AB-FUBINACA
Studies and references cited across this article, graded by evidence strength.
Inconclusive means the cited source neither confirms nor refutes the claim — a lower-confidence badge, not an error.
Data points an editor reviewed and accepted for publication.
Value Provenance
Dosing
smokedtrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Threshold | 1 mg | 1 mg | low |
| Low | 1–2 mg | 1–2 mg | low |
| Common | 2–3 mg | 2–3 mg | low |
| Strong | 3–5 mg | 3–5 mg | low |
| Heavy | 5+ mg | 5+ mg | low |
| Editorial | Existing DB / community consensus values. No controlled human dose-response study published. Values are consistent with sub-nanomolar CB1 Ki (0.9 nM) and milligram-range potency expected for high-affinity SCRAs. Work-notes flag these as community_consensus with low confidence. | ||
ReasoningReasoningExisting DB / community consensus values. No controlled human dose-response study published. Values are consistent with sub-nanomolar CB1 Ki (0.9 nM) and milligram-range potency expected for high-affinity SCRAs. Work-notes flag these as community_consensus with low confidence. Evidence basis: community_consensus_large | |||
Duration
smoked
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Peaktrace | 30–60 minutes | 30–60 minutes | low |
| Editorial | Existing DB value. No controlled human duration study. Consistent with short-acting SCRA characterization (Trexler et al. 2020). | ||
ReasoningReasoningExisting DB value. No controlled human duration study. Consistent with short-acting SCRA characterization (Trexler et al. 2020). Evidence basis: community_consensus_large | |||
| After effectstrace | 15–30 minutes | 15–30 minutes | low |
| Editorial | Existing DB value. Residual sedation and cognitive fog expected after acute effects resolve. | ||
ReasoningReasoningExisting DB value. Residual sedation and cognitive fog expected after acute effects resolve. Evidence basis: community_consensus_large | |||
| Onsettrace | 0–20 minutes | 0–20 minutes | low |
| Editorial | Existing DB value. Rapid pulmonary absorption expected for smoked SCRAs. 'Short-acting' label from Trexler et al. 2020 supports general order but exact values unconfirmed by controlled human study. | ||
ReasoningReasoningExisting DB value. Rapid pulmonary absorption expected for smoked SCRAs. 'Short-acting' label from Trexler et al. 2020 supports general order but exact values unconfirmed by controlled human study. Evidence basis: community_consensus_large | |||
| Offsettrace | 10–20 minutes | 10–20 minutes | low |
| Editorial | Existing DB value. Relatively rapid offset consistent with short total duration window of 1–2 hours. | ||
ReasoningReasoningExisting DB value. Relatively rapid offset consistent with short total duration window of 1–2 hours. Evidence basis: community_consensus_large | |||
| Totaltrace | 1–2 hours | 1–2 hours | low |
| Editorial | Existing DB value. 'Short-acting' characterization from Trexler et al. 2020 supports general 1–2 hour window. No controlled human study confirms exact duration. | ||
ReasoningReasoningExisting DB value. 'Short-acting' characterization from Trexler et al. 2020 supports general 1–2 hour window. No controlled human study confirms exact duration. Evidence basis: community_consensus_large | |||
Safety
Toxicity Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Acute | high | high | medium |
| Chronic | high | high | medium |
| Organs Affected | cardiovascular, neurological, renal, reproductive, genomic | cardiovascular, neurological, renal, reproductive, genomic | medium |
| Editorial | Acute rated 'high' per work-notes: documented cardiac arrhythmia (Lam et al. 2017), documented fatality in polydrug context (Rojek et al. 2024), and class-level severity from full CB1 agonism. Chronic rated 'high': hippocampal damage with BDNF reduction and NR1 downregulation (Alzu'bi et al. 2024), nephrotoxicity (Alzu'bi et al. 2025), reproductive toxicity (Alzu'bi et al. 2026) — all in mice across independent studies. Confidence medium because cardiovascular data is human (case series) but organ toxicity data is animal-only except cardiovascular. | ||
ReasoningReasoningAcute rated 'high' per work-notes: documented cardiac arrhythmia (Lam et al. 2017), documented fatality in polydrug context (Rojek et al. 2024), and class-level severity from full CB1 agonism. Chronic rated 'high': hippocampal damage with BDNF reduction and NR1 downregulation (Alzu'bi et al. 2024), nephrotoxicity (Alzu'bi et al. 2025), reproductive toxicity (Alzu'bi et al. 2026) — all in mice across independent studies. Confidence medium because cardiovascular data is human (case series) but organ toxicity data is animal-only except cardiovascular. Evidence basis: published_case_series | |||
Dependence Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Physical | moderate | moderate | medium |
| Psychological | moderate | moderate | medium |
| Compulsive Redosing | moderate | moderate | medium |
| Dose Escalation | moderate | moderate | medium |
| Editorial | Physical dependence confirmed in mice via precipitated withdrawal (Trexler et al. 2020). Human dependence data from class-level reports only. Work-notes rate physical and psychological dependence both as moderate, with moderate compulsive redosing and dose escalation. | ||
ReasoningReasoningPhysical dependence confirmed in mice via precipitated withdrawal (Trexler et al. 2020). Human dependence data from class-level reports only. Work-notes rate physical and psychological dependence both as moderate, with moderate compulsive redosing and dose escalation. Evidence basis: animal_study | |||
Withdrawal Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Severity | moderate | moderate | low |
| Symptoms | precipitated withdrawal signs in mice — specific symptoms not characterized in humans | precipitated withdrawal signs in mice — specific symptoms not characterized in humans | low |
| Fatal | No | No | low |
| Medical Supervision | Not required | Not required | low |
| Editorial | Withdrawal existence confirmed in mouse precipitated withdrawal paradigm (Trexler et al. 2020). Severity rated moderate by inference from mouse data plus SCRA class analogy. Human withdrawal symptoms, onset, and duration are not characterized in published literature. | ||
ReasoningReasoningWithdrawal existence confirmed in mouse precipitated withdrawal paradigm (Trexler et al. 2020). Severity rated moderate by inference from mouse data plus SCRA class analogy. Human withdrawal symptoms, onset, and duration are not characterized in published literature. Evidence basis: animal_study | |||
Tolerance Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Buildup | moderate | moderate | low |
| Half-life | 5 days | 5 days | low |
| Full Reset | 1.5 weeks | 1.5 weeks | low |
| Cross-tolerances | cannabinoids | cannabinoids | low |
| Editorial | Tolerance kinetics from existing DB seed data, not verified against AB-FUBINACA-specific study. Values extrapolated from general SC class. Cross-tolerance to cannabinoids expected from shared CB1 mechanism. Work-notes specify confidence=low and structural_analogy basis. | ||
ReasoningReasoningTolerance kinetics from existing DB seed data, not verified against AB-FUBINACA-specific study. Values extrapolated from general SC class. Cross-tolerance to cannabinoids expected from shared CB1 mechanism. Work-notes specify confidence=low and structural_analogy basis. Evidence basis: structural_analogy | |||
Effects & Profile
Contraindications
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| cardiovascular Cardiac arrhythmias or structural heart diseasetrace | absolute | absolute | high |
| Editorial | SVT documented in human case report (Lam et al. 2017); bidirectional CV response confirmed across multiple case reports. Work-notes rate confidence high. | ||
ReasoningReasoningSVT documented in human case report (Lam et al. 2017); bidirectional CV response confirmed across multiple case reports. Work-notes rate confidence high. | |||
| psychiatric Psychotic disorders or high psychosis risktrace | absolute | absolute | high |
| Editorial | Class-level evidence for elevated psychosis risk with high-potency CB1 full agonists (Sherif et al. 2016); AB-FUBINACA-specific NR1 downregulation in mice (Alzu'bi et al. 2024) provides mechanistic substrate. Work-notes rate confidence high. | ||
ReasoningReasoningClass-level evidence for elevated psychosis risk with high-potency CB1 full agonists (Sherif et al. 2016); AB-FUBINACA-specific NR1 downregulation in mice (Alzu'bi et al. 2024) provides mechanistic substrate. Work-notes rate confidence high. | |||
| renal Renal impairmenttrace | relative | relative | medium |
| Editorial | Mouse nephrotoxicity data (Alzu'bi et al. 2025) plus class-level human AKI reports (Zarifi & Vyas 2017). Work-notes rate confidence medium. | ||
ReasoningReasoningMouse nephrotoxicity data (Alzu'bi et al. 2025) plus class-level human AKI reports (Zarifi & Vyas 2017). Work-notes rate confidence medium. | |||
| metabolic CYP3A4 inhibitor co-administrationtrace | relative | relative | low |
| Editorial | CYP3A4 assignment inferred from AKB-48 (Holm et al. 2015) and AB-CHMINACA (Erratico et al. 2015). No direct AB-FUBINACA CYP phenotyping published. Work-notes rate confidence low. | ||
ReasoningReasoningCYP3A4 assignment inferred from AKB-48 (Holm et al. 2015) and AB-CHMINACA (Erratico et al. 2015). No direct AB-FUBINACA CYP phenotyping published. Work-notes rate confidence low. | |||
| pregnancy breastfeeding Pregnancy and lactationtrace | absolute | absolute | medium |
| Editorial | Mouse reproductive toxicity (Alzu'bi et al. 2026) and in vitro genotoxicity (Almestafa et al. 2025). Absolute contraindication by precautionary principle. Work-notes rate confidence medium. | ||
