generation run 2026-05-09
60 min completedmodel pipeline-v5plan not recordedrun/15ca6f12…Selection
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3 further caveats recorded as free text — readable on the working page
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- 20 source keys (listed under Sources)
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20 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed Central | Dark Classics in Chemical Neuroscience NBOMes | 1 | 1 | Authoritative historical overview including synthesis history and toxicity data |
| 2 | PubMed | NBOMe series phenethylamine psychedelic serotonin receptor | 5 | 2 | Comprehensive receptor binding profiles and forensic case data |
| 3 | PubMed | Suzuki NBOMe toxicities review literature 2015 | 1 | 1 | Clinical toxicology review for the NBOMe class |
| 4 | ClinicalTrials.gov · absence | 25N-NBOMe NBOMe psychedelic | 0 | 0 | N/A - no trials exist |
| 5 | WebSearch | 25N-NBOMe legal status scheduling DEA UK | 10 | 3 | Legal status not available through PubMed |
| 6 | PubMed | NBOMe new psychoactive substance toxicity emergency seizure hyperthermia | 10 | 2 | Clinical toxicology data for NBOMe class |
| 7 | PubMed | 25N-NBOMe pharmacology receptor binding | 1 | 1 | Primary pharmacology paper with specific 25N-NBOMe receptor data |
| 8 | OpenAlex | NBOMe phenethylamine serotonin 2A receptor pharmacology psychedelic | 10 | 2 | Highly cited authoritative reviews on NBOMe pharmacology and toxicology |
| 9 | PubMed | NBOMe designer drug forensic analysis identification | 9 | 2 | Grafinger paper is specifically about 25N-NBOMe metabolism - key finding |
| 10 | WebSearch/Erowid | NBOMe series legal status international | 10 | 1 | Definitive jurisdiction-by-jurisdiction legal status listing |
| 11 | PubMed · absence | 25N-NBOMe toxicity overdose case report death | 0 | 0 | No specific case reports found for 25N-NBOMe |
| 12 | PubChem | 25N-NBOMe | 1 | 1 | Primary chemical identity verification |
| 13 | PsychonautWiki | 25N-NBOMe dose duration effects chemistry | 1 | 1 | Community-sourced dose/duration data; only available source for compound-specific dose information |
| 14 | PubMed | 25I-NBOMe CIMBI-5 PET radioligand serotonin 5-HT2A brain imaging | 1 | 1 | Historical context for NBOMe development as scientific research tools before recreational spread |
| 15 | Multiple | 25N-NBOMe chemical identity verification | 3 | 1 | Chemical identity verification |
| 16 | PubMed | NBOMe serotonin syndrome NPS systematic review | 8 | 1 | Key serotonin syndrome interaction risk documentation |
| 17 | WebSearch | 25N-NBOMe 2C-N NBOMe psychedelic effects dose experience report | 10 | 2 | Community dose data and harm reduction context |
| 18 | Erowid/WebSearch | NBOMe 25N legal status scheduling international jurisdictions | 1 | 2 | Comprehensive jurisdiction-by-jurisdiction legal status documentation |
| 19 | PubMed | Gil-Martins NBOMe neurotoxicity phenethylamine cytotoxicity mitochondrial 2024 | 1 | 1 | Mechanistic neurotoxicity data for NBOMe class |
| 20 | ClinicalTrials.gov · absence | 25N-NBOMe NBOMe psychedelic | 0 | 0 | Confirms no clinical development status |
65 claims by section — every cited sentence, checked against its source
safety14 · 9 ok
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
The typical severe presentation for NBOMe intoxication includes hallucinations with violent agitation, serotonergic and sympathomimetic signs (mydriasis, tachycardia, hypertension, hyperthermia, diaphoresis), seizures, excited delirium, rhabdomyolysis with elevated creatine kinase, acute kidney injury, metabolic acidosis, disseminated intravascular coagulation, and in severe cases, multiorgan failure and coma.supported
