generation run 2026-05-08
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24 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubChem | 25D-NBOMe | 1 | 1 | Primary chemical identity confirmation |
| 2 | PubMed | 25x-NBOMe receptor binding pharmacology serotonin | 1 | 1 | Highly relevant comprehensive review |
| 3 | PubMed | 2C-D 2,5-dimethoxy-4-methylphenethylamine pharmacology psychedelic | 1 | 1 | Relevant as 25D-NBOMe is the N-benzyl derivative of 2C-D |
| 4 | ClinicalTrials.gov · absence | 25D-NBOMe NBOMe phenethylamine | 0 | 0 | No registered trials |
| 5 | PubMed | NBOMes-Highly Potent Toxic Alternatives LSD Zawilska | 1 | 1 | Comprehensive review, highly cited |
| 6 | OpenAlex | 25x-NBOMe pharmacology serotonin receptor hallucinogen | 10 | 3 | Wallach 2023 identifies 5-HT2A signaling pathways relevant to NBOMe class; Demin 2022 provides in vivo behavioral data |
| 7 | PubMed | 25I-NBOMe 25C-NBOMe fatality toxicology forensic | 1 | 1 | Important toxicology case report for the NBOMe class |
| 8 | PubMed | NBOMe vasoconstriction serotonin syndrome hyperthermia rhabdomyolysis | 1 | 1 | Landmark review with toxicity case analysis |
| 9 | PubMed | 25D-NBOMe NBOMe phenethylamine psychedelic | 4 | 4 | All four directly relevant to 25D-NBOMe |
| 10 | Crossref via verify_doi | 10.1021/acschemneuro.3c00196 | 1 | 1 | Only primary study specifically on 25D-NBOMe abuse potential and dopaminergic mechanism |
| 11 | OpenAlex | NBOMe N-benzyl phenethylamine first synthesis history Ralf Heim 2003 | 4 | 1 | Important fatality case report for class toxicity context |
| 12 | Web | NBOMe discovery Ralf Heim Free University Berlin 2003 synthesis | 10 | 0 | Historical context for NBOMe class discovery |
| 13 | PubMed | 25C-NBOMe preliminary pharmacology psychoactive effects toxicity | 1 | 1 | Clinical review of closely related NBOMe compound; class pharmacology |
| 14 | PubMed | 25I-NBOMe metabolism in vitro demethylation hydroxylation phase I metabolites | 2 | 2 | Primary data on NBOMe metabolic pathways |
| 15 | Web | 25D-NBOMe legal status scheduling DEA controlled substance US UK Australia | 10 | 0 | Legal status context for 25D-NBOMe |
| 16 | PubMed | 25D-NBOMe reinforcing rewarding dopaminergic neurochemical Lee | 1 | 1 | Primary substance-specific source for abuse potential and dopaminergic pharmacology |
| 17 | PubMed | Receptor interaction profiles N-2-methoxybenzyl NBOMe 2C drugs Rickli Liechti | 1 | 1 | Key comparative pharmacology paper for NBOMe receptor profiles |
| 18 | PubMed | 25I-NBOMe Australia death case fatal forensic | 1 | 1 | Regional fatality case for class toxicity data |
| 19 | PubMed | Luethi Liechti designer drugs mechanism action adverse effects 2020 | 1 | 1 | Highly cited review covering NBOMe mechanism and adverse effects |
| 20 | PubMed | novel psychoactive substance emergency management benzodiazepine seizures treatment | 3 | 1 | Emergency management protocol for NPS including NBOMe-class compounds |
| 21 | OpenAlex | 25I-NBOMe 25C-NBOMe clinical intoxication hospital case series management | 8 | 2 | Best available clinical management guidance for NBOMe class |
| 22 | PubChem/Brief | 25D-NBOMe chemical identity cross-reference | 1 | 1 | Fills major gaps in chemical identity section of brief |
| 23 | Erowid | — | 1 | 1 | Only available specific 25D-NBOMe user report with dose details; user-report level evidence |
| 24 | PubMed | Caspar Brandt Stoever Meyer Maurer NBOMe 25B 25C metabolic fate urine | 1 | 1 | Primary CYP enzyme data applicable to 25D-NBOMe metabolism |
82 claims by section — every cited sentence, checked against its source
safety21 · 17 ok
The most significant substance-specific toxicity finding is hERG potassium channel inhibition, demonstrated by Yoon and colleagues (2019) in the only direct cardiac study of 25D-NBOMesupported
