25E-NBOH
4-ethyl-2,5-dimethoxy-N-(2-hydroxybenzyl)phenethylamine
Viewing r1 — May 7, 2026 — CURRENT
Back to HistoryInteractions, related substances, and reports reflect the current entry and are not shown for historical revisions.
25E-NBOH (2C-E-NBOH) is a synthetic psychedelic of the phenethylamine class. It is an N-benzyl derivative of 2C-E, distinguished from the related NBOMe series by a hydroxyl group on the benzyl ring. 25E-NBOH is a full agonist at serotonin 5-HT₂A receptors,[1] producing its effects by disrupting the brain's default filtering of sensory and cognitive input.
Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
LSD, psilocybin, mescaline +4 moreLSD, psilocybin, mescaline, DMT, DOx series, 25x-NBOMe compounds, 25x-NBOH compounds show less
The NBOH scaffold was developed around 2009–2010 by Martin Hansen as part of a program to create brain-imaging agents for serotonin receptors.[2] 25E-NBOH appeared on research chemical markets approximately 2018–2019,[3] following the scheduling of structurally related NBOMe compounds. It circulates primarily on blotter paper and remains unscheduled under international drug treaties, though several countries have banned it individually.
Subjective effects include geometric visual patterns, color enhancement, cognitive stimulation, and body load. The experience pairs unusual analytical clarity — verbal fluency and self-awareness remain relatively intact — with pronounced physical tension from vasoconstriction that distinguishes it from classical psychedelics. Muscle soreness, cold extremities, and nausea are characteristic unsought effects.
No physical dependence has been documented, and the toxic dose in humans is unknown — one source references fatal cases without clinical details.[4] The primary acute risks are cardiovascular: vasoconstriction from adrenoceptor activity can produce dangerous blood pressure elevation, compounded by seizure and overheating risk at the class level.[5] No clinical studies have been conducted; the current understanding rests on a single animal pharmacology study, metabolic profiling, and community reports.
History[edit]
Discovery
The parent compound 2C-E was first synthesized and documented by Alexander Shulgin in PiHKAL.[6] The NBOH (N-(2-hydroxybenzyl)) modification was developed around 2009–2010 by Martin Hansen and colleagues at the University of Copenhagen, who sought to create agonist PET radioligands for imaging serotonin 5-HT₂A receptors in living brain tissue.[2] 25CN-NBOH emerged as the program's most pharmacologically significant compound,[7][8] while 25E-NBOH and other members of the series received less individual characterization.
Market Emergence and Forensic Detection
After several NBOMe compounds were placed into Schedule I in the United States in 2013,[9] the structurally distinct NBOH series entered the research chemical market as an alternative. 25E-NBOH appeared around 2018–2019.[3] Its first forensic identification came from blotter papers seized by Brazilian police in 2017–2018, characterized using multiple spectroscopic techniques,[10] following a similar identification of 25I-NBOH in Brazil the previous year.[11]
Analytical Challenges
Early forensic identification was complicated by 25E-NBOH's thermolability — it breaks down into its parent compound 2C-E under the heat of standard gas chromatography.[12][10] This property likely caused underreporting of its presence in seized materials and necessitated liquid chromatography or NMR-based methods for definitive identification.
