generation run 2026-04-25
56 min completedmodel pipeline-v5plan not recordedrun/07fd79d2…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
none raised on this run
Reproduce
- inputs
- 32 source keys (listed under Sources)
- plan
- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
- streams
- 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 | PubMed | 25I-NBOMe fatality death poisoning | 7 | 7 | All highly relevant case reports and toxicity reviews selected |
| 2 | OpenAlex | 25I-NBOMe NBOMe pharmacology serotonin | 10 | 6 | Selected highly-cited review and primary research papers covering NBOMe pharmacology, designer drugs context, and 5-HT2A signaling |
| 3 | PubMed | 25I-NBOMe pharmacology receptor binding | 6 | 5 | Selected core pharmacology papers with binding data; discarded primate PET imaging paper as less directly relevant to article |
| 4 | PubMed | NBOMe hallucinogen intoxication adverse effects clinical | 5 | 5 | Selected all for metabolism, metabolite biomarkers, and clinical toxicology data |
| 5 | PubChem | 25I-NBOMe | 1 | 4 | All core chemical identity data confirmed via PubChem API |
| 6 | PubMed | 25I-NBOMe metabolism CYP enzyme pharmacokinetics | 2 | 2 | Primary CYP metabolism studies for 25I-NBOMe |
| 7 | PubMed | NBOMe head twitch response mouse hallucinogen potency dose | 2 | 2 | Key behavioral pharmacology papers demonstrating 25I-NBOMe potency |
| 8 | Web/Erowid | 25I-NBOMe legal status jurisdictions scheduling | 10 | 1 | Most comprehensive legal status data available |
| 9 | PubMed | 25I-NBOMe urine blood analytical detection forensic | 2 | 2 | Analytical detection methods for toxicological screening |
| 10 | Web/DEA Federal Register | 25I-NBOMe Schedule I DEA emergency scheduling 2013 United States UK | 5 | 2 | Critical legal status data for multiple jurisdictions |
| 11 | PubMed | 5-HT2A receptor downregulation tolerance serotonin hallucinogens mechanism | 2 | 2 | Mechanism of tolerance development to 5-HT2A agonists - applicable to 25I-NBOMe class |
| 12 | Web | 25I-NBOMe synthesis history Ralf Heim Berlin 2003 dissertation NBOMe series first described | 8 | 1 | Essential synthesis history data not available in PubMed |
| 13 | PubMed | NBOMe 5-HT2A receptor agonist binding affinity subnanomolar human serotonin | 2 | 1 | Core binding affinity data for NBOMe class at multiple receptor subtypes |
| 14 | ClinicalTrials.gov · absence | 25I-NBOMe NBOMe hallucinogen | 0 | — | Confirms absence of clinical trials |
| 15 | Web | 25I-NBOMe CAS number physical properties melting point | 8 | 3 | Physical property data not available via API tools |
| 16 | PubChem REST API | CID 10251906 SMILES InChI properties | 1 | 3 | Complete chemical identity data for seed data verification |
| 17 | PubMed | neurotoxicological profile hallucinogenic compound 25I-NBOMe Scientific Reports 2022 | 1 | 1 | First in vivo brain neurotoxicity study specifically for 25I-NBOMe |
| 18 | Web | 25I-NBOMe binding affinity Ki 5-HT2A subnanomolar published study | 8 | 2 | Confirmed adrenergic receptor binding and approximate 5-HT2A Ki range |
| 19 | Frontiers in Neuroscience | 25I-NBOMe binding affinity dose information adrenergic receptor | 1 | 3 | Specific receptor binding profile data for adrenergic classification |
102 claims by section — every cited sentence, checked against its source
safety37 · 22 ok
Unlike classical psychedelics such as LSD — which has no confirmed direct pharmacological fatalities at normal doses — 25I-NBOMe has been causally implicated in multiple analytically confirmed deaths.supported
Reviews five LSD-attributed deaths; one likely caused by drug substituted for LSD with strong temperature effects (e.g. 25I-NBOMe). j.forsciint.2018.01.006
Claim in safety — inconclusiveinconclusiveworking →