25D-NBOMe inhibited hERG potassium channels. j.toxlet.2019.01.004
PAK1, a biomarker of cardiac stress, was downregulatedsupported
PAK1 downregulated. j.toxlet.2019.01.004
Halberstadt (2017) reviewed 51 published cases of NBOMe toxicity, identifying rhabdomyolysis as a relatively common complication of severe intoxication, linked to seizures, hyperthermia, and sustained vasoconstrictionsupported
Analysis of 51 cases of NBOMe toxicity. Rhabdomyolysis common complication of severe toxicity, linked to seizures, hyperthermia, and vasoconstriction. 7854_2016_64
The broader toxicity profile documented for the NBOMe class includes:supported
Adverse effects: hallucinations, confusion, seizures, excited delirium, sympathomimetic signs. Rhabdomyolysis, DIC, hypoglycemia, metabolic acidosis, multiorgan failure reported. fnins.2020.00078
The broader toxicity profile documented for the NBOMe class includes:supported
Common adverse effects: tachycardia, anxiety, hypertension, seizures. Preclinical: developmental impairments, cytotoxicity, cardiovascular toxicity. 10408444.2023.2194907
Multiple fatalities have been attributed to 25I-NBOMe, 25B-NBOMe, and 25C-NBOMesupported
First confirmed 25I-NBOMe related death from Australia. j.forsciint.2015.02.010
Claim in safety — inconclusiveinconclusiveworking →
Multiple fatalities have been attributed to 25I-NBOMe, 25B-NBOMe, and 25C-NBOMesupported
First quantification of 25C-NBOMe in biological specimens from fatal intoxication. j.forsciint.2015.03.012
Morini and colleagues (2017) documented 25D-NBOMe as a component of mixed-NBOMe blotter preparations found in a fatality case, though the decedent tested positive for 25C-NBOMe and 25H-NBOMe rather than 25D-NBOMe specifically.supported
LC-MS/MS method for 5 NBOMes (25B-, 25C-, 25D-, 25H-, 25I-NBOMe). Blood positive for 25C- and 25H-NBOMe. j.forsciint.2017.08.028
Gil-Martins and colleagues (2024) demonstrated that NBOMe compounds produce higher cytotoxicity than their parent 2C compounds in neuronal cell lines, with lipophilicity as the primary determinantsupported
NBOMe drugs showed higher cytotoxicity than parent 2C compounds, correlating with lipophilicity. jox14020044
Wojtas and Gołembiowska (2024) reported genotoxicity markers and microglial activation following chronic NBOMe administration in ratssupported
Chronic administration: rapid tolerance development, genotoxicity, microglial activation. ijms25010241
Psychological risks are inferred from class-level literature for NBOMe compounds:supported
Reviews NBOMe structure-activity relationships, behavioral pharmacology, metabolism, and toxicity. 7854_2016_64
Psychological risks are inferred from class-level literature for NBOMe compounds:supported
Adverse effects: hallucinations, confusion, seizures, excited delirium, sympathomimetic signs. fnins.2020.00078
Claim in safety — inconclusiveinconclusiveworking →
Wojtas and Gołembiowska (2024) confirmed rapid tolerance development with chronic NBOMe administration in rodent modelssupported
Chronic administration: rapid tolerance development, genotoxicity, microglial activation. ijms25010241
Lee and colleagues (2023) established reinforcing properties in rats via intravenous self-administration (IVSA) at 0.03 mg/kg and conditioned place preference (CPP) at 1 mg/kg, with dopaminergic neurochemical changes in the nucleus accumbens as the underlying mechanismsupported
IVSA test showed increased self-administration at 0.03 mg/kg in rats; CPP showed rewarding effects at 1 mg/kg in mice. Microdialysis: increased extracellular DA, DOPAC, HVA in NAc. acschemneuro.3c00196
Claim in safety — inconclusiveinconclusiveworking →
