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Psychedex

25B-NBOH

4-bromo-2,5-dimethoxy-N-(2-hydroxybenzyl)phenethylamine

Sources
28
4 strong · 20 moderate · 4 weak

Studies and references cited across this article, graded by evidence strength.

Claims checked
88
61verified2partial24inconclusive1not supported

Inconclusive means the cited source neither confirms nor refutes the claim — a lower-confidence badge, not an error.

Generated
May 7, 2026 · pipeline-v5
Values approved
164/168 (98%)

Data points an editor reviewed and accepted for publication.

01

Value Provenance

Dosing

sublingualtrace

FieldPublishedAI ProposedConfidence
Threshold100 µg100 µglow
Low200–400 µg200–400 µglow
Common400–800 µg400–800 µglow
Strong800–1000 µg800–1000 µglow
Heavy1000+ µg1000+ µglow
Editorial

No published clinical dose-finding study exists for 25B-NBOH. Values derived from community consensus (PsychonautWiki user reports) and structural analog inference (25I-NBOH forensic blotter doses 300–1000 µg, Arantes 2017). Consistent with NBOH/NBOMe class microgram-range activity. All dose ranges are safety-critical and require strong editorial caveat before publication.

Reasoning

No published clinical dose-finding study exists for 25B-NBOH. Values derived from community consensus (PsychonautWiki user reports) and structural analog inference (25I-NBOH forensic blotter doses 300–1000 µg, Arantes 2017). Consistent with NBOH/NBOMe class microgram-range activity. All dose ranges are safety-critical and require strong editorial caveat before publication.

Evidence basis: community_consensus_large

Duration

sublingual

FieldPublishedAI ProposedConfidence
Onsettrace15–45 minutes15–45 minuteslow
Editorial

Community consensus (PsychonautWiki). Sublingual absorption bypasses first-pass metabolism, producing faster onset than oral 2C-B. No published human PK study for 25B-NBOH.

Reasoning

Community consensus (PsychonautWiki). Sublingual absorption bypasses first-pass metabolism, producing faster onset than oral 2C-B. No published human PK study for 25B-NBOH.

Evidence basis: community_consensus_large

Come uptrace30–60 minutes30–60 minuteslow
Editorial

Community consensus (PsychonautWiki). No published duration data for 25B-NBOH.

Reasoning

Community consensus (PsychonautWiki). No published duration data for 25B-NBOH.

Evidence basis: community_consensus_large

Peaktrace2–3 hours2–3 hourslow
Editorial

Community consensus (PsychonautWiki). Consistent with 2C-B peak duration by structural analogy (Mallaroni 2023).

Reasoning

Community consensus (PsychonautWiki). Consistent with 2C-B peak duration by structural analogy (Mallaroni 2023).

Evidence basis: community_consensus_large

Offsettrace1–2 hours1–2 hourslow
Editorial

Community consensus (PsychonautWiki). No published human data.

Reasoning

Community consensus (PsychonautWiki). No published human data.

Evidence basis: community_consensus_large

Totaltrace4–6 hours4–6 hourslow
Editorial

Estimated by class analogy with 2C-B (Mallaroni 2023: subjective effects of 2C-B largely resolve within 6 hours) plus community consensus. No published human duration study for 25B-NBOH.

Reasoning

Estimated by class analogy with 2C-B (Mallaroni 2023: subjective effects of 2C-B largely resolve within 6 hours) plus community consensus. No published human duration study for 25B-NBOH.

Evidence basis: structural_analogy

After effectstrace2–6 hours2–6 hourslow
Editorial

Community consensus (PsychonautWiki). Residual stimulation, possible headache, delayed sleep. No published data.

Reasoning

Community consensus (PsychonautWiki). Residual stimulation, possible headache, delayed sleep. No published data.

Evidence basis: community_consensus_large

Safety

Toxicity Profiletrace

FieldPublishedAI ProposedConfidence
Acutehighhighmedium
Chronicmoderatemoderatemedium
Organs Affectedcardiovascular, neurological, renalcardiovascular, neurological, renalmedium
Editorial

Acute rated 'high' per work-notes: Ivory 2022 poisoning cluster provides direct 25B-NBOH clinical toxicity data; Yoon 2022 cardiovascular data from 25I-NBOH/25C-NBOH analogs; multiple class fatalities documented (Halberstadt 2017, Zawilska 2020). Chronic downgraded from work-notes 'high' to 'moderate' per evidence discount rule: no chronic 25B-NBOH data exists; only class-level chronic evidence from 25I-NBOMe repeated dosing (Herian 2021 — memory deficiency, motor reduction, anxiety in rats). Chronic assessment is entirely analog-inferred, warranting one-level downgrade.

Reasoning

Acute rated 'high' per work-notes: Ivory 2022 poisoning cluster provides direct 25B-NBOH clinical toxicity data; Yoon 2022 cardiovascular data from 25I-NBOH/25C-NBOH analogs; multiple class fatalities documented (Halberstadt 2017, Zawilska 2020). Chronic downgraded from work-notes 'high' to 'moderate' per evidence discount rule: no chronic 25B-NBOH data exists; only class-level chronic evidence from 25I-NBOMe repeated dosing (Herian 2021 — memory deficiency, motor reduction, anxiety in rats). Chronic assessment is entirely analog-inferred, warranting one-level downgrade.

Evidence basis: published_case_series

Dependence Profiletrace

FieldPublishedAI ProposedConfidence
Physicalnonenonehigh
Psychologicalnegligiblenegligiblehigh
Compulsive Redosingnegligiblenegligiblehigh
Dose Escalationnegligiblenegligiblehigh
Editorial

Class-level evidence is strong and consistent for serotonergic psychedelics: no dopaminergic reward engagement (Eshleman 2018), rapid tolerance prevents escalation (De la Fuente Revenga 2022). No published dependence or withdrawal reports for any NBOH compound.

Reasoning

Class-level evidence is strong and consistent for serotonergic psychedelics: no dopaminergic reward engagement (Eshleman 2018), rapid tolerance prevents escalation (De la Fuente Revenga 2022). No published dependence or withdrawal reports for any NBOH compound.

Evidence basis: structural_analogy

Withdrawal Profiletrace

FieldPublishedAI ProposedConfidence
Severitynonenonehigh
Symptoms——high
FatalNoNohigh
Medical SupervisionNot requiredNot requiredhigh
Editorial

No withdrawal syndrome documented for any serotonergic psychedelic. 25B-NBOH lacks dopaminergic reward pathway engagement (Eshleman 2018) and does not produce physical dependence.

Reasoning

No withdrawal syndrome documented for any serotonergic psychedelic. 25B-NBOH lacks dopaminergic reward pathway engagement (Eshleman 2018) and does not produce physical dependence.

Evidence basis: structural_analogy

Tolerance Profiletrace

FieldPublishedAI ProposedConfidence
Builduprapidrapidmedium
Half-life7 days7 daysmedium
Full Reset14 days14 daysmedium
Cross-tolerancesLSD, psilocybin, DMT, DOx compounds, mescaline, other serotonergic psychedelicsLSD, psilocybin, DMT, DOx compounds, mescaline, other serotonergic psychedelicsmedium
Editorial

Mechanism supported by De la Fuente Revenga 2022 (single-dose tolerance, β-arrestin 2-independent 5-HT₂A downregulation). Timeline values are community consensus consistent with class pharmacology but not 25B-NBOH-specific.

Reasoning

Mechanism supported by De la Fuente Revenga 2022 (single-dose tolerance, β-arrestin 2-independent 5-HT₂A downregulation). Timeline values are community consensus consistent with class pharmacology but not 25B-NBOH-specific.

Evidence basis: community_consensus_large

Effects & Profile

Contraindications

FieldPublishedAI ProposedConfidence
cardiovascular Pre-existing cardiac disease or Long QT syndrometraceabsoluteabsolutemedium
Editorial

Cardiovascular toxicity data from structural analogs 25I-NBOH/25C-NBOH (Yoon 2022) plus documented tachycardia/hypertension in Ivory 2022 poisoning cluster. No 25B-NBOH-specific cardiac study, but class evidence is strong.

Reasoning

Cardiovascular toxicity data from structural analogs 25I-NBOH/25C-NBOH (Yoon 2022) plus documented tachycardia/hypertension in Ivory 2022 poisoning cluster. No 25B-NBOH-specific cardiac study, but class evidence is strong.

neurological Epilepsy or reduced seizure thresholdtraceabsoluteabsolutemedium
Editorial

Class-level seizure association documented in Halberstadt 2017 and Zawilska 2020. No substance-specific case but mechanistically expected from potent 5-HT₂A agonism.

Reasoning

Class-level seizure association documented in Halberstadt 2017 and Zawilska 2020. No substance-specific case but mechanistically expected from potent 5-HT₂A agonism.

other Concurrent MAO inhibitor therapytraceabsoluteabsolutehigh
Editorial

Class-level serotonin syndrome mechanism is well-established for serotonergic psychedelics combined with MAOIs. Pelletier 2024 provides closest published NBOH-class serotonin syndrome case.

Reasoning

Class-level serotonin syndrome mechanism is well-established for serotonergic psychedelics combined with MAOIs. Pelletier 2024 provides closest published NBOH-class serotonin syndrome case.

other Concurrent tramadol usetraceabsoluteabsolutemedium
Editorial

Mechanistically sound serotonin syndrome risk from dual serotonergic mechanisms. Classified as 'dangerous' in seed data. No substance-specific case report exists — class-inferred.

Reasoning

Mechanistically sound serotonin syndrome risk from dual serotonergic mechanisms. Classified as 'dangerous' in seed data. No substance-specific case report exists — class-inferred.

psychiatric Psychotic disorderstracerelativerelativemedium
Editorial

Standard class-level contraindication for all potent 5-HT₂A agonists. No 25B-NBOH-specific psychiatric case data, but the mechanism is well-established.

Reasoning

Standard class-level contraindication for all potent 5-HT₂A agonists. No 25B-NBOH-specific psychiatric case data, but the mechanism is well-established.

other Concurrent lithium therapytraceabsoluteabsolutelow
Editorial

Class-level warning for 5-HT₂A agonists + lithium. No substance-specific data — low confidence but absolute severity given potential for seizures.

Reasoning

Class-level warning for 5-HT₂A agonists + lithium. No substance-specific data — low confidence but absolute severity given potential for seizures.

pregnancy breastfeeding Pregnancy or lactationtraceabsoluteabsolutelow
Editorial

Precautionary absolute contraindication. No reproductive safety data exist. The compound's pharmacological profile (potent 5-HT₂A/₂C agonism, sympathomimetic activation) warrants exclusion.

Reasoning

Precautionary absolute contraindication. No reproductive safety data exist. The compound's pharmacological profile (potent 5-HT₂A/₂C agonism, sympathomimetic activation) warrants exclusion.

Timeline Phases

sublingual

FieldPublishedAI ProposedConfidence
Onsettrace600–1800 sec(i=0.10)600–1800 sec(i=0.10)low
Editorial

No published human PK or duration study for 25B-NBOH. Timeline derived from community consensus (PsychonautWiki) and structural analogy with 2C-B duration (Mallaroni 2023: effects resolve within 6 hours). Onset faster than oral 2C-B due to sublingual bypass of first-pass metabolism. All phase durations are class-inferred and require editorial review.

Reasoning

No published human PK or duration study for 25B-NBOH. Timeline derived from community consensus (PsychonautWiki) and structural analogy with 2C-B duration (Mallaroni 2023: effects resolve within 6 hours). Onset faster than oral 2C-B due to sublingual bypass of first-pass metabolism. All phase durations are class-inferred and require editorial review.

Evidence basis: community_consensus_large

Come uptrace900–2700 sec(i=0.50)900–2700 sec(i=0.50)low
Editorial

No published human PK or duration study for 25B-NBOH. Timeline derived from community consensus (PsychonautWiki) and structural analogy with 2C-B duration (Mallaroni 2023: effects resolve within 6 hours). Onset faster than oral 2C-B due to sublingual bypass of first-pass metabolism. All phase durations are class-inferred and require editorial review.

Reasoning

No published human PK or duration study for 25B-NBOH. Timeline derived from community consensus (PsychonautWiki) and structural analogy with 2C-B duration (Mallaroni 2023: effects resolve within 6 hours). Onset faster than oral 2C-B due to sublingual bypass of first-pass metabolism. All phase durations are class-inferred and require editorial review.

Evidence basis: community_consensus_large

Peaktrace5400–10800 sec(i=1.00)5400–10800 sec(i=1.00)low
Editorial

No published human PK or duration study for 25B-NBOH. Timeline derived from community consensus (PsychonautWiki) and structural analogy with 2C-B duration (Mallaroni 2023: effects resolve within 6 hours). Onset faster than oral 2C-B due to sublingual bypass of first-pass metabolism. All phase durations are class-inferred and require editorial review.

Reasoning

No published human PK or duration study for 25B-NBOH. Timeline derived from community consensus (PsychonautWiki) and structural analogy with 2C-B duration (Mallaroni 2023: effects resolve within 6 hours). Onset faster than oral 2C-B due to sublingual bypass of first-pass metabolism. All phase durations are class-inferred and require editorial review.

Evidence basis: community_consensus_large

Resolutiontrace3600–7200 sec(i=0.40)3600–7200 sec(i=0.40)low
Editorial

No published human PK or duration study for 25B-NBOH. Timeline derived from community consensus (PsychonautWiki) and structural analogy with 2C-B duration (Mallaroni 2023: effects resolve within 6 hours). Onset faster than oral 2C-B due to sublingual bypass of first-pass metabolism. All phase durations are class-inferred and require editorial review.