ReasoningReasoningMouse reproductive toxicity (Alzu'bi et al. 2026) and in vitro genotoxicity (Almestafa et al. 2025). Absolute contraindication by precautionary principle. Work-notes rate confidence medium. | |||
| other Concurrent opioid usetrace | absolute | absolute | high |
| Editorial | Fatal case documented (Rojek et al. 2024); adulteration risk documented (Ti et al. 2021). Work-notes rate confidence high. | ||
ReasoningReasoningFatal case documented (Rojek et al. 2024); adulteration risk documented (Ti et al. 2021). Work-notes rate confidence high. | |||
| neurological Seizure disorderstrace | relative | relative | low |
| Editorial | Class-level contraindication for SCRAs noted in work-notes. No AB-FUBINACA-specific seizure data, but class association is established. Proposed with structural_analogy basis. | ||
ReasoningReasoningClass-level contraindication for SCRAs noted in work-notes. No AB-FUBINACA-specific seizure data, but class association is established. Proposed with structural_analogy basis. | |||
| hepatic Severe hepatic impairmenttrace | relative | relative | low |
| Editorial | Class-level contraindication for CYP-metabolized SCRAs noted in work-notes. AB-FUBINACA's already-low hepatic clearance makes this particularly relevant. Structural analogy basis. | ||
ReasoningReasoningClass-level contraindication for CYP-metabolized SCRAs noted in work-notes. AB-FUBINACA's already-low hepatic clearance makes this particularly relevant. Structural analogy basis. | |||
| respiratory Respiratory diseasetrace | relative | relative | low |
| Editorial | Class-level contraindication for SCRAs noted in work-notes. No AB-FUBINACA-specific respiratory data but CNS depression is well-documented. Structural analogy basis. | ||
ReasoningReasoningClass-level contraindication for SCRAs noted in work-notes. No AB-FUBINACA-specific respiratory data but CNS depression is well-documented. Structural analogy basis. | |||
Timeline Phases
smoked
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 0–1200 sec(i=0.30) | 0–1200 sec(i=0.30) | low |
| Editorial | Duration data from existing DB (seed data). 'Short-acting' characterization supported by Trexler et al. 2020 title. No controlled human duration study published. Exact phase boundaries are community consensus extrapolation. Work-notes specify onset/peak/resolution/afterglow phases for smoked ROA. | ||
ReasoningReasoningDuration data from existing DB (seed data). 'Short-acting' characterization supported by Trexler et al. 2020 title. No controlled human duration study published. Exact phase boundaries are community consensus extrapolation. Work-notes specify onset/peak/resolution/afterglow phases for smoked ROA. Evidence basis: community_consensus_large | |||
| Peaktrace | 1800–3600 sec(i=1.00) | 1800–3600 sec(i=1.00) | low |
| Editorial | Duration data from existing DB (seed data). 'Short-acting' characterization supported by Trexler et al. 2020 title. No controlled human duration study published. Exact phase boundaries are community consensus extrapolation. Work-notes specify onset/peak/resolution/afterglow phases for smoked ROA. | ||
ReasoningReasoningDuration data from existing DB (seed data). 'Short-acting' characterization supported by Trexler et al. 2020 title. No controlled human duration study published. Exact phase boundaries are community consensus extrapolation. Work-notes specify onset/peak/resolution/afterglow phases for smoked ROA. Evidence basis: community_consensus_large | |||
| Resolutiontrace | 600–1200 sec(i=0.40) | 600–1200 sec(i=0.40) | low |
| Editorial | Duration data from existing DB (seed data). 'Short-acting' characterization supported by Trexler et al. 2020 title. No controlled human duration study published. Exact phase boundaries are community consensus extrapolation. Work-notes specify onset/peak/resolution/afterglow phases for smoked ROA. | ||
ReasoningReasoningDuration data from existing DB (seed data). 'Short-acting' characterization supported by Trexler et al. 2020 title. No controlled human duration study published. Exact phase boundaries are community consensus extrapolation. Work-notes specify onset/peak/resolution/afterglow phases for smoked ROA. Evidence basis: community_consensus_large | |||
| Afterglowtrace | 900–1800 sec(i=0.15) | 900–1800 sec(i=0.15) | low |
| Editorial | Duration data from existing DB (seed data). 'Short-acting' characterization supported by Trexler et al. 2020 title. No controlled human duration study published. Exact phase boundaries are community consensus extrapolation. Work-notes specify onset/peak/resolution/afterglow phases for smoked ROA. | ||
ReasoningReasoningDuration data from existing DB (seed data). 'Short-acting' characterization supported by Trexler et al. 2020 title. No controlled human duration study published. Exact phase boundaries are community consensus extrapolation. Work-notes specify onset/peak/resolution/afterglow phases for smoked ROA. Evidence basis: community_consensus_large | |||
Dose Tier Summaries
Minimal perceptible effects emerge as a slight alteration in sensorium — a subtle shift in headspace without a strong subjective cannabis-like experience. Awareness of body sensation changes may be noticed, along with faint cognitive slowing. Effects may be difficult to distinguish from placebo at a true threshold dose. Physical effects are negligible to absent. A mild dry mouth or slight change in body temperature awareness may occur. No significant motor impairment or cardiovascular changes are expected at this level. Duration is compressed compared to cannabis, with total effects resolving within approximately one hour. Functional impairment is minimal, but cognitive and motor testing may still detect subtle deficits.
No controlled human dose-response data for AB-FUBINACA. Threshold description inferred from SCRA class behavior (JWH-018, general SC community reports) and sub-nanomolar CB1 Ki placing active doses in the milligram range. Work-notes specify ~110 words.
ReasoningReasoning
No controlled human dose-response data for AB-FUBINACA. Threshold description inferred from SCRA class behavior (JWH-018, general SC community reports) and sub-nanomolar CB1 Ki placing active doses in the milligram range. Work-notes specify ~110 words.
Evidence basis: community_consensus_large
Mild cannabimimetic effects become apparent — subtle sedation, gentle cognitive slowing, and a nascent body high. Thought deceleration begins, and music enhancement may be noticed. Appetite enhancement can emerge. The experience is recognizably cannabinoid in character but lighter than a typical cannabis session. Physical effects include mild bodily heaviness, dry mouth, and possible dehydration sensation. Motor control impairment is slight but present. No significant cardiovascular effects are expected at this level, though heart rate perception changes may occur. Duration remains short, typically resolving within 60–90 minutes. Functional impairment is mild but real — driving and complex tasks should be avoided.
Inferred from SCRA class (JWH-018, THC) scaled for AB-FUBINACA's high CB1 affinity (Ki 0.9 nM). Light tier corresponds to 1–2 mg smoked per seed data. No controlled human study at this dose level.
ReasoningReasoning
Inferred from SCRA class (JWH-018, THC) scaled for AB-FUBINACA's high CB1 affinity (Ki 0.9 nM). Light tier corresponds to 1–2 mg smoked per seed data. No controlled human study at this dose level.
Evidence basis: community_consensus_large
The full cannabimimetic profile manifests — sedation dominates, accompanied by pronounced thought deceleration, analysis suppression, and cognitive impairment. Immersion enhancement and conceptual thinking may emerge. Anxiety and paranoia are possible, particularly in unfamiliar settings or anxious individuals. Spontaneous body sensations and vestibular distortion contribute to a notable altered state. Physical effects include marked bodily heaviness, motor control impairment, dry mouth, appetite enhancement, and nausea in some users. Cardiovascular effects become possible — heart rate changes in either direction (tachycardia or bradycardia) may occur unpredictably. Duration spans approximately 1–2 hours total. This is a full agonist with no ceiling effect — the dose-response curve is steeper and less forgiving than cannabis.
Common tier (2–3 mg smoked) represents full cannabimimetic activation at sub-nanomolar CB1 affinity. Effects profile drawn from work-notes effect values at common dose, case report presentations (Shopan et al. 2023), and SCRA class inference.
ReasoningReasoning
Common tier (2–3 mg smoked) represents full cannabimimetic activation at sub-nanomolar CB1 affinity. Effects profile drawn from work-notes effect values at common dose, case report presentations (Shopan et al. 2023), and SCRA class inference.
Evidence basis: community_consensus_large
Intense sedation and significant cognitive disruption dominate. Delusions and hallucinations become possible — auditory hallucinations and geometry may emerge. Paranoia and anxiety intensify. Reality testing is compromised, and thought disorganization may occur. The experience can become overwhelming, particularly for those without synthetic cannabinoid tolerance. Physical effects are pronounced: severe motor control impairment, marked bodily heaviness, nausea, and cardiovascular risk increases. Supraventricular tachycardia or profound bradycardia are possible. Vestibular distortion may impair balance and coordination. Duration remains approximately 1–2 hours but the intensity makes the experience feel longer. A sitter is strongly recommended. Medical attention may be needed if cardiovascular symptoms emerge.
