generation run 2026-05-07
62 min completedmodel pipeline-v5plan not recordedrun/ece7415d…Selection
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16 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubChem | 25C-NBOH | 1 | 1 | Primary chemical identity verification |
| 2 | OpenAlex | NBOH 25I-NBOH metabolism toxicology forensic | 46 | 4 | Kristofic 2016 documents 25C-NBOH as metabolite detected in overdose; Eshleman 2018 has NBOH receptor pharmacology data |
| 3 | PubMed · absence | 25C-NBOH serotonin receptor psychedelic pharmacology | 0 | — | — |
| 4 | PubMed | NBOH new psychoactive substance serotonin 5-HT2A receptor | 3 | 3 | All directly relevant to NBOH pharmacology and metabolism |
| 5 | OpenAlex | 25C-NBOH NBOH phenethylamine psychedelic | 44 | 3 | Machado 2019 is the primary characterization paper for 25C-NBOH; Zawilska 2020 covers NBOMe/NBOH toxicology comprehensively |
| 6 | PubMed | PMID 31657895 | 1 | 1 | Comprehensive review including NBOMes and NBOH class history, chemistry, pharmacology |
| 7 | PubMed | 25C-NBOMe pharmacology toxicity hallucinogen case | 6 | 5 | Directly relevant to toxicity and safety sections for 25C-NBOH class |
| 8 | OpenAlex | NBOMe serotonin 5-HT2A binding affinity Ki structure activity relationship | 33 | 3 | All provide class-level data applicable to 25C-NBOH by structural analogy |
| 9 | OpenAlex | tramadol serotonin syndrome serotonergic toxicity opioid | 520 | 2 | Directly relevant to tramadol interaction risk documented in brief |
| 10 | PubMed | synthesis structure activity relationships N-benzyl phenethylamines 5-HT2A 2C agonists 2014 | 2 | 2 | Primary SAR papers for NBOH class; Hansen is lead synthesizer of NBOH class compounds |
| 11 | WebSearch | 25C-NBOH legal status United States DEA scheduled controlled substance federal law | 10 | 1 | Legal status information for NBOH class; key distinction between NBOMe (scheduled) and NBOH (potentially unscheduled federally) |
| 12 | PubMed | PMID 24397362 | 1 | 1 | Primary discovery paper for NBOH class pharmacology; first SAR study by Copenhagen group |
| 13 | WebSearch | EMCDDA 25C-NBOH 25B-NBOH early warning NBOH new psychoactive substance | 10 | 2 | Only paper specifically testing 25C-NBOH in vivo cardiotoxicity studies |
| 14 | PubMed | NBOH phenethylamine cardiomyocyte QT interval hERG PAK1 cardiovascular toxicity 2021 2022 | 1 | 1 | Only substance-specific 25C-NBOH pharmacological/toxicological study found |
| 15 | WebSearch/Erowid | 25C-NBOH legal status UK USA EU Canada Australia scheduling | 10 | — | Key legal status distinctions between NBOMe (widely scheduled) and NBOH (more limited scheduling) |
| 16 | ClinicalTrials.gov · absence | NBOH 25C phenethylamine psychedelic | 0 | — | Confirms absence of clinical trial data |
76 claims by section — every cited sentence, checked against its source
safety26 · 19 ok
Tang et al. reported severe intoxication associated with analytically confirmed 25C-NBOMe use.supported
Two severe intoxication cases involving 25B-NBOMe and 25C-NBOMe. Clinical features documented. 15563650.2014.909932
Andreasen et al. reported the first fatal poisoning quantifying 25C-NBOMe — a young male who died 12 hours after ingestion with signs of serotonin toxicity (ante-mortem blood concentration 0.81 µg/kg).supported
Fatal overdose of 25C-NBOMe in a young male who died 12h after ingestion with serotonin toxicity signs. Blood 0.81 µg/kg ante-mortem. First quantification of 25C-NBOMe in fatal intoxication case. j.forsciint.2015.03.012
Morini et al. documented a teenager who drowned after agitation and confusion following ingestion of 25C-NBOMe and 25H-NBOMe (peripheral blood 25C-NBOMe concentration 2.80 ng/mL, described as potentially toxic).supported
Teenager drowned after ingesting 25C-NBOMe and 25H-NBOMe blotter. 25C-NBOMe 2.80 ng/mL peripheral blood... Blood levels considered potentially toxic. j.forsciint.2017.08.028
Kristofic et al. detected 25C-NBOH in the blood and urine alongside 25C-NBOMe in a fatal case, confirming in vivo human exposure to 25C-NBOH as a metabolite.supported
LC-QTOF screen detected 25C-NBOMe, 25C-NBOH (as metabolite) and 2C-C in blood and urine. bkw035
