentiated serotonergic effects when combined with monoamine oxidase inhibitors (MAOIs) or selective serotonin reuptake inhibitors (SSRIs), potentially precipitating serotonin syndrome characterized by hyperthermia, tachycardia, hypertension, and seizures.^[37] This interaction arises from NBOMe-induced elevations in extracellular serotonin levels in brain regions such as the frontal cortex and nucleus accumbens, which compound the impaired serotonin metabolism or reuptake inhibition caused by these agents.^[46] A case report documented serotonin syndrome in a patient following 25B-NBOMe ingestion, with postmortem plasma levels of 3.15 ng/mL at admission, underscoring the compound's standalone serotonergic potency that could amplify with co-ingestants.^[37] The metabolism of 25B-NBOMe is predominantly mediated by cytochrome P450 2D6 (CYP2D6), accounting for approximately 69% of hepatic net clearance, with low K_m values indicating high substrate affinity.^[47] Consequently, CYP2D6 inhibitors such as quinidine, fluoxetine, or paroxetine may extend exposure duration, particularly in individuals with poor metabolizer phenotypes due to genetic polymorphisms, thereby heightening toxicity risks despite the involvement of multiple CYP isoforms mitigating overall interaction severity.^[47] Combinations with stimulants, including amphetamines or cocaine, may result in additive vasoconstriction and cardiovascular strain, as 25B-NBOMe exhibits affinity for α₁-adrenergic receptors contributing to hypertension and tachycardia, effects exacerbated by catecholamine release from stimulants.^[16] Polydrug use involving depressants like alcohol or opioids has been observed in toxicity reports, where unpredictable synergies may worsen agitation, seizures, or overall physiological burden, though mechanistic details specific to 25B-NBOMe remain limited to observational data from user patterns rather than controlled studies.^[37]

Contraindications with other substances

Combination with stimulants, such as MDMA, substantially elevates the risk of severe cardiovascular complications and potentially fatal outcomes due to additive effects on blood pressure and heart rate.^[48] This interaction has been highlighted in alerts for structurally similar NBOMe analogs, where synergistic toxicity amplifies vasoconstriction and tachycardia inherent to 25B-NBOMe.^[24] Alcohol co-ingestion poses a particular hazard by inducing disinhibition and impaired decision-making, which can result in dosing errors with 25B-NBOMe—a compound active at sub-milligram levels prone to overdose.^[24] Case reports of NBOMe intoxications frequently involve ethanol, contributing to escalated behavioral risks and delayed recognition of toxicity.^[29] Polysubstance use is prevalent in documented 25B-NBOMe fatalities and intoxications, with over two-thirds of analyzed cases featuring concurrent ingestion of cannabis, amphetamines, or other hallucinogens, complicating causal attribution but consistently worsening prognosis through intensified neuroexcitation and metabolic stress.^[43]^[23] Combining 25B-NBOMe with other serotonergic psychedelics may further heighten psychotic features, as evidenced by cluster reports of agitation and hallucinations in poly-intoxications.^[23] Caution is warranted with cardiac medications like beta-blockers, which may obscure tachycardic warning signs without alleviating 25B-NBOMe's vasoconstrictive effects, potentially leading to undetected hypertensive crises in vulnerable individuals.^[49] Empirical data from NBOMe case series underscore the need to avoid such pairings absent clinical oversight.^[50]