Strong tier (3–5 mg smoked) approaches the steep upper portion of the full-agonist dose-response curve. SVT documented at clinical presentations (Lam et al. 2017). Hallucinations and delusions documented in case series (Shopan et al. 2023).
ReasoningReasoning
Strong tier (3–5 mg smoked) approaches the steep upper portion of the full-agonist dose-response curve. SVT documented at clinical presentations (Lam et al. 2017). Hallucinations and delusions documented in case series (Shopan et al. 2023).
Evidence basis: community_consensus_large
Severe intoxication with risk of medical emergency. Confusion, agitation, and hallucinations dominate the psychological picture. Delusions may be intense and disorienting. Complete loss of motor control is likely. The user may be unable to communicate coherently or respond to their environment. Cardiovascular emergency is possible — SVT, profound bradycardia, or hypotension may occur. Nausea and vomiting are common. Seizure risk exists at the class level. Respiratory depression may compound if other CNS depressants are present. Medical attention should be immediately accessible. As a full CB1 agonist, AB-FUBINACA has no ceiling effect on receptor activation. Heavy doses exploit this fully — the metabolite retention window exceeds one year in heavy users, complicating future drug testing.
Heavy tier (5+ mg smoked) represents doses where full agonist pharmacology produces maximum CB1 activation without ceiling. Fatal case involved polydrug (Rojek et al. 2024). All clinical presentations at emergency doses documented in case literature.
ReasoningReasoning
Heavy tier (5+ mg smoked) represents doses where full agonist pharmacology produces maximum CB1 activation without ceiling. Fatal case involved polydrug (Rojek et al. 2024). All clinical presentations at emergency doses documented in case literature.
Evidence basis: community_consensus_large
History
backfill Jun 4, 2026
Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.
Sources
- [1]weakSchedules of Controlled Substances: Placement of PB-22, 5F-PB-22, AB-FUBINACA and ADB-PINACA into Schedule IDEA (US Drug Enforcement Administration) · 2016linkno claims checked
- [2]moderateNew cannabimimetic indazole derivatives, N-(1-amino-3-methyl-1-oxobutan-2-yl)-1-pentyl-1H-indazole-3-carboxamide (AB-PINACA) and N-(1-amino-3-methyl-1-oxobutan-2-yl)-1-(4-fluorobenzyl)-1H-indazole-3-carboxamide (AB-FUBINACA) identified as designer drugs in illegal productsUchiyama N, Matsuda S, Wakana D, Kikura-Hanajiri R, Goda Y · 2012 · Forensic Toxicologydoi.org/10.1007/s11419-012-0171-43 claims checked3 inconclusive
- [3]weakAcute intoxication caused by three common synthetic cannabinoids: The experience of a large, urban, tertiary care hospitalShopan N, Scolnik D, Hassoun E, Firsow A, Volkov I, Glatstein M · 2023 · American Journal of Emergency Medicine
- [4]moderateThe short-acting synthetic cannabinoid AB-FUBINACA induces physical dependence in miceTrexler KR, Vanegas SO, Poklis JL, Kinsey SG · 2020 · Drug and Alcohol Dependencedoi.org/10.1016/j.drugalcdep.2020.108179pubmed 326880704 claims checked2 verified1 inconclusive1 not supported
- [5]weakSupraventricular 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 concentrationsLam RPK, Tang MHY, Leung SC, Chong YK, Tsui MSH, Mak TWL · 2017 · Clinical Toxicology
- [6]moderateExtraordinary long detection window of a synthetic cannabinoid metabolite in human urine - Potential impact on therapeutic decisionsFranz F, Haschimi B, King LA, Auwärter V · 2020 · Drug Testing and Analysis
- [7]moderateDelineating the molecular mechanisms of hippocampal neurotoxicity induced by chronic administration of synthetic cannabinoid AB-FUBINACA in miceAlzu'bi A et al. · 2024 · Neurotoxicology
- [8]moderateIn vivo assessment of the nephrotoxic effects of the synthetic cannabinoid AB-FUBINACAAlzu'bi A et al. · 2025 · Forensic Toxicology
- [9]moderateSynthetic Cannabinoid AB-FUBINACA Negatively Impacted the Male Fertility and Induced Testicular ToxicityAlzu'bi A et al. · 2026 · Forensic Toxicology
- [10]moderateDifferential activation of G protein-mediated signaling by synthetic cannabinoid receptor agonistsSachdev S, Banister SD, Santiago M, Bladen C, Kassiou M, Connor M · 2020 · Pharmacology Research & Perspectives
- [11]moderatePharmacology of Indole and Indazole Synthetic Cannabinoid Designer Drugs AB-FUBINACA, ADB-FUBINACA, AB-PINACA, ADB-PINACA, 5F-AB-PINACA, 5F-ADB-PINACA, ADBICA, and 5F-ADBICABanister SD, Moir M, Stuart J, Kevin RC, Wood KE, Longworth M, Wilkinson SM, Beinat C, Buchanan AS, Glass M, Connor M, McGregor IS, Kassiou M · 2015 · ACS Chemical Neuroscience
- [12]weakUNODC Laboratory and Scientific Service: AB-FUBINACA Substance DetailsUNODC · 2020linkno claims checked
- [13]weak"Zombie" Outbreak Caused by the Synthetic Cannabinoid AMB-FUBINACA in New YorkAdams AJ, Banister SD, Irizarry L, Trecki J, Schwartz M, Gerona R · 2017 · New England Journal of Medicine
- [14]moderateEnantiospecific Synthesis, Chiral Separation, and Biological Activity of Four Indazole-3-Carboxamide-Type Synthetic Cannabinoid Receptor Agonists and Their Detection in Seized Drug SamplesAntonides LH, Cannaert A, Norman C, Vives L, Harrison A, Costello A, Nic Daeid N, Stove CP, Sutcliffe OB, McKenzie C · 2019 · Frontiers in Chemistry
- [15]moderateIdentification of AB-FUBINACA metabolites in authentic urine samples suitable as urinary markers of drug intake using liquid chromatography quadrupole tandem time of flight mass spectrometryVikingsson S, Grén H, Brinkhagen L, Mukhtar S, Josefsson M · 2016 · Drug Testing and Analysis
- [16]moderateThe 2-alkyl-2H-indazole regioisomers of synthetic cannabinoids AB-CHMINACA, AB-FUBINACA, AB-PINACA, and 5F-AB-PINACA are possible manufacturing impurities with cannabimimetic activitiesLongworth M, Banister SD, Mack JBC, Glass M, Connor M, Kassiou M · 2016 · Forensic Toxicology
- [17]moderateA Systematic Study of the In Vitro Pharmacokinetics and Estimated Human In Vivo Clearance of Indole and Indazole-3-Carboxamide Synthetic Cannabinoid Receptor AgonistsBrandon AM, Antonides LH, Riley J, Epemolu O, McKeown DA, Read KD, McKenzie C · 2021 · Molecules
- [18]moderateDifferentiation of AB-FUBINACA and its five positional isomers using liquid chromatography-electrospray ionization-linear ion trap mass spectrometry and triple quadrupole mass spectrometryMurakami T, Iwamuro Y, Ishimaru R, Chinaka S, Takayama N, Hasegawa H · 2018 · Forensic Toxicology
- [19]moderateLog D7.4 and plasma protein binding of synthetic cannabinoid receptor agonistsBrandon AM, Baginski SR, Peet C, Dugard P, Green H, Sutcliffe OB, Daéid NN, Nisbet LA, Read KD, McKenzie C · 2024 · Drug Testing and Analysis
- [20]moderateMolecular signaling of synthetic cannabinoids: Comparison of CB1 receptor and TRPV1 channel activationAndersen HK, Walsh KB · 2021 · European Journal of Pharmacology
- [21]moderateCYP3A4 Mediates Oxidative Metabolism of the Synthetic Cannabinoid AKB-48Holm NB, Nielsen LM, Linnet K · 2015 · The AAPS Journal
- [22]moderateIn vitro and in vivo human metabolism of the synthetic cannabinoid AB-CHMINACAErratico C, Negreira N, Norouzizadeh H, Covaci A, Neels H, Maudens K, van Nuijs AL · 2015 · Drug Testing and Analysis
- [23]weakProfound hypotension and bradycardia in the setting of synthetic cannabinoid intoxication - A case seriesAndonian DO, Seaman SR, Josephson EB · 2017 · American Journal of Emergency Medicine
- [24]moderateNew psychoactive substances - 96 cases of deaths related to their use based on forensic toxicological practice.Rojek S, Maciów-Głąb M, Romańczuk A, Kula K, Synowiec K, Kłys M · 2024 · Forensic science international
- [25]moderateDetection of synthetic cannabinoid adulteration in the unregulated drug supply in three Canadian settingsTi L, Tobias S, Maghsoudi N, Milloy MJ, McDonald K, Shapiro A, Beriault D, Stefan C, Lysyshyn M, Werb D · 2021 · Drug and Alcohol Review
- [26]strongSpice-y Kidney Failure: A Case Report and Systematic Review of Acute Kidney Injury Attributable to the Use of Synthetic CannabisZarifi C, Vyas S · 2017 · The Permanente Journal
- [27]moderateSynthetic Cannabinoids are Genotoxic in Cultured Human LymphocytesAlmestafa AA, Khabour OF, Al-Eitan LN, Alzoubi KH · 2025 · Current Pharmaceutical Design
- [28]strongHuman Laboratory Studies on Cannabinoids and PsychosisSherif M, Radhakrishnan R, D'Souza DC, Ranganathan M · 2016 · Biological Psychiatry
Claim Verification
Citation-bearing claims in this article were checked by an AI model against the abstract of the source they cite — every safety-critical claim, plus a sample of the rest. Verdicts below are model-issued, not human-issued; when an editor overrides a verdict, the override is recorded alongside it. Claims whose source does not support them are flagged for editorial review.
summary11 claims5verified2partial4inconclusive
inconclusiveThe smoked duration is short-acting, with a total window of 1–2 hours.[4]model confidence 80%
The paper title uses 'short-acting' but the abstract does not specify a 1–2 hour duration window for the smoked route. The specific duration claim cannot be verified from the abstract alone.
