generation run 2026-04-25
73 min completedmodel pipeline-v5plan not recordedrun/5b6eac1b…Selection
Verification
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- seen / partial
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The model's own caveats
none raised on this run
Reproduce
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- 25 source keys (listed under Sources)
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- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
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- none — agent transcripts are persisted from 2026-09 onward
19 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubChem | 25B-NBOMe | 1 | 1 | Confirms chemical identity of 25B-NBOMe |
| 2 | PubMed | 25B-NBOMe pharmacology receptor binding | 4 | 4 | All directly relevant to 25B-NBOMe pharmacology |
| 3 | PubMed | Cimbi-36 5-HT2A PET radioligand synthesis evaluation | 3 | 3 | Core Cimbi-36 = 25B-NBOMe scientific literature |
| 4 | PubMed | NBOMe hallucinogen fatality death intoxication case report | 1 | 1 | Analogue fatality case with relevant class toxicology data |
| 5 | PubMed · absence | 25B-NBOMe toxicity overdose case report | 0 | — | No specific results; broadened search strategy |
| 6 | PubMed | 25I-NBOMe 25B-NBOMe intoxication hospital clinical presentation | 1 | 1 | Direct 25B-NBOMe clinical case |
| 7 | ClinicalTrials.gov · absence | 25B-NBOMe NBOMe Cimbi-36 | 0 | — | No trials registered |
| 8 | OpenAlex | Cimbi-36 25B-NBOMe serotonin receptor binding pharmacology citations sort | 17 | 4 | Key metabolism, analytical, and behavioral papers |
| 9 | OpenAlex | 25B-NBOMe NBOMe psychedelic pharmacology (citations sort) | 10 | 4 | High-citation papers most relevant to 25B-NBOMe pharmacology and toxicology |
| 10 | WebSearch | 25B-NBOMe DEA scheduling controlled substance legal status US UK Australia | 10 | 2 | Legal scheduling history confirmed |
| 11 | ECDD Repository | — | 1 | 1 | WHO ECDD official assessment with legal and abuse data |
| 12 | WebSearch | 25B-NBOMe Ki value 5-HT2A receptor binding affinity nanomolar | 10 | 2 | Key binding affinity papers with specific Ki/EC50 values |
| 13 | ClinicalTrials.gov | Cimbi-36 serotonin 5-HT2A PET brain imaging | 5 | 2 | Completed and active trials using 25B-NBOMe as radioligand |
| 14 | WebSearch | 25B-NBOMe discovery history synthesis Braden Heim NBOMe first synthesized | 10 | 1 | Primary source for discovery history |
| 15 | DOI verification | — | 1 | 1 | Verified 25B-NBOMe-specific fatality case report |
| 16 | PubMed | 25B-NBOMe cluster toxicity N-bomb case series | 1 | 1 | Largest 25B-NBOMe-specific clinical case series; treatment guidance |
| 17 | PubMed | 25B-NBOMe 25C-NBOMe severe intoxication analytically confirmed | 1 | 1 | Direct 25B-NBOMe clinical intoxication case report |
| 18 | WebSearch | 25B-NBOMe reagent test Ehrlich Hofmann testing identification harm reduction | 10 | 1 | Harm reduction testing guidance for 25B-NBOMe identification |
| 19 | PubMed | fatal intoxications 25B-NBOMe 25I-NBOMe Indiana 2014 | 1 | 1 | 25B-NBOMe specific fatality with quantified blood levels |
97 claims by section — every cited sentence, checked against its source
safety34 · 23 ok
Claim in safety — inconclusiveinconclusiveworking →
The documented predominance of violent agitation suggests heightened risk in individuals with impulse control disorders.supported
Hallucinations and violent agitation predominate. 15563650.2015.1115056
Postmortem cardiac blood concentration: 3.14 ng/mL.supported
Postmortem cardiac blood concentration: 3.14 ng/mL. ijpbs.9870
A teenage male in Indiana (2014) died with 25B-NBOMe confirmed in postmortem heart blood at 1.59 ng/mL by UPLC-MS/MS. Autopsy findings were consistent with acute drug poisoning.supported
Two teenage male deaths in Indiana 2014. Case 1: 25B-NBOMe in postmortem heart blood at 1.59 ng/mL. UPLC-MS/MS analysis. bkv058