Reasoning

No published human PK or duration study for 25B-NBOH. Timeline derived from community consensus (PsychonautWiki) and structural analogy with 2C-B duration (Mallaroni 2023: effects resolve within 6 hours). Onset faster than oral 2C-B due to sublingual bypass of first-pass metabolism. All phase durations are class-inferred and require editorial review.

Evidence basis: community_consensus_large

Afterglowtrace7200–18000 sec(i=0.10)7200–18000 sec(i=0.10)low
Editorial

No published human PK or duration study for 25B-NBOH. Timeline derived from community consensus (PsychonautWiki) and structural analogy with 2C-B duration (Mallaroni 2023: effects resolve within 6 hours). Onset faster than oral 2C-B due to sublingual bypass of first-pass metabolism. All phase durations are class-inferred and require editorial review.

Reasoning

No published human PK or duration study for 25B-NBOH. Timeline derived from community consensus (PsychonautWiki) and structural analogy with 2C-B duration (Mallaroni 2023: effects resolve within 6 hours). Onset faster than oral 2C-B due to sublingual bypass of first-pass metabolism. All phase durations are class-inferred and require editorial review.

Evidence basis: community_consensus_large

Dose Tier Summaries

thresholdtrace
low

Subtle perceptual shifts emerge — faint brightening of colors, mild enhancement of visual acuity, and a slight sharpening of ambient sounds. A gentle body awareness develops, possibly accompanied by a light mood lift or vague sense of novelty enhancement. Effects may be ambiguous and difficult to distinguish from placebo at this level. Physically, mild stimulation and slight pupil dilation may be present but are often unnoticed. Appetite suppression is minimal or absent. Functional impairment is negligible — most users would appear and feel baseline to outside observers. The sublingual route means onset is faster than oral psychedelics; a bitter or metallic taste on the blotter is an incidental identification feature of NBOH compounds.

Editorial

No clinical dose-finding data for 25B-NBOH. Threshold effects inferred from community consensus (PsychonautWiki) and structural analogy with 2C-B threshold experiences. All values require editorial review.

Reasoning

No clinical dose-finding data for 25B-NBOH. Threshold effects inferred from community consensus (PsychonautWiki) and structural analogy with 2C-B threshold experiences. All values require editorial review.

Evidence basis: community_consensus_large

lighttrace
low

Noticeable perceptual changes appear — color enhancement becomes clear, surfaces may show faint visual drifting or environmental patterning, and brightness alteration shifts the visual field. Auditory enhancement makes music more engaging. Mild tracers may appear in peripheral vision. Body sensations become apparent: light stimulation, spontaneous body sensations (tingling or warmth), and the beginnings of muscle tension. Heart rate increases mildly as sympathomimetic activation begins. Appetite suppression is moderate. A sense of bodily lightness may emerge. Cognitive effects are present but manageable — thought acceleration, novelty enhancement, and a growing emotional openness. Most users remain functionally capable, though driving and complex tasks should be avoided.

Editorial

Derived from community consensus (PsychonautWiki) and structural analogy with 2C-B light-dose experiences (Papaseit 2018). No clinical data for 25B-NBOH at any dose level.

Reasoning

Derived from community consensus (PsychonautWiki) and structural analogy with 2C-B light-dose experiences (Papaseit 2018). No clinical data for 25B-NBOH at any dose level.

Evidence basis: community_consensus_large

commontrace
low

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.

Editorial

Community consensus (PsychonautWiki) plus structural analogy with 2C-B common-dose phenomenology (Mallaroni 2023, Papaseit 2018). Sympathomimetic features supported by Ivory 2022 clinical data. No controlled human study at this dose level.

Reasoning

Community consensus (PsychonautWiki) plus structural analogy with 2C-B common-dose phenomenology (Mallaroni 2023, Papaseit 2018). Sympathomimetic features supported by Ivory 2022 clinical data. No controlled human study at this dose level.

Evidence basis: community_consensus_large

strongtrace
low

Intense visual phenomena dominate — vivid geometry, visual morphing, object transformations, and internal hallucinations become immersive. Visual recursion, visual scenery slicing, and synesthesia may emerge. External hallucinations are possible. Auditory hallucinations may accompany visual distortions. Sympathomimetic activation is pronounced: tachycardia, hypertension, significant muscle tension, and temperature dysregulation require attention. Vasoconstriction intensifies. Restlessness and involuntary body movements may occur. The cardiovascular load at this level begins to approach clinical concern, particularly for individuals with undiagnosed cardiac vulnerabilities. Profound cognitive shifts occur — ego dissolution may begin, thought loops and thought disorganization emerge, and confusion is common. Anxiety and paranoia are possible. Decision impairment makes the experience difficult to manage without prior psychedelic experience. Personal insight and unity and interconnectedness may characterize positive experiences.

Editorial

Extrapolated from community reports and structural analogy with 2C-B and 25I-NBOH strong-dose experiences. Cardiovascular concerns supported by Yoon 2022 analog data and Ivory 2022 clinical findings. No clinical data at this dose level.

Reasoning

Extrapolated from community reports and structural analogy with 2C-B and 25I-NBOH strong-dose experiences. Cardiovascular concerns supported by Yoon 2022 analog data and Ivory 2022 clinical findings. No clinical data at this dose level.

Evidence basis: structural_analogy

heavytrace
low

Overwhelming sensory and cognitive effects. Visual and auditory hallucinations may become indistinguishable from reality. Complete ego dissolution, delirium, and loss of behavioral control are possible. Reality testing impairment is severe — the user may be unable to communicate coherently or respond to their environment. Serious cardiovascular risk escalates — tachycardia, hypertension, and QT prolongation (demonstrated for NBOH analogs by Yoon 2022) create conditions for potentially fatal cardiac arrhythmia. Seizure risk elevates significantly. Hyperthermia and rhabdomyolysis are possible complications of severe toxicity, as documented in NBOMe/NBOH class fatality reviews. This dose range carries medical emergency potential. No LD₅₀ has been established, and the margin between strong and life-threatening doses is unknown. The class-level statement 'potentially fatal at heavy dosages' is not confirmed by a 25B-NBOH-specific fatality but is consistent with multiple NBOMe/NBOH class deaths.

Editorial

Heavy dose effects extrapolated from NBOMe/NBOH class toxicology reviews (Halberstadt 2017, Zawilska 2020), Ivory 2022 poisoning cluster, and Yoon 2022 cardiovascular data. No 25B-NBOH-specific heavy-dose human data. All claims are class-derived.

Reasoning

Heavy dose effects extrapolated from NBOMe/NBOH class toxicology reviews (Halberstadt 2017, Zawilska 2020), Ivory 2022 poisoning cluster, and Yoon 2022 cardiovascular data. No 25B-NBOH-specific heavy-dose human data. All claims are class-derived.

Evidence basis: structural_analogy

02

History

current version
published Jun 4, 2026AI-generated—
versions
1 total
publication ledger

backfill Jun 4, 2026

Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.

full version history suggest a correctioncontact@psychedex.org
03

Sources

4 strong · 20 moderate · 4 weak
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    moderate
    Synthesis and Structure-Activity Relationships of N-Benzyl Phenethylamines as 5-HT2A/2C Agonists
    Hansen M, Phonekeo K, Paine JS, Leth-Petersen S, Begtrup M, Brauner-Osborne H, Kristensen JL · 2014 · ACS Chemical Neuroscience
    doi.org/10.1021/cn400216upubmed 243973623 claims checked2 verified1 inconclusive
  2. [2]
    moderate
    Identification of new NBOH drugs in seized blotter papers: 25B-NBOH, 25C-NBOH, and 25E-NBOH
    Machado Y, Coelho Neto J, Lordeiro RA, Alves RB, Piccin E · 2019 · Forensic Toxicology
    doi.org/10.1007/s11419-019-00509-78 claims checked2 verified1 partial5 inconclusive
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    weak
    A cluster of 25B-NBOH poisonings following exposure to powder sold as lysergic acid diethylamide (LSD)
    Ivory ST, Rotella JA, Schumann J, Greene SL · 2022 · Clinical Toxicology
    doi.org/10.1080/15563650.2022.2053150pubmed 353438588 claims checked4 verified4 inconclusive
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    moderate
    Neurochemical pharmacology of psychoactive substituted N-benzylphenethylamines: High potency agonists at 5-HT2A receptors.
    Eshleman AJ, Wolfrum KM, Reed JF, Kim SO, Johnson RA, Janowsky A · 2018 · Biochemical Pharmacology
    doi.org/10.1016/j.bcp.2018.09.024pubmed 302611755 claims checked5 verified
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    moderate
    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
    Yoon KS, Cha HJ, Choi SO, Lee JM · 2022 · Toxicology Letters
    doi.org/10.1016/j.toxlet.2021.11.016pubmed 348438744 claims checked4 verified
  6. [6]
    moderate
    NBOMes-Highly Potent and Toxic Alternatives of LSD
    Zawilska JB, Kacela M, Adamowicz P · 2020 · Frontiers in Neuroscience
    doi.org/10.3389/fnins.2020.00078pubmed 321748037 claims checked4 verified3 inconclusive
  7. [7]
    strong
    Pharmacology and Toxicology of N-Benzylphenethylamine (NBOMe) Hallucinogens
    Halberstadt AL · 2017 · Current Topics in Behavioral Neurosciences
    doi.org/10.1007/7854_2016_64pubmed 280975287 claims checked4 verified3 inconclusive
  8. [8]
    strong
    Locomotor and discriminative stimulus effects of NBOH hallucinogens in rodents
    Munir DD, Shetty RA, Gatch MB, Sumien N, Hill RD, Priddy JA, Forster MJ · 2025 · Behavioural Pharmacology
    doi.org/10.1097/fbp.0000000000000802pubmed 396420354 claims checked3 verified1 inconclusive
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    weak
    25B-NBOH New Drug Monograph
    Center for Forensic Science Research and Education (CFSRE) · 2023
    linkno claims checked
  10. [10]
    moderate
    Synthesis and pharmacological evaluation of N-benzyl substituted 4-bromo-2,5-dimethoxyphenethylamines as 5-HT2A/2C partial agonists
    Hansen M, Jacobsen SE, Plunkett S, Liebscher GE, McCorvy JD, Brauner-Osborne H, Kristensen JL · 2015 · Bioorganic & Medicinal Chemistry
    doi.org/10.1016/j.bmc.2014.12.011pubmed 2558309910 claims checked7 verified3 inconclusive
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    moderate
    Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice
    de la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J · 2022 · ACS Chemical Neuroscience
    doi.org/10.1021/acschemneuro.2c00170pubmed 359008764 claims checked3 verified1 not supported
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    moderate
    25I-NBOH: a new potent serotonin 5-HT2A receptor agonist identified in blotter paper seizures in Brazil
    Arantes LC, Junior EF, de Souza LF, Cardoso AC, Alcantara TLF, Liao LM, Machado Y, Lordeiro RA, Neto JC, Andrade AFB · 2017 · Forensic Toxicology
    doi.org/10.1007/s11419-017-0357-xpubmed 28706567no claims checked
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    weak
    UNODC Substance Details: 25B-NBOH
    United Nations Office on Drugs and Crime · 2023
    linkno claims checked
  14. [14]
    moderate
    Simultaneous analysis of 2Cs, 25-NBOHs, 25-NBOMes and LSD in seized exhibits using liquid chromatography-tandem mass spectrometry: A targeted approach
    Chia XWS, Ong MC, Yeo YYC, Ho YJ, Binte Ahmad Nasir EI, Tan LJ, Chua PY, Yap TWA, Lim JLW · 2019 · Forensic Science International
    doi.org/10.1016/j.forsciint.2019.05.036pubmed 312341103 claims checked3 verified
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    moderate
    Metabolic characterization of 25X-NBOH and 25X-NBOMe phenethylamines based on UHPLC-Q-Exactive Orbitrap MS in human liver microsomes.
    Xiang J, Wen D, Zhai W, Zhao J, Xiang P, Ma C, Shi Y · 2024 · Journal of Pharmaceutical and Biomedical Analysis
    doi.org/10.1016/j.jpba.2024.116020pubmed 383594934 claims checked3 verified1 inconclusive
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    moderate
    Characterization of the hepatic cytochrome P450 enzymes involved in the metabolism of 25I-NBOMe and 25I-NBOH
    Nielsen LM, Holm NB, Leth-Petersen S, Kristensen JL, Olsen L, Linnet K · 2017 · Drug Testing and Analysis
    doi.org/10.1002/dta.2031pubmed 274007395 claims checked4 verified1 inconclusive
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    Liquid chromatography-tandam mass spectrometry-based pharmacokinetic and metabolic analysis of 4-bromo-2,5-dimethoxyphenethylamine and its metabolites in human plasma
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    doi.org/10.1016/j.dmd.2025.100086pubmed 404089053 claims checked3 verified
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    Behavioral arrest and a characteristic slow waveform are hallmark responses to selective 5-HT2A receptor activation
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    doi.org/10.1038/s41598-021-81552-6pubmed 334793682 claims checked1 verified1 inconclusive
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    moderate
    Identification of psychedelic new psychoactive substances (NPS) showing biased agonism at the 5-HT2AR through simultaneous use of β-arrestin 2 and miniGαq bioassays
    Pottie E, Dedecker P, Stove CP · 2020 · Biochemical Pharmacology
    doi.org/10.1016/j.bcp.2020.114251pubmed 329980001 claim checked1 verified
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    moderate
    Receptor interaction profiles of novel N-2-methoxybenzyl (NBOMe) derivatives of 2,5-dimethoxy-substituted phenethylamines (2C drugs)
    Rickli A, Luethi D, Reinisch J, Buchy D, Hoener MC, Liechti ME · 2015 · Neuropharmacology
    doi.org/10.1016/j.neuropharm.2015.08.034pubmed 26318099no claims checked
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    moderate
    Identification of 5-HT2A receptor signaling pathways associated with psychedelic potential
    Wallach J, Cao AB, Calkins MM, Heim AJ, Lanham JK, et al. · 2023 · Nature Communications
    doi.org/10.1038/s41467-023-44016-1pubmed 381021072 claims checked2 verified
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    moderate
    Psychedelics elicit their effects by 5-HT2A receptor-mediated Gi signalling
    Xu Z, Wang H, Yu J et al. · 2026 · Nature
    doi.org/10.1038/s41586-025-10061-7pubmed 41606342no claims checked
  23. [23]
    moderate
    Metabolic fate and detectability of 25B-NBOMe and 25C-NBOMe in human and rat urine by GC-MS, LC-MSn, and LC-HR-MS/MS approaches.
    Caspar AT, Brandt SD, Stoever AE, Meyer MR, Maurer HH · 2017 · Journal of Pharmaceutical and Biomedical Analysis
    doi.org/10.1016/j.jpba.2016.11.040pubmed 279151931 claim checked1 verified
  24. [24]
    weak
    Severe 25E-NBOH intoxication associated with MDPHP intake: a case report, metabolism study, and literature review
    Pelletier R, Gicquel T, Carvelli J, Balaz P, Pelissier-Alicot AL, Morel I, Bottinelli C, Solas C, Le Dare B, Fabresse N · 2024 · International Journal of Legal Medicine
    doi.org/10.1007/s00414-023-03151-6pubmed 381174183 claims checked3 verified
  25. [25]
    strong
    Assessment of the Acute Effects of 2C-B vs. Psilocybin on Subjective Experience, Mood, and Cognition
    Mallaroni P, Mason NL, Reckweg JT, Paci R, Ritscher S, Toennes SW, Theunissen EL, Kuypers KPC, Ramaekers JG · 2023 · Clinical Pharmacology and Therapeutics
    doi.org/10.1002/cpt.2958pubmed 372531612 claims checked1 verified1 inconclusive
  26. [26]
    moderate
    Acute Pharmacological Effects of 2C-B in Humans: An Observational Study
    Papaseit E, Farre M, Perez-Mana C, Torrens M, Ventura M, Pujadas M, de la Torre R, Gonzalez D · 2018 · Frontiers in Pharmacology
    doi.org/10.3389/fphar.2018.00206pubmed 29593537no claims checked
  27. [27]
    moderate
    Interactions between classic psychedelics and serotonergic antidepressants: Effects on the acute psychedelic subjective experience, well-being and depressive symptoms from a prospective survey study
    Barbut Siva J, Barba T, Kettner H, et al. · 2024 · Journal of Psychopharmacology
    doi.org/10.1177/02698811231224217pubmed 382810751 claim checked1 verified
  28. [28]
    moderate
    Psychedelic experience dose-dependently modulated by cannabis: results of a prospective online survey
    Kuc J, Kettner H, Rosas F, Erritzoe D, Haijen E, Kaelen M, Nutt D, Carhart-Harris RL · 2022 · Psychopharmacology
    doi.org/10.1007/s00213-021-05999-1pubmed 347343141 claim checked1 partial
04