The clinical toxidrome of severe 25I-NBOMe intoxication includes sympathomimetic signs (tachycardia, hypertension, hyperthermia, mydriasis, diaphoresis), neurological effects (agitation, disorientation, violent or aggressive behavior, excited delirium, generalized tonic-clonic seizures), and severe complications including rhabdomyolysis, acute kidney injury secondary to rhabdomyolysis, disseminated intravascular coagulation, metabolic acidosis, hypoglycemia, multiorgan failure, and cardiopulmonary arrest.supported
adverse effects include visual hallucinations, agitation, violent behavior, seizures, excited delirium, rhabdomyolysis, DIC, metabolic acidosis, multiorgan failure. fnins.2020.00078
Claim in safety — inconclusiveinconclusiveworking →
Halberstadt (2017) reviewed 51 documented cases of NBOMe toxicity and identified rhabdomyolysis as a common complication, likely driven by the combination of seizure activity, hyperthermia, and vasoconstriction.supported
Based on review of 51 cases of NBOMe toxicity; rhabdomyolysis identified as common complication. 7854_2016_64
Two rave-party deaths (21-year-old male, 15-year-old female) described by Walterscheid et al. — the 21-year-old displayed sudden violent rage followed by unresponsiveness. Initial toxicology detected only marijuana; 25I-NBOMe was identified subsequently by TOF-MS and tandem-MS.supported
Two rave party deaths: 21yo male (rage/aggression before becoming unresponsive) and 15yo female. 25I-NBOMe identified by TOF-MS and confirmed by tandem-MS. Marijuana the only other drug detected initially. 15563650.2014.909932
A 19-year-old male traumatic death following blotter paper ingestion — the first complete postmortem tissue distribution study, with peripheral blood concentration of 405 pg/mL, liver 7.2 ng/g, and brain 2.54 ng/g.supported
First postmortem tissue distribution case of 25I-NBOMe. 19yo male ingested blotter paper. Peripheral blood 405 pg/mL... brain 2.54 ng/g, liver 7.2 ng/g. j.forsciint.2013.10.015
Two teenage males in Indiana (2014), with postmortem heart blood concentration of 19.8 ng/mL.supported
Two teenage male deaths in Indiana 2014. 25I-NBOMe detected in postmortem heart blood at 19.8 ng/mL in case 2. bkv058
An Australian case with postmortem aortic blood concentration of approximately 28 ng/mL — the highest postmortem concentration reported.supported
First Australian 25I-NBOMe fatal case. Postmortem aortic blood concentration: approximately 28 µg/L — much higher than non-fatal cases. j.forsciint.2015.02.010
A 15-year-old male in Washington State who co-ingested 25I-NBOMe and psilocin, progressing from seizures and vomiting to cardiopulmonary arrest, multiorgan failure, and death three days later; antemortem blood concentration was 0.76 ng/mL.supported
15-year-old male ingested 25I-NBOMe and mushrooms, developed seizures and vomiting, died 3 days later of multi-system organ failure following cardiopulmonary arrest. Antemortem blood confirmed 25I-NBOMe at 0.76 ng/mL. bkv092
Claim in safety — inconclusiveinconclusiveworking →
In rats, chronic 25I-NBOMe administration produces oxidative DNA damage detectable 72 hours after chronic treatment, reduces glial cell counts in the frontal cortex and medial prefrontal cortex, but does not reduce neural cell counts or cause detectable apoptosis at the same time pointssupported
Oxidative DNA damage detected 72h after chronic treatment. Decrease in glial (not neural) cells in frontal and medial prefrontal cortex. No apoptotic signal at same timepoint. s41598-022-07069-8
This misidentification is a critical safety concern that has directly contributed to multiple fatalitiessupported
Establishes that extreme hyperthermia leading to death was likely caused by 25I-NBOMe sold as LSD. j.forsciint.2018.01.006
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
At higher doses, excited delirium syndrome — characterized by uncontrollable violent behavior, extreme agitation, and apparent imperviousness to pain — has been documented in multiple case reports.supported
