generation run 2026-05-11
63 min completedmodel pipeline-v5plan not recordedrun/98a1fd38…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
- sparse_evidence
- safety_data_unverified
Reproduce
- inputs
- 28 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
20 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | OpenAlex | AB-FUBINACA synthetic cannabinoid | 10 | 3 | Banister 2015 is landmark pharmacology paper; Luethi & Liechti 2020 provides broader NPS context; Diao & Huestis covers SC metabolism strategies |
| 2 | ClinicalTrials.gov · absence | AB-FUBINACA synthetic cannabinoid | 0 | 0 | No trials found; as expected for a prohibited research chemical |
| 3 | PubMed | AB-FUBINACA metabolism metabolites urinary detection | 2 | 2 | Critical for metabolism section; 15 metabolites identified in urine |
| 4 | PubMed | AB-FUBINACA toxicity adverse effects case report | 1 | 1 | Key clinical case report with quantitative serum concentrations |
| 5 | PubMed | AB-FUBINACA synthetic cannabinoid pharmacology | 15 | 15 | All highly relevant to AB-FUBINACA pharmacology, toxicology, PK, and safety |
| 6 | PubChem | AB-FUBINACA | 1 | 1 | Single exact match for AB-FUBINACA; confirms molecular formula and weight |
| 7 | PubMed | PMID 26134475 | 1 | 1 | Primary pharmacology reference confirming CB1 agonism with nM potency |
| 8 | OpenAlex | AB-FUBINACA metabolism pharmacokinetics | 8 | 2 | Metabolism review and CYP enzyme data for SCRA class |
| 9 | Web/Wikipedia | AB-FUBINACA Pfizer patent origin pharmaceutical history | 10 | 1 | Historical origin data; pharmacological values from patent |
| 10 | DOI verification/Crossref | 10.1007/s11419-012-0171-4 | 1 | 1 | Discovery paper; first forensic identification |
| 11 | UNODC | AB-FUBINACA substance details | 1 | 1 | Official CAS number and international scheduling confirmation |
| 12 | Web/Federal Register | AB-FUBINACA DEA Schedule I emergency scheduling history legal status | 10 | 1 | Authoritative US legal status information |
| 13 | PubMed | PMIDs 26134475, 32688070, 31944614, 28393558 | 4 | 4 | All key primary sources for AB-FUBINACA |
| 14 | Web | Zombie mass overdose New York Brooklyn 2016 AB-FUBINACA | 10 | 1 | Contextual clarification; AMB-FUBINACA vs AB-FUBINACA distinction |
| 15 | Crossref/DOI | 10.1056/NEJMoa1610300 | 1 | 1 | api_verified confirmation of NEJM citation |
| 16 | Research synthesis | All pharmacological, toxicological, and legal data for AB-FUBINACA | — | 1 | Final data extraction and synthesis step |
| 17 | Web/UNODC | AB-FUBINACA UNODC substance details legal status | 1 | 1 | Official international scheduling and CAS number confirmation |
| 18 | PubMed | PMID 27973993 - NEJM zombie outbreak AMB-FUBINACA | 1 | 1 | Critical distinction: AMB-FUBINACA vs AB-FUBINACA |
| 19 | Web | AB-FUBINACA Canada Australia legal status | 10 | 0 | Gap identified - Canada and Australia status unconfirmed |
| 20 | PubChem CID 58124325 | AB-FUBINACA CID 58124325 | 1 | 1 | Chemical identity verification from authoritative database |
90 claims by section — every cited sentence, checked against its source
safety29 · 16 ok
In vivo assessment in mice demonstrates nephrotoxic effects consistent with acute kidney injury (AKI) pathologysupported
In vivo assessment of AKI from AB-FUBINACA exposure in mice. Associated with pathogenesis of AKI. s11419-024-00699-9
AKI has been reported in human synthetic cannabinoid users across the SCRA class, though no AB-FUBINACA-specific human renal case has been published.supported
Case report and systematic review of AKI from synthetic cannabinoid use. 16-160
Claim in safety — inconclusiveinconclusiveworking →
Cardiovascular toxicity manifests as supraventricular tachycardia (SVT) — documented in a patient who ingested e-cigarette fluid containing AB-FUBINACA and ADB-FUBINACA — and, in separate case series, as profound bradycardia and hypotensionsupported
Supraventricular tachycardia and acute confusion following ingestion of e-cigarette fluid containing AB-FUBINACA and ADB-FUBINACA: a case report with quantitative analysis of serum drug concentrations 15563650.2017.1307385
Cardiovascular toxicity manifests as supraventricular tachycardia (SVT) — documented in a patient who ingested e-cigarette fluid containing AB-FUBINACA and ADB-FUBINACA — and, in separate case series, as profound bradycardia and hypotensionsupported
