25C-NBOH
4-chloro-2,5-dimethoxy-N-(2-hydroxybenzyl)phenethylamine
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25C-NBOH is a synthetic psychedelic of the phenethylamine class. It is a structural variant of 25C-NBOMe, differing by a single chemical group on the benzyl ring. It activates serotonin receptors in the brain, producing the visual and cognitive shifts characteristic of serotonergic psychedelics.[1][2]
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The NBOH compound class was developed through systematic research into N-benzyl phenethylamine pharmacology.[3] 25C-NBOH appeared on the novel psychoactive substance market between 2014 and 2017, first identified in blotter papers seized by Brazilian law enforcement.[4] It remains unscheduled under United Nations drug conventions, though Brazil and some US states have added specific NBOH compounds to controlled schedules.
Subjective effects include geometric visual patterns, color enhancement, emotional intensification, conceptual thinking, and a sense of boundary dissolution. The experience is more visually driven and physically stimulating than tryptamine psychedelics, with a narrow gap between threshold and strong effects — small dose changes produce large shifts in intensity. Nausea, anxious fixation, and a numbing or metallic taste from the blotter are common unwanted effects.
25C-NBOH does not produce physical dependence, but animal studies document dangerous heart rhythm changes and heart cell death.[5] Active in microgram quantities with a steep dose-response curve, the compound shares a structural class with 25C-NBOMe, for which documented fatalities exist.[6][7] No clinical studies exist — the safety profile rests on a single animal study, class-level data, and forensic reports.
History[edit]
Discovery
The N-benzyl phenethylamine psychedelic class originates from Ralf Heim's 2002 patent.[2] The NBOH variant was developed by Martin Hansen and Jesper Kristensen through systematic research across 48 N-benzyl phenethylamines.[3][8] 25C-NBOH has no recorded date of first synthesis — its existence follows from the systematic compound series.
Market emergence
25C-NBOH appeared on the novel psychoactive substance market between 2014 and 2017. Machado et al. published the first forensic identification, detecting it in blotter papers seized by Brazilian law enforcement.[4] By the late 2010s, NBOH compounds had become the dominant hallucinogens in seized Brazilian blotter papers, displacing both LSD and NBOMe compounds.
Regulatory history
No NBOH compounds appear in any United Nations drug control conventions.[4] Brazil scheduled 25C-NBOH in December 2018.[9] In the United States it is not directly scheduled federally, though the Federal Analogue Act may apply given its structural similarity to the Schedule I compound 25C-NBOMe.
The name 25C-NBOH encodes its chemistry: "25" marks the N-benzyl substitution pattern, "C" identifies the 4-chloro substituent from the parent compound 2C-C, and "NBOH" specifies the ortho-hydroxybenzyl group.
Chemistry[edit]
Structural class
25C-NBOH belongs to the N-benzyl phenethylamine class, built on the parent compound 2C-C (2,5-dimethoxy-4-chlorophenethylamine). Attaching a 2-hydroxybenzyl group to the nitrogen dramatically increases binding strength at serotonin receptors.[3] The molecular formula is C₁₇H₂₀ClNO₃ (molecular weight 321.8 g/mol).
The NBOH designation marks the ortho-hydroxyl group on the benzyl ring — one functional group different from the NBOMe series, which carries an ortho-methoxy group instead.[12] The free phenol makes 25C-NBOH susceptible to oxidative breakdown,[12] and standard gas chromatography can cause the molecule to decompose and be misidentified as the parent compound 2C-C — liquid chromatography is required for reliable identification.[4][13]
Pharmacology[edit]
Mechanism of action
25C-NBOH is presumed to produce its effects through strong activation of serotonin receptors in the brain.[2][14] No binding data have been published for 25C-NBOH specifically — the mechanism is inferred from research on related N-benzyl phenethylamines[3] and from studies of the closely related 25I-NBOH, which showed potent serotonin receptor activation with very little stimulant activity.[1] That receptor activation triggers a calcium-signaling cascade inside neurons; this specific pathway is what produces psychedelic effects.[15]
Pharmacokinetics
Sublingual absorption is the primary documented route — the blotter is held under the tongue, absorbing through the oral mucosa and bypassing the liver's first-pass processing.[4] The compound is primarily broken down by an enzyme called CYP2D6, distinct from the related 25C-NBOMe, which uses a different enzyme.[12]
25C-NBOH is also produced in the body when 25C-NBOMe is consumed.[11][10] No human pharmacokinetic studies have been published; duration figures from user reports (5–7 hours total, 15–45 minutes onset sublingual) remain unconfirmed.safety citation needed
Neuroscience[edit]
No direct neuroimaging or neurochemical data exist for 25C-NBOH. The following draws on established mechanisms for serotonergic psychedelics and preclinical data from the NBOH class.