The name "25E-NBOH" follows systematic research chemical nomenclature: "25" refers to the 2,5-dimethoxy substitution pattern, "E" denotes the 4-ethyl group (from 2C-E), and "NBOH" indicates the N-(2-hydroxybenzyl) modification. The NBOH suffix distinguishes the series from NBOMe (N-(2-methoxybenzyl)) compounds — a single functional group difference (hydroxyl vs methoxy) that created a distinct legal identity while retaining comparable pharmacological potency.[9]
Chemistry[edit]
Structural Class
25E-NBOH belongs to the N-benzylphenethylamine class, a family of potent serotonergic psychedelics created by attaching an N-benzyl group to 2C-x phenethylamines. The structural lineage runs from mescaline through 2C-E (4-ethyl-2,5-dimethoxyphenethylamine) to 25E-NBOH, where an N-(2-hydroxybenzyl) group is added to the nitrogen. This N-benzyl addition dramatically increases binding affinity at 5-HT₂A receptors compared to the parent 2C-E.[5]
The compound differs from its NBOMe counterpart (25E-NBOMe) by a single functional group: a free hydroxyl on the benzyl ring rather than a methoxy group. This change retains potent 5-HT₂A activity while creating a pharmacologically and legally distinct compound.[9]
Molecular Properties
| Molecular formula | C₁₉H₂₅NO₃ |
| Molecular weight | 315.4 g/mol |
The molecule combines a 2,5-dimethoxy-4-ethylphenethylamine backbone (the 2C-E scaffold) linked through a secondary amine to a 2-hydroxybenzyl group. Key features include two aromatic methoxy groups, an ethyl substituent at the 4-position, and a phenolic hydroxyl on the N-benzyl ring. The compound contains no chirality centers.
Physical Properties
No published data exist for melting point, solubility, or stability of 25E-NBOH. It is distributed on blotter paper for sublingual use, implying adequate stability in dry solid form at room temperature.
A critical property is thermolability: 25E-NBOH degrades to 2C-E under the heat of standard gas chromatography (inlet temperatures of 250–300°C).[12][11][10] The thermal breakdown pathway cleaves the N-benzyl bond, regenerating the parent 2C-E molecule. This property is shared across the NBOH class and requires liquid chromatography or NMR for reliable identification.
Pharmacology[edit]
Mechanism of Action
25E-NBOH produces psychedelic effects primarily through agonism at serotonin 5-HT₂A receptors.[1][5] It has been confirmed as a high-affinity full agonist at both 5-HT₂A and 5-HT₂C receptors,[1] though no specific binding affinity values have been published for this compound.
Recent structural work has shown that the hallucinogenic effects of 5-HT₂A agonists depend on non-canonical Gᵢ signalling rather than the Gq pathway.[13] Whether 25E-NBOH shows preference between these signalling pathways has not been investigated. Studies on the closely related 25CN-NBOH provide a structural framework for understanding how N-benzylphenethylamines balance different downstream signalling routes.[14][15]
Secondary effects likely include binding at alpha-1A adrenoceptors, documented for the NBOMe class at meaningful potency.[16][17] This receptor target is responsible for the vasoconstriction and cardiovascular stimulation that characterize the phenethylamine body load.
Pharmacokinetics
No human pharmacokinetic data exist for 25E-NBOH. Bioavailability, time to peak effect, plasma half-life, and elimination pathways have not been measured in any species.
Metabolic profiling has been conducted in laboratory settings. Vágnerová et al. mapped the metabolic pathway of 25E-NBOH in human liver preparations and animal models, confirming that 2C-E (the parent phenethylamine) is produced as a metabolite through cleavage of the N-benzyl group.[3] Xiang et al. independently identified additional metabolites using high-resolution mass spectrometry.[4]
The sublingual route — standard for blotter paper delivery — partially bypasses liver metabolism, which may explain the compound's activity at very low doses despite expected metabolic vulnerability. By analogy with the closely related 25CN-NBOH, NBOH compounds show moderate susceptibility to liver metabolism.[18][9]
Neuroscience[edit]
Where It Acts
No direct brain imaging or electrophysiology data exist for 25E-NBOH. Its neural effects are inferred from its confirmed serotonin 2A receptor agonist pharmacology.[1] 5-HT₂A receptors concentrate on pyramidal neurons in the prefrontal cortex, where their activation triggers glutamate release and disrupts the brain's normal hierarchical processing of sensory information.
At the network level, serotonergic psychedelics reduce connectivity within the default mode network (associated with ego dissolution), impair thalamic filtering of sensory input (producing enhanced perception), and increase communication between brain regions that do not normally interact (underlying unusual associative thinking and synesthesia-like phenomena).
