25B-NBOH
4-bromo-2,5-dimethoxy-N-(2-hydroxybenzyl)phenethylamine
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25B-NBOH (2C-B-NBOH) is an emerging synthetic psychedelic of the phenethylamine class. It is a microgram-potency derivative of 2C-B, distinguished from 25B-NBOMe by a hydroxyl group on its N-benzyl ring. 25B-NBOH is a 5-HT₂A receptor agonist, producing its effects by disrupting serotonin-mediated sensory filtering in the cortex.
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The NBOH scaffold was developed at the University of Copenhagen in 2014 as part of systematic structure-activity research on phenethylamines.[1] By 2017, 25B-NBOH had appeared in forensic seizures across Brazil and Europe, becoming a predominant hallucinogen on blotter papers in parts of Brazil.[2] It remains unscheduled under United Nations conventions and circulates in unregulated markets, often misrepresented as LSD.[3]
Subjective effects include geometric visual patterns, color enhancement, emotional intensification, and sympathomimetic activation. The experience carries a pronounced physical edge — elevated heart rate, blood pressure, and pupil dilation overlay the psychedelic state, distinguishing it from classical serotonergic psychedelics with lower cardiovascular load.[3] Agitation, anxiety, and nausea are common unsought effects.
25B-NBOH produces no physical dependence and is not habit-forming,[4] but no lethal dose or therapeutic index has been established. Cardiovascular toxicity is the defining acute risk — structural analogs inhibit cardiac ion channels,[5] and multiple fatalities are documented across the broader NBOMe/NBOH class.[6][7] The evidence base is extremely thin: one animal behavioral study,[8] one clinical poisoning cluster,[3] and in vitro binding data — no controlled human studies have been conducted.
History[edit]
Discovery
The NBOH scaffold emerged from systematic structure-activity work by Hansen and colleagues at the University of Copenhagen, who synthesized 48 N-benzyl phenethylamine derivatives and demonstrated that N-benzyl substitution dramatically increased 5-HT₂A binding affinity.[1] The specific pharmacological profile of 25B-NBOH — built on the 2C-B backbone with an ortho-hydroxybenzyl N-substituent — was characterized the following year.[9]
Market emergence
25B-NBOH first appeared in forensic seizures in Brazil between 2017 and 2018, alongside several other NBOH compounds.[2] Through approximately 2014–2019, NBOH compounds became the predominant hallucinogens on blotter papers in certain Brazilian regions, largely displacing LSD in the unregulated market.[2] A 2022 poisoning cluster in Australia — caused by 25B-NBOH powder sold as LSD — underscored the compound's role as an adulterant and the critical importance of drug checking services.[3]
Regulatory response
Sweden scheduled 25B-NBOH in January 2016, and Brazil followed in December 2018. The United Kingdom covers it as a Class A substance under N-benzylphenethylamine catch-all provisions, while Germany controls it under the Neue-psychoaktive-Stoffe-Gesetz. In the United States, the compound is not specifically listed but may fall under the Federal Analogue Act. As of 2019, 25B-NBOH was not controlled under United Nations drug conventions.[2]
The name 25B-NBOH follows systematic naming conventions for N-benzylphenethylamines: 25 denotes the 2,5-dimethoxy substitution pattern, B indicates the 4-bromo substituent (from 2C-B), and NBOH specifies the N-(2-hydroxybenzyl) group. The compound is also referenced as 2C-B-NBOH and NBOH-2C-B in forensic and academic literature. No widely recognized street names exist; the substance typically circulates on blotter paper sold under generic or misleading labels.
Chemistry[edit]
Structural class
25B-NBOH belongs to the 25x-NBOH series — the N-(2-hydroxybenzyl) derivatives of the 2C-x phenethylamine family. The compound is built from the 2C-B backbone (4-bromo-2,5-dimethoxyphenethylamine) with a 2-hydroxybenzyl group attached to the amine nitrogen. This N-benzyl substitution converts the moderate-potency parent phenethylamine into a high-potency serotonin 2A receptor agonist active in the microgram range.[1]
The NBOH series is the hydroxyl counterpart of the NBOMe series: where 25B-NBOMe bears a methoxy group on the N-benzyl ring, 25B-NBOH bears a free hydroxyl at the same position. This single functional group difference alters the compound's metabolic and analytical profile.