adverse effects include visual hallucinations, agitation, violent behavior, seizures, excited delirium, rhabdomyolysis, DIC, metabolic acidosis, multiorgan failure. fnins.2020.00078
At higher doses, excited delirium syndrome — characterized by uncontrollable violent behavior, extreme agitation, and apparent imperviousness to pain — has been documented in multiple case reports.supported
21yo male (rage/aggression before becoming unresponsive)... External contusions prominent. 15563650.2014.909932
In mice, tolerance to the head-twitch response is observable 24 hours after a single administrationsupported
Tolerance within 24h of single administration. acschemneuro.2c00170
Claim in safety — inconclusiveinconclusiveworking →
The mechanism involves decreased 5-HT₂A receptor density; notably, 5-HT₂C does not downregulate in parallel, making receptor selectivity relevant to the pattern of tolerance development.supported
5-HT2A receptor downregulation (not 5-HT2C) is mechanism of tolerance to hallucinogenic phenethylamines. pmid:10435391
Cross-tolerance exists across the serotonergic psychedelic class via shared 5-HT₂A downregulation. 25I-NBOMe produces cross-tolerance with LSD, psilocin, DMT, mescaline, and other 5-HT₂A agonists.supported
Cross-tolerance between DOI and LSD. 5-HT2A downregulation confirmed. acschemneuro.2c00170
Claim in safety — inconclusiveinconclusiveworking →
Serotonin toxicity features have been documented in a fatal case involving the closely related analog 25C-NBOMesupported
Fatal 25C-NBOMe case: young male died ~12h after ingestion with signs of serotonin toxicity. j.forsciint.2015.03.012
Claim in safety — inconclusiveinconclusiveworking →
Tramadol presents a specific dual-mechanism danger: it has direct serotonergic activity (SERT inhibition and serotonin release), lowers the seizure threshold (as does 25I-NBOMe), and is metabolized primarily by CYP2D6 — the same enzyme responsible for 61% of 25I-NBOMe hepatic clearancesupported
CYP2D6 main contributor to hepatic clearance for 25I-NBOMe (61%). j.toxlet.2017.12.017
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — not_supportednot supportedworking →
Multiple fatal case reports detected THC or carboxy-THC alongside 25I-NBOMe, but no pharmacological interaction study specific to this combination has been publishedsupported
Marijuana the only other drug detected initially. 15563650.2014.909932
CYP2D6 poor metabolizers face inherently higher exposure from any given dose.supported
CYP2D6 main contributor to hepatic clearance for 25I-NBOMe (61%). Polymorphically expressed CYPs may cause inter-individual variation. j.toxlet.2017.12.017
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Hepatic impairment is a relative contraindication due to the compound's extensive hepatic metabolism via polymorphic CYP enzymes; impaired clearance could increase exposure unpredictably.supported
CYP2D6 main contributor to hepatic clearance for 25I-NBOMe (61%). CYP2C19 also involved. Polymorphically expressed CYPs may cause inter-individual variation. j.toxlet.2017.12.017
Concurrent use of CYP2D6 or CYP3A4 inhibitors is a relative contraindication for the same metabolic reasons.supported
CYP2D6 main contributor to hepatic clearance for 25I-NBOMe (61%). CYP2C19 also involved. j.toxlet.2017.12.017
Concurrent use of CYP2D6 or CYP3A4 inhibitors is a relative contraindication for the same metabolic reasons.supported
Major CYPs for 25I-NBOMe: CYP3A4 and CYP2D6... CYP3A4 inhibitors could cause drug-drug interactions. dta.2031
Claim in safety — inconclusiveinconclusiveworking →
pharmacology23 · 18 ok
A total of 68 metabolites have been identified.supported
68 metabolites identified. s00216-015-8828-6
Claim in pharmacology — inconclusiveinconclusiveworking →