History

Discovery and early research

The development of 25B-NBOMe stemmed from research into selective serotonin 5-HT_2A receptor ligands within the phenethylamine class. In 1994, Richard A. Glennon and colleagues at Virginia Commonwealth University synthesized initial N-benzylphenethylamine derivatives, including analogs of 2C-B, demonstrating that benzyl substitution markedly increased binding affinity for the 5-HT_2A receptor compared to unsubstituted counterparts.^[9] Ralf Heim advanced this work during his 2003 doctoral thesis at the Free University of Berlin, synthesizing 25B-NBOMe by attaching an N-(2-methoxybenzyl) group to the 2C-B scaffold. This modification aimed to create potent, selective 5-HT_2A agonists for use as pharmacological tools in studying receptor function, with the ortho-methoxy substitution enhancing affinity and receptor specificity.^[9]^[7] Early pharmacological evaluations focused on in vitro radioligand binding assays, revealing 25B-NBOMe's high potency at the 5-HT_2A receptor (K_i = 0.8 nM) and greater selectivity over alpha-adrenergic receptors relative to parent 2C-series compounds, which exhibited more pronounced off-target interactions.^[9] Further structure-activity studies by David E. Nichols and coworkers in 2006 corroborated these findings, establishing the compound's profile as a full agonist suitable for probing 5-HT_2A-mediated effects in cellular models.^[9]

Rise in recreational markets (2010s onward)

25B-NBOMe, part of the NBOMe series, entered recreational markets around 2010 as a potent hallucinogen sold online and misrepresented as LSD on blotter paper, capitalizing on demand for cheap psychedelic alternatives.^[9] Early adoption accelerated in 2012, with users reporting sublingual or buccal administration for effects mimicking LSD but with higher potency, leading to its nickname "N-Bomb" alongside congeners like 25I-NBOMe.^[7] By 2013, widespread substitution for LSD in festival and party settings contributed to a surge in use, as evidenced by U.S. poison control reports of NBOMe exposures rising sharply that year.^[9] Popularity peaked between 2012 and 2015, driven by online vendors and darknet marketplaces offering it as "legal acid" or blotter tabs at doses far exceeding safe thresholds, often 500-1000 micrograms versus LSD's 100 micrograms.^[7] DEA data documented 924 law enforcement encounters with 25B-NBOMe specifically from January 2014 to April 2018, reflecting heightened trafficking during this period, while European agencies noted NBOMe detections in seizures comprising 0.03% of global hallucinogen confiscations from 2011-2017.^[3] Key incidents, such as cluster overdoses at Portugal's Boom Festival in 2014 where NBOMes were sold as LSD, amplified visibility and prompted harm reduction testing initiatives.^[51] Post-2015, recreational prevalence declined due to accumulating reports of severe toxicity and fatalities— including two confirmed 25B-NBOMe deaths in Indiana that year—coupled with U.S. emergency scheduling in November 2013 and international controls in 2015, eroding vendor supply and user trust.^[9] ^[52] Despite this, 25B-NBOMe persisted in niche dark web sales targeting experienced users aware of dosing risks, though overall market share waned as awareness of its narrow therapeutic window deterred casual adoption.^[7]

Controversies and public perceptions

Misidentification as LSD and overdose incidents

25B-NBOMe, like other compounds in the NBOMe series, has been commonly distributed on blotter paper mimicking LSD packaging, leading users to ingest it under the false assumption of equivalent dosing and safety profiles.^[29] Typical LSD blotters contain 50–150 μg of active material, whereas NBOMe blotters are frequently dosed at 500–1500 μg or higher, prompting naive users to consume multiple tabs when initial effects seem subdued, resulting in acute toxicity.^[29] This misidentification exploits perceptual similarities in hallucinogenic onset while disregarding NBOMe's narrower therapeutic window and higher vasoconstrictive risks.^[7] In a systematic review of 20 confirmed NBOMe intoxication cases from 2012–2014, 4 instances (20%) involved substances believed to be LSD, with toxicology screens via HPLC-MS/MS verifying NBOMe presence; two of these ended in fatalities, and one in a suicide attempt following ingestion of blotters labeled as "acid."^[29] For 25B-NBOMe specifically, two analytically confirmed intoxications were documented in this period, aligning with broader patterns of mislabeling.^[29] Prevalence data from U.S. surveys indicate NBOMe use among 2.6% of 22,289 past-year drug users, with 93.5% reporting first exposure in 2012 or later, coinciding with surges in blotter-based sales misrepresented as LSD.^[29] Notable clusters underscore dosing error harms: In Christchurch, New Zealand, 10 patients presented in two 2015 episodes (4 cases initially, followed by 6 over 12 hours), having ingested 25B-NBOMe sold as "synthetic LSD"; all exhibited agitation, tachycardia, and hallucinations, with 7 requiring benzodiazepine sedation but no fatalities in this series.^[44] Toxicology confirmed 25B-NBOMe via plasma levels of 0.7–10.1 ng/mL, highlighting batch-related mislabeling in party settings.^[44] Such incidents, verified through forensic analysis, demonstrate how assumed LSD equivalence amplifies overdose risks, with users often insufflating or swallowing tabs without appreciating the compound's potency.^[29]

