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25B-NBOMe
4-bromo-2,5-dimethoxy-N-(2-methoxybenzyl)phenethylamine
25B-NBOMe — N-Bomb, Smiles — is a synthetic psychedelic of the phenethylamine class. It is the N-benzylated derivative of 2C-B, active at roughly one-fiftieth its dose. It activates serotonin receptors in the brain, producing the visual distortions and cognitive shifts characteristic of classical psychedelics.[1]
25B-NBOMe — N-Bomb, Smiles — is a synthetic psychedelic of the phenethylamine class. It is the N-benzylated derivative of 2C-B, active at roughly one-fiftieth the dose of its parent compound. 25B-NBOMe is a full 5-HT₂A receptor agonist, producing its effects by directly activating the brain's primary serotonin-driven psychedelic pathway.[1]
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Ralf Heim first synthesized 25B-NBOMe in 2003 during doctoral research into potent serotonin-binding compounds.[2] It spread into recreational markets in the early 2010s, sold on blotter paper as LSD, and a wave of intoxications and deaths prompted emergency scheduling in the US in 2013. It is now internationally controlled, though it also serves as a licensed brain-imaging research agent called Cimbi-36.[3]
Subjective effects include geometric visual patterns, color enhancement, thought acceleration, emotional lability, and intense physical stimulation. The experience is more bodily aggressive than most classical psychedelics — potent psychedelic perceptual shifts collide with a heavy cardiovascular load that feels physically punishing. Severe nausea, vasoconstriction, muscle tension, and violent agitation are characteristic unsought effects.[4]
No physical dependence has been documented, but 25B-NBOMe carries critical acute toxicity — fatal blood concentrations overlap with non-fatal ones, leaving no safe threshold definable.[5][6][4] It also activates adrenergic receptors, constricting blood vessels and producing cardiac arrhythmia risk not seen with classical psychedelics.[1] The evidence base rests on emergency case reports and animal research; no controlled human studies exist.[7]
History[edit]
Discovery
Ralf Heim first synthesized 25B-NBOMe in 2003 at the Free University of Berlin, as part of doctoral research into N-benzylphenethylamine compounds with dramatically enhanced serotonin receptor binding.[2] Attaching an N-methoxybenzyl group to 2C-B transformed a moderately potent psychedelic into one active at sub-milligram doses. David Nichols's laboratory later explored these compounds as tools for mapping serotonin receptor binding.[8]
Research significance
Separately from recreational interest, the CIMBI group developed 25B-NBOMe as the first agonist PET radioligand capable of imaging active serotonin receptors in living human brains.[3] This gave the compound a rare dual existence: a controlled substance and a licensed scientific tool used in neuroscience research worldwide.
Prohibition and scheduling
25B-NBOMe appeared on recreational markets in the early 2010s alongside 25I-NBOMe and 25C-NBOMe, sold on blotter paper visually indistinguishable from LSD.[7][9] Reports of severe intoxications and deaths prompted the US DEA to emergency-schedule all three compounds in November 2013.[10] International control followed in 2015.[11]
The name NBOMe comes from the N-2-methoxybenzyl structural modification that defines the class. Street names include "N-Bomb" (a phonetic abbreviation), "Smiles," and "Solaris."[7] The research designation "Cimbi-36" comes from the Copenhagen group that developed it as a brain-imaging tool. Among NBOMe compounds, 25B-NBOMe is less discussed than 25I-NBOMe but carries the same reputation for unpredictable toxicity and dangerously narrow safety margins.
Chemistry[edit]
Structural class
25B-NBOMe belongs to the N-benzylphenethylamine series — the same chemical family as 25I-NBOMe and 25C-NBOMe.[1] It is derived from 2C-B by adding an N-(2-methoxybenzyl) group to its nitrogen atom; this single structural change dramatically amplifies serotonin receptor binding and drops the active dose to the sub-milligram range.[2]
Molecular properties
| Molecular formula | C₁₈H₂₂BrNO₃ |
| Molecular weight | 380.3 g/mol |
Pharmacology[edit]
Mechanism of action
25B-NBOMe is a full agonist at serotonin receptors — the same receptors activated by LSD, psilocin, and mescaline.[7][12] It binds with exceptional strength and activates them completely, placing it among the most potent synthetic serotonergic psychedelics known.[1]
Beyond serotonin, 25B-NBOMe activates adrenergic receptors — the receptors normally triggered by epinephrine.[1] This constricts blood vessels, raises blood pressure, and accelerates the heart rate, producing the heavy cardiovascular body load that distinguishes NBOMe intoxication from classical tryptamine psychedelics.
Pharmacokinetics
No human pharmacokinetic data exist at recreational doses.safety citation needed The only human data come from brain imaging studies using the compound at tracer doses, confirming it reaches serotonin receptor regions as expected.[3] The compound is taken sublingually or nasally; metabolism generates dozens of breakdown products, so forensic detection targets metabolites rather than the parent molecule.[13]
Neuroscience[edit]
Where it acts
25B-NBOMe activates serotonin receptors concentrated in the prefrontal cortex — the same population targeted by all classical psychedelics.[7][12] This disrupts the brain system responsible for habitual self-referential thinking, loosening perceptual boundaries and — at higher doses — eroding the sense of self. Brain imaging confirmed the expected distribution, with highest binding in frontal, temporal, and parietal regions.[3]
Why it matters
Current models of psychedelic action suggest that serotonin receptor activation reduces the brain's reliance on its existing models of reality, allowing raw sensory input to flow more freely. As an extremely potent activator, 25B-NBOMe produces particularly robust disruption — though no brain imaging during active intoxication has been done to confirm this.
The pronounced agitation documented in clinical cases may reflect simultaneous release of dopamine, acetylcholine, and glutamate alongside serotonin — a broader neurochemical disruption than most classical psychedelics produce.[14]
Whether 25B-NBOMe promotes structural brain plasticity — as documented for other serotonergic psychedelics — is unknown. A subtle DNA-damaging signal detected in rat studies[14] raises the possibility that any such effects could be accompanied by cellular harm. The dopamine reward signal observed in animal self-administration studies[15] — unusual for classical psychedelics — has not been investigated in humans.