Where it acts
As a presumed serotonin receptor activator, 25C-NBOH is expected to act on neurons in the prefrontal cortex, disrupting the brain's normal filtering of sensory information.[2] Studies using 25I-NBOH as a research probe documented slow brainwave patterns and behavioral arrest in rodents — signatures of selective cortical activation.[16] Across the broader psychedelic literature, this class of receptor activation consistently dissolves the brain's default network and increases global connectivity.citation needed
Why it matters
This receptor activation may loosen the brain's confidence in its existing predictions, allowing raw sensory input greater influence over perception — accounting for pattern recognition enhancement, geometric visuals, and conceptual fluidity.citation needed The same receptors also drive rapid structural changes in neurons — new connections and branches — a property called neuroplasticity.citation needed Whether 25C-NBOH shares this capacity has not been tested.
Key unknowns include whether 25C-NBOH promotes neuroplasticity at relevant doses, what its signaling bias profile looks like compared to related compounds, and whether genetic variation in CYP2D6[12] alters brain exposure. The relationship between its documented cardiac effects[5] and autonomic changes during the psychedelic state also remains unexplored.
Subjective Effects[edit]
The 25C-NBOH experience is defined by intense visual activity and somatic stimulation. Colors deepen, surfaces shift and ripple, and geometry emerge with eyes open or closed. The mental character leans outward — toward sensation — rather than inward. Dose sensitivity is extreme: a narrow range separates threshold from overwhelming intensity.
Within the serotonergic psychedelic landscape, 25C-NBOH sits closest to 25C-NBOMe in character — comparable potency and duration, with a more abrupt onset and offset than LSD. The N-benzyl phenethylamine class generally produces a more visually saturated, physically charged experience than tryptamines like psilocybin, with less of the psychological weight and introspective depth.
Effect Grid
A common dose produces a full psychedelic experience. Visual effects are pronounced — geometry, visual drifting, color enhancement, tracers, and symmetrical texture repetition are clearly present. Internal hallucinations may emerge. Cognitive effects include conceptual thinking, thought connectivity, pattern recognition enhancement, and emotional enhancement. Set and setting become major modulators of the experience.
Physical effects are notable: stimulation and wakefulness are reliable, with muscle tension, vasoconstriction, and possible temperature dysregulation. Nausea may occur during the come-up. Appetite is suppressed.
Full functional impairment — do not drive or operate machinery. Total duration approximately 5–7 hours with extended aftereffects possible over subsequent days.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Tracers · Brightness alteration · Music enhancement · Symmetrical texture repetition · Environmental patterning · Visual breathing · Perspective distortion · Auditory enhancement · Depth perception distortion · Visual diffraction · Light sensitivity · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Visual haze / noise · Visual morphing · Holotropic state · Auditory distortion · Auditory misinterpretation · Proprioceptive distortion · Visual melting · Visual acuity enhancement · Visual magnification · Peripheral misidentification · Synesthesia · After-images · Dreaming enhancement · Touch enhancement · Visual processing acceleration · Vestibular distortion · Touch suppression · Tinnitus · Flashbacks · Object transformations · Internal hallucinations · Visual recursion · Environmental orbism / cubism · Object activation · Visual scenery slicing · External hallucinations · Visual processing suppression · Auditory hallucinations · Perspective hallucinations · Gustatory hallucination · Visual flipping · Persisting hallucinations
Environmental patterning · Visual breathing · Perspective distortion · Auditory enhancement · Depth perception distortion · Visual diffraction · Light sensitivity · Peripheral vision distortion · Sound sensitivity · Spatial disorientation · Visual haze / noise · Visual morphing · Holotropic state · Auditory distortion · Auditory misinterpretation · Proprioceptive distortion · Visual melting · Visual acuity enhancement · Visual magnification · Peripheral misidentification · Synesthesia · After-images · Dreaming enhancement · Touch enhancement · Visual processing acceleration · Vestibular distortion · Touch suppression · Tinnitus · Flashbacks · Object transformations · Internal hallucinations · Visual recursion · Environmental orbism / cubism · Object activation · Visual scenery slicing · External hallucinations · Visual processing suppression · Auditory hallucinations · Perspective hallucinations · Gustatory hallucination · Visual flipping · Persisting hallucinations