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
The broader NBOMe class toxicity case series documents seizures, excited delirium, rhabdomyolysis (with secondary acute kidney injury), disseminated intravascular coagulation (DIC), hypoglycemia, metabolic acidosis, and multiorgan failure as severe outcomessupported
Covers... sympathomimetic effects, rhabdomyolysis, DIC, multiorgan failure. fnins.2020.00078
Yoon et al. provide the only published toxicological data directly testing 25C-NBOH:supported
25I-NBOH and 25C-NBOH cardiotoxicity evaluated via MTT assay, rat ECG, Langendorff test, hERG assay. j.toxlet.2021.11.016
The same group previously demonstrated analogous QT prolongation for 25C-NBOMe and 25D-NBOMe in rat models, with PAK1 involvement documented for the NBOMe series.supported
25C-NBOMe 0.75 mg/kg prolonged QT intervals in rat ECG. PAK1 down-regulated by both compounds. j.toxlet.2019.01.004
The same group previously demonstrated analogous QT prolongation for 25C-NBOMe and 25D-NBOMe in rat models, with PAK1 involvement documented for the NBOMe series.supported
QTc interval prolonged at 1.0 and 3.0 mg/kg IV. PAK1 downregulated in rat hearts and H9c2 cells. 01480545.2020.1784924
The NBOMe/NBOH class produces a sympathomimetic toxidrome at supratherapeutic doses: tachycardia, hypertension, hyperthermia, and mydriasissupported
Covers visual/auditory hallucinations, sympathomimetic effects, rhabdomyolysis, DIC, multiorgan failure. fnins.2020.00078
In the clinical case series reported by Gee et al. for 25B-NBOMe, 7 of 10 patients required high-dose benzodiazepine sedation for agitation, with peak plasma concentrations of 0.7–10.1 ng/mL.supported
10-patient case series... Peak plasma 0.7-10.1 ng/mL. Benzodiazepine sedation required in 7/10. 15563650.2015.1115056
Claim in safety — inconclusiveinconclusiveworking →
Class-level evidence from NBOMe intoxication reports documents acute psychological distress including severe anxiety, paranoia, agitation, confusion, and uncontrollable violent behavior at high doses.supported
Hallucinations, violent agitation, mydriasis, tachycardia, hypertension, hyperthermia. 15563650.2015.1115056
Claim in safety — inconclusiveinconclusiveworking →
The mechanism is presumed to involve rapid 5-HT₂A receptor downregulation and desensitization following agonist exposure, consistent with the established pharmacology of serotonergic psychedelics and with the receptor tachyphylaxis mechanism described by Wallach et al. for β-arrestin-recruiting 5-HT₂A ligands.supported
Beta-arrestin-biased ligands block psychedelic effects and induce tachyphylaxis. s41467-023-44016-1
The negligible monoamine transporter activity documented for 25I-NBOH (low-to-mid micromolar affinity at DAT, SERT, and NET) is consistent with minimal stimulant-type reinforcement potentialsupported
Minimal transporter activity. j.bcp.2018.09.024
The most significant interaction risk involves co-administration with drugs that increase central serotonergic tone. Tramadol combines serotonin reuptake inhibition with weak µ-opioid agonism; the addition of a potent 5-HT₂A full agonist substantially elevates serotonin syndrome risksupported
Tramadol inhibits serotonin and norepinephrine reuptake; serotonin syndrome risk, especially with serotonergic co-medications. pmid:26218943
Serotonin syndrome presents as a triad of neuromuscular excitation (clonus, hyperreflexia, myoclonus, rigidity), autonomic dysfunction (hyperthermia, tachycardia, diaphoresis), and altered mental status, with severe cases progressing to rapid-onset hyperthermia, muscle rigidity, and multiorgan failuresupported
Serotonin toxicity clinical features: neuromuscular excitation, autonomic stimulation, altered mental status. j.1326-5377.2007.tb01282.x
Claim in safety — inconclusiveinconclusiveworking →
By analogy with 25I-NBOH, CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion, quinidine) could reduce the metabolic clearance of 25C-NBOH and increase plasma concentrationssupported
Major CYPs: CYP2D6 for 25I-NBOH. dta.2031