Why It Matters
The REBUS model proposes that psychedelics loosen the brain's top-down predictions, allowing raw sensory data greater influence on conscious experience — consistent with the visual distortions and conceptual flexibility reported with 25E-NBOH. The related compound 25C-NBF has demonstrated psychoplastogenic properties (promoting neural growth) and rapid antidepressant effects in rodents,[19] suggesting the N-benzylphenethylamine class may share the neuroplasticity-promoting capacity documented for classical psychedelics.
Several questions remain unanswered for 25E-NBOH specifically: whether it promotes structural brain changes (neuroplasticity) at sub-hallucinogenic doses, what its signalling bias profile looks like compared to other NBOH members, and whether the active metabolite 2C-E contributes meaningfully to the subjective experience or is present only at negligible concentrations.
Subjective Effects[edit]
The 25E-NBOH experience is defined by a distinctive tension between mental lucidity and physical discomfort. Users consistently report that analytical capacity and verbal fluency remain relatively intact even as visual perception becomes profoundly altered — a clear-headed quality that separates it from the cognitive dissolution characteristic of high-dose tryptamines. The experience intensifies proportionally with dose, progressing from mild visual enhancement at threshold to pronounced pattern recognition and transpersonal phenomena at higher levels. Set and setting strongly modulate the psychological character, but the somatic dimension — muscle tightness, cold extremities, a bodily pressure from vasoconstriction — is pharmacologically intrinsic and present across the dose range.
Compared to 2C-E, which requires milligram oral doses and lasts considerably longer, 25E-NBOH is active at microgram sublingual doses with a more compressed timeline. It is more stimulating and visually oriented than psilocybin, but carries a cardiovascular body load more reminiscent of the NBOMe series than of classical tryptamine psychedelics.
Effect Grid
Full psychedelic visual field emerges — visual drifting and morphing are prominent, geometric overlays appear on surfaces, color enhancement is vivid, and tracers follow moving objects. Internal hallucinations become accessible with closed eyes. Time alteration is pronounced; minutes may feel stretched or compressed unpredictably.
Cognitive effects include enhanced thought connectivity, pattern recognition enhancement, creativity enhancement, and introspective depth. The characteristic clear-headedness of 25E-NBOH is maintained — analytical capacity persists alongside perceptual disruption, distinguishing this from tryptamine psychedelics at equivalent intensity.
Vasoconstriction is notable at this tier — muscle soreness, cold extremities, and bodily pressure are commonly reported. Stimulation is pronounced. Temperature dysregulation may occur. Total duration is 4–6 hours.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual breathing · Tracers · Music enhancement · Brightness alteration · Environmental patterning · Symmetrical texture repetition · After-images · Auditory distortion · Auditory enhancement · Depth perception distortion · Light sensitivity · Perspective distortion · Sound sensitivity · Visual morphing · Touch enhancement · Visual acuity enhancement · Auditory misinterpretation · Peripheral vision distortion · Spatial disorientation · Visual diffraction · Visual haze / noise · Visual melting · Synesthesia · Peripheral misidentification · Proprioceptive distortion · Vestibular distortion · Olfactory enhancement · Taste enhancement · Visual processing acceleration · Visual magnification · Flashbacks · Object transformations · Internal hallucinations · Object activation · Visual recursion · Environmental orbism / cubism · External hallucinations · Visual scenery slicing · Auditory hallucinations · Perspective hallucinations · Visual flipping · Persisting hallucinations
Environmental patterning · Symmetrical texture repetition · After-images · Auditory distortion · Auditory enhancement · Depth perception distortion · Light sensitivity · Perspective distortion · Sound sensitivity · Visual morphing · Touch enhancement · Visual acuity enhancement · Auditory misinterpretation · Peripheral vision distortion · Spatial disorientation · Visual diffraction · Visual haze / noise · Visual melting · Synesthesia · Peripheral misidentification · Proprioceptive distortion · Vestibular distortion · Olfactory enhancement · Taste enhancement · Visual processing acceleration · Visual magnification · Flashbacks · Object transformations · Internal hallucinations · Object activation · Visual recursion · Environmental orbism / cubism · External hallucinations · Visual scenery slicing · Auditory hallucinations · Perspective hallucinations · Visual flipping · Persisting hallucinations