Case series: bradycardia and hypotension toxidrome from synthetic cannabinoid (K2) use in NYC 2015. Normalized with IV fluids over 6-7h. j.ajem.2017.01.011
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Chronic AB-FUBINACA administration in mice produces hippocampal damage characterized by increased oxidative stress, neuroinflammation, elevated apoptosis markers, reduced BDNF expression, and decreased NR1 subunit expression of NMDA receptorssupported
Chronic AB-FUBINACA induced recognition memory impairment, hippocampal histopathological changes, increased oxidative stress, neuroinflammation, apoptosis markers, reduced BDNF, and decreased NR1 subunit of NMDA receptors. j.neuro.2024.05.009
Subacute AB-FUBINACA exposure in mice impairs male fertility and causes testicular histopathological damagesupported
Subacute exposure to AB-FUBINACA in mice caused male fertility impairment and testicular toxicity. s11419-025-00739-y
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
High-potency CB1 full agonists carry elevated psychosis risk compared to cannabissupported
Review of controlled lab studies showing cannabinoid agonists produce schizophrenia-like symptoms; patients with schizophrenia are more vulnerable. j.biopsych.2016.01.011
The NMDA NR1 downregulation observed in chronic mouse exposure provides a plausible mechanistic substrate for psychotomimetic effects but does not establish causation in humans.supported
Decreased NR1 subunit of NMDA receptors. j.neuro.2024.05.009
Physical dependence develops in mice following repeated AB-FUBINACA administration, as demonstrated through precipitated withdrawal paradigmssupported
Physical dependence demonstrated in mice. j.drugalcdep.2020.108179
Claim in safety — not_supportednot supportedworking →
The extraordinarily long urinary detection window (potentially >1 year in heavy users) has direct implications for monitoring abstinence during addiction treatment: urine drug screens cannot reliably distinguish recent use from residual excretion in former heavy users.supported
Metabolite detectable in urine >1 year in heavy users. Title: Extraordinary long detection window — Potential impact on therapeutic decisions. dta.2770
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Both interactions are inferred from the structural analogy-based CYP assignment and have not been clinically evaluated.supported
CYP3A4 is the major CYP enzyme responsible for oxidative metabolism of the indazole-carboxamide synthetic cannabinoid AKB-48. DDIs possible with CYP3A4 inhibitors. s12248-015-9788-7
SVT has been documented during AB-FUBINACA exposure, and the bidirectional cardiovascular response (tachyarrhythmia or bradycardia) is unpredictablesupported
Supraventricular tachycardia and acute confusion following ingestion of e-cigarette fluid containing AB-FUBINACA and ADB-FUBINACA. 15563650.2017.1307385
All high-potency CB1 full agonists carry elevated psychosis risk compared to cannabissupported
Review of controlled lab studies showing cannabinoid agonists produce schizophrenia-like symptoms; patients with schizophrenia are more vulnerable. j.biopsych.2016.01.011
Animal data demonstrate nephrotoxic potential, and the SCRA class is associated with AKI in humanssupported
In vivo assessment of AKI from AB-FUBINACA exposure in mice. Associated with pathogenesis of AKI. s11419-024-00699-9
Animal data demonstrate nephrotoxic potential, and the SCRA class is associated with AKI in humanssupported
Case report and systematic review of AKI from synthetic cannabinoid use. 16-160
Animal data show male reproductive toxicity, and genotoxicity has been demonstrated in human cell cultures.supported
Subacute exposure to AB-FUBINACA in mice caused male fertility impairment and testicular toxicity. s11419-025-00739-y
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
pharmacology17 · 11 ok
Claim in pharmacology — inconclusiveinconclusiveworking →
Functional potency measured by fluorometric membrane potential assay places CB1 EC50 in the range of 1.8–11.6 nM and CB2 EC50 in the range of 3.2–21.1 nM, depending on the assay system.partially supported
AB-FUBINACA acts as high-potency agonist at CB1 (EC50 = 2.1-11.6 nM) and CB2 (EC50 = 5.6-21.1 nM). s11419-016-0316-y