Tang et al. documented two cases of severe intoxication with analytically confirmed 25B-NBOMe and 25C-NBOMe requiring hospitalization.supported
Two acute intoxication cases with analytically confirmed 25B-NBOMe and 25C-NBOMe. 15563650.2014.909932
Peak plasma concentrations ranged from 0.7 to 10.1 ng/mL.supported
Peak plasma 0.7-10.1 ng/mL by LC-MS/MS. 15563650.2015.1115056
The overlap between fatal blood levels (1.59–3.14 ng/mL) and non-fatal plasma levels (up to 10.1 ng/mL) means no safe blood concentration threshold can be definedsupported
Case 1: 25B-NBOMe in postmortem heart blood at 1.59 ng/mL. bkv058
The overlap between fatal blood levels (1.59–3.14 ng/mL) and non-fatal plasma levels (up to 10.1 ng/mL) means no safe blood concentration threshold can be definedsupported
Postmortem cardiac blood concentration: 3.14 ng/mL. ijpbs.9870
The overlap between fatal blood levels (1.59–3.14 ng/mL) and non-fatal plasma levels (up to 10.1 ng/mL) means no safe blood concentration threshold can be definedsupported
Peak plasma 0.7-10.1 ng/mL by LC-MS/MS. No seizures or death in this series. 15563650.2015.1115056
The α₁-adrenergic receptor binding of NBOMe compounds (class Ki 0.3–0.9 µM) produces clinically significant vasoconstriction and hypertensionsupported
Alpha-1 receptor Ki: 0.3-0.9 µM (explains cardiovascular effects). j.neuropharm.2015.08.034
Cardiac arrhythmia (ventricular fibrillation) was the documented cause of death in the Al-Imam casepartially supported
Cause of death: cardiac arrest from cardiac arrhythmia. ijpbs.9870
Claim in safety — inconclusiveinconclusiveworking →
Documented complications include rhabdomyolysis, acute kidney injury, disseminated intravascular coagulation (DIC), metabolic acidosis, and multiorgan failurepartially supported
Hyperthermia, rhabdomyolysis, kidney injury observed. 15563650.2015.1115056
Claim in safety — inconclusiveinconclusiveworking →
Fatal cases involving related NBOMe compounds (25C-NBOMe) demonstrate similar multiorgan pathology.supported
Fatal overdose: young male died 12h after ingestion with serotonin toxicity signs. 25C-NBOMe and demethylated/glucuronidated metabolites identified. j.forsciint.2015.03.012
Fatal cases involving related NBOMe compounds (25C-NBOMe) demonstrate similar multiorgan pathology.supported
Teenager drowned after becoming agitated/confused after NBOMe use. 25C-NBOMe and 25H-NBOMe detected in blood/urine. j.forsciint.2017.08.028
25B-NBOMe demonstrated a subtle genotoxic effect in the comet assay at tested doses in rats — less pronounced than MDMA but not absentpartially supported
Showed subtle genotoxic effect. s12640-020-00297-8
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Case reports document confusion, disorientation, anxiety, panic, fear, and violent agitation as predominant featuressupported
Hallucinations and violent agitation predominate; serotonergic/stimulant signs (mydriasis, tachycardia, hypertension, hyperthermia). 15563650.2015.1115056
Violent agitation was present in 10 of 10 patients in the Gee case series, a frequency exceeding typical reports for classical serotonergic psychedelics and possibly related to the compound's additional α₁-adrenergic and multi-transmitter release profile.partially supported
Hallucinations and violent agitation predominate. 15563650.2015.1115056
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
In preclinical models, 25B-NBOMe demonstrated rewarding and reinforcing properties (conditioned place preference and self-administration) mediated through a dopaminergic mechanism — blocked by D₁ and D₂ antagonists but not by ketanserinsupported
25B-NBOMe elicited CPP and self-administration. DRD1/DRD2 antagonists blocked CPP but not 5-HT2A antagonist. adb.12850
Claim in safety — inconclusiveinconclusiveworking →