Subjective Effects[edit]
The 25B-NBOMe experience is defined by two pharmacological forces acting together. Potent serotonin activation drives vivid perceptual distortions, accelerated thought, and emotional enhancement. Layered beneath is a heavy cardiovascular load — the body tightening, the heart racing — making the experience feel physically demanding in a way most psychedelics do not.
Compared to 2C-B — its parent compound — 25B-NBOMe lasts longer and carries a much heavier physical signature. Relative to LSD, the experience is more physically demanding, with stronger vasoconstriction and muscle tension defining the character of the come-up and plateau.
Synthesized by Ralf Heim in 2003 during doctoral research on phenethylamine pharmacology,[2] 25B-NBOMe was later developed as a PET brain-imaging radioligand under the designation Cimbi-36.[3] It appeared on recreational markets in the early 2010s, sold on blotter paper mimicking LSD, prompting US emergency scheduling in 2013. It is now Schedule I in the United States and internationally controlled under the UN 1971 Convention.
Subjective effects include geometric visual patterns, color enhancement, thought acceleration, and violent agitation. The experience is defined by a collision between intense psychedelic perceptual shifts and a heavy, physically punishing body load driven by pronounced cardiovascular stimulation — more bodily aggressive than most classical psychedelics. Severe nausea, vasoconstriction, muscle tension, and uncontrollable agitation are characteristic unsought effects.[4]
No physical dependence has been documented, but 25B-NBOMe carries critical acute toxicity — fatalities occur at blood levels overlapping with non-fatal concentrations, leaving no safe threshold definable.[5][6][4] α₁-Adrenergic activity produces vasoconstriction and cardiac arrhythmia risk absent from classical tryptamine psychedelics,[1] while dopaminergic reward signaling in animal models raises unresolved questions about dependence.[7] No controlled human studies exist; the evidence base rests on emergency case reports, preclinical pharmacology, and sub-pharmacological PET imaging.[8]
History[edit]
Discovery
Ralf Heim first synthesized 25B-NBOMe in 2003 at the Free University of Berlin, as part of doctoral research into N-benzylphenethylamine structure-activity relationships.[2] Heim demonstrated that attaching a 2-methoxybenzyl group to the nitrogen of 2C-B — a phenethylamine psychedelic previously synthesized by Alexander Shulgin — dramatically increased serotonin receptor binding. David Nichols's laboratory at Purdue University subsequently explored these compounds as tools for mapping receptor binding conformations.[9]
Research significance
Independently of recreational interest, the Copenhagen Image and Molecular Pharmacology (CIMBI) group developed 25B-NBOMe as [¹¹C]Cimbi-36 — the first agonist PET radioligand validated for imaging serotonin 5-HT₂A receptors in living humans.[3] This gave the compound a dual identity rare among psychoactive drugs: controlled substance and licensed research tool. PET studies using Cimbi-36 have since contributed to understanding serotonin receptor distribution across healthy and clinical populations.
Prohibition and scheduling
25B-NBOMe appeared on recreational markets in the early 2010s alongside 25I-NBOMe and 25C-NBOMe, sold on blotter paper often indistinguishable from LSD.[8][10] Reports of severe intoxications and deaths prompted the US DEA to emergency-schedule all three compounds in November 2013.[11] The WHO Expert Committee on Drug Dependence recommended international control in 2014,[12] and 25B-NBOMe was placed in Schedule I of the UN 1971 Convention effective March 2015.
The name NBOMe derives from the N-2-methoxybenzyl structural modification that defines the class. Street names include "N-Bomb" (a phonetic abbreviation), "Smiles" (origin unclear), and "Solaris".[8] The designation "Cimbi-36" comes from the Copenhagen Image and Molecular Pharmacology group that developed it as a brain-imaging tool. Among NBOMe compounds, 25B-NBOMe is less widely discussed than 25I-NBOMe but carries the same reputation for unpredictable toxicity and dangerously narrow safety margins.
Chemistry[edit]
Structural class
25B-NBOMe belongs to the N-benzylphenethylamine series, formed by attaching an N-(2-methoxybenzyl) group to the parent compound 2C-B (2,5-dimethoxy-4-bromophenethylamine). This single structural modification transforms a moderately potent psychedelic into one active at sub-milligram doses — the N-benzyl addition dramatically increases serotonin receptor binding.[1]
The molecule features a 2,5-dimethoxyphenyl ring with a bromine atom at the 4-position, connected through an ethylamine chain to an N-(2-methoxyphenyl)methyl group. Three methoxy groups are present: two on the phenethylamine ring and one on the N-benzyl moiety. The 2-methoxy position on the benzyl group is the critical feature responsible for the potency enhancement — the central finding of Heim's original research.[2]
Molecular properties
| Molecular formula | C₁₈H₂₂BrNO₃ |
| Molecular weight | 380.3 g/mol |
Related compounds
Within the NBOMe series, variation occurs at the 4-position of the phenethylamine ring: 25I-NBOMe carries iodine, 25C-NBOMe carries chlorine, and 25B-NBOMe carries bromine. These halogen substitutions alter receptor affinity and selectivity while preserving the core pharmacophore. Conformationally constrained analogues have been synthesized for research purposes, with some showing enhanced receptor selectivity,[9] but these are distinct laboratory compounds not encountered in recreational contexts.
Stereochemistry
25B-NBOMe does not contain a chirality center in its standard form. The secondary amine nitrogen is not a stereocenter, meaning the compound exists as a single achiral species under normal conditions.
Physical properties
No published characterization of melting point, solubility, or stability exists in peer-reviewed literature. NBOMe compounds degrade in biological samples, potentially causing underestimation of true concentrations in stored specimens.[8] The compound has been distributed on blotter paper and as tablets,[13] indicating sufficient stability for handling under normal conditions.