Co-administration with stimulants enhances hyperthermia risk — a concern substantiated by the NBOMe class toxicity literature, where hyperthermia is a documented contributor to fatal outcomes.supported
Covers visual/auditory hallucinations, sympathomimetic effects, rhabdomyolysis, DIC, multiorgan failure. fnins.2020.00078
Cardiac conditions (absolute): The documented QT prolongation and cardiomyocyte toxicity make pre-existing cardiac arrhythmias, congenital long QT syndrome, and structural heart disease absolute contraindications. Concurrent use of other QT-prolonging medications amplifies this risk.supported
Both significantly increased QT and RR intervals in rat ECG. Both compounds decreased H9c2 cardiomyocyte viability. j.toxlet.2021.11.016
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Hepatic impairment (relative): CYP2D6-dependent metabolism suggests that hepatic impairment could reduce clearance, though the direct glucuronidation pathway provides partial metabolic redundancy.supported
Major CYPs: CYP2D6 for 25I-NBOH. 25I-NBOH also liable to direct glucuronidation. dta.2031
pharmacology12 · 11 ok
As a member of the N-benzyl phenethylamine class, 25C-NBOH is presumed to act primarily through potent agonism at the 5-HT₂A receptor, the principal pharmacological target mediating psychedelic effectssupported
NBOMe class yielded 25CN-NBOH, most selective 5-HT2A agonist. acschemneuro.9b00528
As a member of the N-benzyl phenethylamine class, 25C-NBOH is presumed to act primarily through potent agonism at the 5-HT₂A receptor, the principal pharmacological target mediating psychedelic effectssupported
Comprehensive review of NBOMe pharmacological properties, pattern of use, metabolism, desired effects. fnins.2020.00078
All mechanistic characterization is inferred from the class-level SAR established by Hansen et al. across 48 N-benzyl phenethylamine compounds and from direct pharmacological studies of the closely related analogue 25I-NBOH.supported
48-compound SAR study of N-benzyl phenethylamines. cn400216u
All mechanistic characterization is inferred from the class-level SAR established by Hansen et al. across 48 N-benzyl phenethylamine compounds and from direct pharmacological studies of the closely related analogue 25I-NBOH.supported
Receptor pharmacology of NBOMe and NBOH substituted phenethylamines including 25I-NBOH. j.bcp.2018.09.024
Claim in pharmacology — inconclusiveinconclusiveworking →
Wallach et al. established that Gq-signaling efficacy, rather than β-arrestin 2 recruitment, predicts psychedelic potential as measured by mouse head-twitch response magnitude; β-arrestin-biased 5-HT₂A ligands blocked psychedelic effects and induced receptor tachyphylaxissupported
5-HT2A Gq-signaling (not beta-arrestin2) efficacy predicts psychedelic potential. Beta-arrestin-biased ligands block psychedelic effects and induce tachyphylaxis. s41467-023-44016-1
Pottie et al. identified biased agonism within the NBOH class, with the 25H-NBOH analogue showing statistically significant preference for β-arrestin 2 recruitment over miniGαq activation compared to an LSD referencesupported
25H-NBOH and related NBOMes show biased agonism at 5-HT2A receptor, preferentially recruiting β-arrestin 2 over miniGαq. j.bcp.2020.114251
Eshleman et al. characterized 25I-NBOH as showing full efficacy at both 5-HT₂A and 5-HT₂C receptors with subnanomolar to low-nanomolar affinity, very low potency at 5-HT₁A, lower affinity at 5-HT₂B, and negligible activity at monoamine transporters (low-to-mid micromolar)supported
Very high affinity for 5-HT2A and 5-HT2C; subnanomolar to low nanomolar potencies. Low potency at 5-HT1A, 5-HT2B. Minimal transporter activity. j.bcp.2018.09.024
Sublingual administration is the primary documented route, based on forensic characterization of seized blotter paperssupported
First identification and structural elucidation of 25B-NBOH, 25C-NBOH, and 25E-NBOH in seized blotter papers. s11419-019-00509-7
Nielsen et al. characterized the hepatic cytochrome P450 metabolism of 25I-NBOH in human liver microsomessupported
CYP metabolism study of 25I-NBOMe and 25I-NBOH in human liver microsomes. dta.2031