Molecular properties
| Molecular formula | C₁₇H₂₀BrNO₃ |
| Molecular weight | 366.2 g/mol |
The structure comprises a 2,5-dimethoxyphenethylamine core bearing a bromine at the 4-position and an N-(2-hydroxybenzyl) group. Key functional groups include two aromatic methoxy groups, an aromatic bromine, a secondary amine, and a phenolic hydroxyl on the N-benzyl ring.
Stereochemistry
25B-NBOH contains no classical chirality center in its free-base form. In the broader N-benzylphenethylamine class, compounds bearing a chiral alpha-carbon typically show stereoselective receptor binding, but 25B-NBOH lacks this substituent. No enantiomer-resolved binding data have been published.
Analytical identification
A critical property for forensic and clinical settings is thermolability: 25B-NBOH degrades to its parent compound 2C-B under standard gas chromatography conditions.[2][10] Routine GC-MS screening will therefore misidentify 25B-NBOH as 2C-B — a clinically and forensically significant pitfall. Accurate identification requires liquid chromatography–tandem mass spectrometry (LC-MS/MS) or nuclear magnetic resonance spectroscopy.[10]
Pharmacology[edit]
Mechanism of action
25B-NBOH produces its psychedelic effects primarily through activation of serotonin 5-HT₂A receptors, consistent with the broader N-benzylphenethylamine class.[7][6] The compound binds 5-HT₂A with high affinity and 5-HT₂C with even higher affinity.[9][11] This unusually strong 5-HT₂C binding may indicate partial agonism at 5-HT₂A, as the original characterization noted that NBOH compounds were generally less efficacious agonists than previously reported N-benzyl phenethylamines.[9]
Affinity at other targets is substantially lower. Monoamine transporters (dopamine, serotonin, norepinephrine) bind only at concentrations far above the active dose range, indicating no meaningful stimulant contribution.[4]
The only published animal study directly testing 25B-NBOH confirmed its hallucinogenic behavioral profile: in rats trained to recognize DOM (a reference psychedelic), 25B-NBOH fully substituted for DOM's effects with potency exceeding both DOM and several NBOMe analogs.[8] The compound also decreased spontaneous movement in mice, similar in magnitude to DOM.[8]
Pharmacokinetics
No human pharmacokinetic studies have been published. Half-life, time to peak concentration, bioavailability, and plasma concentration profiles remain entirely uncharacterized in humans.
NBOH compounds are inactive or nearly inactive when swallowed at standard doses, due to extensive first-pass metabolism in the liver.[2][11] In unregulated settings, administration occurs via sublingual absorption from blotter papers or by insufflation — both routes bypass first-pass metabolism and allow the compound to reach the bloodstream intact.
Metabolism studies in human liver microsomes identified multiple biotransformation pathways including demethylation, hydroxylation, and glucuronidation. Three metabolites — designated B2-1, B2-2, and B6 — were identified as recommended biomarkers for forensic detection.[12] By analogy with the closely related 25I-NBOH, CYP2D6 is likely the primary enzyme responsible for clearance.[13] The parent compound 2C-B is metabolized through multiple enzymatic pathways, with primary metabolites that do not activate serotonin receptors.[14]
Neuroscience[edit]
Where it acts
No direct neuroimaging or electrophysiological studies have been published for 25B-NBOH in humans. Based on its confirmed 5-HT₂A agonism,[8] the compound is expected to disrupt activity in prefrontal cortex layer V pyramidal neurons — the same population targeted by LSD and psilocybin. Class-level neuroimaging for serotonergic psychedelics shows dissolution of the default mode network, disruption of thalamic filtering, and increased global functional connectivity — changes collectively experienced as broadened, less-filtered conscious awareness.
A related NBOH compound (25I-NBOH) produced characteristic slow waveforms and behavioral arrest in animal EEG studies, providing a class-level neural fingerprint for selective 5-HT₂A engagement.[15]
Why it matters
Serotonergic psychedelics as a class promote structural neuroplasticity — rapid dendritic spine growth through BDNF and mTOR pathways — raising the possibility that compounds like 25B-NBOH could function as psychoplastogens. No neuroplasticity data exist for 25B-NBOH specifically, and whether its possible partial agonism[9] affects neuroplastogenic potential remains unknown.