Pharmacology[edit]
Mechanism of action
25B-NBOMe acts as a full agonist at the 5-HT₂A serotonin receptor — the same molecular target engaged by LSD, psilocin, and mescaline.[8][14] It binds this receptor with exceptionally high affinity and activates it with strong efficacy, placing it among the most potent synthetic serotonergic psychedelics known.[1]
The hallucinogenic mechanism is confirmed by rodent studies: the head twitch response — a validated behavioral marker of psychedelic activity — is fully blocked by the selective 5-HT₂A antagonist ketanserin.[7] In rats, the compound simultaneously increased levels of dopamine, serotonin, acetylcholine, and glutamate across the frontal cortex, striatum, and nucleus accumbens,[15] a broader neurochemical release profile than most classical psychedelics.
Beyond perception, 25B-NBOMe binds α₁-adrenergic receptors, producing vasoconstriction, elevated blood pressure, and rapid heart rate.[1] This adrenergic component drives the pronounced cardiovascular body load that distinguishes NBOMe intoxication from classical tryptamine psychedelics. The binding profile predicts "strong hallucinogenic effects, similar to LSD, but possibly more stimulant properties because of α₁ receptor interactions".[1]
The compound also demonstrates rewarding properties in animal models through a dopaminergic mechanism. Rodents showed conditioned place preference and self-administration behavior that was blocked by dopamine antagonists but not by ketanserin[7] — indicating that any reinforcement operate through dopamine pathways rather than the serotonin system responsible for psychedelic perception.
Pharmacokinetics
No human pharmacokinetic data exist for 25B-NBOMe at recreational doses.safety citation needed Bioavailability, peak blood levels, half-life, and distribution volume are entirely uncharacterized. The only human data come from PET imaging studies using [¹¹C]Cimbi-36 at sub-pharmacological tracer doses, which confirmed high brain uptake matching known serotonin receptor distribution.[3]
Known active routes are sublingual/buccal and insufflated. Oral bioavailability has not been published, though extensive first-pass liver metabolism makes poor oral absorption structurally plausible. Active routes bypass this first-pass metabolism, which is why sublingual and nasal administration are effective at sub-milligram doses.
Metabolism studies identified 66 metabolites in rat and human urine, with the parent compound largely undetectable — metabolites serve as the primary targets for forensic detection.[16] The compound is processed through multiple liver enzyme pathways, meaning other drugs that compete for these pathways could theoretically alter blood levels and toxicity risk.
Neuroscience[edit]
Where it acts
As a potent serotonin 2A receptor agonist, 25B-NBOMe activates serotonin receptors concentrated on layer V pyramidal neurons in the prefrontal cortex — the same population targeted by all classical psychedelics.[8][14] This activation enhances glutamate release and disrupts the coherence of the default mode network, the brain system underlying habitual self-referential thought. The subjective correlate is ego dissolution and the loosening of perceptual boundaries.
PET imaging with [¹¹C]Cimbi-36 confirmed the expected cortical binding distribution in healthy volunteers, with highest uptake in frontal, temporal, and parietal cortex.[3]
Why it matters
The REBUS (Relaxed Beliefs Under Psychedelics) model offers the most relevant interpretive framework: 5-HT₂A agonism reduces the brain's reliance on existing models of reality, allowing raw sensory input to flow more freely and producing the characteristic loosening of perceptual and cognitive constraints. As an extremely potent agonist at this receptor, 25B-NBOMe would be predicted to produce particularly robust disruption — though no direct neuroimaging during intoxication exists to test this.
The broader multi-transmitter release profile — dopamine, serotonin, acetylcholine, and glutamate simultaneously[15] — may explain the more prominent agitation and stimulant character reported in clinical presentations compared to simpler serotonergic psychedelics.
Several fundamental questions remain unanswered. Whether 25B-NBOMe promotes structural neuroplasticity (as documented for other 5-HT₂A agonists) is unknown, and a subtle genotoxic signal in rat studies[15] raises the possibility that any such effects could be accompanied by DNA damage. The dopaminergic reward signal demonstrated in rodent self-administration[7] — atypical for classical psychedelics — has not been investigated in humans.
Subjective Effects[edit]
The 25B-NBOMe experience is shaped by two pharmacological forces pulling in tandem: potent serotonin receptor activation driving classical psychedelic perceptual and cognitive shifts, and adrenergic stimulation layering a pronounced cardiovascular body load over the entire experience. The result feels more physically aggressive and bodily demanding than most serotonergic psychedelics. At lower doses, perceptual shifts and mood changes predominate; at higher doses, the stimulant and vasoconstrictive effects intensify alongside the psychedelic ones, narrowing the space between desired experience and medical emergency. All human experiential data come from uncontrolled settings — set and setting remain unstudied for this compound.
Compared to its parent compound 2C-B, 25B-NBOMe is active at roughly one-fiftieth the dose, with longer duration and a heavier cardiovascular signature. Relative to LSD, the experience carries more prominent vasoconstriction and physical tension, with a narrower margin between desired effects and serious adverse events.
Effect Grid
At common doses, the full psychedelic experience manifests: pronounced open- and closed-eye visuals including geometric patterning, color shifting, object morphing and drifting, and enhanced pattern recognition. Time distortion becomes significant — minutes may feel like hours. Thought acceleration and increased conceptual connectivity produce novel associations. Emotional responses intensify substantially; empathy and introspection may alternate with anxiety or paranoia depending on set and setting.
The sympathomimetic component becomes prominent: tachycardia, hypertension, mydriasis, increased body temperature, and peripheral vasoconstriction (cold extremities). Jaw clenching, muscle tension, and restlessness are common. Nausea may occur, particularly during the come-up.