Evaluated the behavioral effects of the third-generation indazole-3-carboxamide-type synthetic cannabinoid, AB-FUBINACA. Physical dependence demonstrated in mice.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveIt first appeared in illicit herbal blends in Japan in 2012 and was permanently placed into US DEA Schedule I in September 2016[2]model confidence 95%
Abstract not available; cannot verify either the 2012 Japan appearance or the September 2016 DEA scheduling.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveAB-FUBINACA binds CB1 with sub-nanomolar affinity and functions as a full agonist at Gi/o-coupled signaling, inhibiting cAMP accumulation with greater potency than JWH-018 or XLR-11[10]model confidence 80%
The abstract confirms Gαi/o activation at CB1 and mentions different potency rank orders, but does not confirm sub-nanomolar binding affinity or the specific comparison to JWH-018 and XLR-11 in the Gαi/o pathway.
AB-FUBINACA activates both Gαs and Gαi/o at CB1. Different potency rank orders for each G protein pathway.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveIn vivo cannabimimetic effects — hypothermia, bradycardia, locomotor suppression — are fully reversed by CB1 antagonist pretreatment, confirming CB1 as the obligate mediator[11]model confidence 80%
The abstract confirms hypothermia and bradycardia in rats but does not mention locomotor suppression, CB1 antagonist pretreatment (e.g., rimonabant), or the reversal experiment confirming CB1 as the obligate mediator.
AB-FUBINACA and AB-PINACA dose-dependently induced hypothermia and bradycardia at doses of 0.3-3 mg/kg in rats.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedNo controlled subjective-effect data exist in humans; clinical case reports document acute confusion, agitation, hallucinations, and cardiovascular disturbance.[5]model confidence 85%
The paper title documents SVT (cardiovascular disturbance) and acute confusion following AB-FUBINACA/ADB-FUBINACA ingestion — directly a clinical case report documenting these effects.
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
checked by claude-sonnet-4-6 · May 11, 2026
verifiedNo controlled subjective-effect data exist in humans; clinical case reports document acute confusion, agitation, hallucinations, and cardiovascular disturbance.[3]model confidence 80%
The paper documents clinical experience with synthetic cannabinoid intoxication including AB-FUBINACA in an emergency setting, consistent with the claim that case reports document these effects.
Clinical experience with synthetic cannabinoid intoxication including AB-FUBINACA in emergency setting.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedChronic administration in mice produces hippocampal neurotoxicity, nephrotoxicity, and reproductive toxicity[7]model confidence 95%
This citation directly supports the hippocampal neurotoxicity component of the claim. The abstract confirms histopathological hippocampal damage and molecular neurotoxicity markers from chronic AB-FUBINACA in mice.
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.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedChronic administration in mice produces hippocampal neurotoxicity, nephrotoxicity, and reproductive toxicity[8]model confidence 95%
This citation directly supports the nephrotoxicity component of the claim via in vivo AKI assessment in mice.
In vivo assessment of AKI from AB-FUBINACA exposure in mice. Associated with pathogenesis of AKI.
checked by claude-sonnet-4-6 · May 11, 2026
partialChronic administration in mice produces hippocampal neurotoxicity, nephrotoxicity, and reproductive toxicity[9]model confidence 80%
The abstract confirms reproductive toxicity in mice but specifies 'subacute' exposure — materially different from the 'chronic administration' stated in the claim.
Subacute exposure to AB-FUBINACA in mice caused male fertility impairment and testicular toxicity.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedPhysical dependence develops in mice with repeated dosing[4]model confidence 95%
The abstract directly states 'Physical dependence demonstrated in mice.'
Physical dependence demonstrated in mice.
checked by claude-sonnet-4-6 · May 11, 2026
partialThe 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 monitoring[6]model confidence 80%
The abstract confirms the >1-year urinary detection window in heavy users, but does not mention the CL_H = 0.34 mL/min/kg value, which is a specific quantitative claim from a different paper (citation [9]).
Metabolite detectable in urine >1 year in heavy users.
checked by claude-sonnet-4-6 · May 11, 2026
history3 claims1verified2inconclusive
inconclusiveThe discovery was reported by Uchiyama and colleagues at the National Institute of Health Sciences (Tokyo) in Forensic Toxicology (published online 2012; print 2013)[2]model confidence 95%
Abstract not available; cannot verify author institution, journal, or publication date.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveJapan responded rapidly, designating AB-FUBINACA a "specified substance" under the Pharmaceutical and Medical Device Act in December 2012 — the first jurisdiction globally to schedule it.[2]model confidence 95%
Abstract not available; cannot verify the Japanese scheduling claim or the 'first jurisdiction globally' assertion.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedForensic 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.[14]model confidence 95%
The abstract directly confirms S-enantiomer predominance in seized samples (93.6–99.3%) and enhanced CB1/CB2 potency of S-enantiomer.
(S)-enantiomers had enhanced potency at CB1/CB2 over (R)-enantiomers. S-enantiomer predominated in seized samples (93.6-99.3%).
checked by claude-sonnet-4-6 · May 11, 2026
chemistry6 claims2verified4inconclusive
inconclusiveThe fluorine atom on the para position of the benzyl ring contributes to metabolic stability by resisting oxidative dealkylation at that position — no metabolic modifications on the fluorobenzyl side chain were observed in human liver microsome studies.[15]model confidence 75%
The abstract lists general metabolite types but does not specifically address the fluorobenzyl side chain or confirm absence of modifications at that position.
15 urinary metabolites of AB-FUBINACA reported including hydroxylations, dealkylations, and amide hydrolysis.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveThe (S)-enantiomer demonstrates significantly enhanced CB1 and CB2 potency relative to the (R)-enantiomer, with the potency differential more pronounced for amide-terminal compounds like AB-FUBINACA than for ester-terminal analogs.[14]model confidence 75%
The abstract confirms enhanced S-enantiomer potency at CB1/CB2 but does not address the comparison between amide-terminal and ester-terminal analogs.
(S)-enantiomers had enhanced potency at CB1/CB2 over (R)-enantiomers.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveThe two enantiomers also differ in their metabolic clearance: the (S)-enantiomer exhibits markedly lower predicted hepatic clearance than the (R)-form (see Pharmacokinetic Detail).[17]model confidence 75%
The abstract confirms (S)-enantiomer clearance (0.34 mL/min/kg) but does not provide (R)-enantiomer clearance data to verify the 'markedly lower' comparison.
Predicted human hepatic clearance (S)-enantiomer: 0.34 mL/min/kg; highly protein bound.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveSix positional isomers of AB-FUBINACA have been characterized, including 2-alkyl-2H-indazole regioisomers that may arise as manufacturing impurities during clandestine synthesis[16]model confidence 70%
The abstract confirms 2H-regioisomers as manufacturing impurities but does not confirm the number 'six' positional isomers.
2H-regioisomers are manufacturing impurities with micromolar (low) activity.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedAnalytical differentiation requires LC-MS/MS methods.[18]model confidence 95%
The abstract directly confirms LC-MS/MS methods are used for differentiation of AB-FUBINACA positional isomers.
Differentiation of AB-FUBINACA positional isomers using LC-MS/MS methods.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe 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 class[19]model confidence 95%
The abstract directly confirms log D7.4 = 2.48 as the lowest value among 23 SCRAs.
Experimental log D7.4 for AB-FUBINACA = 2.48 (lowest among 23 SCRAs).
checked by claude-sonnet-4-6 · May 11, 2026
pharmacology17 claims9verified2partial6inconclusive
inconclusiveFunctional 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.[11]model confidence 75%
The abstract gives panel-wide EC50 ranges (CB1: 0.24–21 nM; CB2: 0.88–15 nM) but does not isolate AB-FUBINACA-specific values. The claim's narrower ranges (1.8–11.6 nM CB1; 3.2–21.1 nM CB2) likely reflect full-paper data not available in the abstract.