The N-(2-methoxybenzyl) modification of the 2C-I scaffold produces a marked increase in 5-HT₂A binding affinity relative to the parent compoundsupported
Reviews structure-activity relationships, behavioral pharmacology, metabolism, and toxicity of NBOMe hallucinogens including 25I-NBOMe. Subnanomolar 5-HT2A affinity noted. 7854_2016_64
The N-(2-methoxybenzyl) modification of the 2C-I scaffold produces a marked increase in 5-HT₂A binding affinity relative to the parent compoundsupported
NBOMes displayed higher affinity for 5-HT2A than 2C counterparts j.neuropharm.2018.02.033
Published affinity data place Ki values in the subnanomolar to low-nanomolar range (0.5–1.6 nM for the NBOMe series), with greater than 1,000-fold selectivity for 5-HT₂A over 5-HT₁A.supported
Ki values in low nanomolar range at 5-HT2A/2C; >1000-fold selectivity over 5-HT1A fnins.2020.00078
Activation of the Gq pathway — rather than β-arrestin-2 recruitment — predicts psychedelic potential; compounds with sufficient Gq efficacy produce hallucinogen-like behavior in rodent models, and 5-HT₂A Gq-efficacy strongly predicts head-twitch response magnitudesupported
5-HT2A-Gq (not beta-arrestin2) signaling predicts psychedelic potential via head-twitch response. s41467-023-44016-1
In mouse head-twitch response studies, 25I-NBOMe was 14-fold more potent than 2C-I at subcutaneous doses of 0.1–1 mg/kg; the selective 5-HT₂A antagonist M100907 completely reversed the HTR, confirming exclusive 5-HT₂A dependence of this behavioral endpoint.supported
25I-NBOMe induced head-twitch response in C57BL/6J mice at 0.1-1 mg/kg SC. 14-fold higher potency than 2C-I. M100907 (selective 5-HT2A antagonist) completely blocked response. j.neuropharm.2013.08.025
Hallucinogenic activity appears linked to increased glutamate release mediated via cortical 5-HT₂A receptors, with 5-HT₂C and 5-HT₁A activity modulating overall effects.supported
Hallucinogenic activity linked to GLU release via cortical 5-HT2A receptors. s12640-019-00033-x
Claim in pharmacology — inconclusiveinconclusiveworking →
Off-target µ opioid receptor (MOR) activation has been demonstrated at high concentrations in vitro via NanoBiT β-arrestin-2 assay, though physiologically relevant MOR opioid toxicity is considered unlikely at recreational concentrations.supported
25I-NBOMe shown to activate MOR (µ opioid receptor) at high concentrations via NanoBiT β-arrestin2 and Ca2+ release assays. Authors conclude MOR opioid toxicity unlikely at physiologically relevant concentrations. s00204-023-03465-9
NBOMes display markedly lower affinity, potency, and efficacy at 5-HT₂B compared to 5-HT₂A or 5-HT₂C, reducing theoretical cardiac valvulopathy risk relative to compounds with high 5-HT₂B activitysupported
higher 5-HT2A affinity than 2C counterparts; lower efficacy at 5-HT2B fnins.2020.00078
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Primary metabolite biomarkers for urine detection include 2-O-desmethyl-5-I-NBOMe (M5, recommended as the primary urine screening biomarker), 5-O-desmethyl-2-I-NBOMe, and seven glucuronidated Phase II metabolitessupported
Major metabolites: 2-O-desmethyl-5-I-NBOMe (M5) and 5-O-desmethyl-2-I-NBOMe. Seven phase II glucuronidated metabolites identified. Recommends M5 as primary biomarker. bkv079
The parent compound is often undetectable in urine; detection relies on metabolites analyzed by LC-MS methods (not GC-MS), with β-glucuronidase enzymatic hydrolysis recommended before screening.supported
Recommends M5 as primary biomarker and β-glucuronidase hydrolysis prior to screening. bkv079
The parent compound is often undetectable in urine; detection relies on metabolites analyzed by LC-MS methods (not GC-MS), with β-glucuronidase enzymatic hydrolysis recommended before screening.supported
Detectable only by LC-MS approaches. s00216-015-8828-6
CYP2D6 is the main contributor to hepatic clearance, accounting for approximately 61% of metabolismsupported