The REBUS framework (Relaxed Beliefs Under Psychedelics) offers the most explanatory model: psychedelics relax the brain's confidence in its own predictions, allowing bottom-up sensory signals greater influence on conscious experience. 25B-NBOH's 5-HT₂A agonism is consistent with this mechanism, though partial agonism may produce a less complete effect than full agonists.
- Does 25B-NBOH's apparent partial agonism at 5-HT₂A translate into a qualitatively different experience or lower ceiling on psychedelic intensity compared to full agonists?
- Why does 25B-NBOH show greater behavioral potency than 25I-NBOH in animals despite 25I-NBOH's higher in vitro efficacy — do pharmacokinetic differences, signaling bias, or receptor residence time explain the gap?
- Does the NBOH class's β-arrestin 2 signaling bias[16] produce measurably different neural activation patterns compared to other psychedelic classes?
Subjective Effects[edit]
25B-NBOH produces a psychedelic experience colored by notable physical activation. Users encounter visual and auditory distortions alongside a somatic signature — racing heart, elevated blood pressure, dilated pupils — that sits heavier in the body than classical psychedelics like LSD or psilocybin.[3] Set and setting strongly modulate the qualitative character; the compound's oral inactivity means route of administration is itself a critical variable, as swallowing a blotter may produce no effect at all.
Within the phenethylamine landscape, 25B-NBOH occupies a position between its parent compound 2C-B — orally active, moderate potency, well-characterized — and 25B-NBOMe, which shares microgram-range potency but carries a more extensively documented toxicity record. The NBOH series sits at an intermediate structural point: extreme potency without oral activity, cardiovascular risk exceeding classical psychedelics, and far less human data than either comparator.
Effect Grid
A full psychedelic experience unfolds. Visual effects are prominent — clear visual drifting, color enhancement and alteration, symmetrical texture repetition, and emerging geometry. Internal hallucinations may appear with eyes closed. Auditory distortion and music enhancement are notable. Depth perception distortion and perspective distortion alter spatial awareness.
The body load is pronounced and distinctly sympathomimetic. Tachycardia, muscle tension, temperature dysregulation, and vasoconstriction are typical. Pupil dilation is marked. Nausea may occur during the come-up. Stimulation and wakefulness are sustained throughout the 4–6 hour duration. Dehydration sensation and dry mouth are common.
Cognitive alteration is significant — thought connectivity, conceptual thinking, pattern recognition enhancement, and immersion enhancement reshape mental processing. Emotional enhancement and empathy enhancement color the experience. Time alteration is noticeable. Anxiety may surface, particularly during the ascent phase.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual breathing · Tracers · Brightness alteration · Auditory enhancement · Symmetrical texture repetition · Visual diffraction · Environmental patterning · Light sensitivity · Sound sensitivity · Visual morphing · Holotropic state · Depth perception distortion · Perspective distortion · After-images · Peripheral vision distortion · Spatial disorientation · Touch enhancement · Visual haze / noise · Visual melting · Visual acuity enhancement · Visual magnification · Peripheral misidentification · Auditory distortion · Auditory misinterpretation · Proprioceptive distortion · Vestibular distortion · Synesthesia · Touch suppression · Visual recursion · Object transformations · Environmental orbism / cubism · Object activation · Internal hallucinations · Visual scenery slicing · External hallucinations · Perspective hallucinations · Visual processing suppression · Auditory hallucinations · Gustatory hallucination
Symmetrical texture repetition · Visual diffraction · Environmental patterning · Light sensitivity · Sound sensitivity · Visual morphing · Holotropic state · Depth perception distortion · Perspective distortion · After-images · Peripheral vision distortion · Spatial disorientation · Touch enhancement · Visual haze / noise · Visual melting · Visual acuity enhancement · Visual magnification · Peripheral misidentification · Auditory distortion · Auditory misinterpretation · Proprioceptive distortion · Vestibular distortion · Synesthesia · Touch suppression · Visual recursion · Object transformations · Environmental orbism / cubism · Object activation · Internal hallucinations · Visual scenery slicing · External hallucinations · Perspective hallucinations · Visual processing suppression · Auditory hallucinations · Gustatory hallucination