Sleep is impossible for 8–10 hours. The experience demands a full day's commitment and a controlled environment.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Symmetrical texture repetition · Environmental patterning · Visual breathing · Tracers · Music enhancement · After-images · Brightness alteration · Depth perception distortion · Perspective distortion · Visual morphing · Holotropic state · Auditory distortion · Auditory enhancement · Light sensitivity · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Visual melting · Visual acuity enhancement · Auditory misinterpretation · Proprioceptive distortion · Synesthesia · Touch enhancement · Visual diffraction · Visual haze / noise · Visual processing acceleration · Peripheral misidentification · Vestibular distortion · Touch suppression · Visual magnification · Flashbacks · Object transformations · Internal hallucinations · Visual recursion · Visual scenery slicing · Environmental orbism / cubism · External hallucinations · Object activation · Auditory hallucinations · Perspective hallucinations · Visual flipping · Persisting hallucinations
Music enhancement · After-images · Brightness alteration · Depth perception distortion · Perspective distortion · Visual morphing · Holotropic state · Auditory distortion · Auditory enhancement · Light sensitivity · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Visual melting · Visual acuity enhancement · Auditory misinterpretation · Proprioceptive distortion · Synesthesia · Touch enhancement · Visual diffraction · Visual haze / noise · Visual processing acceleration · Peripheral misidentification · Vestibular distortion · Touch suppression · Visual magnification · Flashbacks · Object transformations · Internal hallucinations · Visual recursion · Visual scenery slicing · Environmental orbism / cubism · External hallucinations · Object activation · Auditory hallucinations · Perspective hallucinations · Visual flipping · Persisting hallucinations
Wakefulness · Spontaneous body sensations · Body high · Insomnia · Muscle tension · Restlessness · Tingling / electric sensations · Bodily lightness · Nausea · Appetite suppression · Dry mouth · Excessive sweating · Heart rate perception changes · Vibrations / buzzing · Bodily pressures · Body schema distortion · Dehydration sensation · Dizziness · Headache · Laughter fits · Motor control impairment · Seizure threshold reduction · Tactile euphoria · Temperature dysregulation · Sexual arousal enhancement · Breathing alteration · Bruxism · Involuntary body movements · Trembling · Vomiting · Nystagmus (eye wobbles) · Bodily dissociation · Tactile hallucination
Insomnia · Muscle tension · Restlessness · Tingling / electric sensations · Bodily lightness · Nausea · Appetite suppression · Dry mouth · Excessive sweating · Heart rate perception changes · Vibrations / buzzing · Bodily pressures · Body schema distortion · Dehydration sensation · Dizziness · Headache · Laughter fits · Seizure threshold reduction · Tactile euphoria · Temperature dysregulation · Sexual arousal enhancement · Breathing alteration · Bruxism · Involuntary body movements · Trembling · Vomiting · Nystagmus (eye wobbles) · Bodily dissociation · Tactile hallucination
Conceptual thinking · Thought connectivity · Immersion enhancement · Aesthetic enhancement · Cognitive euphoria · Cognitive flexibility · Cognitive impairment · Increased nature relatedness · Introspection enhancement · Multiple thought streams · Openness enhancement · Memory suppression · Analysis enhancement · Cognitive dysphoria · Cognitive fatigue · Confusion · Creativity enhancement · Memory fragmentation · Synchronicity · Thought disorganization · Thought loops · Humor enhancement · Information processing enhancement · Information processing suppression · Language suppression · Focus enhancement · Motivation enhancement · Amnesia · Delirium · Delusions
Aesthetic enhancement · Cognitive euphoria · Cognitive flexibility · Cognitive impairment · Increased nature relatedness · Introspection enhancement · Multiple thought streams · Openness enhancement · Memory suppression · Analysis enhancement · Cognitive dysphoria · Cognitive fatigue · Confusion · Creativity enhancement · Memory fragmentation · Synchronicity · Thought disorganization · Thought loops · Humor enhancement · Information processing enhancement · Information processing suppression · Language suppression · Focus enhancement · Motivation enhancement · Delirium · Delusions
Anxiety · Simultaneous emotions · Empathy enhancement · Dysphoria · Irritability · Catharsis
Irritability · Catharsis
Social connection · Sociability enhancement · Communication suppression · Trust enhancement · Communication enhancement · Flow state · Sociability suppression · Social disconnection · Boundary dissolution · Ego dissolution · Cognitive disconnection · Identity alteration · Telepathic feelings
Communication enhancement · Flow state · Sociability suppression · Social disconnection · Boundary dissolution · Ego dissolution · Cognitive disconnection · Identity alteration · Telepathic feelings
Time cessation
Death-rebirth sequence · Entity contact · Non-dual awareness · Voidness
Timeline
Onset is rapid via insufflation — first effects within 1–10 minutes. Intense nasal burning is typical. The speed of onset contributes to unpredictable dose absorption and overdose risk.
Effects escalate rapidly over 10–30 minutes. The compressed come-up can produce overwhelming anxiety as intensity builds faster than via sublingual administration. Sympathomimetic activation (tachycardia, hypertension) emerges quickly.
Peak intensity for 1. 5–3 hours. Full psychedelic and sympathomimetic effects manifest.
Gradual decline over 1–2 hours. Visual and cognitive effects lessen while cardiovascular stimulation persists.
Effects resolve over 30–90 minutes. Residual stimulation and mild perceptual changes linger.
Residual effects persist 2–8 hours. Cognitive fatigue and mood instability may be present.
⚠ Do not drive or operate machinery for at least 24 hours after insufflated use, as the rapid onset creates risk of residual impairment that may not be subjectively recognized.
Safety[edit]
- Acute toxicity
- Critical
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
Acute toxicity
25B-NBOMe carries critical acute toxicity risk. Blood concentrations that caused death in some users fall within the range found in survivors[5][6][4] — meaning blood levels alone cannot predict who survives. No safe dose threshold can be defined.safety citation needed
In the largest published case series, all ten patients showed hallucinations and violent agitation, with dilated pupils, rapid heart rate, elevated blood pressure, and elevated body temperature. Seven required sedation with benzodiazepines.[4]
Heart and circulation
25B-NBOMe constricts blood vessels and elevates blood pressure through adrenergic receptor activation.[1] Fatal cardiac rhythm disturbance has been documented as a direct cause of death[6] — a risk not present with classical serotonergic psychedelics, which lack significant adrenergic activity.