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Downstream, AB-FUBINACA activates G protein-gated inwardly rectifying potassium (GIRK) channels via CB1supported
AB-FUBINACA activated GIRK channels (CB1 signaling); no significant TRPV1 activation unlike some other SCRAs. j.ejphar.2021.174301
Unlike XLR-11, UR-144, and AM1220, AB-FUBINACA does not significantly activate TRPV1 channels at maximally active CB1 concentrations, indicating a cleaner CB1-selective signaling profile without the "off-target" vanilloid receptor engagement observed in some other SCRAs.supported
No significant TRPV1 activation unlike some other SCRAs. j.ejphar.2021.174301
Claim in pharmacology — inconclusiveinconclusiveworking →
AB-FUBINACA exhibits moderate-to-low microsomal clearance: after 3 hours of incubation with human liver microsomes (HLM), 77% of parent compound signal remained — substantially higher parent retention than most SCRAs tested under identical conditionssupported
77% of parent remained after 3h HLM incubation. dta.1896
Predicted hepatic clearance for the active (S)-enantiomer is 0.34 ± 0.09 mL/min/kg, among the lowest of all SCRAs characterized, whereas the (R)-enantiomer clears approximately 40-fold faster (CL_int = 13.7 ± 4.06 mL/min/kg)partially supported
Predicted human hepatic clearance (S)-enantiomer: 0.34 mL/min/kg; highly protein bound. molecules26051396
Claim in pharmacology — inconclusiveinconclusiveworking →
A controlled oral ingestion study demonstrated biphasic serum concentration-time kinetics consistent with distribution into deeper tissue compartments and slow redistributionsupported
Pharmacokinetic properties of AB-FUBINACA collected from controlled administration study (single oral ingestion). Biphasic serum kinetics observed. dta.2770
An elimination phase exceeding one year after last intake is plausible in cases of extensive prior consumption.supported
Metabolite detectable in urine >1 year in heavy users. dta.2770
Fifteen urinary metabolites have been identified by LC-QTOF-MS in authentic human urine samples, confirmed with HLM incubationsupported
15 urinary metabolites of AB-FUBINACA reported including hydroxylations, dealkylations, and amide hydrolysis. 77% of parent remained after 3h HLM incubation. dta.1896
Claim in pharmacology — inconclusiveinconclusiveworking →
Parent AB-FUBINACA was detectable in 54% of urine samples — a relatively high parent detection rate for SCRAs, consistent with the compound's low microsomal clearance.supported
Parent compound detected in 54% of case samples. dta.1896
By structural analogy with the related indazole-carboxamide AKB-48 and AB-CHMINACA, CYP3A4 is the likely primary enzyme responsible for oxidative hydroxylation, with CYP2D6 and CYP2C19 as potential minor contributorssupported
CYP3A4 is the major CYP enzyme responsible for oxidative metabolism of the indazole-carboxamide synthetic cannabinoid AKB-48. s12248-015-9788-7
By structural analogy with the related indazole-carboxamide AKB-48 and AB-CHMINACA, CYP3A4 is the likely primary enzyme responsible for oxidative hydroxylation, with CYP2D6 and CYP2C19 as potential minor contributorssupported
AB-CHMINACA metabolized by CYP3A4 as most active enzyme; 26 metabolites detected. Structural analog to AB-FUBINACA. dta.1796
summary11 · 7 ok
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
No controlled subjective-effect data exist in humans; clinical case reports document acute confusion, agitation, hallucinations, and cardiovascular disturbance.supported
Supraventricular tachycardia and acute confusion following ingestion of e-cigarette fluid containing AB-FUBINACA and ADB-FUBINACA: a case report with quantitative analysis of serum drug concentrations 15563650.2017.1307385
No controlled subjective-effect data exist in humans; clinical case reports document acute confusion, agitation, hallucinations, and cardiovascular disturbance.supported
Clinical experience with synthetic cannabinoid intoxication including AB-FUBINACA in emergency setting. j.ajem.2023.08.007
Chronic administration in mice produces hippocampal neurotoxicity, nephrotoxicity, and reproductive toxicitysupported
Chronic AB-FUBINACA induced recognition memory impairment, hippocampal histopathological changes, increased oxidative stress, neuroinflammation, apoptosis markers, reduced BDNF, and decreased NR1 subunit of NMDA receptors. j.neuro.2024.05.009