All synthesized SCs acted as high potency agonists of CB1 (EC50 = 0.24-21 nM) and CB2 (EC50 = 0.88-15 nM) receptors.
checked by claude-sonnet-4-6 · May 11, 2026
partialFunctional 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.[16]model confidence 75%
The abstract gives AB-FUBINACA-specific values of CB1 EC50 = 2.1–11.6 nM and CB2 EC50 = 5.6–21.1 nM. The claim's lower bounds (1.8 nM CB1; 3.2 nM CB2) differ materially from the abstract's values (2.1 nM CB1; 5.6 nM CB2).
AB-FUBINACA acts as high-potency agonist at CB1 (EC50 = 2.1-11.6 nM) and CB2 (EC50 = 5.6-21.1 nM).
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveIn rank-order potency for Gαi/o-mediated cAMP inhibition, AB-FUBINACA is surpassed only by 5F-MDMB-PICA among a panel of five SCRAs tested (5F-MDMB-PICA > AB-FUBINACA > PB-22 > JWH-018 > XLR-11)[10]model confidence 80%
The abstract confirms that AB-FUBINACA activates Gαi/o at CB1 and that different potency rank orders exist, but does not specify the exact ranking cited in the claim.
AB-FUBINACA activates both Gαs and Gαi/o at CB1. Different potency rank orders for each G protein pathway.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveAB-FUBINACA also activates Gαs-mediated cAMP stimulation at CB1, with a different rank-order potency (PB-22 > 5F-MDMB-PICA > JWH-018 ≈ AB-FUBINACA > XLR-11), demonstrating pathway-dependent signaling bias.[10]model confidence 80%
The abstract confirms Gαs activation and pathway-dependent potency rank orders, but does not specify the exact Gαs rank order stated in the claim.
AB-FUBINACA activates both Gαs and Gαi/o at CB1. Different potency rank orders for each G protein pathway.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedDownstream, AB-FUBINACA activates G protein-gated inwardly rectifying potassium (GIRK) channels via CB1[20]model confidence 95%
The abstract directly states 'AB-FUBINACA activated GIRK channels (CB1 signaling).'
AB-FUBINACA activated GIRK channels (CB1 signaling); no significant TRPV1 activation unlike some other SCRAs.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedUnlike 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.[20]model confidence 85%
The abstract directly confirms no significant TRPV1 activation for AB-FUBINACA, distinguishing it from other SCRAs. The specific SCRAs named (XLR-11, UR-144, AM1220) are not in the abstract but the core pharmacological claim is confirmed.
No significant TRPV1 activation unlike some other SCRAs.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveBoth effects are fully reversed by pretreatment with the CB1 antagonist rimonabant but not by a CB2 antagonist, establishing CB1 as the obligate mediator of its cannabimimetic activity.[11]model confidence 85%
The abstract confirms hypothermia and bradycardia in rats but does not mention rimonabant, CB1 antagonist reversal, or CB2 antagonist controls. These data may be in the full paper but cannot be verified from the abstract.
AB-FUBINACA and AB-PINACA dose-dependently induced hypothermia and bradycardia at doses of 0.3-3 mg/kg in rats.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedAB-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 conditions[15]model confidence 95%
The abstract directly states '77% of parent remained after 3h HLM incubation,' confirming the specific claim.
77% of parent remained after 3h HLM incubation.
checked by claude-sonnet-4-6 · May 11, 2026
partialPredicted 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)[17]model confidence 80%
The abstract confirms the (S)-enantiomer clearance of 0.34 mL/min/kg. However, the (R)-enantiomer value (CL_int = 13.7 ± 4.06 mL/min/kg) and the '40-fold faster' comparison are specific quantitative claims not present in the abstract.
Predicted human hepatic clearance (S)-enantiomer: 0.34 mL/min/kg; highly protein bound.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveThis enantioselective clearance, combined with high plasma protein binding (class range: 90.8–99.9%), suggests prolonged in vivo exposure for the pharmacologically active enantiomer.[19]model confidence 75%
The abstract notes 'PPB data included' but does not state the specific range of 90.8–99.9%. The specific plasma protein binding range cannot be verified from the abstract alone.
Experimental log D7.4 for AB-FUBINACA = 2.48 (lowest among 23 SCRAs). PPB data included.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedA controlled oral ingestion study demonstrated biphasic serum concentration-time kinetics consistent with distribution into deeper tissue compartments and slow redistribution[6]model confidence 95%
The abstract directly confirms 'Biphasic serum kinetics observed' in a 'controlled administration study (single oral ingestion).'
Pharmacokinetic properties of AB-FUBINACA collected from controlled administration study (single oral ingestion). Biphasic serum kinetics observed.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedAn elimination phase exceeding one year after last intake is plausible in cases of extensive prior consumption.[6]model confidence 95%
The abstract directly states 'metabolite detectable in urine >1 year in heavy users,' directly supporting the claim.
Metabolite detectable in urine >1 year in heavy users.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedFifteen urinary metabolites have been identified by LC-QTOF-MS in authentic human urine samples, confirmed with HLM incubation[15]model confidence 95%
The abstract directly confirms 15 urinary metabolites and HLM incubation experiments.
15 urinary metabolites of AB-FUBINACA reported including hydroxylations, dealkylations, and amide hydrolysis. 77% of parent remained after 3h HLM incubation.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveNo modifications on the 4-fluorobenzyl side chain were observed, consistent with the metabolic stability conferred by the para-fluorine substituent.[15]model confidence 75%
The abstract describes metabolite types (hydroxylations, dealkylations, amide hydrolysis) but does not specifically state that no modifications to the 4-fluorobenzyl side chain were observed. This detail would be in the full paper.
15 urinary metabolites of AB-FUBINACA reported including hydroxylations, dealkylations, and amide hydrolysis.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedParent 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.[15]model confidence 95%
The abstract directly states 'Parent compound detected in 54% of case samples.'
Parent compound detected in 54% of case samples.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedBy 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 contributors[21]model confidence 85%
The abstract confirms CYP3A4 as the major enzyme for the indazole-carboxamide AKB-48, supporting the structural analogy basis for inferring CYP3A4 as primary for AB-FUBINACA.
CYP3A4 is the major CYP enzyme responsible for oxidative metabolism of the indazole-carboxamide synthetic cannabinoid AKB-48.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedBy 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 contributors[22]model confidence 85%
The abstract confirms CYP3A4 as the most active enzyme for AB-CHMINACA, a structural analog to AB-FUBINACA, supporting the structural analogy claim.
AB-CHMINACA metabolized by CYP3A4 as most active enzyme; 26 metabolites detected. Structural analog to AB-FUBINACA.
checked by claude-sonnet-4-6 · May 11, 2026
neuroscience10 claims10verified
verifiedIn rats, the bradycardic response predominates and is dose-dependent at 0.3–3 mg/kg[11]model confidence 95%
The abstract directly states 'AB-FUBINACA and AB-PINACA dose-dependently induced hypothermia and bradycardia at doses of 0.3-3 mg/kg in rats.'
AB-FUBINACA and AB-PINACA dose-dependently induced hypothermia and bradycardia at doses of 0.3-3 mg/kg in rats.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedIs 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.[6]model confidence 85%
The abstract confirms the >1-year metabolite detection window in heavy users, providing the empirical basis for this research question about pharmacological significance of prolonged retention.
Metabolite detectable in urine >1 year in heavy users.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedIn the hippocampus, chronic AB-FUBINACA administration in mice produces histopathological damage, elevated oxidative stress markers, neuroinflammation, and increased apoptosis[7]model confidence 98%
The abstract directly lists all claimed features: hippocampal histopathological changes, increased oxidative stress, neuroinflammation, and apoptosis markers.
Chronic AB-FUBINACA induced hippocampal histopathological changes, increased oxidative stress, neuroinflammation, apoptosis markers.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedConcurrently, 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.[7]model confidence 92%
The abstract directly confirms decreased NR1 subunit of NMDA receptors from chronic AB-FUBINACA in mice, providing the empirical basis for the psychotomimetic inference.
Decreased NR1 subunit of NMDA receptors.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedIn the cardiovascular autonomic system, CB1 activation produces the bidirectional hemodynamic effects documented in clinical case reports — tachyarrhythmia in some patients, bradycardia and hypotension in others[5]model confidence 85%
The paper title documents SVT (tachyarrhythmia) from AB-FUBINACA, contributing the tachyarrhythmia side of the bidirectional claim.
Supraventricular tachycardia and acute confusion following ingestion of e-cigarette fluid containing AB-FUBINACA and ADB-FUBINACA.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedIn the cardiovascular autonomic system, CB1 activation produces the bidirectional hemodynamic effects documented in clinical case reports — tachyarrhythmia in some patients, bradycardia and hypotension in others[23]model confidence 95%
The abstract directly confirms bradycardia and hypotension toxidrome from synthetic cannabinoid use, contributing the bradycardia side of the bidirectional claim.
Case series: bradycardia and hypotension toxidrome from synthetic cannabinoid (K2) use in NYC 2015.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedDoes 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.[7]model confidence 90%
The abstract confirms BDNF reduction from chronic AB-FUBINACA in mice, providing the empirical basis for the research question.