Organ damage
Severe intoxications have produced muscle breakdown, acute kidney injury, dangerous blood clotting failure, and multi-organ failure.[7][4] Muscle breakdown is a relatively common complication, driven by seizures, elevated body temperature, and blood vessel constriction acting together.[7]
Genotoxicity
A subtle DNA-damaging effect was detected in rat studies — less pronounced than MDMA but present.[14] No human data exist.
Detection
Standard drug screening panels do not detect 25B-NBOMe; specialized mass spectrometry testing is required.[16][5] Someone presenting to emergency services may test negative on routine panels despite active intoxication. The compound also degrades in stored biological samples, causing reported blood levels to underestimate actual concentrations.[7]
Psychological risks
Emergency case reports consistently document confusion, disorientation, anxiety, panic, and violent agitation.[4] Violent agitation appeared in every patient in the largest case series — more frequent than typical reports for classical psychedelics, possibly reflecting additional adrenergic and multi-transmitter activity.[4][14]
No data on persisting perceptual disturbances, psychosis, or long-term psychological effects specific to 25B-NBOMe have been published. Given its serotonin receptor activity, standard psychedelic psychological risks — acute distress and potential worsening of latent psychotic conditions — are presumed to apply.inferred
Tolerance and dependence
Tolerance builds rapidly as serotonin receptors downregulate — the same mechanism common to all serotonergic psychedelics.[7] Near-complete tolerance develops within 24 hours, with partial recovery over roughly a week and full reset at approximately two weeks.inferred Complete cross-tolerance exists with LSD, psilocybin, mescaline, and DMT.[7]
No human dependence studies exist.[11] In animal models, 25B-NBOMe produced reward and reinforcing behavior through dopamine pathways — blocked by dopamine antagonists but not by serotonin blockers.[15] This dopaminergic reward signal is atypical for classical psychedelics and leaves open whether 25B-NBOMe carries greater dependence risk than its class membership would suggest.
Drug Interactions
No published interaction studies exist. The following are derived from pharmacological reasoning.
Serotonergic drugs: Combining 25B-NBOMe with MDMA, SSRIs, SNRIs, or MAOIs increases total serotonin load. 25B-NBOMe intoxication already produces agitation, elevated body temperature, and rapid heart rate[7] — effects that overlap with serotonin syndrome, a potentially life-threatening overheating and seizure response. MAOIs carry the highest risk among these combinations.safety citation needed
Stimulants: cocaine and amphetamines constrict blood vessels and stress the heart through catecholamine activation. Combined with 25B-NBOMe’s own vasoconstriction,[1] the risk of dangerously high blood pressure, cardiac rhythm disturbance, and stroke is elevated.safety citation needed
Tramadol: tramadol raises serotonin (adding to serotonin syndrome risk) and lowers the seizure threshold — especially dangerous given that seizures are a documented complication of NBOMe poisoning.[7]safety citation needed
Enzyme inhibitors: 25B-NBOMe is metabolized through multiple liver enzyme pathways.[13] Drugs that strongly inhibit these enzymes could increase blood concentrations and amplify toxicity risk, though no clinical data exist.
Contraindications
10 knownNo substance-specific contraindication data have been published. The following are derived from the pharmacological profile and documented toxicity.
Heart conditions: Documented cardiac fatalities[6] and adrenergic vasoconstriction constitute absolute contraindications for individuals with pre-existing heart rhythm disorders, coronary artery disease, or uncontrolled high blood pressure.
Psychiatric conditions: Contraindicated in individuals with psychotic disorders or a strong family history of psychosis. Bipolar disorder is a relative contraindication. The documented predominance of violent agitation[4] suggests heightened risk in individuals with impulse control disorders.
Seizure disorders: Seizures are documented in NBOMe poisoning.[7] Epilepsy is an absolute contraindication.
Kidney or liver impairment: Extensive liver metabolism[13] and documented acute kidney injury[4] make pre-existing impairment of either organ a relative contraindication.
Pregnancy: Contraindicated. The genotoxic signal in animal studies[14] and potent serotonin receptor activity raise concerns for fetal development.
Harm Reduction[edit]
Forms & Identification
25B-NBOMe is most commonly found on blotter paper, where it is visually indistinguishable from LSD — and frequently sold as LSD.[7] It has also been found in tablet and powder form.[16]
A widely circulated heuristic — "if it's bitter, it's a spitter" — reflects the fact that NBOMe compounds typically produce a bitter, numbing sensation when held in the mouth, while LSD is tasteless. This is not a reliable analytical test, but it provides a useful first signal.
Reagent testing and analytical drug checking services provide more dependable identification. Standard hospital drug screens do not detect NBOMe compounds[16] — someone presenting to emergency services may test negative on routine panels despite active intoxication.
Guidelines
- Test every dose. Reagent testing helps distinguish NBOMe compounds from LSD. Analytical drug checking services provide definitive identification where available.
- Start low. The margin between desired effects and medical emergency is narrower than for most psychedelics. Do not redose before effects are fully established.
- Sublingual over insufflation. Nasal administration produces faster, less controllable onset with greater overdose risk.
- Avoid physical exertion and heat. The cardiovascular load from adrenergic activity is compounded by exercise and high ambient temperature.
- Have a sober sitter present. Violent agitation is common even in otherwise healthy users. A trusted person who can provide reassurance — and call for help if needed — is essential.
- Stay hydrated but do not overhydrate — moderate, steady fluid intake.
Set & Setting
The heavy physical body load and documented frequency of violent agitation[4] make environment especially important. A calm, familiar space with a sober sitter is essential. The extended duration means the environment must remain safe and comfortable for many hours.