Claim Verification

Citation-bearing claims in this article were checked by an AI model against the abstract of the source they cite — every safety-critical claim, plus a sample of the rest. Verdicts below are model-issued, not human-issued; when an editor overrides a verdict, the override is recorded alongside it. Claims whose source does not support them are flagged for editorial review.

summary15 claims8verified1partial6inconclusive
inconclusiveDistinguished from 25B-NBOMe by an N-(2-hydroxybenzyl) group replacing N-(2-methoxybenzyl), the compound is active in the microgram range via sublingual administration and orally inactive at standard doses due to extensive first-pass metabolism.[2]model confidence 85%
Inconclusive

Abstract covers forensic identification and market context for 25B-NBOH in Brazil; does not address the structural distinction (OH vs OCH3), microgram-range activity, oral inactivity, or first-pass metabolism.

First forensic identification and detailed characterization of 25B-NBOH, 25C-NBOH, and 25E-NBOH in seized blotter papers (Brazil, 2017-2018).

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveThe NBOH scaffold was established through structure-activity work at the University of Copenhagen, with 25B-NBOH's receptor profile characterized in 2015[1]model confidence 75%
Inconclusive

Abstract confirms a 48-compound SAR study establishing N-benzyl substitution effects on 5-HT2A, consistent with the scaffold claim, but 'University of Copenhagen' and the year '2015' are not verifiable from the abstract text.

48-compound SAR study using 2C-B phenethylamine scaffold. N-benzyl substitution produces dramatic increase in binding affinity and functional activity at 5-HT2A receptor.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveThe NBOH scaffold was established through structure-activity work at the University of Copenhagen, with 25B-NBOH's receptor profile characterized in 2015[10]model confidence 75%
Inconclusive

Abstract confirms this paper characterizes 25B-NBOH (N-(2-hydroxybenzyl) substituted 2C-B derivatives) at 5-HT2A/2C, consistent with the 2015 characterization claim, but 'University of Copenhagen' is not verifiable from the abstract.

Examines how 5-HT2A/2C affinity is influenced by N-benzyl substitution of 4-bromo-2,5-dimethoxyphenethylamine (2C-B) derivatives. Includes compounds with N-(2-hydroxybenzyl) substitution (25B-NBOH).

checked by claude-sonnet-4-6 · May 7, 2026

partialThe compound appeared in European forensic seizures around June 2016 and became a predominant hallucinogen on blotter papers in parts of Brazil through 2019[2]model confidence 85%
Partial

Abstract directly supports Brazil as a region where NBOH became the predominant hallucinogen, with seizures in 2017-2018. However, 'European forensic seizures around June 2016' is not mentioned in this abstract at all.

NBOH substances have become the main hallucinogenic drug in the region. Not under UN Conventions control as of 2019.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedThe published evidence base comprises one direct in vivo behavioral study, one clinical poisoning cluster, and in vitro binding and metabolism data.[8]model confidence 90%
Verified

This citation IS the direct in vivo behavioral study referenced in the claim, confirming that element of the evidence base.

25B-NBOH, 25C-NBOH, 25E-NBOH, and 25I-NBOH tested in mice (locomotor) and DOM-trained rats (discriminative stimulus).

checked by claude-sonnet-4-6 · May 7, 2026

verifiedThe published evidence base comprises one direct in vivo behavioral study, one clinical poisoning cluster, and in vitro binding and metabolism data.[3]model confidence 90%
Verified

This citation IS the clinical poisoning cluster referenced in the claim, directly confirming that element of the evidence base.

First published report documenting clinical toxicity of NBOH derivatives. Cluster of poisonings from powder sold as LSD.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusive25B-NBOH binds serotonin 5-HT₂A receptors with high affinity (pKi = 8.3, Ki ≈ 5 nM) and 5-HT₂C receptors with subnanomolar affinity (pKi = 9.4, Ki ≈ 0.4 nM)[10]model confidence 80%
Inconclusive

Abstract confirms this paper provides pKi values for 25B-NBOH at 5-HT2A/2C, but the specific numeric values (pKi 8.3, 9.4) are not stated in the abstract text — they would be in the paper's data tables.

Includes compounds with N-(2-hydroxybenzyl) substitution (25B-NBOH). Generally found to be less efficacious partial agonists vs. previously reported N-benzyl phenethylamines.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedIn DOM-trained rats, 25B-NBOH fully substitutes for DOM's discriminative stimulus (≥80% drug-appropriate responding) with potency exceeding DOM and several NBOMe analogs[8]model confidence 98%
Verified

Abstract directly states 25B-NBOH fully substituted for DOM (>=80%) and discriminative stimulus effects were more potent than DOM and 25X-NBOMe compounds.

25B-NBOH, 25C-NBOH, and 25E-NBOH fully substituted for DOM (>=80%). Discriminative stimulus effects more potent than DOM and 25X-NBOMe compounds.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedMonoamine transporter affinity is negligible at pharmacologically relevant concentrations.[4]model confidence 90%
Verified

Abstract states 'low micromolar potency at monoamine transporters' and 'minimal psychostimulant activity.' Since NBOH compounds are active at nanomolar concentrations, micromolar transporter affinity is indeed negligible at pharmacologically relevant doses.

Low micromolar potency at monoamine transporters. Results consistent with hallucinogenic activity, minimal psychostimulant activity.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveClinical toxicology reports document hallucinations, mydriasis, agitation, tachycardia, and hypertension[3]model confidence 80%
Inconclusive

Abstract confirms this is the first published clinical toxicity report for NBOH derivatives with a poisoning cluster, but specific symptoms (hallucinations, mydriasis, agitation, tachycardia, hypertension) are not listed in the abstract text.

First published report documenting clinical toxicity of NBOH derivatives. Cluster of poisonings from powder sold as LSD.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedStructural analogs 25I-NBOH and 25C-NBOH inhibit hERG potassium channels and reduce cardiomyocyte viability in preclinical models, and multiple NBOMe/NBOH-class fatalities are documented, though no confirmed 25B-NBOH-specific death has been published[5]model confidence 95%
Verified

Abstract directly confirms hERG inhibition and decreased cardiomyocyte viability for 25I-NBOH and 25C-NBOH. This citation supports the structural analog cardiovascular toxicity portion of the claim.

25I-NBOH and 25C-NBOH: decreased viability of H9c2 cardiomyocytes (MTT assay), increased QT and RR intervals in rat ECG, 25I-NBOH downregulated PAK1 protein, 25I-NBOH inhibited hERG potassium channels.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedStructural analogs 25I-NBOH and 25C-NBOH inhibit hERG potassium channels and reduce cardiomyocyte viability in preclinical models, and multiple NBOMe/NBOH-class fatalities are documented, though no confirmed 25B-NBOH-specific death has been published[6]model confidence 90%
Verified

Abstract explicitly mentions 'cases of non-fatal and lethal intoxication,' directly supporting the claim that fatalities are documented at the class level.

Comprehensive review of NBOMe compounds including pharmacological properties, pattern of use, metabolism, desired effects, and cases of non-fatal and lethal intoxication.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveStructural analogs 25I-NBOH and 25C-NBOH inhibit hERG potassium channels and reduce cardiomyocyte viability in preclinical models, and multiple NBOMe/NBOH-class fatalities are documented, though no confirmed 25B-NBOH-specific death has been published[7]model confidence 70%
Inconclusive

Review covers 51 NBOMe toxicity cases and discusses rhabdomyolysis/seizures but does not explicitly mention fatalities or hERG inhibition in the abstract. Full text likely contains this data.

Reviews NBOMe structure-activity relationships, behavioral pharmacology, metabolism, and toxicity. Reviews 51 cases of NBOMe toxicity.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedThe compound does not engage dopaminergic reward pathways and is not habit-forming[4]model confidence 88%
Verified

Abstract confirms low micromolar potency at monoamine transporters and minimal psychostimulant activity, supporting the claim that dopaminergic reward pathways are not meaningfully engaged.

Low micromolar potency at monoamine transporters. Results consistent with hallucinogenic activity, minimal psychostimulant activity.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedTolerance develops rapidly via 5-HT₂A receptor downregulation, with cross-tolerance across serotonergic psychedelics[11]model confidence 97%
Verified

Abstract directly states tolerance develops after single dose, cross-tolerance exists between DOI and LSD, and 5-HT2AR downregulation in frontal cortex is the mechanism.

Repeated DOI induces progressive decrease in HTR; tolerance after single dose. Cross-tolerance between DOI and LSD. DOI caused 5-HT2AR downregulation in frontal cortex.

checked by claude-sonnet-4-6 · May 7, 2026

history4 claims4verified
verifiedThe foundational structure-activity work establishing the NBOH scaffold was published in 2014 by Hansen and colleagues at the University of Copenhagen, who synthesized a series of 48 N-benzyl phenethylamine derivatives and demonstrated that N-benzyl substitution of 2,5-dimethoxy-substituted phenethylamines dramatically increased 5-HT₂A binding affinity[1]model confidence 92%
Verified

Abstract directly confirms a 48-compound SAR study and that N-benzyl substitution produces a dramatic increase in 5-HT2A binding affinity and functional activity. Year and institution are not verifiable from the abstract but the scientific content is directly confirmed.

48-compound SAR study using 2C-B phenethylamine scaffold. N-benzyl substitution produces dramatic increase in binding affinity and functional activity at 5-HT2A receptor.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedThe specific pharmacological characterization of 25B-NBOH — employing the 4-bromo-2,5-dimethoxyphenethylamine backbone with an ortho-hydroxybenzyl N-substituent — followed in 2015.[10]model confidence 90%
Verified

Abstract confirms this paper characterizes N-benzyl substituted 4-bromo-2,5-dimethoxyphenethylamine (2C-B) derivatives including N-(2-hydroxybenzyl) substitution (25B-NBOH), consistent with the claim.

Examines how 5-HT2A/2C affinity is influenced by N-benzyl substitution of 4-bromo-2,5-dimethoxyphenethylamine (2C-B) derivatives. Includes compounds with N-(2-hydroxybenzyl) substitution (25B-NBOH).

checked by claude-sonnet-4-6 · May 7, 2026

verifiedThe same Brazilian forensic team subsequently identified 25B-NBOH in seized blotter papers between 2017 and 2018, alongside 25C-NBOH and 25E-NBOH[2]model confidence 99%
Verified

Abstract directly states first forensic identification of 25B-NBOH, 25C-NBOH, and 25E-NBOH in seized blotter papers in Brazil between 2017 and 2018.