CYP2D6 main contributor to hepatic clearance for 25I-NBOMe (61%). j.toxlet.2017.12.017
CYP3A4 is a co-primary enzyme, contributing to hydroxylation and initial metabolic stepssupported
Major CYPs for 25I-NBOMe: CYP3A4 and CYP2D6. Biotransformations include hydroxylation, O-demethylation, N-dealkylation, dehydrogenation. dta.2031
CYP2C19 mediates O-demethylation reactions, while CYP1A2 and CYP2C9 play additional rolessupported
CYP1A2 and CYP3A4 in hydroxylation; CYP2C9 and CYP2C19 in O-demethylation. s00216-015-8828-6
Intrinsic clearance has been estimated at 70.1 mL/min/kg.supported
Intrinsic clearance 70.1 mL/min/kg. dta.2031
Claim in pharmacology — not_supportednot supportedworking →
Strong CYP3A4 inhibitors (e.g., ketoconazole, ritonavir) could increase 25I-NBOMe exposure significantly.supported
CYP3A4 inhibitors could cause drug-drug interactions. dta.2031
25I-NBOMe crosses the blood-brain barrier readily in rats and accumulates in brain tissue (frontal cortex, hippocampus) after multiple administrations.supported
25I-NBOMe crosses BBB easily and accumulates in brain tissue after multiple injections. s41598-022-07069-8
pharmacokinetic-detail8 · 6 ok
The parent compound is rarely detectable in urine; seven glucuronidated metabolites and the primary Phase I metabolite M5 (2-O-desmethyl-5-I-NBOMe) serve as forensic biomarkers.supported
Major metabolites: 2-O-desmethyl-5-I-NBOMe (M5)... Seven phase II glucuronidated metabolites identified. Recommends M5 as primary biomarker. bkv079
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
CYP2D6 poor metabolizers — approximately 5–10% of Caucasian populations — may experience prolonged or intensified effects due to reduced clearancesupported
CYP2D6 main contributor to hepatic clearance for 25I-NBOMe (61%). Polymorphically expressed CYPs may cause inter-individual variation. j.toxlet.2017.12.017
Co-administration of strong CYP3A4 inhibitors (ketoconazole, ritonavir, clarithromycin) could substantially increase 25I-NBOMe plasma exposuresupported
CYP3A4 inhibitors could cause drug-drug interactions. dta.2031
The shared CYP2D6 metabolic pathway creates specific competitive inhibition risk with co-ingested substances metabolized by the same enzyme, including tramadol, codeine, and many antidepressants.supported
Major CYPs for 25I-NBOMe: CYP3A4 and CYP2D6. dta.2031
Reliable detection requires LC-MS or LC-MS/MS methods; GC-MS alone is insufficient for 25I-NBOMe and its metabolites. β-Glucuronidase enzymatic hydrolysis is recommended prior to urine screening to deconjugate Phase II metabolites and increase detection sensitivity.supported
Recommends M5 as primary biomarker and β-glucuronidase hydrolysis prior to screening. bkv079
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Reliable detection requires LC-MS or LC-MS/MS methods; GC-MS alone is insufficient for 25I-NBOMe and its metabolites. β-Glucuronidase enzymatic hydrolysis is recommended prior to urine screening to deconjugate Phase II metabolites and increase detection sensitivity.supported
Recommends M5 as primary biomarker and β-glucuronidase hydrolysis prior to screening. bkv079
comparative-pharmacology7 · 5 ok
LSD has an extremely wide therapeutic index with no confirmed direct pharmacological fatalities at recreational doses; 25I-NBOMe has a critically narrow dose-toxicity margin with multiple documented fatalitiessupported
Reviews five LSD-attributed deaths; one likely caused by drug substituted for LSD with strong temperature effects (e.g. 25I-NBOMe). j.forsciint.2018.01.006
Serotonin toxicity features have been documented in a fatal 25C-NBOMe case, indicating that the toxicological profile extends across the series rather than being unique to 25I-NBOMe.supported
Fatal 25C-NBOMe case: young male died ~12h after ingestion with signs of serotonin toxicity. j.forsciint.2015.03.012