Chronic administration in mice produces hippocampal neurotoxicity, nephrotoxicity, and reproductive toxicitysupported
In vivo assessment of AKI from AB-FUBINACA exposure in mice. Associated with pathogenesis of AKI. s11419-024-00699-9
Chronic administration in mice produces hippocampal neurotoxicity, nephrotoxicity, and reproductive toxicitypartially supported
Subacute exposure to AB-FUBINACA in mice caused male fertility impairment and testicular toxicity. s11419-025-00739-y
Physical dependence develops in mice with repeated dosingsupported
Physical dependence demonstrated in mice. j.drugalcdep.2020.108179
The active (S)-enantiomer exhibits unusually low predicted hepatic clearance (CL_H = 0.34 mL/min/kg), and urinary metabolites remain detectable for over one year in heavy users — an extraordinary elimination window that confounds abstinence monitoringpartially supported
Metabolite detectable in urine >1 year in heavy users. dta.2770
neuroscience10 · 10 ok
In rats, the bradycardic response predominates and is dose-dependent at 0.3–3 mg/kgsupported
AB-FUBINACA and AB-PINACA dose-dependently induced hypothermia and bradycardia at doses of 0.3-3 mg/kg in rats. acschemneuro.5b00112
Is the >1-year urinary retention pharmacologically significant? Does tissue-sequestered AB-FUBINACA maintain low-level CB1 activation during the extended elimination phase, or is the retained material pharmacologically inert metabolite? This has implications for both receptor tolerance maintenance and withdrawal timing.supported
Metabolite detectable in urine >1 year in heavy users. dta.2770
In the hippocampus, chronic AB-FUBINACA administration in mice produces histopathological damage, elevated oxidative stress markers, neuroinflammation, and increased apoptosissupported
Chronic AB-FUBINACA induced hippocampal histopathological changes, increased oxidative stress, neuroinflammation, apoptosis markers. j.neuro.2024.05.009
Concurrently, expression of the NR1 subunit of NMDA receptors decreases — a finding with potential relevance to the psychotomimetic effects of synthetic cannabinoids, as glutamatergic hypofunction at NMDA receptors is implicated in psychosis pathogenesis.supported
Decreased NR1 subunit of NMDA receptors. j.neuro.2024.05.009
In the cardiovascular autonomic system, CB1 activation produces the bidirectional hemodynamic effects documented in clinical case reports — tachyarrhythmia in some patients, bradycardia and hypotension in otherssupported
Supraventricular tachycardia and acute confusion following ingestion of e-cigarette fluid containing AB-FUBINACA and ADB-FUBINACA. 15563650.2017.1307385
In the cardiovascular autonomic system, CB1 activation produces the bidirectional hemodynamic effects documented in clinical case reports — tachyarrhythmia in some patients, bradycardia and hypotension in otherssupported
Case series: bradycardia and hypotension toxidrome from synthetic cannabinoid (K2) use in NYC 2015. j.ajem.2017.01.011
Does AB-FUBINACA produce neuroplasticity changes distinct from THC? Full vs partial CB1 agonism may differentially affect BDNF-TrkB-mTOR signaling cascades. The observed BDNF reduction in chronic mouse exposure suggests neurotoxicity rather than neuroplasticity, but acute and chronic effects may diverge.supported
Reduced BDNF. j.neuro.2024.05.009
What explains the bidirectional cardiovascular response? SVT in one patient, bradycardia in another, dose-dependent bradycardia in rats. The dose-response, temporal, and individual-difference factors governing this divergence are uncharacterized.supported
Case series: bradycardia and hypotension toxidrome from synthetic cannabinoid (K2) use in NYC 2015. j.ajem.2017.01.011
What explains the bidirectional cardiovascular response? SVT in one patient, bradycardia in another, dose-dependent bradycardia in rats. The dose-response, temporal, and individual-difference factors governing this divergence are uncharacterized.supported
AB-FUBINACA and AB-PINACA dose-dependently induced hypothermia and bradycardia at doses of 0.3-3 mg/kg in rats. acschemneuro.5b00112
What is the true CYP phenotype? The CYP3A4 assignment rests on structural analogy. AB-FUBINACA's unusually low microsomal clearance raises the question of whether its metabolic pathways differ from faster-cleared class members.supported