First forensic identification and detailed characterization of 25B-NBOH, 25C-NBOH, and 25E-NBOH in seized blotter papers (Brazil, 2017-2018).

checked by claude-sonnet-4-6 · May 7, 2026

verifiedA significant public health event occurred in Australia in 2022, when a cluster of 25B-NBOH poisonings resulted from powder sold as LSD, underscoring the compound's role as an adulterant and the critical importance of drug checking services.[3]model confidence 92%
Verified

Abstract confirms cluster of poisonings from powder sold as LSD, consistent with the core claim. Australia and 2022 are not stated in abstract text but the compound identification and cluster nature are confirmed.

Cluster of poisonings from powder sold as LSD.

checked by claude-sonnet-4-6 · May 7, 2026

chemistry2 claims2verified
verifiedThis N-benzyl substitution converts the moderate-potency parent phenethylamine into a high-potency 5-HT₂A receptor agonist active in the microgram range[1]model confidence 93%
Verified

Abstract directly states N-benzyl substitution produces a dramatic increase in binding affinity with highest affinity at 0.29 nM, confirming conversion to high-potency agonist. Subnanomolar affinity is consistent with microgram-range activity.

N-benzyl substitution produces dramatic increase in binding affinity and functional activity at 5-HT2A receptor. Highest affinity at 0.29 nM.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedA critical analytical property is thermolability: 25B-NBOH degrades to its parent phenethylamine 2C-B under standard gas chromatography conditions[14]model confidence 92%
Verified

Abstract describes a non-thermal LC-MS/MS method that avoids thermal degradation misidentification, and explicitly includes both 25-NBOH compounds and their '2C counterparts,' implying thermal degradation produces 2C compounds.

Non-thermal method avoids thermal degradation misidentification. LC-MS/MS method for simultaneous identification of 25-NBOH compounds including 25B-NBOH, 25C-NBOH, 25I-NBOH, their 2C counterparts.

checked by claude-sonnet-4-6 · May 7, 2026

pharmacology11 claims8verified3inconclusive
verified25B-NBOH is a potent agonist at serotonin 5-HT₂A and 5-HT₂C receptors, with psychoactive effects mediated primarily through 5-HT₂A activation — consistent with the broader N-benzylphenethylamine class[7]model confidence 85%
Verified

This comprehensive review of NBOMe/NBOH pharmacology and SAR covers 5-HT2A/2C agonism as a class property, consistent with the claim. The abstract confirms it reviews SAR and behavioral pharmacology for this class.

Reviews NBOMe structure-activity relationships, behavioral pharmacology, metabolism, and toxicity.

checked by claude-sonnet-4-6 · May 7, 2026

verified25B-NBOH is a potent agonist at serotonin 5-HT₂A and 5-HT₂C receptors, with psychoactive effects mediated primarily through 5-HT₂A activation — consistent with the broader N-benzylphenethylamine class[6]model confidence 95%
Verified

Abstract explicitly states Ki values in the low nanomolar range at 5-HT2A/2C with >1000-fold selectivity over 5-HT1A, directly confirming potent 5-HT2A/2C agonism.

Ki values in low nanomolar range at 5-HT2A/2C with >1000-fold selectivity over 5-HT1A.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveCompound-specific binding data from Hansen et al. report a pKi of 8.3 at 5-HT₂A (Ki ≈ 5 nM) and pKi of 9.4 at 5-HT₂C (Ki ≈ 0.4 nM), confirmed by the CFSRE forensic monograph[10]model confidence 80%
Inconclusive

Abstract confirms this paper provides pKi binding data for 25B-NBOH at 5-HT2A/2C, but the specific values (8.3 and 9.4) are not stated in the abstract text and must come from the paper's tables.

Includes compounds with N-(2-hydroxybenzyl) substitution (25B-NBOH). Generally found to be less efficacious partial agonists vs. previously reported N-benzyl phenethylamines.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedThe notably higher affinity at 5-HT₂C relative to 5-HT₂A is unusual within the class and may indicate partial agonism at 5-HT₂A, as the original study noted that compounds in this series "were generally found to be less efficacious agonists than previously reported N-benzyl phenethylamines".[10]model confidence 97%
Verified

The quoted phrase is virtually verbatim from the abstract. The abstract states compounds were 'generally found to be less efficacious partial agonists vs. previously reported N-benzyl phenethylamines.'

Generally found to be less efficacious partial agonists vs. previously reported N-benzyl phenethylamines.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedAt the class level, NBOH compounds exhibit subnanomolar to low nanomolar functional potencies at 5-HT₂A and 5-HT₂C, comparable to LSD[4]model confidence 90%
Verified

Abstract directly states 'subnanomolar to low nanomolar potency' at 5-HT2A/2C for NBOH compounds. The LSD comparison is not in the abstract but does not contradict the primary potency claim.

Full efficacy at 5-HT2A/2C with subnanomolar to low nanomolar potency.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedAffinity at other targets is substantially lower: 5-HT₁A shows very low potency and low efficacy; 5-HT₂B shows reduced affinity relative to 5-HT₂A/₂C; and monoamine transporters (DAT, SERT, NET) bind only at low to mid-micromolar concentrations, indicating minimal psychostimulant contribution.[4]model confidence 88%
Verified

Abstract directly confirms low efficacy at 5-HT1A and low micromolar potency at monoamine transporters. 5-HT2B is not mentioned in the abstract but its absence does not contradict the claim.

Low efficacy at 5-HT1A. Low micromolar potency at monoamine transporters. Results consistent with hallucinogenic activity, minimal psychostimulant activity.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveThe compound also decreased spontaneous locomotor activity in mice, similar in magnitude to DOM.[8]model confidence 75%
Inconclusive

Abstract confirms 25B-NBOH decreased locomotor activity in mice but does not specify that the magnitude was similar to DOM. Magnitude comparison data would be in the paper's figures.

All four decreased locomotor activity.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveOral inactivity. NBOH compounds are inactive or nearly inactive when swallowed at standard doses, attributed to extensive first-pass hepatic metabolism[2]model confidence 80%
Inconclusive

Abstract is about forensic identification of NBOH compounds in seized blotter papers. It does not address oral bioavailability or first-pass metabolism.

First forensic identification and detailed characterization of 25B-NBOH, 25C-NBOH, and 25E-NBOH in seized blotter papers (Brazil, 2017-2018).

checked by claude-sonnet-4-6 · May 7, 2026

verifiedThree metabolites — designated B2-1 (56.61% peak area ratio), B2-2 (17.43%), and B6 (17.78%) — were identified as recommended biomarkers for forensic detection.[15]model confidence 99%
Verified

Abstract directly and exactly states the three metabolites and their peak area ratios: B2-1 (56.61%), B2-2 (17.43%) and B6 (17.78%).

Major metabolites for 25B-NBOH: B2-1 (56.61%), B2-2 (17.43%) and B6 (17.78%).

checked by claude-sonnet-4-6 · May 7, 2026

verifiedNielsen et al. (2017) identified CYP2D6 as the dominant enzyme for 25I-NBOH clearance (CLint = 118.7 mL/min/kg), with additional contributions from direct glucuronidation that may partially offset the impact of CYP2D6 genetic polymorphism[16]model confidence 99%
Verified

Abstract directly confirms CYP2D6 as the major enzyme for 25I-NBOH, intrinsic clearance of 118.7 mL/min/kg, and direct glucuronidation potentially diminishing CYP2D6 polymorphism impact.

Major CYP enzymes for 25I-NBOH: CYP2D6. Intrinsic clearance for 25I-NBOH: 118.7 mL/min/kg. 25I-NBOH also subject to direct glucuronidation, which may diminish impact of CYP2D6 genetic polymorphism.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedThe parent compound 2C-B is metabolized by MAO-A, MAO-B, cytosolic enzymes, and CYP2D6, with primary metabolites that do not activate 5-HT₂A receptors.[17]model confidence 99%
Verified

Abstract directly states MAO-A, MAO-B, cytosolic enzymes, and CYP2D6 as metabolic enzymes for 2C-B, and that metabolites BDMPAA and B-2-HMPAA do not activate 5-HT2AR.

Key metabolic enzymes: MAO-A, MAO-B, cytosolic enzymes, CYP2D6. Metabolites BDMPAA and B-2-HMPAA do not activate 5-HT2AR.

checked by claude-sonnet-4-6 · May 7, 2026

receptor pharmacology4 claims4verified
verifiedCompound-specific binding data for 25B-NBOH derive from Hansen et al. (2015), who characterized a series of N-benzyl substituted 4-bromo-2,5-dimethoxyphenethylamines:[10]model confidence 95%
Verified

Abstract confirms this paper is specifically about characterizing N-benzyl substituted 4-bromo-2,5-dimethoxyphenethylamines including 25B-NBOH, directly matching the claim.

Examines how 5-HT2A/2C affinity is influenced by N-benzyl substitution of 4-bromo-2,5-dimethoxyphenethylamine (2C-B) derivatives. Includes compounds with N-(2-hydroxybenzyl) substitution (25B-NBOH).

checked by claude-sonnet-4-6 · May 7, 2026

verifiedHansen et al. noted that compounds in this series were generally less efficacious agonists than previously characterized N-benzyl phenethylamines, raising the possibility that 25B-NBOH functions as a partial agonist at 5-HT₂A[10]model confidence 98%
Verified

Abstract directly states compounds were 'generally found to be less efficacious partial agonists vs. previously reported N-benzyl phenethylamines,' fully supporting the claim.

Generally found to be less efficacious partial agonists vs. previously reported N-benzyl phenethylamines.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedWallach et al. (2023) identified 5-HT₂A–Gq efficacy — rather than β-arrestin2 recruitment — as the primary predictor of psychedelic potential as measured by head-twitch response in mice[21]model confidence 99%
Verified

Abstract directly states 5-HT2A-Gq (not beta-arrestin2) efficacy predicts psychedelic potential via head-twitch response in mice.

5-HT2A-Gq (not beta-arrestin2) efficacy predicts psychedelic potential via head-twitch response in mice.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedPottie et al. (2020) showed that NBOH compounds — specifically 25H-NBOH and structurally related analogs — exhibit statistically significant β-arrestin 2 preference over miniGαq relative to LSD[19]model confidence 99%
Verified

Abstract directly states 25H-NBOH shows statistically significant β-arrestin 2 bias over miniGαq at 5-HT2AR compared to LSD.

25H-NBOH shows statistically significant β-arrestin 2 bias over miniGαq at 5-HT2AR compared to LSD.

checked by claude-sonnet-4-6 · May 7, 2026

neuroscience6 claims5verified1inconclusive
verifiedThe neural mechanisms described below are inferred from 25B-NBOH's confirmed 5-HT₂A agonism and from class-level neuroscience data for serotonergic psychedelics.[8]model confidence 90%
Verified

Abstract confirms 25B-NBOH fully substitutes for DOM (a 5-HT2A agonist) in discriminative stimulus assays, providing direct in vivo evidence of 5-HT2A agonism.

25B-NBOH fully substituted for DOM (>=80%). Discriminative stimulus effects more potent than DOM and 25X-NBOMe compounds.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedContreras et al. (2021) used 25I-NBOH as a selective 5-HT₂A agonist tool compound to characterize EEG and behavioral correlates of receptor activation, identifying behavioral arrest and a characteristic slow waveform as hallmark responses to selective 5-HT₂A engagement[18]model confidence 99%
Verified

Abstract directly confirms behavioral arrest and characteristic EEG waveforms as hallmarks of 5-HT2AR activation, using 25I-NBOH as the tool compound.

Behavioral arrest preceding HTR by precise interval; characteristic EEG waveforms (Phase 1: 3.5-4.5 Hz, Phase 2: 2.5-3.2 Hz). Suggests behavioral arrest and EEG waveforms are hallmarks of 5-HT2AR activation.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedXu et al. (2026) identified non-canonical Gi signaling through the 5-HT₂A receptor as essential for hallucinogenic effects, while Wallach et al. (2023) found that Gq efficacy predicts psychedelic potential in the head-twitch assay[21]model confidence 95%
Verified

Abstract directly confirms the Wallach et al. finding: Gq (not beta-arrestin2) efficacy predicts psychedelic potential via head-twitch response. This citation supports the Wallach et al. portion of the claim.

5-HT2A-Gq (not beta-arrestin2) efficacy predicts psychedelic potential via head-twitch response in mice.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedWhether the compound's possible partial agonism at 5-HT₂A affects its neuroplastogenic potential relative to full agonists remains an open question.[10]model confidence 88%
Verified

Abstract provides the basis for partial agonism (less efficacious agonists in this series), which logically underpins the open question about neuroplastogenic potential. The citation supports the partial agonism premise.

Generally found to be less efficacious partial agonists vs. previously reported N-benzyl phenethylamines.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedDe la Fuente Revenga et al. (2022) demonstrated that tolerance to 5-HT₂A agonist head-twitch response can develop after a single dose, driven by receptor downregulation in the frontal cortex through a β-arrestin 2-independent mechanism[11]model confidence 99%
Verified

Abstract directly confirms all three mechanistic components: single-dose tolerance, frontal cortex 5-HT2AR downregulation, and beta-arrestin-2 independence.