Debates on inherent vs. adulterated toxicity

Debates persist regarding whether the toxicity of 25B-NBOMe primarily stems from the compound itself or from adulterants in illicit formulations. Empirical autopsy data indicate that fatalities have occurred with analytically confirmed presence of 25B-NBOMe as the primary or sole agent, at postmortem blood concentrations as low as 0.18 ng/mL in serum and up to 19.8 ng/mL in peripheral blood, levels consistent with pharmacological overdose rather than requiring contaminants for lethality.^[53]^[29] In documented cases, co-detection of adulterants or other substances appears in fewer than 20% of NBOMe-related fatalities, with most involving isolated 25B-NBOMe intoxication, undermining narratives attributing risks solely to impurities.^[54] Preclinical studies further support inherent toxicity, demonstrating acute adverse effects in rodents at doses reflecting a narrow therapeutic index; for instance, escalating administrations up to 10 mg/kg in rats elicited dose-dependent wet-dog shakes and behavioral disruptions indicative of serotonergic overstimulation, with lethality thresholds aligning closely to recreational human equivalents when scaled by potency.^[46] This margin is exacerbated by 25B-NBOMe's high-efficacy agonism at 5-HT2A receptors, where binding affinities in the low nanomolar range drive vasoconstriction, seizures, and cardiovascular collapse through direct receptor-mediated mechanisms, independent of synthesis quality or added substances.^[55] Harm reduction perspectives sometimes minimize risks by emphasizing adulterated batches as the main culprit, yet this overlooks causal pharmacology: the compound's ultrapotent partial agonism induces autonomic instability and neuroexcitation at microgram doses, as evidenced by consistent toxidromes in pure-analyte confirmed exposures.^[7] Such claims, often propagated in user forums without rigorous toxicology backing, fail to account for postmortem redistribution dynamics that still yield toxicologically significant levels from unadulterated intake.^[56] Prioritizing empirical blood analytics and receptor kinetics over anecdotal purity attributions better aligns with observed outcomes.

Legal status

International scheduling

In March 2015, the United Nations Commission on Narcotic Drugs added 25B-NBOMe to Schedule I of the 1971 Convention on Psychotropic Substances, classifying it alongside other substances with high potential for abuse, no recognized medical value, and unsafe use without supervision.^[57] This decision followed a 2014 review by the World Health Organization's Expert Committee on Drug Dependence, which cited the compound's structural relation to the Schedule II phenethylamine 2C-B, its potent agonism at serotonin 5-HT_2A receptors, and emerging reports of recreational misuse leading to acute toxicity and fatalities.^[58] Prior to formal scheduling, 25B-NBOMe was monitored as a new psychoactive substance under frameworks like the European Monitoring Centre for Drugs and Drug Addiction's Early Warning System, with NBOMe derivatives first notified in 2011 and risk assessments by 2013 highlighting their hallucinogenic effects akin to LSD but with greater overdose risks due to narrow therapeutic windows.^[59] International control efforts emphasized its analog status to scheduled hallucinogens under the 1971 Convention, enabling provisional restrictions in signatory states based on evidence of abuse patterns and public health harms rather than established therapeutic utility.^[60]