Both compounds produce vasoconstriction, and both carry independent cardiotoxicity risk — 25D-NBOMe through hERG channel inhibition and QT prolongation, cocaine through sodium channel blockade and catecholamine-driven demand ischemiasupported
25D-NBOMe inhibited hERG potassium channels. Both compounds have potential cardiotoxicity especially cardiac rhythm. j.toxlet.2019.01.004
Claim in safety — inconclusiveinconclusiveworking →
Pre-existing cardiac arrhythmia or prolonged QT interval: hERG channel inhibition by 25D-NBOMe creates direct risk of torsades de pointes in individuals with congenital or acquired long QT syndrome.supported
25D-NBOMe inhibited hERG potassium channels. At 2.0 mg/kg 25D-NBOMe... prolonged QT intervals in rat ECG. j.toxlet.2019.01.004
Seizure disorders: NBOMe compounds lower seizure threshold at supratherapeutic doses.supported
Rhabdomyolysis common complication of severe toxicity, linked to seizures, hyperthermia, and vasoconstriction. 7854_2016_64
pharmacology20 · 13 ok
The addition of the N-(2-methoxybenzyl) group to the 2C-D scaffold produces a marked increase in 5-HT₂A binding affinity and hallucinogenic potency, with subnanomolar to low-nanomolar Ki values in radioligand displacement assays.supported
Full efficacy at 5-HT2A and 5-HT2C; subnanomolar to low nanomolar potency similar to LSD. j.bcp.2018.09.024
25D-NBOMe is a full agonist at the serotonin 5-HT₂A receptor, the primary molecular target responsible for psychedelic effectssupported
Full efficacy at 5-HT2A and 5-HT2C; subnanomolar to low nanomolar potency similar to LSD. j.bcp.2018.09.024
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
The compound demonstrates full agonist activity at 5-HT₂C receptors with potency comparable to LSD and serotoninsupported
Full efficacy at 5-HT2A and 5-HT2C; subnanomolar to low nanomolar potency similar to LSD. j.bcp.2018.09.024
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Potency at 5-HT₁A is very low, with greater than 1,000-fold selectivity for 5-HT₂A over 5-HT₁Asupported
>1000-fold selectivity for 5-HT2A vs 5-HT1A. fnins.2020.00078
Interactions with monoamine transporters (DAT, SERT, NET) occur only at low-to-mid micromolar concentrations — pharmacologically insignificant at psychedelic doses — consistent with a hallucinogenic rather than psychostimulant mechanism.supported
Low-to-mid micromolar at monoamine transporters. Results consistent with hallucinogenic activity, little psychostimulant activity. j.bcp.2018.09.024
NBOMe compounds as a class exhibit additional affinity at adrenergic, dopamine, and histamine receptors, though quantitative binding data at these targets have not been published specifically for 25D-NBOMesupported
Multi-receptor affinity (5-HT, dopamine, adrenergic, histamine). 10408444.2023.2194907
The only primary preclinical study conducted specifically on 25D-NBOMe — by Lee and colleagues (2023) — demonstrated that intraperitoneal administration at progressive doses (1, 3, 10 mg/kg) in rats increased extracellular dopamine, DOPAC, and HVA in the nucleus accumbens via microdialysis, with concurrent alterations in DRD1, DRD2, tyrosine hydroxylase, DAT, and phospho-DAT expressionsupported
Microdialysis: increased extracellular DA, DOPAC, HVA in NAc. Western blot: altered DRD1, DRD2, TH, DAT, p-DAT expression in NAc. acschemneuro.3c00196
Yoon and colleagues (2019) performed the only substance-specific cardiac investigation of 25D-NBOMe, demonstrating hERG (human Ether-à-go-go-Related Gene) potassium channel inhibition — the molecular mechanism underlying drug-induced QT prolongationsupported
25D-NBOMe inhibited hERG potassium channels. Both compounds have potential cardiotoxicity especially cardiac rhythm. j.toxlet.2019.01.004