Body high · Spontaneous body sensations · Muscle tension · Appetite suppression · Dry mouth · Restlessness · Heart rate perception changes · Physical fatigue · Tactile euphoria · Tingling / electric sensations · Nausea · Dehydration sensation · Sexual arousal enhancement · Bodily lightness · Body schema distortion · Dizziness · Excessive sweating · Insomnia · Laughter fits · Motor control impairment · Vibrations / buzzing · Headache · Involuntary body movements · Nystagmus (eye wobbles) · Trembling · Abnormal heartbeat · Increased urination · Seizure threshold reduction · Tactile hallucination
Appetite suppression · Dry mouth · Restlessness · Heart rate perception changes · Physical fatigue · Tactile euphoria · Tingling / electric sensations · Nausea · Dehydration sensation · Sexual arousal enhancement · Bodily lightness · Body schema distortion · Dizziness · Excessive sweating · Insomnia · Laughter fits · Vibrations / buzzing · Headache · Involuntary body movements · Nystagmus (eye wobbles) · Trembling · Abnormal heartbeat · Increased urination · Seizure threshold reduction · Tactile hallucination
Conceptual thinking · Novelty enhancement · Cognitive euphoria · Cognitive flexibility · Introspection enhancement · Multiple thought streams · Openness enhancement · Thought connectivity · Thought acceleration · Cognitive impairment · Focus suppression · Creativity enhancement · Memory suppression · Humor enhancement · Analysis enhancement · Confusion · Information processing suppression · Memory fragmentation · Synchronicity · Thought disorganization · Thought loops · Amnesia
Cognitive flexibility · Introspection enhancement · Multiple thought streams · Openness enhancement · Thought connectivity · Thought acceleration · Cognitive impairment · Focus suppression · Creativity enhancement · Memory suppression · Humor enhancement · Analysis enhancement · Confusion · Information processing suppression · Memory fragmentation · Synchronicity · Thought disorganization · Thought loops
Simultaneous emotions · Anxiety · Catharsis
Trust enhancement · Communication enhancement · Sociability enhancement · Depersonalization · Boundary dissolution · Cognitive disconnection · Identity alteration · Ego dissolution
Boundary dissolution · Cognitive disconnection · Identity alteration · Ego dissolution
Transpersonal visions · Entity contact
Timeline
First awareness of effects; sublingual numbness and bitter/metallic taste from blotter; initial sympathomimetic stirring with slight heart rate increase.
Rapid intensification of visual and cognitive effects. Body load builds — muscle tension, tachycardia, nausea possible. Anxiety is common during the ascent as effects accelerate.
Full expression of perceptual, cognitive, and somatic effects. Maximum sympathomimetic activation — tachycardia, mydriasis, hypertension. Most intense visual phenomena including geometry, drifting, and color enhancement.
Gradual reduction in visual intensity; cognitive effects persist longer than perceptual distortions. Body load recedes. Emotional processing may continue.
Residual cognitive openness, mild stimulation, possible physical fatigue. Headache may emerge. Sleep may be delayed by residual wakefulness.
Safety[edit]
- Acute toxicity
- High
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · DMT
Toxicity
Acute toxicity
No lethal dose has been established for 25B-NBOH in any species, and no therapeutic index can be calculated. The compound carries high acute toxicity risk based on class-level evidence.inferred Multiple fatalities have been attributed to the broader NBOMe/NBOH class,[7][6] and poisoning cases involving 25B-NBOH have been referenced in the literature.[12]
No peer-reviewed report of a confirmed fatality attributable specifically to 25B-NBOH alone has been identified. The Australian poisoning cluster documented hallucinations, dilated pupils, rapid heart rate, elevated blood pressure, and agitation from 25B-NBOH sold as LSD.[3][11]
Heart and circulation
Cardiovascular toxicity is the best-characterized acute risk for the NBOH class. Structural analogs 25I-NBOH and 25C-NBOH reduce heart cell viability, increase QT and RR intervals in animal heart recordings, and — in the case of 25I-NBOH — inhibit hERG potassium channels.[5] Rapid heart rate and elevated blood pressure are documented clinical findings in 25B-NBOH poisoning.[3]
These effects carry particular risk for individuals with pre-existing heart conditions, QT prolongation, or concurrent use of medications that prolong the QT interval.
