25B-NBOMe
4-bromo-2,5-dimethoxy-N-(2-methoxybenzyl)phenethylamine
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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]
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LSD, psilocybin, mescaline +4 moreLSD, psilocybin, mescaline, DMT, 25I-NBOMe, 25C-NBOMe, 2C-B show less
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.
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
No 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.
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