Spontaneous body sensations · Body high · Muscle tension · Wakefulness · Appetite suppression · Dry mouth · Tingling / electric sensations · Excessive sweating · Nausea · Dizziness · Headache · Heart rate perception changes · Insomnia · Laughter fits · Motor control impairment · Physical fatigue · Restlessness · Tactile euphoria · Vibrations / buzzing · Bruxism · Sexual arousal enhancement · Dehydration sensation · Bodily lightness · Bodily pressures · Body schema distortion · Breathing alteration · Salivation · Trembling · Abnormal heartbeat · Increased urination · Diarrhea · Involuntary body movements · Nystagmus (eye wobbles) · Vomiting · Motor control enhancement · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Wakefulness · Appetite suppression · Dry mouth · Tingling / electric sensations · Excessive sweating · Nausea · Dizziness · Headache · Heart rate perception changes · Insomnia · Laughter fits · Physical fatigue · Restlessness · Tactile euphoria · Vibrations / buzzing · Bruxism · Sexual arousal enhancement · Dehydration sensation · Bodily lightness · Bodily pressures · Body schema distortion · Breathing alteration · Salivation · Trembling · Abnormal heartbeat · Increased urination · Diarrhea · Involuntary body movements · Nystagmus (eye wobbles) · Vomiting · Motor control enhancement · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Conceptual thinking · Memory suppression · Thought connectivity · Immersion enhancement · Cognitive euphoria · Cognitive flexibility · Introspection enhancement · Multiple thought streams · Openness enhancement · Creativity enhancement · Thought acceleration · Cognitive fatigue · Cognitive impairment · Focus suppression · Humor enhancement · Increased nature relatedness · Memory fragmentation · Thought disorganization · Thought loops · Analysis enhancement · Information processing enhancement · Analysis suppression · Confusion · Information processing suppression · Memory replays · Motivation suppression · Synchronicity · Focus enhancement · Motivation enhancement · Cognitive dysphoria · Thought deceleration · Delusions of sobriety · Delusions · Amnesia
Immersion enhancement · Cognitive euphoria · Cognitive flexibility · Introspection enhancement · Multiple thought streams · Openness enhancement · Creativity enhancement · Thought acceleration · Cognitive fatigue · Cognitive impairment · Focus suppression · Humor enhancement · Increased nature relatedness · Memory fragmentation · Thought disorganization · Thought loops · Analysis enhancement · Information processing enhancement · Analysis suppression · Confusion · Information processing suppression · Memory replays · Motivation suppression · Synchronicity · Focus enhancement · Motivation enhancement · Cognitive dysphoria · Thought deceleration · Delusions · Amnesia
Simultaneous emotions · Anxiety · Empathy enhancement · Catharsis · Dysphoria · Irritability
Dysphoria · Irritability
Disinhibition · Social connection · Automaticity · Trust enhancement · Communication enhancement · Flow state · Sociability enhancement · Communication suppression · Sociability suppression · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Communication enhancement · Flow state · Sociability enhancement · Communication suppression · Sociability suppression · Social disconnection · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Time cessation
Transpersonal memory access · Transpersonal visions · Entity contact
Anticipatory response · Recursive awareness
Timeline
First alerts emerge — mild stimulation, slight visual sharpening, awareness of blotter taste. Vasoconstriction may begin as faint peripheral tightness.
Progressive intensification of visual and somatic effects. Color enhancement becomes noticeable, geometric hints appear. Vasoconstriction establishes; transitional anxiety possible as intensity builds.
Full expression of visual, cognitive, and somatic effects. Geometry, color enhancement, visual drifting, and morphing at maximum intensity. Thought connectivity and pattern recognition prominent.