Literature review of NBOMe toxicities covering adverse effects, clinical presentations, and fatalities across the compound class. j.psym.2014.11.002
In vitro evidence indicates that NBOMe compounds exhibit higher cytotoxicity than their 2C counterparts in differentiated SH-SY5Y neuronal cells and rat cortical culturessupported
NBOMe drugs show higher cytotoxicity than 2C counterparts correlating with lipophilicity. jox14020044
Acute psychological adverse effects documented across the NBOMe class include severe anxiety, panic, paranoia, confusion, agitation, violent behavior, and excited deliriumsupported
Hallucinations, violent agitation, mydriasis, tachycardia, hypertension, hyperthermia. 7/10 required benzodiazepines. 15563650.2015.1115056
Acute psychological adverse effects documented across the NBOMe class include severe anxiety, panic, paranoia, confusion, agitation, violent behavior, and excited deliriumsupported
Literature review of NBOMe toxicities covering adverse effects, clinical presentations, and fatalities across the compound class. j.psym.2014.11.002
Claim in safety — inconclusiveinconclusiveworking →
Serotonin syndrome has been documented for NBOMe compounds in a systematic review.supported
Systematic review of NPS and serotonin syndrome. NBOMe compounds (25I-NBOMe) identified in clinical SS cases. j.expneurol.2021.113638
Based on CYP phenotyping of 25I-NBOMe, inhibitors of CYP2C9 and CYP2C19 (fluconazole, fluvoxamine, omeprazole) could reduce 25N-NBOMe clearance, increasing systemic exposure and toxicity risksupported
CYP2C9, CYP2C19 in O-demethylation. s00216-015-8828-6
Claim in safety — inconclusiveinconclusiveworking →
Seizure disorders — Seizures are documented in multiple NBOMe intoxication casessupported
Literature review of NBOMe toxicities covering adverse effects, clinical presentations, and fatalities across the compound class. j.psym.2014.11.002
Concurrent serotonergic medication — MAOIs, SSRIs, SNRIs, tramadol, and other serotonergic agents are contraindicated due to serotonin syndrome risk.supported
NBOMe compounds (25I-NBOMe) identified in clinical SS cases. Describes classic triad: altered mental status, neuromuscular effects, autonomic hyperactivity. j.expneurol.2021.113638
CYP2C9/CYP2C19 inhibitor co-administration — Reduced metabolic clearance may increase 25N-NBOMe exposure and toxicity risksupported
CYP2C9, CYP2C19 in O-demethylation. s00216-015-8828-6
Claim in safety — inconclusiveinconclusiveworking →
pharmacokinetic-detail12 · 9 ok
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Inhibitors of these enzymes (e.g., fluconazole, fluvoxamine, omeprazole) could reduce metabolic clearance and increase systemic exposure, elevating toxicity risksupported
CYP1A2, CYP3A4 involved in hydroxylation; CYP2C9, CYP2C19 in O-demethylation. s00216-015-8828-6
Inhibitors of these enzymes (e.g., fluconazole, fluvoxamine, omeprazole) could reduce metabolic clearance and increase systemic exposure, elevating toxicity risksupported
Main pathways: oxidative deamination, N-dealkylation, O-demethylation, hydroxylation. dta.2446
Grafinger and colleagues conducted the only primary study of 25N-NBOMe metabolism, investigating phase I biotransformation in pooled human liver microsomes (pHLM) and the fungal model Cunninghamella elegans.supported
24 phase I metabolites of 25N-NBOMe detected in pooled human liver microsomes; 9 in C. elegans. dta.2446
This reductive pathway was not observed for 25D-NBOMe or 25E-NBOMe studied in the same investigationsupported
Unique to 25N-NBOMe: nitro group reduction and N-acetylation of primary aromatic amine. dta.2446
N-dealkylation of the methoxybenzyl group yields the parent compound 2C-N (2,5-dimethoxy-4-nitrophenethylamine) as a metabolite, consistent with the metabolic pattern across the NBOMe series.supported