Caspar et al. confirmed that O-demethylation of 25C-NBOMe produces 25C-NBOH as a principal metabolite in both human and rat systems, and Kristofic et al. detected 25C-NBOH in the blood and urine of a 25C-NBOMe fatality case, confirming in vivo human exposure to 25C-NBOH as a metabolite.supported
Main pathways: O-demethylation (producing NBOH metabolites)... [for 25B-NBOMe and 25C-NBOMe]. j.jpba.2016.11.040
Caspar et al. confirmed that O-demethylation of 25C-NBOMe produces 25C-NBOH as a principal metabolite in both human and rat systems, and Kristofic et al. detected 25C-NBOH in the blood and urine of a 25C-NBOMe fatality case, confirming in vivo human exposure to 25C-NBOH as a metabolite.supported
LC-QTOF screen detected 25C-NBOMe, 25C-NBOH (as metabolite) and 2C-C in blood and urine. bkw035
comparative-pharmacology7 · 6 ok
Cardiotoxicity: Yoon et al. documented QT prolongation and cardiomyocyte toxicity for both 25C-NBOH and 25I-NBOH in rat models. The same group demonstrated analogous cardiac effects for 25C-NBOMe. Notably, 25C-NBOH had no effect on PAK1 protein expression in H9c2 cells, whereas 25I-NBOH affected PAK1, suggesting partially different cardiotoxic mechanisms even within the NBOH series.supported
Both significantly increased QT and RR intervals in rat ECG. 25I-NBOH inhibited hERG potassium channels and downregulated PAK1; 25C-NBOH had no PAK1 effect. j.toxlet.2021.11.016
Cardiotoxicity: Yoon et al. documented QT prolongation and cardiomyocyte toxicity for both 25C-NBOH and 25I-NBOH in rat models. The same group demonstrated analogous cardiac effects for 25C-NBOMe. Notably, 25C-NBOH had no effect on PAK1 protein expression in H9c2 cells, whereas 25I-NBOH affected PAK1, suggesting partially different cardiotoxic mechanisms even within the NBOH series.supported
25C-NBOMe 0.75 mg/kg prolonged QT intervals in rat ECG. PAK1 down-regulated by both compounds. j.toxlet.2019.01.004
Metabolic relationship: 25C-NBOH is the principal O-demethylation metabolite of 25C-NBOMe, meaning individuals who consume 25C-NBOMe generate 25C-NBOH endogenously.supported
Main pathways: O-demethylation (producing NBOH metabolites)... [title: Metabolic fate of 25B-NBOMe and 25C-NBOMe]. j.jpba.2016.11.040
Metabolism: NBOH compounds are primarily metabolized by CYP2D6, while NBOMe compounds rely on CYP3A4. NBOH compounds are additionally susceptible to direct glucuronidation at the phenol group — a pathway unavailable to NBOMes.supported
Major CYPs: CYP3A4 for 25I-NBOMe and CYP2D6 for 25I-NBOH. 25I-NBOH also liable to direct glucuronidation. dta.2031
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Cardiotoxicity: Both compounds produced QT prolongation in rat ECG studies, but their mechanisms partially diverge — 25I-NBOH affected PAK1 expression, 25C-NBOH did not.supported
Both significantly increased QT and RR intervals in rat ECG. 25I-NBOH inhibited hERG potassium channels and downregulated PAK1; 25C-NBOH had no PAK1 effect. j.toxlet.2021.11.016
25CN-NBOH (the 4-cyano variant) was developed as a pharmacological tool for its superior 5-HT₂A selectivity over 5-HT₂Csupported
Review of 25CN-NBOH discovery and pharmacological profile as highly selective 5-HT2A agonist. cmdc.202100395
history7 · 5 ok
Claim in history — inconclusiveinconclusiveworking →
Kristensen, and colleagues as part of a systematic medicinal chemistry programme investigating structure-activity relationships of N-benzyl phenethylamines at 5-HT₂A and 5-HT₂C receptorssupported
48-compound SAR study of N-benzyl phenethylamines. Best 5-HT2A binding affinity 0.29 nM. N-benzyl substitution including 2-OH (NBOH) conferred high affinity. cn400216u
The NBOH scaffold emerged as a key pharmacological tool variant alongside NBOMe, ultimately yielding 25CN-NBOH — a highly selective 5-HT₂A agonist now used as a standard pharmacological probe.supported
Review of 25CN-NBOH discovery and pharmacological profile as highly selective 5-HT2A agonist. Outlines major findings from animal studies. cmdc.202100395
The first published forensic identification came from Machado et al., who detected 25B-NBOH, 25C-NBOH, and 25E-NBOH in blotter papers seized by Brazilian law enforcement between 2017 and 2018supported