Country-specific regulations

In the United States, 25B-NBOMe was temporarily scheduled as a Schedule I controlled substance under the Controlled Substances Act by the Drug Enforcement Administration (DEA) on November 15, 2013, due to its high potential for abuse, lack of accepted medical use, and safety concerns; this emergency placement was made permanent on November 13, 2015.^[61]^[62] Enforcement efforts have included monitoring through the National Forensic Laboratory Information System (NFLIS), which identified 689 reports of NBOMe compounds, including 25B-NBOMe, from law enforcement submissions between June 2011 and March 2013.^[63] In the United Kingdom, 25B-NBOMe falls under Class A classification pursuant to the Misuse of Drugs Act 1971 via the N-benzylphenethylamine catch-all provision, following Advisory Council on the Misuse of Drugs (ACMD) recommendations for control as a hallucinogenic substance akin to LSD in November 2013 and a temporary ban announced in June 2013.^[64]^[65] Canada added 25B-NBOMe to Schedule III of the Controlled Drugs and Substances Act effective October 31, 2016, prohibiting its production, possession, trafficking, and importation.^[66] Russia banned 25B-NBOMe as a narcotic drug effective May 5, 2015, under federal legislation on controlled substances. In China, it was designated a controlled substance in October 2015. Seizures of 25B-NBOMe remain documented in controlled jurisdictions, such as trace amounts on blotters in European countries including Hungary in 2013, reflecting ongoing enforcement challenges despite scheduling.^[67] In regions lacking specific national bans, such as certain developing countries without analogous controls, the substance's availability persists through online vendors and unregulated markets, contributing to sporadic global distribution.^[68]