LSD has significant 5-HT₁A activity and a broader receptor profile; 25I-NBOMe achieves greater than 1,000-fold 5-HT₂A/5-HT₁A selectivitysupported
>1000-fold selectivity over 5-HT1A fnins.2020.00078
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Both substances produce cross-tolerance via the shared 5-HT₂A downregulation mechanismsupported
Cross-tolerance between DOI and LSD. 5-HT2A downregulation confirmed. acschemneuro.2c00170
The potency of mouse HTR correlates well with human hallucinogenic potency across both compound classes.supported
Strong positive correlation (r=0.9448) between HTR potency in mice and hallucinogenic potency in humans across 36 compounds. Supports translational validity of mouse model for predicting human potency of hallucinogens including NBOMes. j.neuropharm.2019.107933
summary7 · 5 ok
Claim in summary — inconclusiveinconclusiveworking →
First synthesized in 2003 by Ralf Heim at the Free University of Berlin as part of a series of N-(2-methoxybenzyl) phenethylamine ligands, 25I-NBOMe was subsequently developed as the ¹¹C-radiolabeled PET radiotracer CIMBI-5 for in vivo imaging of 5-HT₂A receptors in the high-affinity agonist statesupported
First published synthesis and evaluation of 11C-CIMBI-5 (the radiolabeled form of 25I-NBOMe) as a 5-HT2A receptor agonist PET tracer. jnumed.109.074021
It appeared on the recreational drug market around 2010, frequently sold on blotter paper and misrepresented as LSDsupported
Establishes that extreme hyperthermia leading to death was likely caused by 25I-NBOMe sold as LSD. j.forsciint.2018.01.006
25I-NBOMe binds the 5-HT₂A receptor with subnanomolar to low-nanomolar affinity (Ki 0.5–1.6 nM for the NBOMe series), achieving 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
In rodent models, hallucinogenic activity is mediated through 5-HT₂A–Gq/11 signaling in prefrontal cortex, with glutamate release as the downstream effector; the selective 5-HT₂A antagonist M100907 completely abolishes the head-twitch responsesupported
M100907 (selective 5-HT2A antagonist) completely blocked response. Confirms 5-HT2A mechanism. j.neuropharm.2013.08.025
Claim in summary — inconclusiveinconclusiveworking →
Tolerance develops rapidly via 5-HT₂A receptor downregulation, with cross-tolerance across the serotonergic psychedelic classsupported
Tolerance within 24h of single administration. Cross-tolerance between DOI and LSD. 5-HT2A downregulation confirmed. acschemneuro.2c00170
receptor-pharmacology6 · 5 ok
All binding data derive from review-level compilations and in vitro functional assayssupported
25I-NBOMe shown to activate MOR at high concentrations via NanoBiT β-arrestin2 and Ca2+ release assays. s00204-023-03465-9
All binding data derive from review-level compilations and in vitro functional assayssupported
Comprehensive review: Ki values in low nanomolar range at 5-HT2A/2C; >1000-fold selectivity over 5-HT1A fnins.2020.00078
All binding data derive from review-level compilations and in vitro functional assayssupported
Reviews structure-activity relationships, behavioral pharmacology, metabolism, and toxicity of NBOMe hallucinogens including 25I-NBOMe. 7854_2016_64
Claim in receptor-pharmacology — not_supportednot supportedworking →
The defining pharmacological feature of the NBOMe modification is the dramatic enhancement of 5-HT₂A affinity relative to the parent 2C compound. 25I-NBOMe was 14-fold more potent than 2C-I in the mouse head-twitch response, a validated behavioral proxy for human hallucinogenic activitysupported
14-fold higher potency than 2C-I. M100907 (selective 5-HT2A antagonist) completely blocked response. Confirms 5-HT2A mechanism. j.neuropharm.2013.08.025
Psychedelic potential in the NBOMe series correlates with Gq/11 signaling efficacy at 5-HT₂A rather than β-arrestin-2 recruitmentsupported