Cardiovascular stress makes physical exertion and hot environments genuine medical risks. Rest, shade, and minimizing physical demands are practical measures during the experience.
Aftercare & integration. The cardiovascular demands of 25B-NBOMe can leave the body depleted. Rest, adequate hydration, and nutritious food in the 24–48 hours following use support physical recovery. Muscle soreness may indicate low-grade muscle stress even in cases that did not require medical attention.
If the experience involved agitation, fear, or loss of control, processing may help. Journaling, talking with a trusted person, or consulting a therapist experienced with psychedelic-related distress can aid recovery. If anxiety, perceptual disturbances, or mood instability persist beyond a few days, professional evaluation is advisable.
Recovery & Support
Classical serotonergic psychedelics are generally non-habit-forming, but 25B-NBOMe’s dopamine reward component[15] introduces uncertainty about compulsive use patterns. Anyone finding it difficult to stop or reduce use should seek professional support.
Harm reduction organizations, psychedelic peer support services, and substance use counselors familiar with novel psychoactive substances can provide appropriate guidance. Crisis lines and online peer communities offer anonymous, judgment-free support.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Chest pain, irregular heartbeat, or extremely rapid pulse
- Seizure or uncontrollable muscle rigidity
- Body temperature that feels dangerously hot to touch
- Complete loss of contact with reality or self-harm behavior
- Blue or grey skin coloring
- Loss of consciousness
Immediate steps:
- 1. Call emergency services immediately if any of the above signs appear. Do not wait.
- 2. Keep the person in a cool, quiet environment.
- 3. If unconscious and breathing, place in the recovery position.
- 4. Do not restrain unless there is immediate danger of self-harm — restraint can worsen muscle breakdown and overheating.
- 5. Do not induce vomiting.
- 6. Remove excess clothing to help manage body temperature.
What to tell the dispatcher:
State the substance (25B-NBOMe or "NBOMe"), estimated amount and time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
No reversal agent exists for NBOMe intoxication. Hospital treatment is supportive — benzodiazepines for agitation and seizures, active cooling for elevated body temperature, intravenous fluids for kidney protection.
Legal Status[edit]
25B-NBOMe is internationally controlled under Schedule I of the United Nations Convention on Psychotropic Substances (1971), following a WHO Expert Committee recommendation in 2014.[11] Its dual existence as a controlled substance and an approved PET research agent creates a distinctive regulatory situation in which research use continues under appropriate licensing.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Emergency scheduled November 15, 2013 alongside 25I-NBOMe and 25C-NBOMe;[10] permanent placement November 2015[17] |
| International | Schedule I, UN 1971 Convention | Effective March 2015 following WHO ECDD recommendation[11] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled via N-benzylphenethylamine catch-all provisioncitation needed |
| Australia | Schedule 1 (Criminal Code) | Controlled Drugs Legislation Amendment Regulation 2014[11] |
| New Zealand | Class B controlled drug | Scheduled December 2016citation needed |
| Canada | Status unconfirmed | Not verified via published sourcecitation needed |
| European Union | EMCDDA Early Warning System | Individual member state scheduling varies following international control |
Analogue act considerations
In the United States, 25B-NBOMe is explicitly scheduled and no longer relies on structural analog provisions. In jurisdictions where it is not specifically named, structural similarity to scheduled phenethylamines may subject it to analogue laws if intended for human consumption.
Legal status changes frequently and varies by jurisdiction. This information reflects publicly available records and is not legal advice. Verify current local regulations before drawing any conclusions.
Safety[edit]
- Acute toxicity
- Critical
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Low
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
Acute toxicity
25B-NBOMe carries critical acute toxicity risk. No lethal dose has been established in any species, and no safe dose threshold can be defined.safety citation needed The gap between a dose that produces desired effects and one that triggers life-threatening complications is unpredictably narrow.
Published fatalities include a 17-year-old who died from cardiac arrest after ingesting three tablets, with postmortem blood levels of 3.14 ng/mL,[6] and a teenager in Indiana with confirmed blood levels of 1.59 ng/mL.[5] These fatal concentrations overlap with non-fatal levels reaching 10.1 ng/mL in surviving patients[4] — meaning blood concentration alone does not predict who lives and who dies.
In the largest published case series (10 patients), all exhibited hallucinations and violent agitation, with universal signs of serotonin and stimulant excess: dilated pupils, rapid heart rate, elevated blood pressure, and elevated body temperature. Seven required sedation with benzodiazepines.[4]
Heart and circulation
The adrenergic receptor binding of NBOMe compounds produces clinically significant blood vessel constriction and elevated blood pressure.[1] Fatal cardiac rhythm disturbance (ventricular fibrillation) is documented as a direct cause of death.[6] This cardiovascular toxicity profile distinguishes NBOMes from classical tryptamine and lysergamide psychedelics, which lack significant adrenergic activity.
Organ damage
Severe cases have produced muscle breakdown, acute kidney injury, disseminated intravascular coagulation, severe metabolic imbalance, and multi-organ failure.[8][4] Muscle breakdown is a relatively common complication, driven by the combination of seizures, elevated body temperature, and blood vessel constriction.[8]
Genotoxicity
A subtle genotoxic effect was detected in rat studies — less pronounced than MDMA but present.[15] No human data exist.