References

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Neurochemical and Behavioral Effects of a New Hallucinogenic ...
Dec 18, 2020 · Our findings indicate that 25B-NBOMe shows hallucinogenic activity in the wide range of doses. The changes in neurotransmitter levels may be ...
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https://www.caymanchem.com/product/12047
[3]
[PDF] 25I-NBOMe, 25C-NBOMe, and 25B-NBOMe
25I-NBOMe, 25C-NBOMe, and 25B-NBOMe target the same serotonin (5-HT) receptor subtype (5-HT2A) as many other hallucinogens, including schedule I hallucinogens ...
[4]
25B-NBOMe, a novel N-2-methoxybenzyl ... - PubMed
Nov 20, 2019 · 25B-NBOMe, a novel N-2-methoxybenzyl-phenethylamine (NBOMe) derivative, may induce rewarding and reinforcing effects via a dopaminergic ...
[5]
Case series: toxicity from 25B-NBOMe – a cluster of N-bomb cases
In our series, 25B-NBOMe intoxication caused hallucinations with violent agitation. Serotinergic/sympathetic signs were observed; mydriasis, tachycardia, ...
[6]
Neurochemical and Behavioral Effects of a New Hallucinogenic ...
Dec 18, 2020 · Our findings indicate that 25B-NBOMe shows hallucinogenic activity in the wide range of doses. The changes in neurotransmitter levels may be ...
[7]
NBOMes–Highly Potent and Toxic Alternatives of LSD - Frontiers
Feb 25, 2020 · 25B-NBOMe also fully substituted for MDMA. In both tests, the dose-effect curves for 25B-NBOMe had an inverted U-shape. It is suggested that 25B ...
[8]
25B‐NBOMe, a novel N‐2‐methoxybenzyl‐phenethylamine ...
Nov 20, 2019 · Repeated treatment of 25B-NBOMe increased the DRD1 and reduced the DRD2 protein levels in the NAcc. In addition, it also reduced the DAT and ...<|separator|>
[9]
Dark Classics in Chemical Neuroscience: NBOMes - PMC
CYP2D6 is the main contributor to the hepatic clearance of most NBOMes, as exemplified by 25B-NBOMe, where the 2D6 isoenzyme is responsible for 69% of the ...
[10]
The role of mitochondrial dysfunction and calcium dysregulation in ...
Apr 25, 2025 · ... (25B-NBOMe) [8,9]. 2C drugs are usually ... Both drugs were isolated as hydrochloride salts to improve their solubility and stability.
[11]
Quick Test for Determination of N-Bombs (Phenethylamine ...
Aug 29, 2019 · Scheme 1. Scheme 1. Synthesis of 25F-, 25C-, 25B-, and 25I-NBOMe·HCl Derivatives (2a–d) from Their Corresponding Phenethylamine ...<|separator|>
[12]
Synthesis of 25X-BOMes and 25X-NBOHs (X = H, I, Br) for ...
Mar 2, 2021 · Three NBOMes (25H-, 25I- and 25B-NBOMe) were synthesized with 7–33% overall yield. •. The X-ray structures of 25H-, 25I- and 25B-NBOH.HCl were ...
[13]
Analysis of 25I-NBOMe, 25B-NBOMe, 25C ... - PubMed Central
Sep 16, 2015 · 25I-NBOMe blotter papers usually contain higher doses of 500–800 µg, apparently due to low bioavailability of the drug. Psychoactive drugs of ...Missing: solubility | Show results with:solubility
[14]
Analysis of 25I-NBOMe, 25B-NBOMe, 25C-NBOMe and Other ...
Sep 16, 2015 · The 25H-NBOMe imine and 25I-NBOMe imine produced product ions similar to each other through the same fragmentation pattern (Figure 2). Each of ...
[15]
Scheme 1. Synthesis of 25F-, 25C-, 25B-, and 25I-NBOMe·HCl ...
25‐NBOMe compounds are just one of these new substance groups that pose a public health risk in many countries around the world.
[16]
Receptor interaction profiles of novel N-2-methoxybenzyl (NBOMe ...
The N-2-methoxybenzyl substitution of 2C drugs increased the binding affinity at serotonergic 5-HT2A, 5-HT2C, adrenergic α1, dopaminergic D1-3, and ...
[17]
Toxicodynamic insights of 2C and NBOMe drugs – Is there abuse ...
For instance, if the substituent is a bromine, the resulting compound is known as 25B-NBOMe (Fig. 1). NBOMe drugs are generally more potent in inducing ...
[18]
Metabolic Fate of Hallucinogenic NBOMes - ACS Publications
Dec 15, 2015 · We have identified the phase I and phase II metabolites of 25B-NBOMe in pigs as well as in humans. We find that the primary route of metabolism is 5′- ...<|separator|>