Combined with 25B-NBOMe's α₁-adrenergic vasoconstriction, the risk of hypertensive crisis, cardiac arrhythmia, coronary ischemia, and stroke is mechanistically elevated.supported
Alpha-1 receptor Ki: 0.3-0.9 µM (explains cardiovascular effects). j.neuropharm.2015.08.034
Claim in safety — inconclusiveinconclusiveworking →
CYP-mediated interactions: 25B-NBOMe is metabolized by CYP1A2, CYP3A4, CYP2C9, and CYP2C19supported
CYP1A2/CYP3A4 involved in hydroxylation; CYP2C9/CYP2C19 in O-demethylation. j.jpba.2016.11.040
Cardiovascular conditions: The α₁-adrenergic vasoconstriction and documented cardiac arrhythmia fatalities constitute absolute contraindications for individuals with pre-existing cardiac arrhythmias, congenital or acquired long QT syndrome, coronary artery disease, or uncontrolled hypertension.supported
Cause of death: cardiac arrest from cardiac arrhythmia. Postmortem cardiac blood concentration: 3.14 ng/mL. ijpbs.9870
Claim in safety — inconclusiveinconclusiveworking →
Renal and hepatic impairment: Extensive hepatic metabolism via four CYP enzymes and documented acute kidney injury make hepatic or renal impairment relative contraindications.supported
CYP1A2/CYP3A4 involved in hydroxylation; CYP2C9/CYP2C19 in O-demethylation. j.jpba.2016.11.040
Renal and hepatic impairment: Extensive hepatic metabolism via four CYP enzymes and documented acute kidney injury make hepatic or renal impairment relative contraindications.supported
Hyperthermia, rhabdomyolysis, kidney injury observed. 15563650.2015.1115056
The genotoxic signal in rat comet assays and potent serotonergic activity raise concerns for fetal development, though no teratogenicity data exist.supported
Showed subtle genotoxic effect. s12640-020-00297-8
pharmacology17 · 15 ok
25B-NBOMe acts as a full (or near-full) agonist at the 5-HT₂A receptor, the primary molecular target mediating its psychedelic effectssupported
Ki values in low nanomolar range at 5-HT2A/2C. >1000-fold selectivity over 5-HT1A. fnins.2020.00078
25B-NBOMe acts as a full (or near-full) agonist at the 5-HT₂A receptor, the primary molecular target mediating its psychedelic effectssupported
5-HT2A receptor mediates psychedelic effects. NBOMes class discussed. s00204-020-02693-7
At 5-HT₂A, the compound displays Ki = 0.5 nM and functional activation potency of EC₅₀ = 40 nM, placing it among the most potent synthetic 5-HT₂A agonists knownpartially supported
NBOMes are very potent 5-HT2A agonists (class EC50: 0.04-0.5 µM). j.neuropharm.2015.08.034
Selectivity exceeds 1,000-fold over 5-HT₁A. 5-HT₂A agonism at cortical and subcortical sites drives the hallucinogenic response through the same receptor system engaged by LSD, psilocin, and mescaline.supported
>1000-fold selectivity over 5-HT1A. fnins.2020.00078
Selectivity exceeds 1,000-fold over 5-HT₁A. 5-HT₂A agonism at cortical and subcortical sites drives the hallucinogenic response through the same receptor system engaged by LSD, psilocin, and mescaline.supported
>1000-fold selectivity over 5-HT1A. fnins.2020.00078
Selectivity exceeds 1,000-fold over 5-HT₁A. 5-HT₂A agonism at cortical and subcortical sites drives the hallucinogenic response through the same receptor system engaged by LSD, psilocin, and mescaline.supported
5-HT2A receptor mediates psychedelic effects. NBOMes class discussed. s00204-020-02693-7
Claim in pharmacology — inconclusiveinconclusiveworking →
Zawilska et al. describe NBOMes as "highly efficacious agonists", and Eshleman et al. confirmed full efficacy for structurally related NBOMes in inositol phosphate accumulation assays.supported
Full efficacy at 5-HT2A/2C; subnanomolar to low nanomolar potency. j.bcp.2018.09.024
In rats, 25B-NBOMe increased extracellular dopamine, serotonin, acetylcholine, and glutamate in the frontal cortex, striatum, and nucleus accumbenspartially supported