Gradual recession of visual effects; body load persists. Cognitive clarity returns before perceptual baseline. Stimulation remains notable.
Residual stimulation, mild mood elevation, and possible insomnia. Vasoconstriction resolves. Subtle perceptual brightness may linger.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
No controlled toxicity data, lethal dose values, or safety margin calculations exist for 25E-NBOH in any species.
Xiang et al. state that 25E-NBOH "has caused several poisoning cases and even fatal cases",[4] but provide no case numbers, circumstances, or clinical details. This is the only published reference to fatalities from this specific compound. safety citation needed
Class-Level Risks
The NBOMe/NBOH class shares a toxicity pattern characterized by overstimulation of the sympathetic nervous system and excess serotonin activity. A review of 51 published NBOMe toxicity cases identified the following complications[5]:
- Seizures — documented across multiple compounds in the class
- Dangerous body temperature elevation — can trigger muscle breakdown and organ failure
- Muscle breakdown — linked to seizures, overheating, and sustained vasoconstriction
- Agitation and delirium — including violent behavior and complete disorientation
- Multi-organ failure — the terminal pathway in severe cases
Zawilska et al. confirm this profile and report that NBOMe use has caused deaths.[17] Isbister et al. describe severe toxicity from blotter paper substances in this class.[20]
Cardiovascular Effects
Alpha-1A adrenoceptor binding documented for the NBOMe class[16] produces constriction of blood vessels throughout the body. This can cause high blood pressure, rapid heart rate, and reduced blood flow to the extremities. The serotonergic component adds further cardiovascular risk through coronary vessel constriction.[21]
Analytical Misidentification
25E-NBOH breaks down into 2C-E under standard laboratory testing conditions,[12][10] and 2C-E is also produced as an actual metabolite in the body.[3] This means laboratory detection of 2C-E in a person's system cannot distinguish between 2C-E use and 25E-NBOH use — cases of 25E-NBOH poisoning may be misattributed to 2C-E.
Psychological Risks
No controlled data on psychological adverse events exist for 25E-NBOH. By class analogy with serotonergic psychedelics:
- Acute distress ("bad trip"): anxiety, paranoia, panic, and transient psychotic symptoms are expected at higher doses and in predisposed individuals. The compound's dose sensitivity increases the risk of accidental high-dose exposure.
- Persistent perceptual changes (HPPD): no case reports exist for 25E-NBOH, but risk is established at the class level for N-benzylphenethylamines.
- Psychosis precipitation: serotonin 2A receptor agonists can trigger acute psychotic episodes in individuals with predisposition to psychotic disorders.
- Agitation and delirium: documented for NBOMe class intoxications at high doses.[5]
Tolerance and Dependence
No published tolerance or dependence data exist for 25E-NBOH specifically.
Tolerance
By class pharmacology, rapid tolerance develops through downregulation after a single dose. Research in mice demonstrated that[22]:
- Tolerance is detectable within 24 hours of a single administration
- Repeated dosing over several days produces progressively diminished effects
- Cross-tolerance exists between psychedelic 5-HT₂A agonists — using 25E-NBOH would be expected to reduce the effects of LSD, psilocybin, mescaline, and other serotonergic psychedelics, and vice versa
Dependence
No dependence studies have been conducted for 25E-NBOH.[1] Classical psychedelics as a class show very low reinforcing potential in animal models. The related compound 25C-NBF produced no rewarding or reinforcement in rodents.[19] No evidence of compulsive use, physical dependence, or withdrawal exists for any NBOH compound.
Drug Interactions
MAOIs
Combination with monoamine oxidase inhibitors — both reversible (moclobemide) and irreversible (phenelzine, tranylcypromine) — carries serious serotonin syndrome risk. The combination of 5-HT₂A agonism with elevated serotonin levels from monoamine oxidase inhibition can produce potentially fatal toxicity.[23] No safe combination protocol exists.