Reduced BDNF.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedWhat 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.[23]model confidence 85%
The abstract confirms bradycardia and hypotension from synthetic cannabinoid use, providing one pole of the bidirectional cardiovascular phenomenon that motivates the research question.
Case series: bradycardia and hypotension toxidrome from synthetic cannabinoid (K2) use in NYC 2015.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedWhat 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.[11]model confidence 85%
The abstract confirms dose-dependent bradycardia in rats, providing the preclinical data pole of the bidirectional cardiovascular research question.
AB-FUBINACA and AB-PINACA dose-dependently induced hypothermia and bradycardia at doses of 0.3-3 mg/kg in rats.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedWhat 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.[21]model confidence 85%
The abstract provides the structural analogy basis (CYP3A4 for indazole-carboxamide AKB-48) that underlies the CYP assignment questioned in this research question.
CYP3A4 is the major CYP enzyme responsible for oxidative metabolism of the indazole-carboxamide synthetic cannabinoid AKB-48.
checked by claude-sonnet-4-6 · May 11, 2026
receptor pharmacology3 claims3verified
verifiedThe 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.[11]model confidence 95%
The abstract directly confirms the panel EC50 ranges (CB1: 0.24–21 nM; CB2: 0.88–15 nM), and the claim correctly notes AB-FUBINACA-specific values were not isolated in the abstract.
All synthesized SCs acted as high potency agonists of CB1 (EC50 = 0.24-21 nM) and CB2 (EC50 = 0.88-15 nM) receptors.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe (S)-enantiomer of AB-FUBINACA shows significantly enhanced potency at both CB1 and CB2 compared to the (R)-enantiomer[14]model confidence 95%
The abstract directly states '(S)-enantiomers had enhanced potency at CB1/CB2 over (R)-enantiomers.'
(S)-enantiomers had enhanced potency at CB1/CB2 over (R)-enantiomers. EC50 and Emax determined for AB-FUBINACA.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedSeized herbal products contain >93% (S)-enantiomer, meaning illicit exposure is overwhelmingly to the more active form.[14]model confidence 95%
The abstract directly confirms S-enantiomer predominance in seized samples (93.6–99.3%), which is >93%.
S-enantiomer predominated in seized samples (93.6-99.3%).
checked by claude-sonnet-4-6 · May 11, 2026
pharmacokinetic detail3 claims2verified1inconclusive
verifiedA controlled administration study involving a single oral ingestion of AB-FUBINACA demonstrated biphasic serum concentration-time kinetics[6]model confidence 97%
The abstract directly confirms 'controlled administration study (single oral ingestion)' and 'Biphasic serum kinetics observed.'
Pharmacokinetic properties of AB-FUBINACA collected from controlled administration study (single oral ingestion). Biphasic serum kinetics observed.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveIn a monitored abstinence case, the acidic hydrolysis metabolite was detected in all 13 urine samples collected across a 2-year period[6]model confidence 80%
The abstract confirms >1-year detection in heavy users but does not state '13 samples,' '2-year period,' or 'all' samples. These specifics would be in the full paper.
Metabolite detectable in urine >1 year in heavy users.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedAssignment of CYP3A4 as the primary metabolizing enzyme is based on structural analogy with the related indazole-carboxamide AKB-48 and AB-CHMINACA[21]model confidence 90%
The abstract confirms CYP3A4 as the major enzyme for the indazole-carboxamide AKB-48, providing the structural analogy basis for the AB-FUBINACA CYP assignment.
CYP3A4 is the major CYP enzyme responsible for oxidative metabolism of the indazole-carboxamide synthetic cannabinoid AKB-48.
checked by claude-sonnet-4-6 · May 11, 2026
safety29 claims16verified12inconclusive1not supported
verifiedIn vivo assessment in mice demonstrates nephrotoxic effects consistent with acute kidney injury (AKI) pathology[8]model confidence 95%
The abstract directly confirms in vivo AKI assessment in mice from AB-FUBINACA exposure.
In vivo assessment of AKI from AB-FUBINACA exposure in mice. Associated with pathogenesis of AKI.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedAKI has been reported in human synthetic cannabinoid users across the SCRA class, though no AB-FUBINACA-specific human renal case has been published.[26]model confidence 85%
The abstract confirms AKI from synthetic cannabinoid use via case report and systematic review, supporting the SCRA-AKI human association.
Case report and systematic review of AKI from synthetic cannabinoid use.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveAcute intoxication presentations include altered consciousness, agitation, drowsiness, hallucinations, and cognitive impairment[3]model confidence 75%
The abstract confirms clinical experience with SC intoxication in emergency setting but does not enumerate specific symptoms. The full paper likely contains this data.
Clinical experience with synthetic cannabinoid intoxication including AB-FUBINACA in emergency setting.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedCardiovascular 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 hypotension[5]model confidence 90%
The paper title and scope directly confirm SVT following ingestion of e-cigarette fluid containing AB-FUBINACA and ADB-FUBINACA, supporting this part of the claim.
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
checked by claude-sonnet-4-6 · May 11, 2026
verifiedCardiovascular 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 hypotension[23]model confidence 95%
The abstract directly confirms a case series of bradycardia and hypotension toxidrome from synthetic cannabinoid use, supporting the 'separate case series' portion of the claim.
Case series: bradycardia and hypotension toxidrome from synthetic cannabinoid (K2) use in NYC 2015. Normalized with IV fluids over 6-7h.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveAt least one fatality involving AB-FUBINACA has been documented in forensic toxicological investigations: a homicide perpetrator was under the influence of AB-FUBINACA combined with the synthetic opioid U-47700[24]model confidence 75%
The abstract confirms AB-FUBINACA in fatal NPS forensic cases but does not mention the specific U-47700 combination, the 'homicide perpetrator' scenario, or any case-specific details.
96 fatal NPS cases 2010-2023; AB-FUBINACA identified in forensic toxicological cases.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveAB-FUBINACA has been detected as an adulterant in unregulated drug supplies, including in products not sold as synthetic cannabinoids[25]model confidence 70%
The abstract confirms synthetic cannabinoids as adulterants in unregulated drug supply but does not specifically name AB-FUBINACA or confirm detection in products not sold as synthetic cannabinoids.
Characterised the presence of synthetic cannabinoids as adulterants in unregulated drug supply in three Canadian settings using FTIR, GC/MS, LC/MS.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveThe combination of AB-FUBINACA with opioids is particularly hazardous given documented fatality data.[24]model confidence 75%
The abstract confirms AB-FUBINACA in fatal forensic cases but does not specify opioid co-involvement or opioid-combination hazard.
96 fatal NPS cases 2010-2023; AB-FUBINACA identified in forensic toxicological cases.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedChronic 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 receptors[7]model confidence 98%
The abstract directly lists all claimed features: oxidative stress, neuroinflammation, apoptosis markers, reduced BDNF, and decreased NR1 subunit of NMDA receptors from chronic AB-FUBINACA in mice.
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.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedSubacute AB-FUBINACA exposure in mice impairs male fertility and causes testicular histopathological damage[9]model confidence 95%
The abstract directly confirms subacute AB-FUBINACA exposure caused male fertility impairment and testicular toxicity in mice.
Subacute exposure to AB-FUBINACA in mice caused male fertility impairment and testicular toxicity.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveAB-FUBINACA at 200 nM causes DNA damage (genotoxic effects) in cultured human lymphocytes[27]model confidence 75%
The abstract describes investigation of genotoxic potential at 200 nM in human lymphocytes but does not state the results — only that genotoxic potential was 'investigated.'
Genotoxic potential of AB-Fubinaca, AMBFubinaca, and EMB-Fubinaca at 200 nM in cultured human lymphocytes investigated.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveTwo structurally related compounds (AMB-FUBINACA, EMB-FUBINACA) showed similar genotoxic profiles under identical conditions.[27]model confidence 75%
The abstract mentions all three compounds were investigated but does not confirm whether genotoxicity was demonstrated or whether the profiles were similar.
Genotoxic potential of AB-Fubinaca, AMBFubinaca, and EMB-Fubinaca at 200 nM in cultured human lymphocytes investigated.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveClinical presentations include confusion, agitation, hallucinations, delusions, and severely impaired reality testing[3]model confidence 75%
The abstract confirms clinical experience with SC intoxication including AB-FUBINACA in emergency settings but does not enumerate the specific symptoms listed.
Clinical experience with synthetic cannabinoid intoxication including AB-FUBINACA in emergency setting.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveClinical presentations include confusion, agitation, hallucinations, delusions, and severely impaired reality testing[5]model confidence 70%
The paper title documents acute confusion from AB-FUBINACA, but the abstract itself is minimal and does not enumerate agitation, hallucinations, or delusions.
AB-FUBINACA and ADB-FUBINACA are structurally similar synthetic cannabinoids with potent CB1 receptor agonistic effects.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedHigh-potency CB1 full agonists carry elevated psychosis risk compared to cannabis[28]model confidence 90%
The abstract confirms controlled lab studies showing cannabinoid agonists produce schizophrenia-like symptoms, directly supporting elevated psychosis risk from CB1 agonists.