25B-NBOMe increased DA, 5-HT, and glutamate release in rat frontal cortex, striatum, and nucleus accumbens. s12640-020-00297-8
Claim in pharmacology — not_supportednot supportedworking →
CPP was blocked by the D₁ antagonist SCH23390 and the D₂ antagonist haloperidol, but not by ketanserin, indicating that the rewarding properties operate through a dopaminergic rather than serotonergic mechanismsupported
DRD1/DRD2 antagonists blocked CPP but not 5-HT2A antagonist. Altered dopamine-related proteins in NAcc/VTA. adb.12850
Additional α₁-adrenergic receptor binding (class Ki range 0.3–0.9 µM for the NBOMe series) produces sympathomimetic cardiovascular effects — vasoconstriction, hypertension, and tachycardia — observed consistently in clinical intoxicationssupported
Alpha-1 receptor Ki: 0.3-0.9 µM (explains cardiovascular effects). j.neuropharm.2015.08.034
Rickli et al. noted that "the binding profile of NBOMe drugs predicts strong hallucinogenic effects, similar to LSD, but possibly more stimulant properties because of α₁ receptor interactions".supported
N-methoxybenzyl substitution increases 5-HT2A/2C, alpha-1... Alpha-1 receptor Ki: 0.3-0.9 µM (explains cardiovascular effects). j.neuropharm.2015.08.034
In the first-in-human PET study (n = 29 healthy volunteers), [¹¹C]Cimbi-36 demonstrated high brain uptake with cortical distribution matching known 5-HT₂A receptor topography; cerebellum served as reference tissuesupported
29 healthy volunteers. High brain uptake by 5-HT2A distribution. Ketanserin pretreatment decreased binding in cortical regions. Cerebellum confirmed as reference tissue. jcbfm.2014.68
Radiometabolite analysis identified two metabolite fractions in human plasma: a dominant polar fraction (M1) and a less polar fraction (M2), both arising from O-demethylation.supported
In humans, [11C]Cimbi-36 yields M1 and M2 radiometabolite fractions (O-demethylation products). 0271678x17746179
The definitive metabolism study by Caspar et al. identified 66 metabolites of 25B-NBOMe in rat and human urine using GC-MS, LC-MSⁿ, and LC-HR-MS/MSsupported
66 metabolites identified for 25B-NBOMe. Main pathways: O-demethylation, O,O-bis-demethylation, hydroxylation, glucuronidation, sulfation. j.jpba.2016.11.040
CYP enzyme involvement: CYP1A2 and CYP3A4 catalyze hydroxylation; CYP2C9 and CYP2C19 catalyze O-demethylationsupported
CYP1A2/CYP3A4 involved in hydroxylation; CYP2C9/CYP2C19 in O-demethylation. j.jpba.2016.11.040
summary12 · 10 ok
With a 5-HT₂A receptor affinity of Ki = 0.5 nM, it ranks among the most potent synthetic serotonergic psychedelics characterized, active at sub-milligram doses via sublingual and insufflated routespartially supported
NBOMes are very potent 5-HT2A agonists (class EC50: 0.04-0.5 µM) with high 5-HT2A/5-HT1A selectivity. j.neuropharm.2015.08.034
First synthesized by Ralf Heim in 2003 at the Free University of Berlin as part of structure-activity investigations into N-benzylphenethylamine 5-HT₂A agonists, 25B-NBOMe was independently developed as [¹¹C]Cimbi-36 — the first agonist PET radioligand validated for human 5-HT₂A receptor imagingpartially supported
First agonist PET radioligand for 5-HT2A in humans. jcbfm.2014.68
25B-NBOMe acts as a full agonist at 5-HT₂A receptors (Ki = 0.5 nM, EC₅₀ = 40 nM) with greater than 1,000-fold selectivity over 5-HT₁Apartially supported
NBOMes are very potent 5-HT2A agonists (class EC50: 0.04-0.5 µM) with high 5-HT2A/5-HT1A selectivity. j.neuropharm.2015.08.034
25B-NBOMe acts as a full agonist at 5-HT₂A receptors (Ki = 0.5 nM, EC₅₀ = 40 nM) with greater than 1,000-fold selectivity over 5-HT₁Asupported
Ki values in low nanomolar range at 5-HT2A/2C. >1000-fold selectivity over 5-HT1A. fnins.2020.00078
Additional α₁-adrenergic receptor binding (class Ki 0.3–0.9 µM) produces sympathomimetic cardiovascular effects — vasoconstriction, tachycardia, hypertension — distinguishing NBOMe toxicity from classical tryptamine psychedelicssupported