5-HT2A-Gq (not beta-arrestin2) signaling predicts psychedelic potential via head-twitch response. s41467-023-44016-1
history5 · 2 ok
Claim in history — inconclusiveinconclusiveworking →
The Nichols laboratory at Purdue University further characterized the pharmacology of the NBOMe series, providing benchmark binding affinity and functional data for 25I-NBOMe and related analogs.supported
Comparative pharmacology of N-benzyl phenethylamines (including 2C-I analogs) and tryptamines at 5-HT2A/2B/2C. Provides benchmark binding affinity data for NBOMe series. cn500292d
25I-NBOMe first appeared on the research chemical and recreational drug market approximately in 2010, sold by online vendors as a legal alternative to LSD and other psychedelicssupported
NBOMes available from online vendors since 2010. 7854_2016_64
Claim in history — inconclusiveinconclusiveworking →
Claim in history — not_supportednot supportedworking →
clinical-evidence4 · 3 ok
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Wood et al. (2015) described prevalence and acute toxicity patterns across the NBOMe class in European emergency presentations.supported
Reviews epidemiology and pattern of acute toxicity from 25X-NBOMe series. Covers European, US, and other acute toxicity reports from prior 5 years. 15563650.2015.1004179
The only sanctioned research use of the compound (as CIMBI-5) was as a PET radiotracer administered at trace radioligand doses in neuroimaging studies — not as a psychoactive drug in any therapeutic or investigational contextsupported
Confirms 25I-NBOMe was synthesized as a research tool for brain imaging. jnumed.109.074021
Marchi et al. (2019) published a systematic review of NBOMe clinical and toxicological profiles, compiling case-level data on presenting symptoms, doses ingested (where known), and outcomessupported
Systematic review of NBOMe clinical and toxicological profile. j.psym.2018.11.002
neuroscience3 · 3 ok
The inverted U-shaped dose-response for dopamine and serotonin release — with suppression at the highest tested dose (10 mg/kg) — suggests auto-regulatory feedback via 5-HT₂C and 5-HT₁A receptor activation at supramaximal doses.supported
Inverted U-shaped dose-response for DA and 5-HT; U-shaped for GLU and head-twitch response. s12640-019-00033-x
In rat frontal cortex, 25I-NBOMe dose-dependently increases extracellular dopamine, serotonin, and glutamate, with hallucinogenic behavior correlating most closely with glutamate release mediated by cortical 5-HT₂A receptors on layer V pyramidal neuronssupported
25I-NBOMe at 1, 3, and 10 mg/kg (sc) increased extracellular DA, 5-HT, and GLU in rat frontal cortex. Hallucinogenic activity linked to GLU release via cortical 5-HT2A receptors. s12640-019-00033-x
The compound's Gq/11-biased agonism at 5-HT₂A — rather than β-arrestin-2 recruitment — places it within the signaling framework that predicts psychedelic behavioral outcomes in rodent models.supported
5-HT2A-Gq (not beta-arrestin2) signaling predicts psychedelic potential via head-twitch response. Beta-arrestin-biased 5-HT2A agonists block psychedelic effects. s41467-023-44016-1
chemistry2 · 2 ok
The parent compound is 2C-I (2-(4-iodo-2,5-dimethoxyphenyl)ethan-1-amine); the addition of the N-benzyl moiety dramatically increases 5-HT₂A receptor affinity, converting micromolar-potency phenethylamines into nanomolar-potency ligandssupported
Reviews structure-activity relationships, behavioral pharmacology, metabolism, and toxicity of NBOMe hallucinogens including 25I-NBOMe. Subnanomolar 5-HT2A affinity noted. 7854_2016_64
The parent compound is 2C-I (2-(4-iodo-2,5-dimethoxyphenyl)ethan-1-amine); the addition of the N-benzyl moiety dramatically increases 5-HT₂A receptor affinity, converting micromolar-potency phenethylamines into nanomolar-potency ligandssupported
NBOMes displayed higher affinity for 5-HT2A than 2C counterparts j.neuropharm.2018.02.033