Seizures and muscle breakdown
Seizures are a recognized complication of NBOMe/NBOH class toxicity.[7][6] Severe muscle breakdown has been documented in NBOMe poisoning cases, secondary to seizures, overheating, and vasoconstriction.[7] No 25B-NBOH-specific case has been published.
Serotonin syndrome
The NBOH class carries inherent risk of serotonin syndrome due to potent serotonin receptor activation. A case involving the structural analog 25E-NBOH combined with MDPHP documented serotonin syndrome.[17] Combination with any serotonin-elevating substance — including tramadol, SSRIs, SNRIs, monoamine oxidase inhibitors, or serotonin releasers — elevates this risk.
Chronic toxicity
No chronic administration studies have been published for 25B-NBOH. Repeated dosing of the related compound 25I-NBOMe in rats over 7 days produced memory suppression, reduced motor activity, and increased anxiety,[18] suggesting potential harm from chronic use within the N-benzylphenethylamine class. Multi-organ failure has been reported in fatal NBOMe cases.[6]
Analytical detection
25B-NBOH degrades to 2C-B under standard gas chromatography conditions,[2][10] meaning clinical and forensic samples may be misidentified without LC-MS/MS testing. Recommended urinary biomarkers are metabolites B2-1, B2-2, and B6.[12]
Psychological risks
No controlled studies have assessed 25B-NBOH's psychological risks. As a potent serotonin 2A receptor agonist, the compound carries the standard psychological risk profile of serotonergic psychedelics: acute anxiety, panic, paranoia, and destabilizing experiences during intoxication. Risk of precipitating or worsening psychotic disorders exists in vulnerable individuals. Hallucinogen persisting perception disorder (HPPD) is possible following use.
The Australian poisoning cluster documented agitation as a clinical finding.[3] That cluster — users who believed they were taking LSD and unknowingly received a different compound at an unknown dose — represents a high-risk scenario for psychological harm due to unexpected effects and inability to calibrate expectations.
Tolerance and dependence
Tolerance develops rapidly. A single dose of a 5-HT₂A agonist can produce measurable tolerance through downregulation in the frontal cortex.[18] Cross-tolerance with other serotonergic psychedelics — LSD, psilocybin, DMT, DOx compounds, mescaline — is expected based on the shared 5-HT₂A mechanism. Tolerance builds almost immediately, halves over approximately one week, and fully resets in approximately two weeks.inferred
Dependence. 25B-NBOH is not habit-forming. Serotonergic psychedelics do not produce compulsive drug-seeking through dopamine reward circuits. NBOH compounds have negligible affinity at monoamine transporters at pharmacologically relevant doses.[4] No reports of 25B-NBOH dependence, withdrawal, or compulsive redosing exist.
Drug interactions
Serotonergic combinations
Any substance that increases serotonin levels — tramadol, SSRIs, SNRIs, MAO inhibitors, serotonin releasers — combined with 25B-NBOH's potent serotonin receptor activation carries serotonin syndrome risk. The tramadol combination is classified as dangerous.inferred MAO inhibitors represent the highest-risk combination: they prevent serotonin breakdown while 25B-NBOH simultaneously activates serotonin receptors, creating conditions for life-threatening crisis.
A case of serotonin syndrome with the structural analog 25E-NBOH combined with MDPHP provides the closest published clinical precedent.[17]
SSRIs and SNRIs
Chronic SSRI use may reduce acute psychedelic effects through serotonin receptor downregulation. Survey data demonstrate reduced acute effects in SSRI users taking psychedelics.[19] Combination at high doses still carries serotonin syndrome risk, particularly with SNRIs and tricyclic antidepressants.
CYP2D6 inhibitors
By analogy with 25I-NBOH,[13] medications that inhibit the CYP2D6 enzyme — including paroxetine, fluoxetine, bupropion, and quinidine — may increase 25B-NBOH blood levels and prolong exposure. Individuals who are CYP2D6 poor metabolizers (~5–10% of Caucasian populations) may experience similar elevated exposure without a drug interaction.