Alpha-1 receptor Ki: 0.3-0.9 µM (explains cardiovascular effects). j.neuropharm.2015.08.034
Claim in summary — not_supportednot supportedworking →
Clinical presentations feature visual and auditory hallucinations, violent agitation (documented in 10/10 patients in the largest case series), and a full sympathomimetic toxidromepartially supported
Hallucinations and violent agitation predominate; serotonergic/stimulant signs (mydriasis, tachycardia, hypertension, hyperthermia). 15563650.2015.1115056
Published fatalities document cardiac arrhythmia at postmortem blood levels of 1.59–3.14 ng/mL, overlapping with non-fatal plasma concentrations reaching 10.1 ng/mL — no reliable toxic threshold is definablepartially supported
Case 1: 25B-NBOMe in postmortem heart blood at 1.59 ng/mL. UPLC-MS/MS analysis. bkv058
Published fatalities document cardiac arrhythmia at postmortem blood levels of 1.59–3.14 ng/mL, overlapping with non-fatal plasma concentrations reaching 10.1 ng/mL — no reliable toxic threshold is definablesupported
Cause of death: cardiac arrest from cardiac arrhythmia. Postmortem cardiac blood concentration: 3.14 ng/mL. ijpbs.9870
Published fatalities document cardiac arrhythmia at postmortem blood levels of 1.59–3.14 ng/mL, overlapping with non-fatal plasma concentrations reaching 10.1 ng/mL — no reliable toxic threshold is definablesupported
Peak plasma 0.7-10.1 ng/mL by LC-MS/MS. No seizures or death in this series. 15563650.2015.1115056
Claim in summary — inconclusiveinconclusiveworking →
No human dependence data exist, though rodent models demonstrate dopaminergic self-administrationsupported
25B-NBOMe elicited CPP and self-administration. Abuse potential via dopaminergic mechanism. adb.12850
neuroscience8 · 6 ok
Does the dopaminergic reward signal translate to human dependence risk? Rodent self-administration via D₁/D₂ mechanisms is atypical for classical psychedelics and has not been investigated in humans.supported
25B-NBOMe elicited CPP and self-administration. DRD1/DRD2 antagonists blocked CPP but not 5-HT2A antagonist. Abuse potential via dopaminergic mechanism. adb.12850
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
PET imaging with [¹¹C]Cimbi-36 in healthy volunteers confirmed cortical binding distribution matching 5-HT₂A receptor topography — highest radioligand uptake in frontal, temporal, and parietal cortex, with cerebellum serving as reference tissuesupported
High brain uptake by 5-HT2A distribution. Ketanserin pretreatment decreased binding in cortical regions. Cerebellum confirmed as reference tissue. jcbfm.2014.68
In rats, 25B-NBOMe simultaneously increased extracellular dopamine, serotonin, acetylcholine, and glutamate concentrations in the frontal cortex, striatum, and nucleus accumbenspartially supported
25B-NBOMe increased DA, 5-HT, and glutamate release in rat frontal cortex, striatum, and nucleus accumbens. s12640-020-00297-8
Dose-dependent anxiogenic effects, impaired short-term memory, and decreased locomotor activity were also documented.supported
Lowered recognition index in NOR test, decreased locomotor activity. Showed subtle genotoxic effect. Anxiogenic properties in LDB test. s12640-020-00297-8
The compound demonstrated subtle genotoxic effects in a rat comet assay, raising the question of whether any neuroplastic effects might be accompanied by DNA damage at pharmacologically active doses.supported
Showed subtle genotoxic effect. s12640-020-00297-8
Does 25B-NBOMe produce neuroplasticity? No dendritogenesis or spinogenesis data exist. The genotoxic signal in rats raises the possibility that neuroplastic effects may be accompanied by cytotoxicity absent with classical psychedelics.supported
Showed subtle genotoxic effect. s12640-020-00297-8
history6 · 5 ok