Main pathways: oxidative deamination, N-dealkylation, O-demethylation, hydroxylation. dta.2446
For the related compound 25I-NBOMe, Caspar and colleagues identified CYP1A2 and CYP3A4 as primarily responsible for hydroxylation, while CYP2C9 and CYP2C19 mediate O-demethylationsupported
CYP1A2, CYP3A4 involved in hydroxylation; CYP2C9, CYP2C19 in O-demethylation. s00216-015-8828-6
Analytical methods for detecting 25N-NBOMe and its metabolites in urine and blood have been described using LC-MS/MS and high-resolution mass spectrometrysupported
HPLC-MS/MS method for 9 NBOMe derivatives in urine. bku005
Claim in pharmacokinetic-detail — not_supportednot supportedworking →
Standard immunoassay panels do not detect NBOMe compounds; liquid chromatography-mass spectrometry is required for identification.supported
Detectable only by LC-MS approaches. s00216-015-8828-6
For the related analog 25B-NBOMe, peak plasma concentrations of 0.7–10.1 ng/mL were measured in a clinical toxicology case seriessupported
Peak plasma 0.7-10.1 ng/mL. 15563650.2015.1115056
pharmacology10 · 8 ok
25N-NBOMe exerts its psychedelic effects primarily through full agonism at the serotonin 5-HT₂A receptorsupported
Comprehensive review of NBOMe pharmacology... Ki values in low nanomolar range at 5-HT2A/2C. fnins.2020.00078
In heterologous expression systems using human receptor subtypes, the compound displays full efficacy and subnanomolar to low-nanomolar potency at 5-HT₂A — comparable to LSD in functional assayssupported
25N-NBOMe shows full efficacy with subnanomolar to low nanomolar potency at 5-HT2A/2C receptors. j.bcp.2018.09.024
The NBOMe series demonstrates full agonist activity at this receptor, in contrast to the parent 2C compounds, which are sometimes characterized as partial agonists.supported
25N-NBOMe shows full efficacy with subnanomolar to low nanomolar potency at 5-HT2A/2C receptors. j.bcp.2018.09.024
The addition of the N-(2-methoxybenzyl) group to the 2C-N scaffold markedly increases 5-HT₂A binding affinity, consistent with the structure-activity relationship observed across the broader NBOMe seriessupported
Comprehensive review of NBOMe pharmacology... Ki values in low nanomolar range at 5-HT2A/2C. fnins.2020.00078
The addition of the N-(2-methoxybenzyl) group to the 2C-N scaffold markedly increases 5-HT₂A binding affinity, consistent with the structure-activity relationship observed across the broader NBOMe seriessupported
In vitro receptor interaction profiles of NBOMe drugs vs 2C drugs and LSD. Binding affinities at multiple receptor types and monoamine transporters. j.neuropharm.2015.08.034
Claim in pharmacology — inconclusiveinconclusiveworking →
In vivo confirmation comes from rat behavioral models, where the effects of NBOMe compounds are fully reversible by the selective 5-HT₂A antagonist M100907supported
5-HT2A antagonist M100907 reversed all behaviors. j.neuropharm.2018.02.033
Hondebrink and colleagues identified α- and β-adrenergic receptors as additional targets for hallucinogenic phenethylamines at concentrations relevant to recreational use, though no study has published specific binding affinity values for 25N-NBOMe at any adrenergic receptor subtypesupported
identifies additional targets including α- and β-adrenergic receptors at concentrations relevant to recreational use for hallucinogenic phenethylamines. j.pharmthera.2017.10.022
Claim in pharmacology — inconclusiveinconclusiveworking →
For the related compound 25B-NBOMe, peak plasma concentrations of 0.7–10.1 ng/mL were measured in a clinical toxicology case seriessupported
Peak plasma 0.7-10.1 ng/mL. 15563650.2015.1115056
receptor-pharmacology9 · 8 ok
Eshleman and colleagues characterized the compound in cell lines heterologously expressing human serotonin receptor subtypes and monoamine transporters:supported