Tolerance after single dose. DOI caused 5-HT2AR downregulation in frontal cortex. Mechanism independent of beta-arrestin-2.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveThe characteristic slow waveform documented with 25I-NBOH may represent a specific electrophysiological marker of altered entropy dynamics in the NBOH class.[18]model confidence 75%
Inconclusive

Abstract confirms characteristic slow EEG waveforms with 25I-NBOH, but 'entropy dynamics' is a theoretical interpretive framework not mentioned in the abstract. The link cannot be verified from the abstract alone.

Characteristic EEG waveforms (Phase 1: 3.5-4.5 Hz, Phase 2: 2.5-3.2 Hz). Suggests behavioral arrest and EEG waveforms are hallmarks of 5-HT2AR activation.

checked by claude-sonnet-4-6 · May 7, 2026

pharmacokinetic detail5 claims4verified1inconclusive
verifiedNielsen et al. (2017) characterized 25I-NBOH metabolism and identified CYP2D6 as the dominant clearance enzyme with an intrinsic clearance (CLint) of 118.7 mL/min/kg[16]model confidence 99%
Verified

Abstract directly states CYP2D6 as major enzyme for 25I-NBOH and CLint of 118.7 mL/min/kg.

Major CYP enzymes for 25I-NBOH: CYP2D6. Intrinsic clearance for 25I-NBOH: 118.7 mL/min/kg.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedThe parent compound 2C-B, studied in humans at 30 mg oral by Thomann et al. (2025), is metabolized by MAO-A, MAO-B, cytosolic enzymes, and CYP2D6[17]model confidence 99%
Verified

Abstract directly confirms 30 mg oral dose study and all four metabolic enzymes (MAO-A, MAO-B, cytosolic enzymes, CYP2D6) for 2C-B.

First human plasma PK study of 2C-B (30 mg oral dose). Key metabolic enzymes: MAO-A, MAO-B, cytosolic enzymes, CYP2D6.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedXiang et al. (2024) conducted the most comprehensive metabolism study for 25B-NBOH using human liver microsomes with UHPLC-Q-Exactive Orbitrap mass spectrometry[15]model confidence 92%
Verified

Abstract confirms human liver microsomes, UHPLC-Q-Exactive Orbitrap MS methodology, and identification of 70 total metabolites for 25B-NBOH, consistent with comprehensive characterization.

Investigated phase I and II metabolism of 25B-NBOH in human liver microsomes. 70 metabolites total. UHPLC-Q-Exactive Orbitrap MS.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedImportantly, 25I-NBOH is also subject to direct glucuronidation — a phase II conjugation pathway that may partially offset the pharmacogenomic impact of CYP2D6 polymorphism by providing an alternative elimination route.[16]model confidence 99%
Verified

Abstract directly states 25I-NBOH is subject to direct glucuronidation which may diminish the impact of CYP2D6 genetic polymorphism.

25I-NBOH also subject to direct glucuronidation, which may diminish impact of CYP2D6 genetic polymorphism.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveNBOH compounds are reported to be inactive or nearly inactive by the oral route at standard doses, attributed to extensive first-pass hepatic metabolism[2]model confidence 80%
Inconclusive

Abstract covers forensic identification of NBOH compounds in seized blotter papers; does not address oral bioavailability or first-pass hepatic metabolism.

First forensic identification and detailed characterization of 25B-NBOH, 25C-NBOH, and 25E-NBOH in seized blotter papers (Brazil, 2017-2018).

checked by claude-sonnet-4-6 · May 7, 2026

effects overview1 claim1inconclusive
inconclusiveThe experience carries pronounced sympathomimetic activation — tachycardia, hypertension, and mydriasis are documented clinical features — that distinguishes the somatic texture from classical serotonergic psychedelics with lower cardiovascular engagement.[3]model confidence 80%
Inconclusive

Abstract confirms this is the first published report of 25B-NBOH clinical toxicity from a poisoning cluster, but does not list specific symptoms (tachycardia, hypertension, mydriasis) in the abstract text.

First published report documenting clinical toxicity of NBOH derivatives. Cluster of poisonings from powder sold as LSD.

checked by claude-sonnet-4-6 · May 7, 2026

clinical evidence2 claims2verified
verifiedA related case report by Pelletier et al. (2024) documented severe intoxication with 25E-NBOH (a structural analog) combined with MDPHP, presenting with serotonin syndrome and loss of consciousness[24]model confidence 99%
Verified

Abstract directly describes a 23-year-old male with serotonergic syndrome and loss of consciousness after consuming 25E-NBOH + MDPHP.

23-year-old male with serotonergic syndrome and loss of consciousness after consuming powder labeled as 25I-NBOH; actually contained 25E-NBOH + MDPHP.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedIvory et al. (2022) reported a cluster of poisonings in Australia resulting from powder sold as LSD that was subsequently identified as 25B-NBOH[3]model confidence 97%
Verified

Abstract directly confirms cluster of poisonings from powder sold as LSD, first published report of 25B-NBOH clinical toxicity.

Cluster of poisonings from powder sold as LSD. 25B-NBOH is a synthetic hallucinogen closely related to the NBOMe family.

checked by claude-sonnet-4-6 · May 7, 2026

comparative pharmacology11 claims8verified3inconclusive
verifiedThe NBOMe class has a substantially more extensive toxicological record, with multiple confirmed fatalities documented in case reports and reviews[6]model confidence 95%
Verified

Abstract explicitly mentions 'cases of non-fatal and lethal intoxication,' directly confirming fatalities are documented in this review.

Cases of non-fatal and lethal intoxication.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusive25B-NBOH is the N-(2-hydroxybenzyl) derivative of 2C-B, and the N-benzyl substitution transforms the pharmacological profile substantially. 2C-B is orally active at doses of 15–25 mg, whereas 25B-NBOH is active in the microgram range via sublingual routes — representing an approximately 30- to 50-fold potency increase at 5-HT₂A[25]model confidence 75%
Inconclusive

Abstract confirms 2C-B is active at 20 mg orally in humans, partially supporting the oral dose range. However, the claim about 25B-NBOH microgram activity and the 30-50 fold potency comparison are not addressed in this abstract.

First double-blind controlled study of 2C-B (20 mg) vs psilocybin (15 mg) in 22 healthy participants. 2C-B produced psychedelic alterations of consciousness.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveThe NBOMe class has a substantially more extensive toxicological record, with multiple confirmed fatalities documented in case reports and reviews[7]model confidence 70%
Inconclusive

Abstract reviews 51 NBOMe toxicity cases but does not explicitly mention fatalities. Full text likely documents fatal cases within the 51 reviewed.

Reviews 51 cases of NBOMe toxicity: rhabdomyolysis is common in severe toxicity, linked to seizures, hyperthermia, vasoconstriction.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedThe N-benzyl modification elevates 5-HT₂A affinity from moderate (2C-B) to low nanomolar (25B-NBOH, Ki ≈ 5 nM).[10]model confidence 88%
Verified

Abstract directly addresses how N-benzyl substitution of 2C-B affects 5-HT2A affinity including for 25B-NBOH, consistent with the claim. Specific Ki values would be in the paper's tables.

Examines how 5-HT2A/2C affinity is influenced by N-benzyl substitution of 4-bromo-2,5-dimethoxyphenethylamine (2C-B) derivatives. Includes compounds with N-(2-hydroxybenzyl) substitution (25B-NBOH).

checked by claude-sonnet-4-6 · May 7, 2026

verifiedMallaroni et al. (2023) found that subjective effects of 2C-B (oral) largely resolve within 6 hours[25]model confidence 99%
Verified

Abstract directly states duration of 2C-B largely resolved within 6 hours.

Duration of 2C-B largely resolved within 6 hours.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedMetabolically, 2C-B is cleared by MAO-A, MAO-B, cytosolic enzymes, and CYP2D6, while 25B-NBOH's dominant CYP enzyme is inferred to be CYP2D6 based on 25I-NBOH data[17]model confidence 97%
Verified

Abstract directly confirms all four metabolic pathways for 2C-B. The 25B-NBOH CYP2D6 inference is accurately presented as an analogy in the claim.

Key metabolic enzymes: MAO-A, MAO-B, cytosolic enzymes, CYP2D6.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedA significant pharmacokinetic divergence exists in CYP enzyme involvement. 25B-NBOMe metabolism is dominated by CYP1A2 and CYP3A4 (hydroxylation) and CYP2C9 and CYP2C19 (O-demethylation), whereas the NBOH series likely relies primarily on CYP2D6[23]model confidence 97%
Verified

Abstract directly states CYP1A2/CYP3A4 involved in hydroxylation and CYP2C9/CYP2C19 in O-demethylation for 25B-NBOMe, confirming the claim.

CYP1A2/CYP3A4 involved in hydroxylation; CYP2C9/CYP2C19 in O-demethylation.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveBoth compounds are thermolabile under GC conditions, degrading to their shared parent phenethylamine 2C-B.[2]model confidence 70%
Inconclusive

Abstract uses both GC-MS and LC-MS/MS for analysis but does not explicitly address thermolability or 2C-B as a degradation product under GC conditions.

First forensic identification and detailed characterization of 25B-NBOH using ATR-FTIR, GC-MS, LC-MS/MS, and NMR.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedBoth compounds are thermolabile under GC conditions, degrading to their shared parent phenethylamine 2C-B.[14]model confidence 92%
Verified

Abstract explicitly describes a non-thermal method that avoids thermal degradation misidentification, and includes both NBOH compounds and their 2C counterparts in the panel, strongly implying GC-induced degradation to 2C compounds.

Non-thermal method avoids thermal degradation misidentification. Simultaneous identification of 25-NBOH compounds and their 2C counterparts.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedIn contrast, 25B-NBOH may function as a partial agonist at 5-HT₂A based on the Hansen et al. (2015) observation of reduced efficacy in the bromo-substituted series.[10]model confidence 97%
Verified

Abstract directly states compounds in this series were 'less efficacious partial agonists,' directly supporting the partial agonism claim for 25B-NBOH.

Generally found to be less efficacious partial agonists vs. previously reported N-benzyl phenethylamines.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedYoon et al. (2022) demonstrated that 25I-NBOH inhibits hERG potassium channels, decreases cardiomyocyte viability, and prolongs QT and RR intervals in rat ECG[5]model confidence 99%
Verified

Abstract directly and exactly confirms all three findings: hERG inhibition, decreased cardiomyocyte viability (MTT assay), and increased QT/RR intervals in rat ECG.

25I-NBOH inhibited hERG potassium channels. Decreased viability of H9c2 cardiomyocytes (MTT assay). Increased QT and RR intervals in rat ECG.

checked by claude-sonnet-4-6 · May 7, 2026

safety26 claims15verified1partial9inconclusive1not supported
inconclusiveMultiple fatalities have been attributed to the broader NBOMe/NBOH class, and Xiang et al. (2024) reference "several poisoning cases and even fatal cases" involving 25B-NBOH[7]model confidence 70%
Inconclusive

Abstract reviews 51 toxicity cases but does not explicitly mention fatalities or the specific Xiang et al. characterization. Full text likely covers fatal outcomes.

Reviews 51 cases of NBOMe toxicity.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedMultiple fatalities have been attributed to the broader NBOMe/NBOH class, and Xiang et al. (2024) reference "several poisoning cases and even fatal cases" involving 25B-NBOH[6]model confidence 92%
Verified

Abstract explicitly mentions 'lethal intoxication' cases, directly supporting that fatalities are documented at the class level.

Cases of non-fatal and lethal intoxication.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveMultiple fatalities have been attributed to the broader NBOMe/NBOH class, and Xiang et al. (2024) reference "several poisoning cases and even fatal cases" involving 25B-NBOH[15]model confidence 70%
Inconclusive

Abstract focuses on in vitro metabolism characterization; does not mention poisoning cases or fatalities. The Xiang et al. claim about referencing fatal cases would be in the paper's introduction, not the abstract.

Investigated phase I and II metabolism of 25B-NBOH, 25E-NBOH, 25H-NBOH, and 25iP-NBOMe in human liver microsomes.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedThe Ivory et al. (2022) poisoning cluster in Australia documents clinical toxicity — hallucinations, mydriasis, tachycardia, hypertension, agitation — from 25B-NBOH sold as LSD, but whether any cases were fatal cannot be determined from the available abstract.[3]model confidence 90%
Verified

Abstract confirms the poisoning cluster and clinical toxicity from 25B-NBOH sold as LSD. The claim accurately represents what the abstract shows and appropriately notes that fatality status cannot be determined from the abstract alone.

First published report documenting clinical toxicity of NBOH derivatives. Cluster of poisonings from powder sold as LSD.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedYoon et al. (2022) demonstrated that 25I-NBOH and 25C-NBOH (structural analogs) decrease viability of H9c2 cardiomyocytes on MTT assay, increase QT and RR intervals in rat ECG, and — in the case of 25I-NBOH — inhibit hERG potassium channels and downregulate PAK1 protein in cardiomyocytes[5]model confidence 99%
Verified

Abstract exactly and directly states all components of the claim: H9c2 viability decrease (MTT), QT/RR prolongation in rat ECG, hERG inhibition by 25I-NBOH, and PAK1 downregulation by 25I-NBOH.

25I-NBOH and 25C-NBOH: decreased viability of H9c2 cardiomyocytes (MTT assay), increased QT and RR intervals in rat ECG, 25I-NBOH downregulated PAK1 protein, 25I-NBOH inhibited hERG potassium channels.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveTachycardia and hypertension are documented clinical findings in the 25B-NBOH poisoning cluster[3]model confidence 80%
Inconclusive

Abstract confirms this is the first clinical toxicity report for NBOH from a poisoning cluster but does not list specific vital sign findings like tachycardia and hypertension.