Juncosa et al. synthesized rigid constrained analogues using 25B-NBOMe as a structural template, mapping optimal binding conformations and demonstrating up to 124-fold selectivity for 5-HT₂A over 5-HT₂C in conformationally locked derivatives.supported
Based on 25B-NBOMe structure. Constrained analogue library to identify optimal pharmacophoric arrangement. (S,S)-9b showed 124-fold selectivity for 5-HT2A over 5-HT2C. cn3000668
Early preclinical work on the related CIMBI-5 radioligand appeared in 2010, and the first clinical human PET study using [¹¹C]Cimbi-36 was published in 2014, validating it as the first agonist radioligand for 5-HT₂A receptor imaging in living humanssupported
CIMBI-5 shows cortex-to-cerebellum binding ratio equal to 18F-altanserin. Promising tool for 5-HT2A agonist binding investigation. Related to Cimbi-36 (25B-NBOMe) development. jnumed.109.074021
Early preclinical work on the related CIMBI-5 radioligand appeared in 2010, and the first clinical human PET study using [¹¹C]Cimbi-36 was published in 2014, validating it as the first agonist radioligand for 5-HT₂A receptor imaging in living humanssupported
First-in-human clinical trial with [11C]Cimbi-36. First agonist PET radioligand for 5-HT2A in humans. jcbfm.2014.68
Claim in history — inconclusiveinconclusiveworking →
Forensic analysis confirmed 25B-NBOMe as the major component on commercially obtained blotter products, with trace amounts of other NBOMe derivatives present as impurities.supported
Three blotter paper products confirmed containing 25I-, 25C-, or 25B-NBOMe as major component, with impurities of other NBOMe derivatives. bkv073
By 2013, reports of severe intoxications and deaths involving NBOMe compounds appeared in the medical literaturesupported
Two acute intoxication cases with analytically confirmed 25B-NBOMe and 25C-NBOMe. NBOMe derivatives have been implicated in clinical intoxications and fatalities. 15563650.2014.909932
comparative-pharmacology5 · 5 ok
Key differences: LSD engages a broader receptor profile including 5-HT₂A, 5-HT₂C, 5-HT₁A, and dopamine D₂ receptors, and forms a "lid" over the 5-HT₂A binding pocket via β-arrestin recruitment, contributing to its prolonged duration. 25B-NBOMe shows >1,000-fold selectivity for 5-HT₂A over 5-HT₁A (LSD has no such selectivity) but carries additional α₁-adrenergic activity producing cardiovascular toxicity not typically associated with LSD at recreational dosespartially supported
N-methoxybenzyl substitution increases 5-HT2A/2C, alpha-1... reduces 5-HT1A binding. Alpha-1 receptor Ki: 0.3-0.9 µM (explains cardiovascular effects). j.neuropharm.2015.08.034
The safety profiles diverge sharply: LSD has no documented lethal dose in humans, whereas 25B-NBOMe has multiple published fatalities.supported
Two teenage male deaths in Indiana 2014. Case 1: 25B-NBOMe in postmortem heart blood at 1.59 ng/mL. bkv058
The safety profiles diverge sharply: LSD has no documented lethal dose in humans, whereas 25B-NBOMe has multiple published fatalities.supported
17-year-old male died after three sublingual 25B-NBOMe tablets. Cause of death: cardiac arrest from cardiac arrhythmia. ijpbs.9870
The N-(2-methoxybenzyl) modification produces a dramatic potency increase at 5-HT₂A (Ki = 0.5 nM for 25B-NBOMe versus substantially higher Ki for 2C-B) while simultaneously reducing 5-HT₁A affinity. 2C-B retains activity as a partial agonist at 5-HT₂A with a broader receptor profile, whereas 25B-NBOMe approaches full agonist efficacy at a single dominant targetpartially supported
N-methoxybenzyl substitution increases 5-HT2A/2C, alpha-1, D1-3, H1 binding affinity vs 2C drugs; reduces 5-HT1A binding. j.neuropharm.2015.08.034
All three share the core N-benzylphenethylamine pharmacophore and the α₁-adrenergic binding that produces their characteristic sympathomimetic toxidromesupported
Alpha-1 receptor Ki: 0.3-0.9 µM (explains cardiovascular effects). j.neuropharm.2015.08.034