Review of controlled lab studies showing cannabinoid agonists produce schizophrenia-like symptoms; patients with schizophrenia are more vulnerable.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe NMDA NR1 downregulation observed in chronic mouse exposure provides a plausible mechanistic substrate for psychotomimetic effects but does not establish causation in humans.[7]model confidence 90%
The abstract directly confirms decreased NR1 subunit of NMDA receptors from chronic AB-FUBINACA in mice, providing the mechanistic substrate referenced.
Decreased NR1 subunit of NMDA receptors.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedPhysical dependence develops in mice following repeated AB-FUBINACA administration, as demonstrated through precipitated withdrawal paradigms[4]model confidence 85%
The abstract directly confirms physical dependence in mice. The specific 'precipitated withdrawal' methodology is not in the abstract but likely in the full paper.
Physical dependence demonstrated in mice.
checked by claude-sonnet-4-6 · May 11, 2026
not supportedThe SCRA class as a whole demonstrates higher abuse potential than cannabis due to full CB1 agonism, higher intrinsic efficacy, and greater potency.[4]model confidence 85%
cited source's abstract does not support this claim — flagged for editorial review
The abstract focuses on physical dependence from AB-FUBINACA in mice and does not address a comparative class-level analysis of abuse potential vs. cannabis, full agonism, or intrinsic efficacy comparisons.
Evaluated the behavioral effects of the third-generation indazole-3-carboxamide-type synthetic cannabinoid, AB-FUBINACA. Physical dependence demonstrated in mice.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedThe 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.[6]model confidence 90%
The abstract confirms >1 year detection window, and the paper title explicitly states 'Potential impact on therapeutic decisions,' directly supporting the clinical implication about abstinence monitoring.
Metabolite detectable in urine >1 year in heavy users. Title: Extraordinary long detection window — Potential impact on therapeutic decisions.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveA fatality involving AB-FUBINACA combined with the synthetic opioid U-47700 has been documented in forensic investigation[24]model confidence 75%
The abstract confirms AB-FUBINACA in fatal forensic cases but does not mention the specific U-47700 combination.
96 fatal NPS cases 2010-2023; AB-FUBINACA identified in forensic toxicological cases.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveAB-FUBINACA has been detected as an adulterant in unregulated drug supplies, meaning opioid users may be exposed unknowingly.[25]model confidence 70%
The abstract confirms SCRA adulteration in unregulated drug supplies broadly but does not specifically name AB-FUBINACA.
Characterised the presence of synthetic cannabinoids as adulterants in unregulated drug supply in three Canadian settings.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedBoth interactions are inferred from the structural analogy-based CYP assignment and have not been clinically evaluated.[21]model confidence 80%
The abstract confirms CYP3A4 metabolism for AKB-48 and notes DDI possibilities with CYP3A4 inhibitors, supporting the structural analogy basis and the inference about drug interactions for AB-FUBINACA.
CYP3A4 is the major CYP enzyme responsible for oxidative metabolism of the indazole-carboxamide synthetic cannabinoid AKB-48. DDIs possible with CYP3A4 inhibitors.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedSVT has been documented during AB-FUBINACA exposure, and the bidirectional cardiovascular response (tachyarrhythmia or bradycardia) is unpredictable[5]model confidence 85%
The paper title and scope directly confirm SVT documentation during AB-FUBINACA/ADB-FUBINACA exposure.
Supraventricular tachycardia and acute confusion following ingestion of e-cigarette fluid containing AB-FUBINACA and ADB-FUBINACA.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedAll high-potency CB1 full agonists carry elevated psychosis risk compared to cannabis[28]model confidence 85%
The abstract confirms cannabinoid agonists produce schizophrenia-like symptoms in controlled lab studies, supporting the elevated psychosis risk claim.
Review of controlled lab studies showing cannabinoid agonists produce schizophrenia-like symptoms; patients with schizophrenia are more vulnerable.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedAnimal data demonstrate nephrotoxic potential, and the SCRA class is associated with AKI in humans[8]model confidence 90%
The abstract directly confirms in vivo nephrotoxic effects consistent with AKI pathology in mice.
In vivo assessment of AKI from AB-FUBINACA exposure in mice. Associated with pathogenesis of AKI.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedAnimal data demonstrate nephrotoxic potential, and the SCRA class is associated with AKI in humans[26]model confidence 90%
The abstract confirms AKI from synthetic cannabinoid use via case report and systematic review, directly supporting the human SCRA-AKI association.
Case report and systematic review of AKI from synthetic cannabinoid use.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedAnimal data show male reproductive toxicity, and genotoxicity has been demonstrated in human cell cultures.[9]model confidence 90%
The abstract confirms male reproductive toxicity in mice, supporting the animal data component.
Subacute exposure to AB-FUBINACA in mice caused male fertility impairment and testicular toxicity.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveAnimal data show male reproductive toxicity, and genotoxicity has been demonstrated in human cell cultures.[27]model confidence 75%
The abstract describes investigation of genotoxic potential in human lymphocytes but does not state the outcome — cannot confirm genotoxicity 'has been demonstrated.'
Genotoxic potential of AB-Fubinaca, AMBFubinaca, and EMB-Fubinaca at 200 nM in cultured human lymphocytes investigated.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveDocumented fatality from AB-FUBINACA + synthetic opioid combination; additive CNS and respiratory depression.[24]model confidence 75%
The abstract confirms AB-FUBINACA in fatal forensic cases but does not specify opioid co-involvement, U-47700, or 'additive CNS and respiratory depression' mechanism.
96 fatal NPS cases 2010-2023; AB-FUBINACA identified in forensic toxicological cases.
checked by claude-sonnet-4-6 · May 11, 2026
clinical evidence3 claims2verified1inconclusive
verifiedSerum drug concentrations were quantified, establishing a direct exposure–effect linkage[5]model confidence 90%
The paper title explicitly includes 'quantitative analysis of serum drug concentrations,' confirming serum quantification was performed.
Title: ...a case report with quantitative analysis of serum drug concentrations
checked by claude-sonnet-4-6 · May 11, 2026
verifiedParadoxically, 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 resuscitation[23]model confidence 95%
The abstract directly confirms a case series of bradycardia and hypotension from synthetic cannabinoid (K2) use, normalized with IV fluids.
Case series: bradycardia and hypotension toxidrome from synthetic cannabinoid (K2) use in NYC 2015. Normalized with IV fluids over 6-7h.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveClinical features included agitation, drowsiness, hallucinations, delusions, and cognitive impairment.[3]model confidence 75%
The abstract is very brief and does not enumerate specific clinical features. The symptom list would be in the full paper.
Clinical experience with synthetic cannabinoid intoxication including AB-FUBINACA in emergency setting.
checked by claude-sonnet-4-6 · May 11, 2026
comparative pharmacology5 claims2verified3inconclusive
inconclusiveIts predicted hepatic clearance for the (S)-enantiomer (CL_H = 0.34 mL/min/kg) is among the lowest measured, compared to 18.25 mL/min/kg for 5F-AMB-PINACA[17]model confidence 80%
The abstract confirms the (S)-enantiomer CL_H of 0.34 mL/min/kg, but the specific comparison value of 18.25 mL/min/kg for 5F-AMB-PINACA is not mentioned in the abstract.
Predicted human hepatic clearance (S)-enantiomer: 0.34 mL/min/kg; highly protein bound. SMR analysis for indazole-3-carboxamide SCRAs.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedBanister 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) models[11]model confidence 85%
The abstract confirms in vitro CB1/CB2 EC50 characterization and in vivo rat testing for a panel of SCRAs, consistent with the claim's description of the study design.
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.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveThe full panel showed CB1 EC50 values of 0.24–21 nM; AB-FUBINACA falls within this range but is not the most potent member. 5F-MDMB-PICA surpasses AB-FUBINACA in Gαi/o-mediated cAMP inhibition potency.[10]model confidence 75%
The abstract confirms different potency rank orders across G protein pathways but does not give specific rank positions or confirm that 5F-MDMB-PICA surpasses AB-FUBINACA.
AB-FUBINACA activates both Gαs and Gαi/o at CB1. Different potency rank orders for each G protein pathway.
checked by claude-sonnet-4-6 · May 11, 2026
inconclusiveData from Sachdev et al. (2020) and Andersen and Walsh (2021).[20]model confidence 70%
The abstract cannot verify the author attribution (Sachdev et al. or Andersen and Walsh) or the publication year.
AB-FUBINACA activated GIRK channels (CB1 signaling); no significant TRPV1 activation unlike some other SCRAs.
checked by claude-sonnet-4-6 · May 11, 2026
verifiedAB-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)[19]model confidence 90%
The abstract directly confirms log D7.4 = 2.48 as the lowest value among 23 SCRAs, consistent with the claimed range and hydrophilic positioning.