PAK1, a cardiotoxicity biomarker, was downregulatedsupported
PAK1 downregulated. j.toxlet.2019.01.004
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
O-demethylation (primary pathway): removal of methoxy groups from both the dimethoxyphenyl ring and the 2-methoxybenzyl moiety, mediated by CYP2C9 and CYP2C19supported
Main pathways: O-demethylation, O,O-bis-demethylation, hydroxylation, glucuronidation, sulfation. CYP1A2 and CYP3A4 in hydroxylation; CYP2C9 and CYP2C19 in O-demethylation. j.jpba.2016.11.040
Hydroxylation (secondary pathway): preferentially at the N-(2-methoxybenzyl) ring, mediated by CYP1A2 and CYP3A4supported
CYP1A2 and CYP3A4 in hydroxylation; CYP2C9 and CYP2C19 in O-demethylation. j.jpba.2016.11.040
Claim in pharmacology — inconclusiveinconclusiveworking →
Additional minor pathways: O,O-bis-demethylation, N-dealkylation, dehydrogenation, and carbonylationsupported
Biotransformations: hydroxylation, O-demethylation, N-dealkylation, dehydrogenation, carbonylation. s00414-018-1904-7
Phase I metabolites undergo extensive Phase II conjugation with glucuronic acid and sulfate prior to urinary excretion.supported
Phase I metabolites conjugated with glucuronic acid and sulfate in human urine. dta.2044
receptor-pharmacology8 · 7 ok
Eshleman and colleagues (2018) provided the most comprehensive characterization of 25D-NBOMe receptor pharmacology, using mammalian cells heterologously expressing human receptor subtypes. 25D-NBOMe demonstrated:supported
Compares mechanisms of action of 25D-NBOMe, 25E-NBOMe, 25H-NBOMe, 25I-NBOH, and 25N-NBOMe. Full efficacy at 5-HT2A and 5-HT2C. j.bcp.2018.09.024
5-HT₂A receptor: Subnanomolar to low-nanomolar binding affinity with full agonist efficacy in IP₁ accumulation assays. Potency comparable to LSD.supported
Full efficacy at 5-HT2A and 5-HT2C; subnanomolar to low nanomolar potency similar to LSD. j.bcp.2018.09.024
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
5-HT₁A receptor: Very low potency and low efficacy in [³⁵S]GTPγS binding assays; pharmacologically insignificant.supported
Low efficacy at 5-HT1A. j.bcp.2018.09.024
The overall receptor selectivity profile — strong 5-HT₂A/2C agonism with minimal transporter activity — is consistent with a purely hallucinogenic mechanism and negligible psychostimulant contribution.supported
Results consistent with hallucinogenic activity, little psychostimulant activity. j.bcp.2018.09.024
Rickli and colleagues (2015) demonstrated that NBOMe derivatives consistently show markedly higher affinity at 5-HT₂A than their parent 2C compounds, with the N-(2-methoxybenzyl) group providing the critical pharmacophoric enhancementsupported
In vitro receptor interaction profiles of novel N-2-methoxybenzyl (NBOMe) derivatives of 2,5-dimethoxy-substituted phenethylamines (2C drugs). j.neuropharm.2015.08.034
NBOMe compounds as a class also exhibit binding at adrenergic (α₁, α₂), dopaminergic (D₁, D₂, D₃), and histaminergic (H₁, H₂) receptorssupported
Multi-receptor affinity (5-HT, dopamine, adrenergic, histamine). 10408444.2023.2194907
Wallach and colleagues (2023) identified that the subjective psychedelic experience correlates specifically with 5-HT₂A → Gq pathway activation rather than β-arrestin recruitmentsupported
Identifies 5-HT2A receptor signaling pathways associated with psychedelic potential. Gq-signaling can be fine-tuned to generate ligands distinct from classical psychedelics. s41467-023-44016-1
pharmacokinetic-detail7 · 2 ok
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Hydroxylation occurs preferentially at the N-(2-methoxybenzyl) aromatic ring, mediated by CYP1A2 and CYP3A4.supported
CYP1A2 and CYP3A4 in hydroxylation; CYP2C9 and CYP2C19 in O-demethylation. j.jpba.2016.11.040