Wakefulness · Body high · Spontaneous body sensations · Muscle tension · Dry mouth · Appetite suppression · Restlessness · Heart rate perception changes · Insomnia · Physical fatigue · Bodily lightness · Nausea · Dehydration sensation · Headache · Dizziness · Laughter fits · Tingling / electric sensations · Vibrations / buzzing · Bodily pressures · Body schema distortion · Breathing alteration · Excessive sweating · Motor control impairment · Tactile euphoria · Sexual arousal enhancement · Bodily heaviness · Involuntary body movements · Nystagmus (eye wobbles) · Trembling · Abnormal heartbeat · Increased urination · Bruxism · Vomiting · Seizure threshold reduction · Tactile hallucination
Muscle tension · Dry mouth · Appetite suppression · Restlessness · Heart rate perception changes · Insomnia · Physical fatigue · Bodily lightness · Nausea · Dehydration sensation · Headache · Dizziness · Laughter fits · Tingling / electric sensations · Vibrations / buzzing · Bodily pressures · Body schema distortion · Breathing alteration · Excessive sweating · Tactile euphoria · Sexual arousal enhancement · Bodily heaviness · Involuntary body movements · Nystagmus (eye wobbles) · Trembling · Abnormal heartbeat · Increased urination · Bruxism · Vomiting · Seizure threshold reduction · Tactile hallucination
Immersion enhancement · Aesthetic enhancement · Openness enhancement · Thought connectivity · Thought acceleration · Cognitive euphoria · Cognitive flexibility · Introspection enhancement · Multiple thought streams · Memory suppression · Cognitive fatigue · Cognitive impairment · Focus suppression · Increased nature relatedness · Thought loops · Creativity enhancement · Humor enhancement · Confusion · Information processing suppression · Memory fragmentation · Synchronicity · Thought disorganization · Analysis enhancement · Cognitive dysphoria · Memory replays · Amnesia
Thought connectivity · Thought acceleration · Cognitive euphoria · Cognitive flexibility · Introspection enhancement · Multiple thought streams · Memory suppression · Cognitive fatigue · Cognitive impairment · Focus suppression · Increased nature relatedness · Thought loops · Creativity enhancement · Humor enhancement · Confusion · Information processing suppression · Memory fragmentation · Synchronicity · Thought disorganization · Analysis enhancement · Cognitive dysphoria · Memory replays
Anxiety · Empathy enhancement · Catharsis · Dysphoria
Depersonalization · Trust enhancement · Communication enhancement · Flow state · Sociability enhancement · Boundary dissolution · Ego dissolution · Cognitive disconnection · Identity alteration
Sociability enhancement · Boundary dissolution · Ego dissolution · Cognitive disconnection · Identity alteration
Transpersonal visions · Entity contact · Death-rebirth sequence
Mindfulness enhancement · Recursive awareness
Timeline
Sublingual absorption begins with characteristic numbing or metallic taste at the administration site. First alerts include mild body awareness, subtle perceptual brightening, and faint stimulation.
Progressive intensification of visual and somatic effects. Body load (nausea, muscle tension) typically peaks during this phase. Geometry and color enhancement emerge.
Full expression of visual geometry, color enhancement, conceptual thinking, and emotional intensification. Maximum perceptual and cognitive alteration. Set and setting exert strongest influence on experiential direction.
Gradual reduction in visual intensity and cognitive alteration. Stimulation and wakefulness may persist after visual effects resolve. Appetite begins to return.
Residual mood and perceptual shifts over hours to days. Enhanced pattern recognition, altered emotional baseline, and mild visual anomalies may persist. The extended aftereffect period (up to several days per user reports) may reflect 5-HT2A receptor downregulation.
Safety[edit]
- Acute toxicity
- Moderate
- 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 · mesc
Toxicity
Acute toxicity
No lethal dose or controlled toxicity data exist for 25C-NBOH in any species. No published fatality has been specifically attributed to 25C-NBOH as the primary substance consumed.safety citation needed
The risk of lethality is extrapolated from 25C-NBOMe deaths: a young male died 12 hours after ingestion with signs of serotonin syndrome,[6] and a teenager drowned following confusion and agitation after ingesting 25C-NBOMe and 25H-NBOMe.[7] At high doses the NBOMe/NBOH class can produce seizures, extreme agitation, muscle breakdown, blood clotting disorders, and multi-organ failure.[17][18][14]
Heart toxicity
The only published study directly testing 25C-NBOH found significant cardiac effects in animals.[5] It dramatically reduced the survival of heart muscle cells and caused QT prolongation — a dangerous disruption to heart rhythm — and slowed heart rate in live rats. Human cardiac safety is unknown.