Characterizes 25D-, 25E-, 25H-NBOMe, 25I-NBOH, and 25N-NBOMe at 5-HT1A, 5-HT2A, 5-HT2B, 5-HT2C receptors and monoamine transporters. j.bcp.2018.09.024
Rickli and colleagues provided a complementary broad receptor binding profile across the NBOMe series, comparing NBOMe derivatives to their 2C-drug counterparts and LSDsupported
In vitro receptor interaction profiles of NBOMe drugs vs 2C drugs and LSD. Binding affinities at multiple receptor types and monoamine transporters. j.neuropharm.2015.08.034
The Eshleman paper is the primary source for compound-specific functional potency data; readers requiring exact numeric values should consult the full publication.supported
Characterizes 25D-, 25E-, 25H-NBOMe, 25I-NBOH, and 25N-NBOMe at 5-HT1A, 5-HT2A, 5-HT2B, 5-HT2C receptors and monoamine transporters. 25N-NBOMe shows full efficacy with subnanomolar to low nanomolar potency at 5-HT2A/2C receptors. j.bcp.2018.09.024
25N-NBOMe displays low to mid-micromolar affinity at the dopamine transporter (DAT), serotonin transporter (SERT), and norepinephrine transporter (NET)supported
Low-to-mid micromolar affinity at DAT/SERT/NET. j.bcp.2018.09.024
α- and β-adrenergic receptors have been identified as additional targets for hallucinogenic phenethylamines at concentrations achievable during recreational usesupported
identifies additional targets including α- and β-adrenergic receptors at concentrations relevant to recreational use for hallucinogenic phenethylamines. j.pharmthera.2017.10.022
The N-(2-methoxybenzyl) substituent is the defining structural feature that converts 2C-series phenethylamines from low-potency compounds active at milligram doses into high-potency 5-HT₂A agonists active at microgram dosessupported
Comprehensive review of NBOMe pharmacology... Ki values in low nanomolar range at 5-HT2A/2C. fnins.2020.00078
The N-(2-methoxybenzyl) substituent is the defining structural feature that converts 2C-series phenethylamines from low-potency compounds active at milligram doses into high-potency 5-HT₂A agonists active at microgram dosessupported
SAR study of 48 N-benzyl phenethylamines using 2C-B as template; 5-HT2A affinity ranges from subnanomolar to micromolar. cn400216u
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
As an electron-withdrawing group, –NO₂ alters the electronic properties of the ring system and introduces a unique metabolic vulnerability to enzymatic reduction — a biotransformation pathway not observed for non-nitro NBOMe analogs.supported
Unique to 25N-NBOMe: nitro group reduction and N-acetylation of primary aromatic amine. dta.2446
comparative-pharmacology7 · 4 ok
Gil-Martins and colleagues demonstrated that NBOMe compounds show higher cytotoxicity than their 2C counterparts in differentiated SH-SY5Y neuronal cells and rat cortical cultures, with toxicity correlating with lipophilicity — the N-benzyl substituent increases molecular lipophilicity relative to the parent 2C compounds.supported
NBOMe drugs show higher cytotoxicity than 2C counterparts correlating with lipophilicity. jox14020044
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
This potency shift is consistent across the NBOMe series and reflects the dramatic increase in 5-HT₂A receptor binding affinity conferred by the NBOMe pharmacophore.supported
In vitro receptor interaction profiles of NBOMe drugs vs 2C drugs and LSD. Binding affinities at multiple receptor types and monoamine transporters. j.neuropharm.2015.08.034
While 2C compounds are sometimes described as partial agonists, NBOMe derivatives demonstrate full efficacy in functional assayssupported
25N-NBOMe shows full efficacy with subnanomolar to low nanomolar potency at 5-HT2A/2C receptors. j.bcp.2018.09.024