First identification and structural elucidation of 25B-NBOH, 25C-NBOH, and 25E-NBOH in seized blotter papers... Samples from Brazil 2017-2018. s11419-019-00509-7
Claim in history — inconclusiveinconclusiveworking →
A complicating forensic factor is that 25C-NBOH is the principal O-demethylation metabolite of 25c-nbomesupported
Main pathways: O-demethylation (producing NBOH metabolites)... [for 25B-NBOMe and 25C-NBOMe]. j.jpba.2016.11.040
As of the most recent published regulatory surveys, no NBOH compounds are listed under any United Nations drug control conventionssupported
NBOH substances not under UN Conventions control. s11419-019-00509-7
summary6 · 6 ok
The NBOH scaffold was developed at the University of Copenhagen by Hansen, Kristensen, and colleagues as part of a systematic medicinal chemistry programme characterizing N-benzyl phenethylamine structure-activity relationships at serotonin 5-HT₂A and 5-HT₂C receptors. 25C-NBOH appeared on the novel psychoactive substance market by approximately 2014–2017, first identified in seized blotter papers in Brazilpartially supported
48-compound SAR study of N-benzyl phenethylamines. N-benzyl substitution including 2-OH (NBOH) conferred high affinity. cn400216u
The NBOH scaffold was developed at the University of Copenhagen by Hansen, Kristensen, and colleagues as part of a systematic medicinal chemistry programme characterizing N-benzyl phenethylamine structure-activity relationships at serotonin 5-HT₂A and 5-HT₂C receptors. 25C-NBOH appeared on the novel psychoactive substance market by approximately 2014–2017, first identified in seized blotter papers in Brazilsupported
First identification and structural elucidation of 25B-NBOH, 25C-NBOH, and 25E-NBOH in seized blotter papers... Samples from Brazil 2017-2018. s11419-019-00509-7
25C-NBOH is presumed to act primarily through agonism at the serotonin 5-HT₂A receptor, activating Gq-coupled signaling cascades, with additional activity at 5-HT₂Csupported
Very high affinity for 5-HT2A and 5-HT2C; subnanomolar to low nanomolar potencies in IP accumulation assay. j.bcp.2018.09.024
The only published toxicological study directly testing 25C-NBOH documented significant QT interval prolongation and cardiomyocyte toxicity in rat modelssupported
Both compounds decreased H9c2 cardiomyocyte viability. Both significantly increased QT and RR intervals in rat ECG. j.toxlet.2021.11.016
Fatalities involving the closely related 25c-nbome — of which 25C-NBOH is the principal O-demethylation metabolite — are documented in the forensic literaturesupported
Fatal overdose of 25C-NBOMe in a young male who died 12h after ingestion... 25C-NBOMe and demethylated/glucuronidated metabolites identified. j.forsciint.2015.03.012
Fatalities involving the closely related 25c-nbome — of which 25C-NBOH is the principal O-demethylation metabolite — are documented in the forensic literaturesupported
Teenager drowned after ingesting 25C-NBOMe and 25H-NBOMe blotter. j.forsciint.2017.08.028
chemistry4 · 3 ok
The N-benzylation of 2C-C with a 2-hydroxybenzaldehyde-derived benzyl group produces 25C-NBOH, dramatically increasing 5-HT₂A receptor affinity relative to the parent phenethylamine — a structure-activity relationship systematically characterized across the N-benzyl phenethylamine class.supported
N-benzyl substitution including 2-OH (NBOH) conferred high affinity. cn400216u
This single functional group difference — phenol versus methyl ether — has measurable consequences: lower lipophilicity, altered metabolic susceptibility (the free phenol is a substrate for direct glucuronidation), and different ionization behavior at physiological pH.supported
25I-NBOH also liable to direct glucuronidation. dta.2031
The compound is distributed on the NPS market primarily as blotter paper impregnated with microgram quantitiessupported
First identification and structural elucidation of 25B-NBOH, 25C-NBOH, and 25E-NBOH in seized blotter papers. s11419-019-00509-7
Claim in chemistry — inconclusiveinconclusiveworking →
receptor-pharmacology4 · 4 ok
Hansen et al. conducted the foundational 48-compound SAR study of N-benzyl phenethylamines at 5-HT₂A and 5-HT₂C receptorssupported