Stimulant-like crisis
At excessive doses, the NBOH and NBOMe class produces a stimulant-like emergency: rapid heart rate, high blood pressure, dangerously elevated body temperature, and dilated pupils.[14] In a clinical series involving a related compound, 7 of 10 patients required high-dose sedation for severe agitation.[17]
Psychological Risks
No systematic data exist for 25C-NBOH specifically. Class-level evidence from NBOMe/NBOH intoxications documents severe anxiety, paranoia, confusion, and violent agitation at high doses.[14][17]
Persistent visual disturbances and prolonged psychosis are recognized risks for serotonergic psychedelics as a class and are presumed to apply — particularly given the high potency of N-benzyl phenethylamines.safety citation needed Microgram-range dosing with a steep dose-response curve creates elevated risk of unintentional overdose, compounding both physical and psychological harm.
Tolerance and Dependence
Tolerance builds almost immediately after ingestion, with a reported half-life of approximately one week and full reset at two weeks.safety citation needed The mechanism is presumed to involve rapid serotonin downregulation.[2][15]
25C-NBOH is not considered habit-forming. Serotonergic psychedelics do not activate the brain's reward circuits, and the compound shows negligible activity at the transporters responsible for reinforcing drug use.[1]
Drug Interactions
The interaction profile stems from two features: potent serotonin receptor activation and CYP2D6-dependent metabolism. No substance-specific interaction studies have been published.
Serotonergic combinations
The most dangerous interaction involves drugs that raise serotonin levels. Combining 25C-NBOH with tramadol, monoamine oxidase inhibitors, SSRIs, SNRIs, or triptans substantially elevates the risk of serotonin syndrome[19][20] — a potentially fatal condition involving muscle rigidity, dangerously high body temperature, rapid heart rate, and altered consciousness.
Metabolic interactions
Drugs that inhibit CYP2D6 — including fluoxetine, paroxetine, bupropion, and quinidine — slow the breakdown of 25C-NBOH and raise blood levels.[12] Several of these also increase serotonin, creating a double risk through both slowed elimination and increased serotonergic activity.
Stimulants
Combining with stimulants raises the risk of dangerously elevated body temperature — a documented contributor to fatal outcomes in the NBOMe class.[14]
Cannabis
The interaction with cannabis is uncharacterized. Cannabis commonly intensifies subjective psychedelic effects, but no specific safety data exist for this combination.
Contraindications
No substance-specific contraindication data have been published. The following are inferred from the compound's pharmacological profile and class-level evidence:
- Heart conditions: Documented QT prolongation[5] and heart cell toxicity make pre-existing heart rhythm disorders, long QT syndrome, and structural heart disease absolute contraindications. Other QT-prolonging medications amplify this risk.
- Seizure disorders: Seizures are documented in NBOMe/NBOH class intoxications.[17][18] Pre-existing epilepsy is an absolute contraindication.
- Psychiatric conditions: Personal or family history of psychosis is a relative contraindication.
- MAO inhibitor therapy: Concurrent use creates life-threatening serotonin syndrome risk.
- Liver impairment: CYP2D6-dependent metabolism[12] suggests impaired clearance, though direct glucuronidation provides partial redundancy.
- Pregnancy: No reproductive toxicity data exist. Standard precautionary contraindication applies.
Harm Reduction[edit]
Forms & Identification
The blotter format is visually indistinguishable from LSD, NBOMe compounds, and other NBOH variants. A bitter, numbing, or metallic taste on the tongue confirms the substance is not LSD, which is tasteless. This taste test cannot distinguish between different N-benzyl compounds — quantitative laboratory testing is the only reliable method for confirming identity and dose.
Guidelines
- Test every sample with reagent kits before use — the blotter format carries high substitution risk
- Start with the lowest reported active dose and wait the full onset period (up to 45 minutes sublingual) before considering any increase
- Do not redose — tolerance builds immediately, and redosing during a slow onset accounts for a significant proportion of adverse experiences
- Ensure access to water and a comfortable place to sit or lie down
- Avoid driving, swimming, heights, and any environment where impaired coordination poses physical danger
- Keep the setting calm and the group small — overstimulation amplifies anxiety at high effect levels
- Have a sober companion present who knows what substance was taken and at what dose
Set & Setting
The steep dose-response curve and microgram-level potency make environmental preparation especially important. A familiar, physically safe, low-stimulation environment reduces the likelihood of anxiety escalation. A trusted, sober companion is strongly recommended, particularly for anyone without prior experience with high-potency phenethylamine psychedelics.