Detection
Standard drug screening panels do not detect 25B-NBOMe; specialized mass spectrometry testing is required for identification.[13][5] The compound degrades in stored biological samples, potentially leading to underestimation of actual levels.[8]
Psychological risks
No controlled data characterize the psychological risk profile. Emergency case reports document confusion, disorientation, anxiety, panic, and violent agitation as predominant features.[4] Violent agitation appeared in all ten patients in the largest case series — a frequency exceeding typical reports for classical psychedelics, possibly related to the compound's additional adrenergic and multi-transmitter activity.[4][15]
No data on HPPD (HPPD), psychosis precipitation, or longer-term psychological consequences specific to 25B-NBOMe have been published. Given its serotonin receptor activity, standard psychedelic psychological risks — acute distress, potential worsening of latent psychotic conditions, and destabilization in vulnerable individuals — are presumed to apply.inferred
Tolerance and dependence
Tolerance develops rapidly through serotonin downregulation — the same mechanism across all serotonergic psychedelics.[8] Community-sourced estimates suggest near-complete tolerance within 24 hours, partial recovery over approximately one week, and full reset at roughly two weeks.inferred
Complete cross-tolerance exists with other serotonergic psychedelics including LSD, psilocybin, mescaline, and DMT.[8]
No human dependence studies exist.[12] In animal models, 25B-NBOMe produced rewarding and reinforcing behavior mediated through dopamine pathways — blocked by dopamine antagonists but not by serotonin receptor blockers.[7] This dopaminergic reward signal is atypical for classical psychedelics and leaves open whether 25B-NBOMe carries greater dependence risk than its class membership would suggest.
Drug Interactions
No published interaction studies exist. The following are derived from pharmacological reasoning.
Serotonergic drugs: Combination with serotonin-releasing agents (MDMA), serotonin reuptake inhibitors (SSRIs, SNRIs), or monoamine oxidase inhibitors (MAOIs) increases total serotonergic load. NBOMe intoxication already presents with features overlapping serotonin syndrome — agitation, elevated body temperature, rapid heart rate[8] — making differentiation from primary toxicity impossible. MAOIs represent the highest-risk serotonergic combination.safety citation needed
Stimulants: cocaine and amphetamines produce cardiovascular stimulation through catecholamine pathways. Combined with 25B-NBOMe's blood vessel constriction,[1] the risk of dangerously high blood pressure, cardiac rhythm disturbance, and stroke is elevated.safety citation needed
Tramadol: Combines serotonergic activity (serotonin syndrome risk) with seizure threshold reduction — especially dangerous given that seizures are a documented complication of NBOMe poisoning.[8]safety citation needed
Enzyme inhibitors: 25B-NBOMe is processed by multiple liver enzyme pathways.[16] Drugs that strongly inhibit these enzymes could theoretically increase blood levels and toxicity risk, though no clinical data exist.
Contraindications
10 knownNo substance-specific contraindication data have been published. The following are derived from pharmacological profile and documented toxicity:
Heart conditions: The documented cardiac rhythm disturbance fatalities[6] and adrenergic vasoconstriction constitute absolute contraindications for individuals with pre-existing heart rhythm disorders, coronary artery disease, or uncontrolled high blood pressure.
Psychiatric conditions: As with all potent serotonin 2A receptor agonists, contraindicated in individuals with psychotic disorders or strong family history of psychosis. Bipolar disorder represents a relative contraindication. The documented predominance of violent agitation[4] suggests heightened risk in individuals with impulse control disorders.
Seizure disorders: Seizures are documented in NBOMe poisoning.[8] Epilepsy is an absolute contraindication.
Kidney or liver impairment: Extensive liver metabolism[16] and documented acute kidney injury[4] make pre-existing impairment of either organ a relative contraindication.
Pregnancy: Contraindicated. The genotoxic signal in animal studies[15] and potent serotonin receptor activity raise concerns for fetal development.
Harm Reduction[edit]
Forms & Identification
25B-NBOMe is most commonly encountered on blotter paper, where it is visually indistinguishable from LSD — and frequently sold as LSD.[8] It has also been found in tablet and powder form.[13] A widely circulated harm reduction heuristic — "if it's bitter, it's a spitter" — reflects the fact that NBOMe compounds typically produce a bitter, numbing sensation when held in the mouth, while LSD is tasteless. This is not a reliable analytical test, but it is a useful first signal.
Reagent testing and analytical drug checking services provide more dependable identification. Standard hospital drug screens do not detect NBOMe compounds[13] — someone presenting to emergency services may test negative on routine panels despite active intoxication.
Guidelines
- Test every dose. Reagent testing helps distinguish NBOMe compounds from LSD. Analytical drug checking services provide definitive identification where available.
- Start low. The margin between desired effects and medical emergency is narrower than for most psychedelics. Redosing before effects are fully established is especially dangerous.
- Sublingual over insufflation. Nasal administration produces faster, less controllable onset with greater overdose risk.
- Avoid physical exertion and heat. The cardiovascular load from adrenergic activity is compounded by exercise and high ambient temperature.
- Have a sober sitter present. Violent agitation is common even in otherwise healthy users. A trusted person who can provide reassurance — and call for help if needed — is essential.
- Stay hydrated but do not overhydrate — moderate, steady fluid intake.
Set & Setting
The pronounced physical body load and documented frequency of violent agitation[4] make environment especially important for this compound. A calm, familiar space with a sober sitter is strongly advisable. The extended duration means the setting must remain safe and comfortable for many hours, and the cardiovascular stress means physical exertion and hot environments increase medical risk.
Aftercare & integration. The cardiovascular and physical demands of 25B-NBOMe intoxication can leave the body depleted. Rest, adequate hydration, and nutritious food in the 24–48 hours following use support physical recovery. Muscle soreness may indicate low-grade muscle stress even in cases that did not require medical attention.
Psychologically, the experience — particularly if it involved agitation, fear, or loss of control — may benefit from processing. Journaling, talking with a trusted person, or consulting a therapist experienced with psychedelic-related distress can help integrate difficult material. If anxiety, perceptual disturbances, or mood instability persist beyond a few days, professional evaluation is advisable.
Recovery & Support
Classical serotonergic psychedelics are generally considered non-habit-forming due to rapid tolerance, but 25B-NBOMe's dopaminergic reward component[7] introduces uncertainty about compulsive use patterns. Anyone finding it difficult to stop or reduce use should seek professional support.