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Phase I metabolites undergo extensive conjugation with glucuronic acid and sulfate, which are the predominant urinary excretion forms.supported
Phase I metabolites conjugated with glucuronic acid and sulfate in human urine. dta.2044
comparative-pharmacology6 · 4 ok
The cardiotoxicity profile of 25D-NBOMe parallels that of 25C-NBOMe: Yoon and colleagues (2019) tested both compounds and found hERG inhibition and QT prolongation for each, with 25C-NBOMe producing cardiac effects at a lower dose (0.75 mg/kg vs. 2.0 mg/kg for 25D-NBOMe).supported
At 2.0 mg/kg 25D-NBOMe and 0.75 mg/kg 25C-NBOMe prolonged QT intervals in rat ECG. 25D-NBOMe inhibited hERG potassium channels. Both compounds have potential cardiotoxicity especially cardiac rhythm. j.toxlet.2019.01.004
Rickli and colleagues (2015) demonstrated that NBOMe derivatives consistently exhibit markedly higher affinity at 5-HT₂A receptors compared to their parent 2C compoundssupported
In vitro receptor interaction profiles of novel N-2-methoxybenzyl (NBOMe) derivatives of 2,5-dimethoxy-substituted phenethylamines (2C drugs). j.neuropharm.2015.08.034
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
25D-NBOMe and LSD share subnanomolar 5-HT₂A affinity and produce overlapping perceptual effectssupported
Subnanomolar to low nanomolar potency similar to LSD. j.bcp.2018.09.024
Safety margin: LSD has an extremely wide therapeutic index; 25D-NBOMe has documented hERG inhibition and a narrow, uncharacterized margin between psychedelic and potentially cardiotoxic doses.supported
25D-NBOMe inhibited hERG potassium channels. Both compounds have potential cardiotoxicity especially cardiac rhythm. j.toxlet.2019.01.004
neuroscience6 · 4 ok
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
The dopaminergic neurochemistry demonstrated by Lee and colleagues (2023) — increased extracellular dopamine, DOPAC, and HVA in the nucleus accumbens, with altered expression of DRD1, DRD2, and tyrosine hydroxylase — introduces a mesolimbic reward pathway component not typically observed with classical psychedelicssupported
Microdialysis: increased extracellular DA, DOPAC, HVA in NAc. Western blot: altered DRD1, DRD2, TH, DAT, p-DAT expression in NAc. acschemneuro.3c00196
Wojtas and Gołembiowska (2024) demonstrated that chronic NBOMe administration in rats (25I- and 25B-NBOMe) significantly affects glutamatergic, dopaminergic, serotonergic, and cholinergic neurotransmission across frontal cortex, striatum, and nucleus accumbens, with concurrent rapid tolerance development, genotoxicity markers, and microglial activationsupported
Reviews 25I-NBOMe and 25B-NBOMe effects on glutamatergic, dopaminergic, serotonergic, and cholinergic neurotransmission. Chronic administration: rapid tolerance development, genotoxicity, microglial activation. ijms25010241
Incentive salience (wanting vs. liking): The dopaminergic reward-circuit activation documented by Lee and colleagues (2023) invites application of incentive salience theory — the distinction between mesolimbic dopamine-mediated "wanting" (compulsive approach behavior) and opioid/endocannabinoid-mediated "liking" (hedonic experience)supported
Microdialysis: increased extracellular DA, DOPAC, HVA in NAc. Demonstrates abuse potential and addictive neurochemical changes. acschemneuro.3c00196
Does the hERG channel inhibition documented in vitro translate to clinically significant QT prolongation at psychedelic doses in humans?supported
25D-NBOMe inhibited hERG potassium channels. At 2.0 mg/kg 25D-NBOMe... prolonged QT intervals in rat ECG. j.toxlet.2019.01.004
summary6 · 6 ok