Aftercare & integration. The 5–7 hour duration typically leaves residual stimulation and altered perception for several hours after the primary effects subside. Sleep may be difficult for 2–4 hours after the experience ends.
Eat light, easily digestible food when appetite returns. Hydrate steadily. Avoid major decisions or demanding tasks for 24 hours.
If the experience was intense or distressing, writing or talking about it within the first few days can help process the content. Recurring intrusive imagery, persistent anxiety, or visual disturbances lasting more than a few days warrant consultation with a mental health professional experienced with psychedelic-related concerns.
Recovery & Support
25C-NBOH does not produce physical dependence, and compulsive use is rare due to rapid tolerance. Repeated use of high-potency psychedelics can reflect broader patterns of psychological difficulty or avoidance.
Speaking with a counselor or therapist can help clarify patterns when psychedelic use has become a way of managing emotional difficulty. Peer support communities such as the Fireside Project offer non-clinical spaces to process difficult experiences.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency
Anxiety, nausea, and confusion are distressing but typically self-limiting. Seek immediate help if any of the following occur: seizure activity, loss of consciousness, chest pain or irregular heartbeat, body temperature that feels dangerously hot, violent agitation or total disconnection from reality with risk of self-harm, or breathing difficulties.
Immediate steps
- Call emergency services immediately if any of the above signs are present
- Move the person to a safe, quiet space away from hazards
- Do not restrain unless there is immediate danger of self-harm — restraint can worsen agitation
- Keep them cool — remove excess clothing, apply cool water if overheating
- If unconscious and breathing, place in the recovery position (on their side, airway clear)
- Do not induce vomiting — sublingual absorption means the substance is already in the bloodstream
- Stay with them until help arrives
What to tell the dispatcher
State the substance name (25C-NBOH or "an NBOH psychedelic compound"), the approximate dose if known, the time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for medical help during a drug emergency.
Legal Status[edit]
25C-NBOH occupies a fragmented regulatory position distinct from its NBOMe structural counterpart. No NBOH compounds are listed under any United Nations drug control conventions,[4] and scheduling has proceeded through national action rather than international treaties.
Legal status information was compiled from published academic sources and government documents. Laws change frequently, and the information below may not reflect current regulations. Verify legal status through official government sources before making decisions based on this information.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United Nations | Not controlled | No NBOH compounds listed under any UN drug control convention[4] |
| United States | Not directly scheduled (federal) | 25C-NBOMe is Schedule I (2013). 25C-NBOH may constitute a Controlled Substance Analogue under the Federal Analogue Act when intended for human consumption. Louisiana: 25I-NBOH specifically listed as Schedule I (June 2013)citation needed |
| United Kingdom | Likely controlled | NBOMe compounds controlled under Class A via 2014 Amendment Order to Misuse of Drugs Act 1971.[21] Whether NBOH compounds fall within the generic definition is unresolved. Psychoactive Substances Act 2016 provides additional blanket coverage |
| Brazil | Controlled | NBOH compounds including 25C-NBOH scheduled December 2018[9] |
| Australia | Variable by state | State-level analogue provisions may apply. No specific national scheduling confirmed for NBOH compounds |
| European Union | Variable by member state | No harmonized EU-level control. May be covered under national generic or blanket NPS legislation in individual member states |
Analogue considerations
25C-NBOH and 25C-NBOMe differ by a single atom but share the same pharmacological target. In jurisdictions with structural analog legislation — such as the US Federal Analogue Act — this similarity may make 25C-NBOH a controlled substance when intended for human consumption, even without specific scheduling.
25C-NBOH is also produced in the body when 25C-NBOMe is consumed.[10][11] Its presence in biological specimens does not confirm which compound was originally taken.
references
- [1] ^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
- [2]
- [3] ^abcdHansen 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
- [4]
- [5] ^abcdYoon 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] ^abcAndreasen MF, Telving R, Rosendal I, Eg MB, Hasselstrøm JB, Andersen LV (2015) A fatal poisoning involving 25C-NBOMe. — Forensic Science International doi:10.1016/j.forsciint.2015.03.012