Cannabis
Cannabis combined with psychedelics increases both mystical and challenging experience scores in a dose-dependent manner.[20] The specific interaction with 25B-NBOH is uncharacterized.
Lithium
Lithium carries a class-level seizure risk warning when combined with 5-HT₂A agonists.citation needed
Contraindications
Pre-existing heart conditions. Cardiac ion channel inhibition and QT prolongation demonstrated for NBOH structural analogs[5] make 25B-NBOH contraindicated in individuals with long QT syndrome, structural heart disease, or concurrent use of QT-prolonging medications.
Seizure disorders. The NBOMe/NBOH class is associated with seizures.[7][6] Individuals with epilepsy or lowered seizure threshold should not use 25B-NBOH.
MAO inhibitor therapy. Potent serotonin receptor activation combined with MAO-mediated serotonin accumulation creates life-threatening serotonin syndrome risk. This is an absolute contraindication.
Tramadol. Classified as dangerous due to dual serotonergic and opioid mechanisms.
Psychiatric vulnerability. Personal or family history of psychotic disorders (schizophrenia, schizoaffective disorder, bipolar I with psychotic features) represents a relative contraindication due to risk of precipitating psychotic episodes.
Lithium therapy. Class-level contraindication for serotonergic psychedelics due to reported seizure risk.citation needed
Pregnancy and lactation. No reproductive toxicity data exist. Use during pregnancy or lactation is contraindicated in the absence of safety data.safety citation needed
Harm Reduction[edit]
Forms & Identification
25B-NBOH's thermolability — degrading to 2C-B under heat[2] — means standard GC-MS drug checking cannot distinguish it from 2C-B. Reagent testing provides a preliminary screen but cannot confirm compound identity with certainty. Only advanced testing methods (LC-MS/MS) can reliably differentiate 25B-NBOH from 2C-B or other NBOH/NBOMe compounds.
Blotter papers containing 25B-NBOH are visually indistinguishable from LSD blotters. The 2022 Australian poisoning cluster resulted from powder sold as LSD,[3] demonstrating that misrepresentation extends across all physical forms.
Guidelines
- Test all material using reagent kits as a first screen. Advanced testing (LC-MS/MS) is the only method that can reliably distinguish 25B-NBOH from 2C-B or NBOMe compounds.
- Start low. No standardized dosing exists. Begin with a threshold dose and allow at least 90 minutes before considering whether effects have fully developed.
- Hold blotter sublingually. The compound is orally inactive — swallowing blotter paper bypasses the active route entirely. Hold under the tongue or against the cheek for 15–30 minutes.
- Do not redose if swallowed. If a blotter is accidentally swallowed, do not take a second dose. The first dose may still absorb partially through mucosal contact.
- Have a sober sitter present who knows the substance and can monitor for cardiovascular distress.
- Stay hydrated and temperature-regulated. Sympathomimetic activation increases heart rate and body temperature.
- Avoid physical exertion during the experience to minimize cardiovascular strain.
Set & Setting
25B-NBOH's pronounced cardiovascular effects and oral inactivity make environment particularly important. A calm, physically safe space with temperature control reduces the risk of compounding sympathomimetic activation with environmental stress. The presence of a sober companion familiar with the compound's properties — including its route-dependent activity and cardiovascular signature — is strongly recommended.
The compound's oral inactivity creates a specific redosing trap: if a blotter is swallowed rather than held sublingually, no effects emerge, and the temptation to take another dose is high. Understanding this pharmacological quirk before use prevents dangerous dose stacking.
Aftercare & integration. The days following a 25B-NBOH experience may include residual visual effects, mood fluctuation, and physical fatigue from sustained cardiovascular activation. Prioritize sleep, nutrition, and low-stimulation environments during the 24–48 hours after use.
If the experience was psychologically difficult — marked by anxiety, paranoid ideation, or destabilizing perceptual effects — structured reflection can help process the material. Journaling, conversation with a trusted person, or sessions with a psychedelic-informed therapist are appropriate integration tools. Persistent perceptual disturbances lasting beyond a few days may indicate HPPD and warrant professional evaluation.