As the N-(2-methoxybenzyl) derivative of 2C-D, it exhibits subnanomolar to low-nanomolar affinity at the human 5-HT₂A receptor with full agonist efficacy, placing it among the highest-potency serotonergic psychedelics characterizedsupported
Full efficacy at 5-HT2A and 5-HT2C; subnanomolar to low nanomolar potency similar to LSD. j.bcp.2018.09.024
The NBOMe class originated in academic receptor pharmacology research at the Free University of Berlin (c. 2000–2003) and was further developed as pharmacological tools in the Nichols laboratory at Purdue University. 25D-NBOMe entered online research chemical markets around 2010 and was first analytically identified in seized blotter papers in 2013supported
First analytical characterization of 25D-NBOMe, 25E-NBOMe, and 25G-NBOMe identified in seized blotter papers. dta.1397
The compound's primary research significance derives from a single preclinical study demonstrating dopaminergic reward-circuit activation and abuse potential in rodents, a finding that distinguishes NBOMe compounds from classical psychedelics lacking reinforcing properties.supported
IVSA test showed increased self-administration at 0.03 mg/kg in rats; CPP showed rewarding effects at 1 mg/kg in mice. Microdialysis: increased extracellular DA, DOPAC, HVA in NAc. acschemneuro.3c00196
25D-NBOMe produces psychedelic effects through full agonism at the 5-HT₂A receptor, activating Gq/11-coupled inositol phosphate signaling in cortical neuronssupported
Identifies 5-HT2A receptor signaling pathways associated with psychedelic potential. Gq-signaling can be fine-tuned to generate ligands distinct from classical psychedelics. s41467-023-44016-1
Substance-specific cardiotoxicity data confirm hERG potassium channel inhibition and QT interval prolongation in rats.supported
At 2.0 mg/kg 25D-NBOMe and 0.75 mg/kg 25C-NBOMe prolonged QT intervals in rat ECG. 25D-NBOMe inhibited hERG potassium channels. j.toxlet.2019.01.004
Tolerance develops rapidly through 5-HT₂A receptor downregulation, with cross-tolerance expected across serotonergic psychedelicssupported
Chronic administration: rapid tolerance development, genotoxicity, microglial activation. ijms25010241
history4 · 3 ok
Poklis and colleagues developed a validated urine screening method for nine NBOMe compounds including 25D-NBOMe in 2014, responding to an outbreak of N-benzylphenethylamine abuse and overdose cases in Virginia, United Statessupported
HPLC-MS/MS method for identification and quantification of nine NBOMe drugs in human urine including 25D-NBOMe... Developed in response to outbreak of N-benzyl-phenethylamine abuse in Virginia. bku005
Morini and colleagues documented 25D-NBOMe as a component of mixed-NBOMe blotter preparations in a 2017 forensic case involving a teenage fatality, though the decedent's blood tested positive for 25C-NBOMe and 25H-NBOMe rather than 25D-NBOMe specifically.supported
Teenager died by drowning after agitated/confused state following party. Blotter paper contained NBOMes. LC-MS/MS method for 5 NBOMes (25B-, 25C-, 25D-, 25H-, 25I-NBOMe). Blood positive for 25C- and 25H-NBOMe. j.forsciint.2017.08.028
NBOMe compounds entered online research chemical markets beginning around 2010, distributed primarily on blotter paper in a format visually indistinguishable from LSDsupported
NBOMes available from online vendors since 2010. 7854_2016_64
Claim in history — inconclusiveinconclusiveworking →
chemistry3 · 0 ok
clinical-evidence1 · 1 ok
The compound's documented hERG channel inhibition and QT prolongation risk, combined with the absence of a clearly defined therapeutic application, make initiation of human clinical studies unlikely in the near term.supported
25D-NBOMe inhibited hERG potassium channels. Both compounds have potential cardiotoxicity especially cardiac rhythm. j.toxlet.2019.01.004