48-compound SAR study of N-benzyl phenethylamines. cn400216u
Eshleman et al. characterized the NBOH-class compound 25I-NBOH across a broader receptor panel (5-HT₁A, 5-HT₂A, 5-HT₂B, 5-HT₂C) and monoamine transporters:supported
Receptor pharmacology of NBOMe and NBOH substituted phenethylamines including 25I-NBOH... Low potency at 5-HT1A, 5-HT2B. Minimal transporter activity. j.bcp.2018.09.024
Whether 25C-NBOH shares this β-arrestin bias is unknown — the 4-chloro substituent could shift the bias profile, as ring substitution patterns modulate both affinity and signaling selectivity across the series.supported
Most compounds had low-moderate 1-40-fold selectivity for 5-HT2A vs 5-HT2C; compound 6b showed 100-fold selectivity. cn400216u
Nichols et al. examined a parallel series of N-benzyl tryptamines alongside N-benzyl phenethylamines, confirming that the N-benzyl substitution is a general strategy for enhancing 5-HT₂ receptor affinity across structurally diverse scaffoldssupported
N-benzylated phenethylamine (2C-I) series: high 5-HT2A affinity, EC50 7.6-63 nM for tryptamine congeners. cn500292d
neuroscience3 · 2 ok
Claim in neuroscience — inconclusiveinconclusiveworking →
Contreras et al. used 25I-NBOH as a selective 5-HT₂A agonist probe in rodent electrophysiology studies and documented a characteristic slow cortical waveform and behavioral arrest response following administration — hallmark electrophysiological signatures of selective 5-HT₂A activationsupported
25I-NBOH used as selective 5-HT2A agonist in mice. Behavioral arrest and head twitch response (HTR) documented with EEG. Phase 1 (3.5-4.5 Hz) and Phase 2 (2.5-3.2 Hz) waveforms. s41598-021-81552-6
Given the CYP2D6-dependent metabolism of NBOH compounds, do CYP2D6 poor metabolizers show altered neural response profiles due to higher effective brain exposure?supported
Major CYPs: CYP2D6 for 25I-NBOH. dta.2031
pharmacokinetic-detail3 · 3 ok
Nielsen et al. characterized the hepatic cytochrome P450 enzymes involved in 25I-NBOH metabolism using human liver microsomes and recombinant CYP isoforms:supported
CYP metabolism study of 25I-NBOMe and 25I-NBOH in human liver microsomes. Major CYPs: CYP3A4 for 25I-NBOMe and CYP2D6 for 25I-NBOH. dta.2031
However, the availability of direct glucuronidation as a parallel clearance route may partially buffer this effect.supported
25I-NBOH also liable to direct glucuronidation. dta.2031
Kristofic et al. confirmed the detection of 25C-NBOH in the blood and urine of a deceased individual with documented 25C-NBOMe exposure, providing direct evidence of in vivo human biotransformation.supported
LC-QTOF screen detected 25C-NBOMe, 25C-NBOH (as metabolite) and 2C-C in blood and urine. bkw035
clinical-evidence2 · 2 ok
The published human evidence base for 25C-NBOH consists entirely of forensic case reports in which 25C-NBOH appears either as the suspected ingested substance (identified in seized blotter papers) or as a detected metabolite of 25c-nbome in post-mortem and clinical toxicology specimenssupported
First identification and structural elucidation of 25B-NBOH, 25C-NBOH, and 25E-NBOH in seized blotter papers. s11419-019-00509-7
The published human evidence base for 25C-NBOH consists entirely of forensic case reports in which 25C-NBOH appears either as the suspected ingested substance (identified in seized blotter papers) or as a detected metabolite of 25c-nbome in post-mortem and clinical toxicology specimenssupported
Main pathways: O-demethylation (producing NBOH metabolites)... j.jpba.2016.11.040
legal-status2 · 2 ok
No NBOH compounds are listed under any United Nations drug control conventions, and international scheduling has proceeded through national-level action rather than harmonized treaty obligationssupported
NBOH substances not under UN Conventions control. s11419-019-00509-7
The further complication that 25C-NBOH is a principal metabolite of 25C-NBOMe creates forensic ambiguity: detection of 25C-NBOH in biological specimens does not unambiguously establish that the compound was the substance consumed.supported
LC-QTOF screen detected 25C-NBOMe, 25C-NBOH (as metabolite) and 2C-C in blood and urine. bkw035