Recovery & Support
25B-NBOH does not produce physical dependence, and compulsive use patterns are rare among serotonergic psychedelics due to rapid tolerance. If use has become a coping mechanism or is causing distress, harm reduction services and psychedelic peer support organizations can provide non-judgmental guidance.
For individuals experiencing lasting psychological difficulty — persistent anxiety, depersonalization, or intrusive perceptual changes — professional support from therapists experienced with psychedelic-related concerns is recommended. Crisis support is available through organizations such as the Fireside Project and MAPS integration resources.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: uncomfortable body load and mild anxiety are common and do not require medical intervention. Seek emergency help immediately if any of the following occur: chest pain, irregular heartbeat, seizure, loss of consciousness, severe uncontrolled agitation, self-harm behavior, or body temperature that feels dangerously elevated through clothing.
Immediate steps:
- 1. Call emergency services.
- 2. Place the person in the recovery position if unconscious but breathing.
- 3. Keep them cool if overheating — remove excess clothing, apply cool water.
- 4. Do not restrain unless there is immediate danger of self-harm or harm to others.
- 5. Do not induce vomiting.
- 6. Stay with the person until help arrives.
What to tell the dispatcher: the substance taken (25B-NBOH or "an NBOH psychedelic"), the approximate amount and time of ingestion, and current symptoms. Good Samaritan laws exist in many jurisdictions to protect people who call for help during a drug-related emergency.
No specific reversal agent exists for 25B-NBOH or any serotonergic psychedelic.
Legal Status[edit]
The regulatory status of 25B-NBOH varies across jurisdictions, reflecting the fragmented international response to novel psychoactive substances. The compound is not controlled under United Nations drug conventions as of 2019,[2] though the UNODC maintains a substance database entry.[21] Several jurisdictions have scheduled 25B-NBOH explicitly or captured it under blanket legislation targeting phenethylamine analogs.
All national legal status entries below are derived from web-retrieved sources and should be verified against primary legislative texts before reliance.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not specifically scheduled | Potentially subject to the Federal Analogue Act due to structural similarity to Schedule I 2C compoundscitation needed |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Covered under N-benzylphenethylamine catch-all provisions |
| Sweden | Schedule I (Narcotic Drugs Punishments Act) | Listed since January 26, 2016 |
| Germany | Controlled (NpSG) | Covered under the Neue-psychoaktive-Stoffe-Gesetz (New Psychoactive Substances Act) |
| Canada | Controlled | Covered under phenethylamine blanket-ban legislation |
| Brazil | Prohibited | Scheduled December 2018 |
| Switzerland | Controlled | Listed as controlled substance |
| Australia | Unconfirmed | TGA Poisons Standard status not independently verified; possibly covered under analogue provisionscitation needed |
| International (UN) | Not listed | Not under UN drug conventions as of 2019;[2] UNODC database entry exists[21] |
references
- [1] ^abcHansen M, Phonekeo K, Paine JS, Leth-Petersen S, Begtrup M, Brauner-Osborne H, Kristensen JL (2014) Synthesis and Structure-Activity Relationships of N-Benzyl Phenethylamines as 5-HT2A/2C Agonists — ACS Chemical Neuroscience doi:10.1021/cn400216u
- [2]
- [3]
- [4] ^abcEshleman AJ, Wolfrum KM, Reed JF, Kim SO, Johnson RA, Janowsky A (2018) Neurochemical pharmacology of psychoactive substituted N-benzylphenethylamines: High potency agonists at 5-HT2A receptors. — Biochemical Pharmacology doi:10.1016/j.bcp.2018.09.024
- [5] ^abcYoon KS, Cha HJ, Choi SO, Lee JM (2022) 2-((2-(4-Iodo-2,5-dimethoxyphenyl)ethylamino)methyl)phenol (25I-NBOH) and 2-(((2-(4-chloro-2,5-dimethoxyphenyl)ethyl)amino)methyl)phenol (25C-NBOH) induce adverse effects on the cardiovascular system — Toxicology Letters doi:10.1016/j.toxlet.2021.11.016
- [6]