SSRIs and SNRIs
Chronic SSRI or SNRI use may blunt psychedelic effects through 5-HT₂A receptor downregulation. The interaction in combined serotonergic states is complex and incompletely understood.[23]
Lithium
Lithium combined with psychedelic 5-HT₂A agonists has been associated with increased seizure risk in case reports. safety citation needed
Vasoconstrictive Substances
Combining 25E-NBOH with other substances that constrict blood vessels (amphetamines, cocaine, MDMA, ergotamines) produces additive cardiovascular risk.[5] The combined effect can produce dangerous blood pressure elevation and reduced blood flow to extremities.
Seizure-Threshold-Lowering Agents
Given the seizure risk documented for the NBOMe/NBOH class, combination with substances that independently lower seizure threshold (tramadol, bupropion) represents additive risk. safety citation needed
Contraindications
Absolute
- Concurrent MAOI use: serotonin syndrome risk is mechanistically certain and potentially fatal
- Seizure disorders: seizure threshold reduction is documented at class level[5][17]
- Cardiovascular disease: pre-existing high blood pressure, coronary artery disease, peripheral vascular disease, or structural heart defects — blood vessel constriction from adrenoceptor activity poses direct risk[16]
Relative
- Personal or family history of psychotic disorders: 5-HT₂A agonism can trigger acute psychosis in predisposed individuals
- Concurrent lithium use: seizure risk elevation reported at class level
- Pregnancy: no reproductive safety data exist; effects of 5-HT₂A agonism during fetal development are unknown citation needed
- Concurrent stimulant use: additive cardiovascular risk from combined blood vessel constriction
Harm Reduction[edit]
Forms & Identification
25E-NBOH circulates on blotter paper that is visually indistinguishable from blotters containing LSD, NBOMe compounds, or other substances active at microgram doses. No visual inspection can confirm identity or dosage.
Reagent testing provides preliminary identification but cannot confirm purity or dose. The compound's thermolability means it degrades to 2C-E under heat, which can confuse results from analytical methods that apply thermal energy. Quantitative laboratory analysis is the only way to confirm both identity and dose with certainty.
Guidelines
- Test every batch with reagent kits before use; consider laboratory analysis services for quantitative confirmation
- Start with the lowest available dose — 25E-NBOH is highly dose-sensitive, and small differences in amount can produce substantially different experiences
- Use the sublingual route as intended; do not alter the route of administration
- Have a sober, trusted companion present throughout the experience
- Ensure access to a warm, comfortable environment — vasoconstriction can cause cold extremities and physical discomfort
- Keep a light meal available for after the experience; avoid eating heavily beforehand
- Allow a full recovery day afterward with no obligations
- Wait at least two weeks between uses to allow full tolerance reset
Set & Setting
The clear-headed quality reported for 25E-NBOH does not reduce psychological risk — cognitive lucidity can coexist with intense perceptual distortion and emotional intensity. A calm, familiar environment with a trusted sober companion provides the strongest foundation for a manageable experience.
The pronounced body load (muscle tension, cold extremities, physical pressure) is pharmacologically intrinsic and not a sign that something has gone wrong. Knowing this in advance reduces the likelihood of anxiety spiraling in response to somatic discomfort.
Aftercare & integration. The vasoconstriction-related body load may leave residual muscle soreness for 12–24 hours after the experience. Gentle movement, hydration, and warmth help with physical recovery. Adequate sleep the following night is important — the stimulating quality of the compound may make falling asleep difficult on the day of use.
Psychedelic experiences can surface unexpected emotional material. Journaling, conversation with a trusted person, or professional integration support can help process the experience. If distressing perceptual changes (visual haze / noise, trailing, pattern recognition in blank surfaces) persist beyond a few days, consult a healthcare provider familiar with HPPD.
Recovery & Support
While 25E-NBOH does not produce physical dependence, patterns of frequent psychedelic use can become psychologically habitual. If use is escalating in frequency, occurring in response to emotional distress rather than intentional exploration, or causing conflict in daily life, professional support is appropriate.