[19]
Human biodistribution and radiation dosimetry of the 5-HT 2A ...
Jul 31, 2019 · In its non-labeled form (25B-NBOMe), it is used as a recreational drug that can lead to severe adverse effects, in some cases, with fatal ...
[20]
Human cytochrome P450 kinetic studies on six N-2-methoxybenzyl ...
Mar 15, 2018 · The main contributors to hepatic net clearance were CYP2D6 for 25B-NBOMe ... Another aim was the determination of the Km and Vmax values for the ...
[21]
The NBOMe hallucinogenic drug series: Patterns of use ... - PubMed
The NBOMe compounds are a novel series of hallucinogenic drugs that are potent agonists of the 5-HT2A receptor, have a short history of human consumption ...Missing: pharmacology | Show results with:pharmacology<|separator|>
[22]
[PDF] NBOMe Toxicity and Fatalities: A Review of the Literature
Mar 3, 2022 · In 2014, Lawn et al. performed a large anonymous online survey of NBOMe users, recording a peak psychoactive effect of two hours after oral ...
[23]
Case series: toxicity from 25B-NBOMe--a cluster of N-bomb cases
Dec 1, 2015 · This report describes a series of 10 patients who suffered adverse effects from 25B-NBOMe. Hallucinations and violent agitation predominate along with ...Missing: dissolution | Show results with:dissolution
[24]
NBOMes - Alcohol and Drug Foundation
Jun 6, 2025 · NBOMes (N-methoxybenzyl) are a group of psychedelic drugs. which means they can affect all the senses, altering a person's thinking, sense of time and emotions.
[25]
NBOMes – hi-ground.org
NBOMes such as 25I-NBOMe produces visual effects like LSD, but unlike LSD, 25I has an unpredictable safety profile and seemingly random negative effects. Refer ...
[26]
https://doi.org/10.3109/15563650.2015.1115056
[27]
Neurotoxicological profile of the hallucinogenic compound 25I-NBOMe
The incubation of the rat primary cortical cultures with 25B-NBOMe (30 μM) decreased neuronal activity that did not recover after 19 h of washout period.Missing: solubility | Show results with:solubility
[28]
25C‐NBOMe: Preliminary Data on Pharmacology, Psychoactive ...
Jul 3, 2014 · Common negative physical side effects of 25C-NBOMe include vasoconstriction, nausea, vomiting, headache, irregular heartbeat, sweating, and ...Missing: physiological | Show results with:physiological<|separator|>
[29]
Toxicities associated with NBOMe ingestion, a novel class of potent ...
The most common adverse effects were agitation (85.0%), tachycardia (85.0%), and hypertension (65.0%). Seizures were reported in 8 (40.0%) patients. The most ...Missing: acute | Show results with:acute
[30]
Neurotoxicological profile of the hallucinogenic compound 25I-NBOMe
Feb 21, 2022 · 25I-NBOMe is a new psychoactive substance with strong hallucinogenic properties. Our previous data reported increased release of dopamine, serotonin, and ...
[31]
Mechanistic Insights into the Neurotoxicity of 2,5 ... - MDPI
However, when their levels are excessive, they can cause oxidative stress and damage the cells [28]. ... 25B-NBOMe (about a two-fold increase in ROS levels was ...
[32]
Novel Psychoactive Phenethylamines: Impact on Genetic Material
Dec 17, 2020 · The apoptosis fold increase on TK6 cells after 26 h of treatment with 2C-H, 2C-I, 2C-B, 25B-NBOMe, and MDMA at the indicated concentrations with ...<|separator|>
[33]
Neurotoxic effects of hallucinogenic drugs 25H-NBOMe ... - Cell Press
Jun 27, 2023 · 25H-NBOMe and 25H-NBOH disrupt the balance between neurogenesis and neuronal death in the hippocampus and, although chemically similar, have distinct ...
[34]
The new psychoactive substances 25H-NBOMe and 25H-NBOH ...
Nov 22, 2021 · 25H-NBOMe and 25H-NBOH recreational drugs induces abnormal formation in zebrafish embryos. Biophysical and theoretical studies indicate that these drugs have ...Missing: solubility | Show results with:solubility
[35]
Zebrafish and Artemia salina in vivo evaluation of the recreational ...