CYP3A4 is the major CYP enzyme responsible for oxidative metabolism of the indazole-carboxamide synthetic cannabinoid AKB-48. s12248-015-9788-7
chemistry6 · 2 ok
Claim in chemistry — inconclusiveinconclusiveworking →
Claim in chemistry — inconclusiveinconclusiveworking →
Claim in chemistry — inconclusiveinconclusiveworking →
Claim in chemistry — inconclusiveinconclusiveworking →
Analytical differentiation requires LC-MS/MS methods.supported
Differentiation of AB-FUBINACA positional isomers using LC-MS/MS methods. s11419-018-0410-4
The compound's lipophilicity has been measured as log D₇.₄ = 2.48, the lowest value among 23 SCRAs tested (range: 2.48–4.95), indicating relatively low lipophilicity for its classsupported
Experimental log D7.4 for AB-FUBINACA = 2.48 (lowest among 23 SCRAs). dta.3621
comparative-pharmacology5 · 2 ok
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Banister et al. (2015) characterized a panel of eight indole and indazole SCRAs in both in vitro (fluorometric CB1/CB2 assay) and in vivo (rat biotelemetry) modelssupported
All synthesized SCs acted as high potency agonists of CB1 (EC50 = 0.24-21 nM) and CB2 (EC50 = 0.88-15 nM) receptors. AB-FUBINACA and AB-PINACA dose-dependently induced hypothermia and bradycardia at doses of 0.3-3 mg/kg in rats. acschemneuro.5b00112
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
AB-FUBINACA's low log D₇.₄ (2.48) places it at the hydrophilic extreme of the SCRA class (range: 2.48–4.95 across 23 compounds)supported
Experimental log D7.4 for AB-FUBINACA = 2.48 (lowest among 23 SCRAs). dta.3621
clinical-evidence3 · 2 ok
Serum drug concentrations were quantified, establishing a direct exposure–effect linkagesupported
Title: ...a case report with quantitative analysis of serum drug concentrations 15563650.2017.1307385
Paradoxically, the opposite hemodynamic pattern has also been documented for synthetic cannabinoid intoxication: Andonian et al. (2017) reported a case series of profound bradycardia and hypotension during K2/synthetic cannabinoid exposure, responsive to intravenous fluid resuscitationsupported
Case series: bradycardia and hypotension toxidrome from synthetic cannabinoid (K2) use in NYC 2015. Normalized with IV fluids over 6-7h. j.ajem.2017.01.011
Claim in clinical-evidence — inconclusiveinconclusiveworking →
history3 · 1 ok
Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
Forensic analyses revealed that illicit AB-FUBINACA is produced predominantly (>93%) as the pharmacologically more active (S)-enantiomer, consistent with synthesis from commercially available L-valine precursors.supported
(S)-enantiomers had enhanced potency at CB1/CB2 over (R)-enantiomers. S-enantiomer predominated in seized samples (93.6-99.3%). fchem.2019.00321
pharmacokinetic-detail3 · 2 ok
A controlled administration study involving a single oral ingestion of AB-FUBINACA demonstrated biphasic serum concentration-time kineticssupported
Pharmacokinetic properties of AB-FUBINACA collected from controlled administration study (single oral ingestion). Biphasic serum kinetics observed. dta.2770
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Assignment of CYP3A4 as the primary metabolizing enzyme is based on structural analogy with the related indazole-carboxamide AKB-48 and AB-CHMINACAsupported
CYP3A4 is the major CYP enzyme responsible for oxidative metabolism of the indazole-carboxamide synthetic cannabinoid AKB-48. s12248-015-9788-7
receptor-pharmacology3 · 3 ok
The EC50 range from Banister et al. (2015) places AB-FUBINACA within a panel of eight SCRAs showing CB1 EC50 values of 0.24–21 nM and CB2 EC50 values of 0.88–15 nM, though a specific value for AB-FUBINACA was not isolated in the abstract.supported
All synthesized SCs acted as high potency agonists of CB1 (EC50 = 0.24-21 nM) and CB2 (EC50 = 0.88-15 nM) receptors. acschemneuro.5b00112
The (S)-enantiomer of AB-FUBINACA shows significantly enhanced potency at both CB1 and CB2 compared to the (R)-enantiomersupported
(S)-enantiomers had enhanced potency at CB1/CB2 over (R)-enantiomers. EC50 and Emax determined for AB-FUBINACA. fchem.2019.00321
Seized herbal products contain >93% (S)-enantiomer, meaning illicit exposure is overwhelmingly to the more active form.supported
S-enantiomer predominated in seized samples (93.6-99.3%). fchem.2019.00321