Among NBOMe analogs, 25N-NBOMe is distinguished by the electron-withdrawing nitro group at the 4-position, which introduces a unique metabolic vulnerability — enzymatic nitro reduction followed by N-acetylation — not observed in other series memberssupported
Unique to 25N-NBOMe: nitro group reduction and N-acetylation of primary aromatic amine. dta.2446
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
summary5 · 3 ok
The compound acts as a full-efficacy agonist at the 5-HT₂A receptor with subnanomolar to low-nanomolar potency, placing it among the most potent serotonergic psychedelics characterized to datesupported
25N-NBOMe shows full efficacy with subnanomolar to low nanomolar potency at 5-HT2A/2C receptors. j.bcp.2018.09.024
25N-NBOMe produces its psychedelic effects primarily through full agonism at 5-HT₂A receptors, with additional activity at 5-HT₂Csupported
25N-NBOMe shows full efficacy with subnanomolar to low nanomolar potency at 5-HT2A/2C receptors. j.bcp.2018.09.024
Claim in summary — inconclusiveinconclusiveworking →
The N-2-methoxybenzyl substituent confers markedly greater 5-HT₂A affinity than the parent 2C compounds, and effects are fully reversed by the selective 5-HT₂A antagonist M100907 in animal modelssupported
NBOMes show higher affinity for 5-HT2A than 2C counterparts but weaker functional potency. 5-HT2A antagonist M100907 reversed all behaviors. j.neuropharm.2018.02.033
Claim in summary — inconclusiveinconclusiveworking →
neuroscience4 · 4 ok
As a full agonist at 5-HT₂A with potency comparable to LSD, 25N-NBOMe is expected to produce these downstream neural effectssupported
25N-NBOMe shows full efficacy with subnanomolar to low nanomolar potency at 5-HT2A/2C receptors. j.bcp.2018.09.024
In rat behavioral models, the effects of NBOMe compounds are fully reversed by M100907, confirming that 5-HT₂A activation is the proximate neural trigger.supported
5-HT2A antagonist M100907 reversed all behaviors. j.neuropharm.2018.02.033
The absence of meaningful 5-HT₁A activity in the NBOMe series is potentially significant: 5-HT₁A agonism may modulate the anxiolytic quality of certain psychedelics (notably LSD and ayahuasca), and its absence could contribute to the anxiety-prominent phenomenology reported for NBOMe compounds.supported
In vitro receptor interaction profiles of NBOMe drugs vs 2C drugs and LSD. Binding affinities at multiple receptor types and monoamine transporters. j.neuropharm.2015.08.034
In vitro data from Gil-Martins and colleagues demonstrate that NBOMe compounds induce mitochondrial membrane depolarization, intracellular ATP depletion, and glutathione reduction in neuronal cell modelssupported
Cytotoxic effects via mitochondrial dysfunction, ATP depletion, and GSH reduction. jox14020044
chemistry2 · 2 ok
The class is defined by a phenethylamine backbone bearing methoxy groups at the 2- and 5-positions, a variable substituent at the 4-position (here, a nitro group –NO₂), and an N-(2-methoxybenzyl) extension — the 'NBOMe' moiety — that converts low-affinity 2C-series compounds into high-potency 5-HT₂A agonistssupported
Comprehensive review of NBOMe pharmacology... Ki values in low nanomolar range at 5-HT2A/2C. fnins.2020.00078
While other members carry halogens (–I, –Br, –Cl), methyl, or ethyl groups at this position, the electron-withdrawing nitro group confers distinctive metabolic behavior — most notably, susceptibility to enzymatic reduction to a primary aromatic amine.supported
Unique to 25N-NBOMe: nitro group reduction and N-acetylation of primary aromatic amine. dta.2446
history2 · 1 ok
Claim in history — inconclusiveinconclusiveworking →
This application was pursued most notably with CIMBI-5 (¹¹C-labeled 25I-NBOMe), evaluated by Ettrup and colleagues in 2010.supported
CIMBI-5 (11C-labeled 25I-NBOMe) evaluated as PET radioligand for 5-HT2A receptor. Shows cortical binding displaceable by ketanserin. jnumed.109.074021