First published report documenting clinical toxicity of NBOH derivatives. Cluster of poisonings from powder sold as LSD.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedSeizures are a recognized complication of NBOMe/NBOH class toxicity[7]model confidence 97%
Verified

Abstract directly mentions seizures as a factor linked to rhabdomyolysis in severe NBOMe toxicity cases.

Rhabdomyolysis is common in severe toxicity, linked to seizures, hyperthermia, vasoconstriction.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveSeizures are a recognized complication of NBOMe/NBOH class toxicity[6]model confidence 70%
Inconclusive

Abstract covers NBOMe toxicity comprehensively including lethal intoxication but does not explicitly mention seizures in the abstract text.

Comprehensive review of NBOMe compounds including pharmacological properties, pattern of use, metabolism, desired effects, and cases of non-fatal and lethal intoxication.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedRhabdomyolysis has been documented in severe NBOMe poisoning cases, secondary to seizures, hyperthermia, and vasoconstriction[7]model confidence 99%
Verified

Abstract directly states rhabdomyolysis is common in severe toxicity, explicitly linking it to seizures, hyperthermia, and vasoconstriction.

Rhabdomyolysis is common in severe toxicity, linked to seizures, hyperthermia, vasoconstriction.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedPelletier et al. (2024) documented serotonin syndrome in a case involving 25E-NBOH (structural analog) combined with MDPHP[24]model confidence 99%
Verified

Abstract directly describes serotonergic syndrome in the context of 25E-NBOH + MDPHP intake.

23-year-old male with serotonergic syndrome and loss of consciousness after consuming powder labeled as 25I-NBOH; actually contained 25E-NBOH + MDPHP.

checked by claude-sonnet-4-6 · May 7, 2026

not supportedRepeated administration of 25I-NBOMe in rats over 7 days produced memory deficiency, motor activity reduction, and increased anxiety, suggesting potential neurotoxic consequences of chronic exposure within the N-benzylphenethylamine class[11]model confidence 97%
Not supported

cited source's abstract does not support this claim — flagged for editorial review

Abstract describes tolerance/cross-tolerance studies using DOI and LSD in mice — it does not involve 25I-NBOMe, rats, 7-day dosing protocols, memory deficiency, or anxiety. The claim describes a completely different study.

Repeated DOI induces progressive decrease in HTR; tolerance after single dose. Cross-tolerance between DOI and LSD. No cross-tolerance with non-psychedelic 5-HT2AR agonist lisuride.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveOrgan-specific chronic toxicity (hepatic, renal, pulmonary) has not been investigated for 25B-NBOH; class-level NBOMe data include reports of multiorgan failure in fatal cases.[6]model confidence 70%
Inconclusive

Abstract mentions lethal intoxication cases in a comprehensive review but does not specifically mention multiorgan failure. The detail would be in the full-text case descriptions.

Cases of non-fatal and lethal intoxication.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusive25B-NBOH's thermolability under GC conditions — degrading to 2C-B — means that clinical and forensic samples may be misidentified unless LC-MS/MS is employed[2]model confidence 70%
Inconclusive

Abstract describes analysis using both GC-MS and LC-MS/MS but does not explicitly mention thermolability or 2C-B as a degradation product under GC conditions.

First forensic identification and detailed characterization of 25B-NBOH, 25C-NBOH, and 25E-NBOH in seized blotter papers using ATR-FTIR, GC-MS, LC-MS/MS, and NMR.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedSeizure disorders. The NBOMe/NBOH class is associated with seizures[7]model confidence 97%
Verified

Abstract explicitly mentions seizures as linked to severe NBOMe toxicity and rhabdomyolysis.

Rhabdomyolysis is common in severe toxicity, linked to seizures, hyperthermia, vasoconstriction.

checked by claude-sonnet-4-6 · May 7, 2026

verified25B-NBOH's thermolability under GC conditions — degrading to 2C-B — means that clinical and forensic samples may be misidentified unless LC-MS/MS is employed[14]model confidence 95%
Verified

Abstract explicitly states the LC-MS/MS method is non-thermal and avoids 'thermal degradation misidentification,' directly supporting the thermolability concern under GC conditions.

Non-thermal method avoids thermal degradation misidentification.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedRecommended urinary biomarkers are metabolites B2-1, B2-2, and B6[15]model confidence 95%
Verified

Abstract directly identifies B2-1 (56.61%), B2-2 (17.43%), and B6 (17.78%) as major metabolites for 25B-NBOH, supporting their use as recommended biomarkers.

Major metabolites for 25B-NBOH: B2-1 (56.61%), B2-2 (17.43%) and B6 (17.78%).

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveDirect glucuronidation (demonstrated for 25I-NBOH) may extend the detection window beyond phase I metabolites.[16]model confidence 72%
Inconclusive

Abstract confirms direct glucuronidation for 25I-NBOH but characterizes its significance in terms of CYP2D6 polymorphism impact — not specifically in terms of extending the detection window.

25I-NBOH also subject to direct glucuronidation, which may diminish impact of CYP2D6 genetic polymorphism.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveThe Ivory et al. (2022) poisoning cluster documented agitation as a clinical finding, consistent with acute psychological distress[3]model confidence 80%
Inconclusive

Abstract confirms the poisoning cluster and clinical toxicity documentation but does not list specific symptoms such as agitation.

First published report documenting clinical toxicity of NBOH derivatives. Cluster of poisonings from powder sold as LSD.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedDe la Fuente Revenga et al. (2022) demonstrated that tolerance to 5-HT₂A agonist head-twitch response can develop after a single dose, mediated by receptor downregulation in the frontal cortex through a β-arrestin 2-independent mechanism[11]model confidence 99%
Verified

Abstract directly states: tolerance after single dose; 5-HT2AR downregulation in frontal cortex; mechanism independent of beta-arrestin-2.

Tolerance after single dose. DOI caused 5-HT2AR downregulation in frontal cortex. Mechanism independent of beta-arrestin-2.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedEshleman et al. (2018) confirmed that NBOH compounds have low to mid-micromolar affinities at monoamine transporters (DAT, SERT, NET), indicating no significant dopaminergic reward pathway engagement at pharmacologically relevant doses[4]model confidence 95%
Verified

Abstract directly states low micromolar potency at monoamine transporters and minimal psychostimulant activity, fully supporting the claim.

Low micromolar potency at monoamine transporters. Results consistent with hallucinogenic activity, minimal psychostimulant activity.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedThe Pelletier et al. (2024) case of serotonin syndrome with 25E-NBOH + MDPHP provides the closest published clinical precedent for NBOH serotonin syndrome.[24]model confidence 90%
Verified

Abstract documents serotonin syndrome in a 25E-NBOH + MDPHP case and includes a literature review of NBOH human exposure cases, confirming this paper is the relevant clinical reference for NBOH serotonin syndrome.

23-year-old male with serotonergic syndrome and loss of consciousness after consuming 25E-NBOH + MDPHP. Literature review of NBOH human exposure cases.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedProspective survey data from Barbut Siva et al. (2024) demonstrate reduced acute effects in SSRI users taking psychedelics[27]model confidence 97%
Verified

Abstract directly states SRI use during psychedelic experience is associated with reduced acute subjective effects.

SRI use during psychedelic experience associated with reduced acute subjective effects but similar post-experience improvements in well-being and depressive symptoms.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedCYP2D6 inhibitors. By analogy with 25I-NBOH (where CYP2D6 is the primary metabolic enzyme), pharmacokinetic interactions with CYP2D6 inhibitors — including paroxetine, fluoxetine, bupropion, and quinidine — may increase 25B-NBOH plasma concentrations and prolong exposure, elevating cardiovascular and neurological toxicity risk[16]model confidence 90%
Verified

Abstract confirms CYP2D6 as the dominant enzyme for 25I-NBOH with high CLint, providing the pharmacological basis for the CYP2D6 inhibitor interaction claim. The specific inhibitors listed and the risk inference are reasonable pharmacological extrapolations.

Major CYP enzymes for 25I-NBOH: CYP2D6. Intrinsic clearance for 25I-NBOH: 118.7 mL/min/kg.

checked by claude-sonnet-4-6 · May 7, 2026

partialCannabis used concomitantly with psychedelics dose-dependently increases mystical experience, visual alterations, and ego dissolution scores while also increasing challenging experience scores[28]model confidence 85%
Partial

Abstract directly supports dose-dependent increases in mystical experience, visual alterations, and ego dissolution. However, for challenging experience the abstract states a 'quadratic relationship' — not a simple monotonic increase — meaning challenging experience may peak and then decline, not simply 'increase.'

Cannabis used concomitantly with psychedelics (n=321) associated with dose-dependent increases in mystical experience, visual alterations, and ego dissolution scores. Quadratic relationship for challenging experience.

checked by claude-sonnet-4-6 · May 7, 2026

verifiedPre-existing cardiac conditions. hERG potassium channel inhibition and QT prolongation demonstrated for NBOH structural analogs make 25B-NBOH contraindicated in individuals with congenital or acquired long QT syndrome, structural heart disease, or concurrent use of QT-prolonging medications.[5]model confidence 93%
Verified

Abstract directly confirms hERG inhibition and QT interval prolongation for 25I-NBOH and 25C-NBOH, providing the preclinical basis for the contraindication claim.

25I-NBOH inhibited hERG potassium channels. Increased QT and RR intervals in rat ECG.

checked by claude-sonnet-4-6 · May 7, 2026

inconclusiveSeizure disorders. The NBOMe/NBOH class is associated with seizures[6]model confidence 70%
Inconclusive

Abstract is a comprehensive review covering NBOMe toxicity including lethal intoxication, but does not explicitly mention seizures in the abstract text.

Comprehensive review of NBOMe compounds including pharmacological properties, pattern of use, metabolism, desired effects, and cases of non-fatal and lethal intoxication.

checked by claude-sonnet-4-6 · May 7, 2026

legal status1 claim1verified
verifiedThe compound is not controlled under United Nations drug conventions as of the most recent assessment, though the UNODC maintains a substance database entry[2]model confidence 95%
Verified

Abstract directly states 25B-NBOH is not under UN Conventions control as of 2019, supporting the claim. UNODC database entry is not mentioned but does not contradict.

Not under UN Conventions control as of 2019.

checked by claude-sonnet-4-6 · May 7, 2026

05

Coverage & Gaps

effect links
140 links · 136 approved · 53 audited0/140 with evidence basis
interactions
2 approved pairs0/2 graded
06

Research Trail

substance-article pipeline-v5 May 7, 2026

StepSourceQueryResults
1database lookupPubChem25B-NBOH1 result, 1 selected
selection rationale

Primary source for chemical identity verification.

2literature searchPubMed25B-NBOH phenethylamine psychedelic pharmacology2 results, 2 selected
selection rationale

Both directly relevant to 25B-NBOH - metabolism and clinical toxicity.

3literature searchOpenAlex25B-NBOH NBOH serotonin receptor binding44 results, 4 selected
selection rationale

Selected most-cited and directly relevant papers.

4clinical trial searchClinicalTrials.gov25B-NBOH0 results
selection rationale

No clinical research on this substance.

5literature searchPubMedNBOMe NBOHcompound 5-HT2A agonist hallucinogen binding5 results, 5 selected
selection rationale

All highly relevant to pharmacological mechanism of NBOH compounds including 25B-NBOH.

6literature searchPubMed25I-NBOH 2-(2-(4-iodo-2,5-dimethoxyphenyl)ethylamino)methyl phenol pharmacology3 results, 2 selected
selection rationale

CYP2D6 metabolism for 25I-NBOH strongly relevant to 25B-NBOH by structural analogy; cardiovascular toxicity important for safety section.

7legal status searchWebSearch25B-NBOH legal status scheduling US UK EU Canada Australia 202410 results, 4 selected
selection rationale

Key legal status data across major jurisdictions.

8literature searchPubMedNBOH discriminative stimulus locomotor head twitch hallucinogen 20250 results
selection rationale

Relevant paper found via other search.

9document retrievalWebSearchNBOH discriminative stimulus effects behavioural pharmacology 20255 results, 1 selected
selection rationale

Critical finding: only published animal behavioral study directly testing 25B-NBOH.

10literature searchPubMed25B-NBOMe 2C-B N-benzyl serotonin receptor Ki pKi binding affinity0 results
selection rationale

Values appear in Hansen et al. 2015 (PMID 25583099) for N-benzyl 2C-B derivatives.

11database lookupPubChem25B-NBOH CID 125181394 verification1 result, 1 selected
selection rationale

Primary chemical identity verification.

12document retrievalWebSearch25B-NBOH CFSRE monograph NPS Discovery 20231 result, 1 selected
selection rationale

Official forensic monograph with key chemical/pharmacological data and first detection dates.

13document retrievalWebSearch25B-NBOH dose threshold light common strong heavy microgram effects duration10 results, 1 selected
selection rationale

Only available dose data; user report consensus; to be flagged as unverified by published clinical studies.

14literature searchOpenAlex25B-NBOH 25C-NBOH 25E-NBOH NBOH toxicity poisoning clinical16 results, 1 selected
selection rationale

Closest structural analog case report of serious NBOH toxicity with serotonin syndrome.