Harm reduction organizations, psychedelic peer support services, and substance use counselors familiar with novel psychoactive substances can provide appropriate guidance. Crisis lines and online peer communities offer anonymous, judgment-free support.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Chest pain, irregular heartbeat, or extremely rapid pulse
- Seizure or uncontrollable muscle rigidity
- Body temperature that feels dangerously hot to touch
- Complete loss of contact with reality or self-harm behavior
- Blue or grey skin coloring
- Loss of consciousness
Immediate steps:
- 1. Call emergency services immediately if any of the above signs appear. Do not wait.
- 2. Keep the person in a cool, quiet environment.
- 3. If unconscious and breathing, place in the recovery position.
- 4. Do not restrain unless there is immediate danger of self-harm — restraint can worsen muscle breakdown and overheating.
- 5. Do not induce vomiting.
- 6. Remove excess clothing to help manage body temperature.
What to tell the dispatcher:
State the substance (25B-NBOMe or "NBOMe"), estimated amount and time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
No reversal agent exists for NBOMe intoxication. Hospital treatment is supportive — benzodiazepines for agitation and seizures, active cooling for elevated body temperature, intravenous fluids for kidney protection.
Legal Status[edit]
25B-NBOMe is internationally controlled under Schedule I of the United Nations Convention on Psychotropic Substances (1971), following the recommendation of the WHO Expert Committee on Drug Dependence in 2014.[12] The compound has been individually scheduled or captured under structural analog provisions in most developed nations. Its dual existence as a controlled drug and an approved PET research radioligand (Cimbi-36) creates a distinctive regulatory situation in which research use continues under appropriate licensing.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Emergency scheduled November 15, 2013 alongside 25I-NBOMe and 25C-NBOMe;[11] permanent placement November 2015[17] |
| International | Schedule I, UN 1971 Convention | Effective March 2015 following WHO ECDD recommendation[12] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled via N-benzylphenethylamine catch-all provisioncitation needed |
| Australia | Schedule 1 (Criminal Code) | Controlled Drugs Legislation Amendment Regulation 2014[12] |
| New Zealand | Class B controlled drug | Scheduled December 2016citation needed |
| Canada | Status unconfirmed | Not verified via published sourcecitation needed |
| European Union | EMCDDA Early Warning System | Individual member state scheduling varies following international control |
Analogue act considerations
In the United States, 25B-NBOMe is now explicitly scheduled and no longer relies on the Federal Analogue Act for control. In jurisdictions where it is not specifically named, its structural similarity to scheduled phenethylamines and its pharmacological activity may subject it to analogue provisions if intended for human consumption.
Frequently asked questions
What is 25B-NBOMe?
25B-NBOMe is a synthetic N-benzylphenethylamine psychedelic derived from 2C-B, active at sub-milligram doses via sublingual and insufflated routes. It acts as a full 5-HT₂A receptor agonist (Ki = 0.5 nM) with α₁-adrenergic activity contributing to a sympathomimetic cardiovascular profile.
How long does 25B-NBOMe last?
Total duration by route of administration — Sublingual: 8 – 12 hours; Insufflated: 5 – 8 hours. Ranges vary with dose and individual factors; see the duration table for onset, peak, and after-effect phases.
Where can I find dosage information for 25B-NBOMe?
Psychedex publishes a dosage table for 25B-NBOMe on this page covering these routes of administration: sublingual, insufflated. Dose values are presented only in that table, always alongside their route of administration.
What are dangerous combinations with 25B-NBOMe?
The highest-severity documented interactions for 25B-NBOMe: MAOIs (Lethal), Buspirone (Dangerous), Dopamine agonists (Dangerous), GHB, Baclofen (Dangerous), GHB, GBL (Dangerous). See the interactions section for the full list with mechanisms and severity levels.
Is 25B-NBOMe addictive?
Psychedex records tolerance and dependence data rather than a yes/no rating. Recorded tolerance indicators for 25B-NBOMe: tolerance builds rapid; full reset takes 14 days; cross-tolerance develops with LSD, psilocybin, mescaline, DMT, 25I-NBOMe, 25C-NBOMe, 2C-B. See the article's dependence and safety sections for recorded dependence data.
experience reports
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First-person accounts of subjective effects, timing, and outcomes — submitted for harm reduction.
references
- [1]
- [2]
- [3] ^abcdEttrup A, da Cunha-Bang S, McMahon B, Lehel S, Dyssegaard A, Skibsted AW, et al. (2014) Serotonin 2A receptor agonist binding in the human brain with [11C]Cimbi-36. — Journal of Cerebral Blood Flow and Metabolism doi:10.1038/jcbfm.2014.68
- [4]
- [5] ^abcShanks KG, Sozio T, Behonick GS (2015) Fatal Intoxications with 25B-NBOMe and 25I-NBOMe in Indiana During 2014. — Journal of Analytical Toxicology doi:10.1093/jat/bkv058
- [6] ^abcdAl-Imam A (2018) 25b-NBOMe: A Case Report of Sudden Death and Insightful View of Google Trends Data. — Iranian Journal of Psychiatry and Behavioral Sciences doi:10.5812/ijpbs.9870
references
- [1]
- [2]
- [3] ^abcdEttrup A, da Cunha-Bang S, McMahon B, Lehel S, Dyssegaard A, Skibsted AW, et al. (2014) Serotonin 2A receptor agonist binding in the human brain with [11C]Cimbi-36. — Journal of Cerebral Blood Flow and Metabolism doi:10.1038/jcbfm.2014.68
- [4]
- [5] ^abcShanks KG, Sozio T, Behonick GS (2015) Fatal Intoxications with 25B-NBOMe and 25I-NBOMe in Indiana During 2014. — Journal of Analytical Toxicology doi:10.1093/jat/bkv058
- [6] ^abcdAl-Imam A (2018) 25b-NBOMe: A Case Report of Sudden Death and Insightful View of Google Trends Data. — Iranian Journal of Psychiatry and Behavioral Sciences doi:10.5812/ijpbs.9870