Resources include psychedelic-informed therapists, harm reduction services such as DanceSafe and The Loop, and general substance use support through SAMHSA's National Helpline (1-800-662-4357).
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Uncomfortable physical effects (muscle tension, nausea, mild anxiety) are common and do not alone constitute an emergency. Seek immediate help if any of the following occur: seizure activity, loss of consciousness, chest pain, extreme body temperature (skin very hot to the touch), severe confusion or violent agitation, or sustained panic that the person cannot be talked through.
Immediate steps:
- 1. Call emergency services immediately if seizure, unconsciousness, chest pain, or dangerous body temperature is present
- 2. Keep the person in a cool, quiet environment
- 3. If conscious, encourage slow breathing and provide calm reassurance
- 4. If unconscious and breathing, place in the recovery position (on their side)
- 5. Do not restrain the person unless they are in immediate danger of harming themselves
- 6. Do not induce vomiting
What to tell the dispatcher: Name the substance (25E-NBOH or "a synthetic psychedelic from the NBOH class"), the approximate time of ingestion, the dose if known, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
No reversal agent exists for 25E-NBOH or any serotonergic psychedelic. Treatment is supportive.
Legal Status[edit]
25E-NBOH is not scheduled under any United Nations drug control conventions,[11] leaving regulation to individual nations. Several countries have captured it through broad scheduling language covering N-benzylphenethylamines or substituted phenethylamines, while in others it remains in a legal grey area.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled under the N-benzylphenethylamine catch-all clause; possession and supply are serious criminal offences[24] |
| Brazil | Scheduled (~Dec 2018) | Explicitly controlled following forensic identification of NBOH compounds in seized blotter papers[11][24] |
| Canada | Controlled (CDSA) | Captured under blanket phenethylamine language in the Controlled Drugs and Substances Actcitation needed |
| United States | Not explicitly scheduled | Potentially subject to prosecution under the Federal Analogue Act (21 USC §813) as structurally similar to Schedule I substancescitation needed |
| Australia | Unverified | May be captured under generic phenethylamine scheduling; specific verification unavailablecitation needed |
| European Union | Varies by member state | Germany, Sweden, and other member states have scheduled specific NBOH compounds; no EU-wide scheduling confirmed |
Analog Act Considerations
In the United States, the Federal Analogue Act extends Schedule I/II controls to substances "substantially similar" in structure or effect to a scheduled compound when intended for human consumption. 25E-NBOH is structurally analogous to 25I-NBOMe (Schedule I since 2013) and pharmacologically similar in mechanism and potency. Prosecution under this act is legally plausible but requires case-by-case determination and has not been tested specifically for 25E-NBOH.
references
- [1]
- [2] ^abEttrup A, Hansen M, Santini MA, Paine J, Gillings N, Palner M, Lehel S, Herth MM, Madsen J, Kristensen J, Begtrup M, Knudsen GM (2011) Radiosynthesis and in vivo evaluation of a series of substituted 11C-phenethylamines as 5-HT2A agonist PET tracers — European Journal of Nuclear Medicine and Molecular Imaging doi:10.1007/s00259-010-1686-8
- [3] ^abcdVágnerová M, Palivec P, Mrnává M et al. (2026) Metabolic profile of 25E-NBOH in human liver microsomes, rat urine, and fungus Cunninghamella elegans — Journal of Pharmaceutical and Biomedical Analysis doi:10.1016/j.jpba.2026.117417
- [4] ^abcXiang J, Wen D, Zhai W, Zhao J, Xiang P, Ma C, Shi Y (2024) Metabolic characterization of 25X-NBOH and 25X-NBOMe phenethylamines based on UHPLC-Q-Exactive Orbitrap MS in human liver microsomes. — Journal of Pharmaceutical and Biomedical Analysis doi:10.1016/j.jpba.2024.116020
- [5]
- [6]