Research document (raw, unedited pipeline output)
# Research Output: 25B-NBOH

---

## Chemical Identity

**Verified against PubChem CID 125181394** [Ref 17 (CFSRE); PubChem direct lookup]:

| Property | Value | Source |
|---|---|---|
| PubChem CID | 125181394 | api_verified |
| IUPAC Name | 2-[[2-(4-bromo-2,5-dimethoxyphenyl)ethylamino]methyl]phenol | PubChem |
| Molecular Formula | C₁₇H₂₀BrNO₃ | PubChem |
| Molecular Weight | 366.2 g/mol | PubChem |
| InChIKey | RSUNJYKZRKIBNB-UHFFFAOYSA-N | PubChem |
| CAS Number | Not confirmed via API; 1354632-06-6 reported in trade/vendor sources (unverifiable) | — |

The brief's IUPAC name matches the PubChem record exactly. The brief was missing PubChem CID, molecular formula, molecular weight, and InChIKey — all now confirmed. SMILES was missing from both the brief and the PubChem API response; the canonical structure is derivable from the IUPAC name.

**Common synonyms/alternate names:** 2C-B-NBOH; NBOH-2C-B; BOH-2C-B. The NBOH suffix indicates the N-(2-hydroxybenzyl) group distinguishes it from 25B-NBOMe (N-(2-methoxybenzyl) group).

**Thermolability flag:** 25B-NBOH is thermolabile under standard gas chromatography conditions and degrades to its parent phenethylamine 2C-B (Machado et al. 2019 [Ref 5]; Chia et al. 2019 [Ref 16]). This is a critical analytical point: routine GC-MS screening will misidentify 25B-NBOH as 2C-B. LC-MS/MS or NMR are required for accurate identification.

---

## Pharmacology

### Primary Mechanism

25B-NBOH is a potent agonist at serotonin 5-HT₂A and 5-HT₂C receptors. Its psychoactive effects are mediated primarily through 5-HT₂A receptor activation, consistent with the broader N-benzylphenethylamine class (Halberstadt 2017 [Ref 7]; Zawilska et al. 2020 [Ref 3]).

### Receptor Binding Affinity

**25B-NBOH-specific data:**
- pKi at 5-HT₂A = **8.3** (Ki ≈ 5 nM) — high nanomolar affinity
- pKi at 5-HT₂C = **9.4** (Ki ≈ 0.4 nM) — subnanomolar affinity
- Source: Hansen et al. 2015 [Ref 20], a study of N-benzyl substituted 4-bromo-2,5-dimethoxyphenethylamines (2C-B scaffold). Confirmed by CFSRE monograph [Ref 17] and MedChemExpress product data citing the same source.

**⚠️ FLAG:** These pKi values come from the Hansen 2015 paper [Ref 20] which studied partial agonists in this series. The abstract notes that compounds tested "were generally found to be less efficacious agonists than previously reported N-benzyl phenethylamines." The specific efficacy (Emax) value for 25B-NBOH at 5-HT₂A has not been independently confirmed in a second published study. Editorial attention recommended.

**Class-level data for NBOH compounds (structural analogs):**
NBOH compounds as a class exhibit subnanomolar to low nanomolar potencies at 5-HT₂A, similar to LSD. Eshleman et al. 2018 [Ref 6] found that 25I-NBOH had full efficacy at 5-HT₂A and 5-HT₂C receptors with subnanomolar to low nanomolar functional potencies. Rickli et al. 2015 [Ref 8] characterized the full NBOMe class receptor interaction profile vs. parent 2C drugs and LSD.

- At 5-HT₁A: Very low potency, low efficacy (class data, Eshleman 2018 [Ref 6])
- At 5-HT₂B: Lower affinity, potency, and efficacy vs. 5-HT₂A/2C (Eshleman 2018 [Ref 6])
- At monoamine transporters (DAT, SERT, NET): Low to mid-micromolar affinities — minimal psychostimulant activity (Eshleman 2018 [Ref 6])

### Signaling Mechanism

5-HT₂A receptor activation by psychedelics involves both Gq/11-mediated (IP₃/DAG) and Gi-mediated signaling. Xu et al. 2026 [Ref 10] identified non-canonical Gi signaling as essential for hallucinogenic effects. Wallach et al. 2023 [Ref 15] found that 5-HT₂A-Gq efficacy (not β-arrestin2) predicts psychedelic potential as measured by head-twitch response. Pottie et al. 2020 [Ref 9] showed that NBOH compounds — specifically 25H-NBOH and related analogs — exhibit statistically significant β-arrestin 2 preference over miniGαq relative to LSD. Whether 25B-NBOH specifically shows this bias has not been published but is expected from class structure.

### In Vivo Behavioral Data (Rodents)

Munir et al. 2025 [Ref 13] — the only published animal study directly testing 25B-NBOH — found:
- **Locomotor activity:** 25B-NBOH decreased spontaneous locomotor activity in mice, similar in magnitude to DOM but less potent than 25X-NBOMe compounds
- **Discriminative stimulus:** 25B-NBOH **fully substituted** for DOM in DOM-trained rats (≥80% drug-appropriate responding), confirming hallucinogenic-like activity
- Discriminative stimulus potency was greater than DOM and 25X-NBOMe compounds for 25B-NBOH, 25C-NBOH, and 25E-NBOH (note: 25I-NBOH failed to fully substitute)

This is the critical in vivo pharmacological confirmation of 25B-NBOH's hallucinogenic profile.

### Pharmacokinetics

No human PK studies exist for 25B-NBOH specifically. The following applies by class analogy:

**Route of administration:** NBOH compounds are inactive or nearly inactive when taken orally at standard doses (Machado 2019 [Ref 5]; CFSRE 2023 [Ref 17]). This is attributed to first-pass metabolism. Standard administration is sublingual/buccal (blotter papers held under tongue) or insufflation.

**Parent compound 2C-B (Thomann et al. 2025 [Ref 24]):** In a human clinical study (30 mg oral), 2C-B was metabolized by MAO-A, MAO-B, cytosolic enzymes, and CYP2D6. Primary metabolites (BDMPAA and B-2-HMPAA) did not activate 5-HT₂AR. CYP2D6 is a minor pathway for 2C-B itself.

**For 25I-NBOH (closest published analog):** Nielsen et al. 2017 [Ref 11] identified **CYP2D6 as the primary metabolic enzyme** for 25I-NBOH (CLint = 118.7 mL/min/kg). 25I-NBOH is also subject to direct glucuronidation, which may reduce the impact of CYP2D6 genetic polymorphism. Biotransformations: hydroxylation, O-demethylation, N-dealkylation, dehydrogenation.

**For 25B-NBOH specifically (Xiang et al. 2024 [Ref 1]):** In vitro human liver microsome study identified 25B-NBOH metabolites. Major biotransformations: O-demethylation, hydroxylation, dehydrogenation, N-dehydroxybenzyl, N-demethoxybenzyl, oxidative transformation to ketone and carboxylate, glucuronidation. Recommended biomarkers (high peak area ratio): **B2-1 (56.61%), B2-2 (17.43%), and B6 (17.78%)**. This is the most comprehensive published metabolism study for 25B-NBOH.

**For 25B-NBOMe (methoxy counterpart, Caspar et al. 2017 [Ref 30]):** 66 metabolites identified. Main pathways: O-demethylation, O,O-bis-demethylation, hydroxylation, glucuronidation, sulfation. CYP1A2/CYP3A4 in hydroxylation; CYP2C9/CYP2C19 in O-demethylation. The NBOH vs. NBOMe metabolic difference (CYP2D6 vs. CYP3A4 predominance) is likely significant clinically for drug-drug interactions.

---

## History

### Discovery and Synthesis

25B-NBOH belongs to the 25x-NBOH class of N-benzylphenethylamines, derived by N-(2-hydroxybenzyl) substitution of 2C-B (4-bromo-2,5-dimethoxyphenethylamine). The NBOH class is a structural variant of the NBOMe series, replacing the N-(2-methoxybenzyl) group with N-(2-hydroxybenzyl).

The foundational SAR work establishing the NBOH scaffold was published by Hansen et al. 2014 [Ref 21] at the University of Copenhagen, who prepared a series of 48 N-benzyl phenethylamine compounds and demonstrated that N-benzyl substitution dramatically increased 5-HT₂A binding affinity. The specific 25B-NBOH compound (using 2C-B as the phenethylamine backbone) was characterized pharmacologically by Hansen et al. 2015 [Ref 20].

25I-NBOH (the iodo analog) was the first NBOH compound to appear in forensic seizures, identified in Brazil in 2016-2017 (Arantes et al. 2017 [Ref 22]). The Brazilian team who first reported 25I-NBOH later identified 25B-NBOH in seized blotter papers in Brazil between 2017 and 2018 (Machado et al. 2019 [Ref 5]).

According to the CFSRE NPS Discovery monograph (2023 [Ref 17]), **25B-NBOH first emerged in Europe approximately June 2016**, and was **first detected in the United States in November 2022**. The compound became the main hallucinogenic drug on blotter papers in certain Brazilian regions from 2014 through early 2019 (Machado 2019 [Ref 5]).

### Regulatory/Prohibition Timeline

- **Sweden:** January 26, 2016 — Added to Narcotic Drugs Punishments Act as Schedule I [web-retrieved]
- **Brazil:** December 2018 — Scheduled as prohibited substance [web-retrieved]
- **UK:** Covered by the N-benzylphenethylamine catch-all clause of the Misuse of Drugs Act 1971 (Class A) [web-retrieved]
- **Germany:** Controlled under the NpSG (New Psychoactive Substances Act) [web-retrieved]
- **Switzerland:** Controlled substance [web-retrieved]
- **Canada:** Covered under phenethylamine blanket-ban legislation [web-retrieved]
- **United States:** Not explicitly scheduled under the Controlled Substances Act; potentially subject to the Federal Analogue Act due to structural similarity to scheduled 2C compounds [web-retrieved]
- **UNODC/International:** Not under UN Drug Conventions control as of the Machado 2019 paper; UNODC maintains a substance entry (ID: 481e6364-ed7f-47f1-a48e-8b82298bbd9d) [Ref 27]

---

## Subjective Effects

No controlled human studies of 25B-NBOH have been published. The following is drawn from:
1. The Ivory 2022 poisoning cluster (clinical toxicology, not voluntary reports) [Ref 2]
2. Structural analog 25E-NBOH intoxication case (Pelletier 2024 [Ref 23])
3. Animal behavioral data (Munir 2025 [Ref 13])
4. Class-level data from NBOH/NBOMe literature (Zawilska 2020 [Ref 3], Halberstadt 2017 [Ref 7])
5. Parent compound 2C-B controlled study (Mallaroni 2023 [Ref 31], Papaseit 2018 [Ref 26])
6. User-report aggregates (PsychonautWiki — not peer-reviewed; flagged as such)

### Documented Clinical Effects (Toxicological Context)

Ivory et al. 2022 [Ref 2] — a cluster of 25B-NBOH poisonings in Australia from powder sold as LSD — reported (per CFSRE summary [Ref 17]): **hallucinations, mydriasis, tachycardia, hypertension, and agitation**. This is the only published human clinical toxicology report for 25B-NBOH specifically.

Pelletier et al. 2024 [Ref 23] documented a 25E-NBOH + MDPHP case presenting with **serotonin syndrome and loss of consciousness**. Although this involves a different NBOH analog, it is the most detailed NBOH human case in the literature.

### Effect Profile (Class Inference + Parent Compound)

**Perceptual:** Visual and auditory hallucinations are class-defining for 5-HT₂A agonists. Zawilska et al. 2020 [Ref 3] documents NBOMe class effects including visual and auditory hallucinations. 2C-B human studies (Mallaroni 2023 [Ref 31]; Papaseit 2018 [Ref 26]) documented perceptual changes in colors, shapes, and lights.

**Sympathomimetic:** Mydriasis, tachycardia, hypertension documented in the Ivory 2022 poisoning cluster [Ref 2].

**Stimulation:** 2C-B parent compound associated with euphoria and stimulation (Papaseit 2018 [Ref 26]).

**Duration:** 2C-B largely resolves within 6 hours (Mallaroni 2023 [Ref 31]). NBOH compounds reported by user consensus to have a shorter duration than their NBOMe counterparts. No published pharmacokinetic study defines duration for 25B-NBOH.

**Route of administration:** Sublingual/buccal (standard for blotter papers). Insufflation also reported. Orally inactive at typical doses (NBOH class, first-pass effect) [Ref 5, 17].

### Dose Data

**⚠️ SAFETY FLAG — NO PUBLISHED CLINICAL DOSE DATA:** No controlled human dose-finding study has been conducted for 25B-NBOH. The following derives from:
- Forensic seizure data (25I-NBOH individual blotter doses: 300–1000 µg, Arantes 2017 [Ref 22])
- User-report consensus aggregated at PsychonautWiki (web-retrieved, not peer-reviewed):

| Level | Dose Range |
|---|---|
| Threshold | ~100 µg |
| Light | 200–400 µg |
| Common | 400–800 µg |
| Strong | 800–1,000 µg |
| Heavy | > 1,000 µg |

These figures are consistent with the class (NBOH/NBOMe compounds are active in the microgram range), and with forensic blotter dose data for 25I-NBOH. However, they have not been validated in any published controlled human study and carry high uncertainty. **Flag for editorial review before publishing.**

---

## Safety & Toxicity

### Acute Toxicity

**Seed data states "acute toxicity: high" and "potentially fatal at heavy dosages."** This characterization is supported by class-level evidence but not by a published LD50 study for 25B-NBOH.

The seed data toxicity characterization is **consistent** with:
- Multiple NBOMe fatalities documented in Halberstadt 2017 [Ref 7] (review of 51 NBOMe toxicity cases)
- Zawilska et al. 2020 [Ref 3] documenting deaths from NBOMe use
- Xiang et al. 2024 [Ref 1] noting "25B-NBOH... have caused several poisoning cases and even fatal cases"
- However: no peer-reviewed case report of a confirmed 25B-NBOH fatality was retrieved in this search. Ivory 2022 [Ref 2] documents poisonings; whether any were fatal is not apparent from the available abstract.