25C-NBOMe induces changes in behavioral patterns in Artemia salina and zebrafish animal models. 25C-NBOMe has teratogenic effects on zebrafish development.
[36]
[PDF] Anne Zwartsen - UU Research Portal - Universiteit Utrecht
hallucinogenic phenethylamines 2C-B (IC50 27 μM) and 25B-NBOMe (IC50 2.4 μM) and between the piperazine derivatives BZP (IC50 161 μM) and TFMPP (IC50 19 μM).
[37]
NBOMes–Highly Potent and Toxic Alternatives of LSD - PMC
Feb 26, 2020 · NBOMe compounds are ultrapotent and highly efficacious agonists of serotonin 5-HT 2A and 5-HT 2C receptors (Ki values in low nanomolar range)Missing: solubility | Show results with:solubility
[38]
Chronic psychosis associated with new hallucinogenic drug 25I ...
Jul 19, 2023 · We describe the case of a 30-year-old man who required psychiatric admission after a single NBOMe intake five months earlier. He began with self ...
[39]
Hallucinogenic Persisting Perception Disorder: A Case Series and ...
May 6, 2022 · We report the clinical characteristics and investigation findings of a series of HPPD cases with a literature review of previous case reports.
[40]
25I-NBOMe - ScienceDirect
The study showed long-lasting effects after 25I-NBOMe administration and allowed for the determination of HPPD risk factors.
[41]
Toxicodynamic insights of 2C and NBOMe drugs – Is there abuse ...
Jan 3, 2025 · Furthermore, dopamine levels were also increased in the NAc tissue of C57BL/6 J mice administered with 25B-NBOMe (1 mg/kg for 7 days). In this ...
[42]
Psychoactive substances 25H-NBOMe and 25H-NBOH induce ...
Sep 15, 2023 · Despite their mind-manifesting abilities, psychedelics are considered to be physiologically safe and are not known to lead to dependence or ...Psychoactive Substances... · 1. Introduction · 4. Discussion<|control11|><|separator|>
[43]
25b-NBOMe: A Case Report of Sudden Death and Insightful View of ...
The phenethylamine derivative 25b-NBOMe is a potent hallucinogen and a serotoninergic agonist. Other forms of NBOMe also exist, including 25c-NBOMe and the more ...
[44]
[PDF] Case series: toxicity from 25B-NBOMe – a cluster of N-bomb cases
Dec 1, 2015 · the base 2C-X molecule creates the NBOMe structure. The most common analogues are 25I-NBOMe 25C-NBOMe and 25B-. NBOMe which vary by one ...<|separator|>
[45]
NBOMe Drugs | California Poison Control System
Aug 12, 2015 · NBOMe drugs are N-methoxybenzyl-substituted phenethylamines, potent serotonin agonists, and are more potent than some conventional ...
[46]
Molecular and Medical Aspects of Psychedelics - PMC
Dec 23, 2023 · Furthermore, 25B-NBOMe reduced locomotor activity and induced anxiety in animals; these effects are also akin to those induced by 25I-NBOMe [46] ...
[47]
Human cytochrome P450 kinetic studies on six N-2-methoxybenzyl ...
Mar 15, 2018 · The main contributors to hepatic net clearance were CYP2D6 for 25B-NBOMe (69%), 25C-NBOMe (83%), 25I-NBOMe (61%), 3,4-DMA-NBOMe (89%) as well ...
[48]
25B-NBOH sold as powdered 'LSD' (July 2021) - Health.vic
Other effects may include nausea, headaches, difficulty with or frequent urination, muscle tension, cramps or involuntary movements, and a metallic/bitter taste ...Missing: physiological | Show results with:physiological<|separator|>
[49]
The psychoactive drug 25B-NBOMe recapitulates rhabdomyolysis in ...
Prominent rhabdomyolysis was also reported in two other cases with severe 25B-NBOMe intoxication [9]. Because the patho-physiological mechanism underlying ...Missing: report | Show results with:report
[50]
Evolution of the NBOMes: 25C- and 25B- Sold as 25I-NBOMe - PMC
Clinical effects included tachycardia, hypertension, agitation, hallucinations, seizures and status epilepticus, intraparenchymal hemorrhage, coma, and acute ...
[51]
The detection and prevention of unintentional consumption of DOx ...
Objective: This paper describes the misrepresentation of LSD at Portugal's Boom Festival 2014 and the prevention of unintentional consumption of DOx and 25x- ...
[52]