pharmacokinetic-detail5 · 4 ok
All human PK data derive from its use as [¹¹C]Cimbi-36 at sub-pharmacological tracer doses in PET imaging studiessupported
First-in-human clinical trial with [11C]Cimbi-36. 29 healthy volunteers. jcbfm.2014.68
In the first-in-human study (29 healthy volunteers), [¹¹C]Cimbi-36 showed rapid brain uptake following intravenous injection at tracer dosessupported
First-in-human clinical trial with [11C]Cimbi-36. 29 healthy volunteers. High brain uptake by 5-HT2A distribution. jcbfm.2014.68
Human biodistribution and radiation dosimetry data have been published separately.supported
Seven healthy volunteers underwent 120-min whole-body PET scans. Confirms 25B-NBOMe identity as Cimbi-36. s13550-019-0527-4
Human radiometabolite studies using [¹¹C]Cimbi-36 confirmed two plasma metabolite fractions: polar M1 (dominant) and less polar M2, both products of O-demethylation.supported
In humans, [11C]Cimbi-36 yields M1 and M2 radiometabolite fractions (O-demethylation products). 0271678x17746179
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
receptor-pharmacology5 · 4 ok
The N-benzyl modification produces a dramatic shift in binding profile compared to parent compound 2C-B: 5-HT₂A affinity increases by orders of magnitude while 5-HT₁A affinity decreasessupported
N-methoxybenzyl substitution increases 5-HT2A/2C, alpha-1, D1-3, H1 binding affinity vs 2C drugs; reduces 5-HT1A binding. j.neuropharm.2015.08.034
The resulting selectivity ratio (>1,000-fold 5-HT₂A over 5-HT₁A) exceeds that of most classical psychedelics.supported
>1000-fold selectivity over 5-HT1A. fnins.2020.00078
α₁-Adrenergic receptor binding for the NBOMe series falls in the Ki range of 0.3–0.9 µMsupported
Alpha-1 receptor Ki: 0.3-0.9 µM (explains cardiovascular effects). j.neuropharm.2015.08.034
Affinities at dopamine and norepinephrine transporters are low to mid-micromolar, biochemically inconsistent with significant direct psychostimulant activity through monoamine reuptake inhibition.supported
Low-to-mid micromolar at transporters. Results consistent with hallucinogenic activity, little psychostimulant activity. j.bcp.2018.09.024
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
chemistry3 · 2 ok
The N-benzyl modification dramatically increases 5-HT₂A receptor affinity — 25B-NBOMe binds with Ki = 0.5 nM versus substantially lower affinity for 2C-Bpartially supported
N-methoxybenzyl substitution increases 5-HT2A/2C, alpha-1, D1-3, H1 binding affinity vs 2C drugs. j.neuropharm.2015.08.034
Juncosa et al. created conformationally constrained analogues with introduced stereocenters, demonstrating up to 124-fold selectivity for 5-HT₂A over 5-HT₂C in specific enantiomers, but these are distinct research compounds rather than forms encountered in recreational or clinical contexts.supported
(S,S)-9b showed 124-fold selectivity for 5-HT2A over 5-HT2C. Maps binding conformation of NBOMe class. cn3000668
Claim in chemistry — inconclusiveinconclusiveworking →
clinical-evidence2 · 2 ok
Published results demonstrated selective cortical binding consistent with 5-HT₂A receptor topography, with cerebellum confirmed as a suitable reference tissue.supported
High brain uptake by 5-HT2A distribution. Ketanserin pretreatment decreased binding in cortical regions. Cerebellum confirmed as reference tissue. jcbfm.2014.68
Gee et al. reported the largest 25B-NBOMe-specific clinical series (n = 10): all patients exhibited hallucinations and violent agitation; serotonergic and sympathomimetic signs were universal; 7/10 required benzodiazepine sedation; peak plasma concentrations ranged from 0.7 to 10.1 ng/mL.supported
10-patient observational case series. Hallucinations and violent agitation predominate. 7/10 required benzodiazepine sedation. Peak plasma 0.7-10.1 ng/mL by LC-MS/MS. 15563650.2015.1115056