**⚠️ FLAG:** "Potentially fatal at heavy dosages" is class-level inference. No published confirmed fatality from 25B-NBOH specifically was found. This should be stated as such in the article.

No published LD₅₀ data (animal or human) for 25B-NBOH was found.

### Cardiovascular Toxicity

Yoon et al. 2022 [Ref 12] demonstrated that 25I-NBOH and 25C-NBOH:
- Decreased viability of H9c2 cardiomyocytes (MTT assay)
- Increased QT and RR intervals in rat ECG
- Inhibited hERG potassium channels (25I-NBOH)
- Downregulated PAK1 protein in cardiomyocytes

These findings are highly relevant to 25B-NBOH by structural analogy. Tachycardia and hypertension are documented in the Ivory 2022 cluster [Ref 2, 17].

### Neurological Toxicity

NBOMe class associated with seizures (Halberstadt 2017 [Ref 7]; Zawilska 2020 [Ref 3]). Seizure threshold reduction is listed in the seed data effect profile. Rhabdomyolysis is a documented complication of severe NBOMe toxicity, linked to seizures, hyperthermia, and vasoconstriction (Halberstadt 2017 [Ref 7]).

Herian et al. 2021 [Ref 14] found that repeated 25I-NBOMe administration caused memory deficiency, motor activity reduction, and anxiety — suggesting neurotoxic effects from chronic use. Direct evidence for 25B-NBOH is absent.

### Serotonin Syndrome

Pelletier et al. 2024 [Ref 23] documented serotonin syndrome in a case involving 25E-NBOH (structural analog). The NBOH class carries inherent serotonin syndrome risk due to potent 5-HT₂A/2C agonism. Combination with other serotonergic substances is particularly dangerous.

### Detection Window

Xiang et al. 2024 [Ref 1] identified major metabolite biomarkers for forensic detection of 25B-NBOH: B2-1, B2-2, and B6. Nielsen et al. 2017 [Ref 11] found 25I-NBOH also subject to direct glucuronidation, which extends the detection window beyond phase I metabolites.

---

## Harm Reduction

### Key Safety Points

1. **Oral inactivity:** 25B-NBOH is inactive or near-inactive when swallowed at typical doses (first-pass metabolism). Users who ingest blotter papers expecting no effect may re-dose and overdose. This is a major harm vector documented in the Ivory 2022 cluster [Ref 2] where powder was sold as LSD.

2. **Adulteration and misrepresentation:** The Ivory 2022 cluster [Ref 2] involved powder sold as LSD — meaning users were unaware they were taking 25B-NBOH. Drug checking services should use reagent testing (Marquis, Simon's) or ideally LC-MS (FTIR/NMR) to distinguish NBOH from LSD, which cannot be done reliably by appearance alone.

3. **Analytical misidentification:** GC-MS will misidentify 25B-NBOH as 2C-B due to thermolability (Machado 2019 [Ref 5]; Chia 2019 [Ref 16]). Forensic/clinical labs should use LC-MS/MS for confirmation.

4. **High potency:** Active in the microgram range; dose errors on blotter paper are possible. Analytical determination of blotter content is not possible without instrumentation.

5. **Cardiovascular risk:** Tachycardia, hypertension, QT prolongation documented in class; particularly dangerous in individuals with pre-existing cardiac conditions.

6. **No antidote:** No specific antidote exists. Supportive care: benzodiazepines for agitation/seizures; 5-HT₂A antagonists (e.g., antipsychotics) may help; cyproheptadine for serotonin syndrome features.

### Contraindications (Literature-Supported)

- MAO inhibitors: Risk of serotonin syndrome (class mechanism)
- Tramadol: Classified as dangerous in seed data — tramadol has serotonergic (SERT inhibition) and weak opioid activity; combination with a potent 5-HT₂A agonist carries serotonin syndrome risk
- SSRIs/SNRIs: May blunt psychedelic effects (5-HT₂A downregulation) or cause serotonin syndrome at high doses; prospective survey data (Barbut Siva 2024 [Ref 33]) shows reduced acute effects in SSRI users
- Cardiac conditions: hERG inhibition and QT prolongation risk (Yoon 2022 [Ref 12])
- Lithium: Class-level warning for 5-HT₂A agonists (seizure risk); not 25B-NBOH specific

---

## Tolerance & Dependence

### Tolerance

**Seed data:** Builds almost immediately after ingestion; half-life ~1 week; full reset ~2 weeks; cross-tolerance with psychedelics.

This is **consistent** with published mechanistic data:

de la Fuente Revenga et al. 2022 [Ref 14] demonstrated that tolerance to 5-HT₂A agonist head-twitch response can develop after a single dose and follows a receptor downregulation mechanism in the frontal cortex. Cross-tolerance between psychedelics (DOI and LSD) was confirmed; mechanism is β-arrestin 2-independent.

Herian et al. 2021 [Ref: PMID 34032876] showed tolerance to 25I-NBOMe's hallucinogenic activity after 7-day treatment, with reduced frontal cortex DA, 5-HT, and glutamate responses to challenge doses.

The specific 1-week half-life and 2-week reset timeline in the seed data are plausible based on known 5-HT₂A receptor downregulation and upregulation kinetics but are not verified by a 25B-NBOH-specific published study.

**⚠️ FLAG:** Tolerance half-life and reset timeline are not confirmed in published literature for 25B-NBOH specifically. Derived from class extrapolation and community consensus. Flag for editorial review.

### Cross-Tolerance

Cross-tolerance with other serotonergic psychedelics (LSD, psilocybin, DMT, DOx amphetamines) is expected based on shared 5-HT₂A receptor mechanism. This is consistent with de la Fuente Revenga 2022 [Ref 14] demonstrating DOI/LSD cross-tolerance.

### Dependence

**Seed data:** "Not habit-forming."

This is consistent with the pharmacological profile: serotonergic hallucinogens generally do not produce compulsive drug-seeking behavior. There is no dopamine reward circuit activation at relevant doses (Eshleman 2018 [Ref 6]: low to mid-micromolar potency at monoamine transporters). No published dependence or withdrawal data for 25B-NBOH.

---

## Interactions

### Tramadol — Dangerous (Seed Data Flag)

**Mechanistic basis:** Tramadol inhibits serotonin and norepinephrine reuptake and has weak µ-opioid activity. Combined with the potent 5-HT₂A/2C agonism of 25B-NBOH and any accompanying serotonin release, this combination carries significant serotonin syndrome risk. The Pelletier 2024 [Ref 23] case documented serotonin syndrome with a structurally similar NBOH compound (25E-NBOH) + a stimulant. No published case report specifically documents 25B-NBOH + tramadol serotonin syndrome, but the mechanistic risk is well-established.

**Assessment:** The "dangerous" classification in the seed data is mechanistically sound. No published confirmatory case for this specific combination found. **Flag as class-derived, not substance-specific.**

### Cannabis — Unknown (Seed Data Flag)

Kuc et al. 2021 [Ref 32] found that cannabis used concomitantly with psychedelics dose-dependently increased mystical experience, visual alterations, and ego dissolution scores, while also increasing challenging experience scores. No 25B-NBOH + cannabis study exists. Interaction is plausible but intensity and risk profile are uncertain.

### SSRIs/SNRIs

Prospective survey data (Barbut Siva 2024 [Ref 33]) suggests SSRIs attenuate acute psychedelic effects. Mechanistically, chronic SSRI use downregulates 5-HT₂A receptors, reducing response to agonists. Combining with potent 5-HT₂A agonists may still carry serotonin syndrome risk at high doses, particularly with SNRIs and tricyclics that strongly elevate synaptic 5-HT.

### MAO Inhibitors

Serotonin syndrome risk via excessive 5-HT accumulation combined with 5-HT₂A agonism. Class-level contraindication for all serotonergic hallucinogens. No 25B-NBOH-specific case found.

### CYP2D6 Inhibitors

By analogy with 25I-NBOH (Nielsen 2017 [Ref 11]), CYP2D6 is likely the primary metabolic enzyme for 25B-NBOH. CYP2D6 inhibitors (paroxetine, fluoxetine, bupropion, quinidine) could increase plasma concentrations and risk toxicity. CYP2D6 poor metabolizers may also experience elevated exposure. **Not confirmed for 25B-NBOH specifically; inferred from analog data.**

---

## Legal Status

| Jurisdiction | Status | Notes |
|---|---|---|
| United States | Not explicitly scheduled | Possible Federal Analogue Act applicability; DEA has not specifically scheduled 25B-NBOH |
| United Kingdom | Class A | Covered under N-benzylphenethylamine catch-all in Misuse of Drugs Act 1971 |
| Canada | Controlled | Phenethylamine blanket-ban legislation |
| Germany | Controlled | NpSG (Neue-psychoaktive-Stoffe-Gesetz) |
| Sweden | Schedule I | Listed since January 26, 2016 |
| Switzerland | Controlled | |
| Brazil | Prohibited | Scheduled December 2018 |
| Australia | **Unconfirmed** | TGA Poisons Standard status not independently verified in this research; possibly covered under analogue provisions |
| UN Conventions | Not listed | Not under international drug conventions as of 2019 (Machado 2019 [Ref 5]); UNODC maintains a database entry [Ref 27] |

**All legal status data is web-retrieved and should be verified against primary legislative sources before publication.**

---

## Clinical Trials

No clinical trials involving 25B-NBOH were found in ClinicalTrials.gov (search returned 0 results). No clinical research program is known. No compassionate use or named-patient data identified.

---

## Community Feedback Analysis

No community feedback was submitted in Part A2 of the brief.

---

## Gaps & Flags

### Critical Safety Flags

1. **⚠️ Dose data not published:** The dose ranges in this report (threshold ~100 µg through heavy >1,000 µg) are derived from community reports (PsychonautWiki) and forensic seizure data for structural analogs (25I-NBOH blotter doses 300–1,000 µg, Arantes 2017 [Ref 22]). No controlled human dosing study exists. Any dose table in the article must carry a strong caveat. **Editorial review required.**

2. **⚠️ "Potentially fatal at heavy dosages" — not directly confirmed:** The seed data toxicity characterization is consistent with class evidence (Zawilska 2020 [Ref 3]; Xiang 2024 [Ref 1] noting fatal cases) but no confirmed 25B-NBOH-specific fatality case report was found in this research. The Ivory 2022 paper [Ref 2] describes poisonings but the full clinical outcomes (fatal/non-fatal) are not available from the abstract alone.

3. **⚠️ Tramadol interaction "dangerous" not compound-specific:** Mechanistically sound but no published case report for this specific combination. Label as class-derived inference.

4. **⚠️ pKi binding values (8.3 / 9.4):** Sourced from Hansen 2015 [Ref 20]; should be confirmed from primary paper table before quoting as definitive. The 5-HT₂C > 5-HT₂A affinity pattern (lower pKi at 2A than 2C) is unusual for this class and may indicate partial agonism at 5-HT₂A.

5. **⚠️ Tolerance timeline values (half-life 1 week; reset 2 weeks):** Not confirmed in published 25B-NBOH literature; class-derived from general serotonergic psychedelic data.

### Data Gaps

- **No published human PK data** for 25B-NBOH (half-life, Tmax, bioavailability, volume of distribution, plasma concentrations at therapeutic/toxic doses)
- **No LD₅₀** for 25B-NBOH (animal or human)
- **Duration of effects** not confirmed in a human study; estimated 4–6 hours by class analogy with 2C-B (Mallaroni 2023 [Ref 31]: 2C-B largely resolves within 6 hours)
- **Melting point, aqueous solubility** not retrieved (no published physicochemical data found)
- **Stereochemistry:** 25B-NBOH has a chiral amine center; specific active stereoisomer not characterized in available published literature
- **Australia legal status** not independently confirmed from TGA sources
- **Chronic toxicity data:** No published chronic administration studies in animals or humans for 25B-NBOH
- **Organ-specific toxicity** (hepatotoxicity, nephrotoxicity): No 25B-NBOH-specific data; class data from NBOMe cases includes multiorgan failure (Zawilska 2020 [Ref 3])
- **No published case report with confirmed 25B-NBOH fatality** (though fatal cases referenced indirectly in Xiang 2024 [Ref 1])
- **Oral bioavailability:** Described as inactive by oral route in user reports; no pharmacokinetic study confirms this
- **Primary ROA:** Not specified in the brief; confirmed as sublingual/buccal or insufflation by class literature (not a published clinical study for 25B-NBOH specifically)

### Areas Relying on Structural Analogy

The following sections rely primarily on class inference rather than 25B-NBOH-specific evidence:
- CYP2D6 as primary metabolic enzyme (inferred from 25I-NBOH data, Nielsen 2017 [Ref 11])
- Duration of effects
- Cardiovascular toxicity (inferred from 25I-NBOH / 25C-NBOH data, Yoon 2022 [Ref 12])
- Serotonin syndrome risk mechanism
- Dependence liability ("not habit-forming")
- Tolerance timeline
- Drug interaction risks beyond tramadol

### Substance Characterization Note

25B-NBOH is an **emerging substance** with a thin published literature relative to its more-studied analogs (25I-NBOMe, 25I-NBOH, 25C-NBOMe). The pharmacological characterization as a 5-HT₂A/2C agonist is well-supported; the safety profile is extrapolated from class data and a single clinical cluster report. The 2025 Munir et al. paper [Ref 13] is the only published in vivo study directly testing 25B-NBOH, confirming its hallucinogenic behavioral profile in rodents. Generation agent should clearly mark sections relying on structural analog inference.