[PDF] Global Synthetic Drugs Assessment
In 2015, the EU Early Warning System recorded almost 80,000 seizure cases of NPS, a large increase from the almost 50,000 cases recorded in 2014. Synthetic ...
[53]
Fatal Intoxications with 25B-NBOMe and 25I ... - Oxford Academic
We report two unrelated deaths associated with 25B-NBOMe and 25I-NBOMe in the state of Indiana during 2014 and discuss the detection of these compounds in ...
[54]
Fatalities related to new psychoactive substances in Singapore—A ...
Another case was due to 25B-NBOMe toxicity (post-mortem blood concentration of 10 ng/ml) while the last two cases were deaths related to 5-Fluoro ADB, where ...
[55]
NBOMes-Highly Potent and Toxic Alternatives of LSD - PubMed
Feb 26, 2020 · NBOMe compounds are ultrapotent and highly efficacious agonists of serotonin 5-HT 2A and 5-HT 2C receptors (Ki values in low nanomolar range)
[56]
Experimental Study on the Postmortem Redistribution of the ...
Postmortem 25B‐NBOMe concentrations in the cardiac blood increased by more than 10‐fold at 6‐h postmortem ... toxicity ... Findings indicate that 25B-NBOMe induces ...
[57]
[PDF] Commission on Narcotic Drugs
Mar 17, 2015 · The. Commission decided to include 25B-NBOMe (2C-B-NBOMe), 25C-NBOMe (2C-C-. NBOMe) and 25I-NBOMe (2C-I-NBOMe) in Schedule I of the Convention ...
[58]
[PDF] WHO Expert Committee on Drug Dependence : thirty-sixth report
Jun 20, 2014 · Similarity to known substances and effects on the central nervous system. 25B-NBOMe is structurally related to the phenethylamine 2C-B (Schedule ...
[59]
[PDF] EMCDDA–Europol Joint Report on a new psychoactive substance
As of 12 December 2013, ten '-NBOMe' compounds have been notified to the EU early warning system and it is important to note that –NBOMe compounds can be ...Missing: peak 2012-2015
[60]
Substance Details 25B-NBOMe - unodc
25B-NBOMe ; C18H22BrNO · 380.2762 g/mol · 71/I · 2015 · This substance is included in Schedule I of the 1971 Convention on Psychotropic Substances.Missing: compounds | Show results with:compounds
[61]
Schedules of Controlled Substances: Temporary Placement of ...
Oct 10, 2013 · Synthetic Phenethylamines 25I-NBOMe and 25B-NBOMe were first described by legitimate research laboratories in 2003. Subsequent studies ...
[62]
Schedules of Controlled Substances: Placement of Three Synthetic ...
Nov 13, 2015 · Concerns over the abuse of 25I-NBOMe, 25C-NBOMe, or 25B-NBOMe have prompted state, military, and international control of these substances. 6.Missing: UN | Show results with:UN
[63]
[PDF] statement of - DEA.gov
Sep 25, 2013 · NFLIS has a total of 689 drug reports (June 2011 through March 2013) in which 25I-NBOMe, 25C-NBOMe or 25B-NBOMe were identified from a number of ...
[64]
ACMD recommends permanent ban on two “legal highs” - GOV.UK
Nov 28, 2013 · The Advisory Council on the Misuse of Drugs (ACMD) recommends NBOMe drugs, which have a hallucinogenic affect similar to LSD, are controlled as Class A drugs.
[65]
Government bans 'legal highs' NBOMe and Benzo Fury - BBC News
Jun 4, 2013 · The government has announced a year-long ban on two "legal highs" - known as NBOMe and Benzo Fury - while drugs experts assess their impact.<|separator|>
[66]
Controlled Drugs and Substances Act ( SC 1996, c. 19)
Federal laws of Canada. ... 4-bromo-2,5-dimethoxy-N-(2-methoxybenzyl)phenethylamine (25B-NBOMe). (2). 4 ...
[67]
25B-NBOMe - Wikipedia
25B-NBOMe, also known as NBOMe-2C-B and Cimbi-36, is a psychedelic drug of the 25-NB (NBOMe) family derived from 2C-B. It acts as a potent full agonist for the ...
[68]
[PDF] N-(2-methoxybenzyl)ethanamine (25I-NBOMe)
Molecular weight: 427.28 g/mol (base). Monoisotopic mass: 427.0644 Da. As of 7 ... A recently published report described the characteristics of users of 25B-NBOMe ...
[69]
[PDF] NBOMe Derivatives - Chromservis
The status of these new designer drugs is unregulated in many countries and there are numerous available ana- logues. This challenges both the legislators and ...