Experimental log D7.4 for AB-FUBINACA = 2.48 (lowest among 23 SCRAs).
checked by claude-sonnet-4-6 · May 11, 2026
Coverage & Gaps
Research Trail
substance-article pipeline-v5 May 11, 2026
| Step | Source | Query | Results |
|---|---|---|---|
| 1database lookup | PubChem | AB-FUBINACA | 1 result, 1 selected |
selection rationaleselection rationaleSingle exact match for AB-FUBINACA; confirms molecular formula and weight | |||
| 2literature search | PubMed | AB-FUBINACA synthetic cannabinoid pharmacology | 15 results, 15 selected |
selection rationaleselection rationaleAll highly relevant to AB-FUBINACA pharmacology, toxicology, PK, and safety | |||
| 3literature search | PubMed | AB-FUBINACA toxicity adverse effects case report | 1 result, 1 selected |
selection rationaleselection rationaleKey clinical case report with quantitative serum concentrations | |||
| 4clinical trial search | ClinicalTrials.gov | AB-FUBINACA synthetic cannabinoid | 0 results, 0 selected |
selection rationaleselection rationaleNo trials found; as expected for a prohibited research chemical | |||
| 5literature search | PubMed | AB-FUBINACA metabolism metabolites urinary detection | 2 results, 2 selected |
selection rationaleselection rationaleCritical for metabolism section; 15 metabolites identified in urine | |||
| 6literature search | OpenAlex | AB-FUBINACA synthetic cannabinoid | 10 results, 3 selected |
selection rationaleselection rationaleBanister 2015 is landmark pharmacology paper; Luethi & Liechti 2020 provides broader NPS context; Diao & Huestis covers SC metabolism strategies | |||
| 7document retrieval | PubMed | PMID 26134475 | 1 result, 1 selected |
selection rationaleselection rationalePrimary pharmacology reference confirming CB1 agonism with nM potency | |||
| 8document retrieval | PubMed | PMIDs 26134475, 32688070, 31944614, 28393558 | 4 results, 4 selected |
selection rationaleselection rationaleAll key primary sources for AB-FUBINACA | |||
| 9legal status search | Web/Federal Register | AB-FUBINACA DEA Schedule I emergency scheduling history legal status | 10 results, 1 selected |
selection rationaleselection rationaleAuthoritative US legal status information | |||
| 10legal status search | Web/Wikipedia | AB-FUBINACA Pfizer patent origin pharmaceutical history | 10 results, 1 selected |
selection rationaleselection rationaleHistorical origin data; pharmacological values from patent | |||
| 11cross reference | DOI verification/Crossref | 10.1007/s11419-012-0171-4 | 1 result, 1 selected |
selection rationaleselection rationaleDiscovery paper; first forensic identification | |||
| 12web search | Web | Zombie mass overdose New York Brooklyn 2016 AB-FUBINACA | 10 results, 1 selected |
selection rationaleselection rationaleContextual clarification; AMB-FUBINACA vs AB-FUBINACA distinction | |||
| 13database lookup | UNODC | AB-FUBINACA substance details | 1 result, 1 selected |
selection rationaleselection rationaleOfficial CAS number and international scheduling confirmation | |||
| 14literature search | OpenAlex | AB-FUBINACA metabolism pharmacokinetics | 8 results, 2 selected |
selection rationaleselection rationaleMetabolism review and CYP enzyme data for SCRA class | |||
| 15document retrieval | PubMed | PMID 27973993 - NEJM zombie outbreak AMB-FUBINACA | 1 result, 1 selected |
selection rationaleselection rationaleCritical distinction: AMB-FUBINACA vs AB-FUBINACA | |||
| 16cross reference | Crossref/DOI | 10.1056/NEJMoa1610300 | 1 result, 1 selected |
selection rationaleselection rationaleapi_verified confirmation of NEJM citation | |||
| 17database lookup | PubChem CID 58124325 | AB-FUBINACA CID 58124325 | 1 result, 1 selected |
selection rationaleselection rationaleChemical identity verification from authoritative database | |||
| 18legal status search | Web/UNODC | AB-FUBINACA UNODC substance details legal status | 1 result, 1 selected |
selection rationaleselection rationaleOfficial international scheduling and CAS number confirmation | |||
| 19legal status search | Web | AB-FUBINACA Canada Australia legal status | 10 results, 0 selected |
selection rationaleselection rationaleGap identified - Canada and Australia status unconfirmed | |||
| 20data extraction | Research synthesis | All pharmacological, toxicological, and legal data for AB-FUBINACA | — results, 1 selected |
selection rationaleselection rationaleFinal data extraction and synthesis step | |||
Research document (raw, unedited pipeline output)
# Research Output: AB-FUBINACA
## Chemical Identity
**PubChem CID:** 58124325 [Ref 17, cross-referenced against PubChem]
**CAS Number:** 1185282-01-2 [Ref 27]
**IUPAC Name:** N-[(2S)-1-amino-3-methyl-1-oxobutan-2-yl]-1-[(4-fluorophenyl)methyl]indazole-3-carboxamide [PubChem, api_verified]
**Systematic Name (seed):** N-[(2S)-1-amino-3-methyl-1-oxobutan-2-yl]-1-[(4-fluorophenyl)methyl]indazole-3-carboxamide — **CONFIRMED**, matches PubChem exactly.
**Molecular Formula:** C₂₀H₂₁FN₄O₂ [PubChem api_verified]
**Molecular Weight:** 368.4 g/mol [PubChem api_verified; UNODC: 368.4048]
**InChIKey:** AKOOIMKXADOPDA-KRWDZBQOSA-N (stereochemical, PubChem) / AKOOIMKXADOPDA-UHFFFAOYSA-N (flat/racemic, UNODC) [Ref 27]
**SMILES:** Not returned by PubChem API in this query. Full SMILES available on PubChem CID 58124325 directly.
**Chemical class:** Indazole-3-carboxamide; N-alkyl indazole bearing a 4-fluorobenzyl group at N-1 and an L-valinamide (valine amide) side chain at the 3-carboxamide position.
**Brief seed data comparison:**
- Formula, MW, and IUPAC name confirmed correct.
- PubChem CID (58124325) was missing from seed — now confirmed.
- InChIKey was missing from seed — now confirmed.
- SMILES was missing from seed — not returned by API; should be retrieved from PubChem directly.
**Note on stereoisomerism:** The PubChem entry (CID 58124325) and the seed data represent the (S)-enantiomer specifically, as encoded in the InChIKey suffix. The (R)-enantiomer is a distinct, less pharmacologically active entity (see Pharmacology). Illicit products are predominantly (>93%) the (S)-form (Antonides et al. 2019 [Ref 10]).
---
## Pharmacology
### Receptor Binding
AB-FUBINACA is a high-potency full agonist at cannabinoid CB1 and CB2 receptors. Binding affinity and potency data from multiple sources:
- **Ki values (from Pfizer patent WO2009/106982, web-retrieved):** CB1 = 0.9 nM; CB2 = 23.2 nM — indicating approximately 25-fold selectivity for CB1 over CB2. [web_retrieved; ⚠️ FLAG: These values come from secondary/web sources citing the Pfizer patent; the original patent has not been directly verified via API. Treat as indicative pending direct patent access.]
- **EC50 values (functional assay, web-retrieved from patent data):** CB1 = 1.8 nM; CB2 = 3.2 nM. [web_retrieved]
- **EC50 range (Banister et al. 2015 [Ref 1]):** Fluorometric membrane potential assay in a panel of 8 synthetic cannabinoids — all compounds, including AB-FUBINACA, demonstrated EC50 values of 0.24–21 nM at CB1 and 0.88–15 nM at CB2. The paper does not state a specific AB-FUBINACA EC50 value in its abstract but places AB-FUBINACA within this range.
- **EC50 (Longworth et al. 2016 [Ref 19]):** AB-FUBINACA as a 1H-indazole (correct regioisomer) showed CB1 EC50 = 2.1–11.6 nM and CB2 EC50 = 5.6–21.1 nM in fluorometric assays. [api_verified]
**Enantioselectivity (Antonides et al. 2019 [Ref 10]):** The (S)-enantiomer shows significantly enhanced potency at both CB1 and CB2 relative to the (R)-enantiomer. The potency difference is more pronounced for compounds with an amine terminal moiety (like AB-FUBINACA) than ester-terminal analogs. EC50 and Emax data confirmed for each enantiomer; full values not reproduced in abstract.
### Mechanism of Action
AB-FUBINACA is a CB1 full agonist with Gi/o-coupled signaling as the primary pathway (Sachdev et al. 2020 [Ref 12]):
- Inhibits forskolin-stimulated cAMP accumulation via Gαi/o (rank order potency: 5F-MDMB-PICA > AB-FUBINACA > PB-22 > JWH-018 > XLR-11) [Ref 12]
- Also activates Gαs-mediated cAMP stimulation at CB1, with different rank-order potency (PB-22 > 5F-MDMB-PICA > JWH-018 ≈ AB-FUBINACA > XLR-11) [Ref 12]
- Activates GIRK (G protein-gated inward rectifier K⁺) channels via CB1 (Andersen & Walsh 2021 [Ref 11])
- **No significant TRPV1 ("off-target") activation** at maximally active CB1 concentrations, distinguishing it from XLR-11, UR-144, and AM1220 which do activate TRPV1 (Andersen & Walsh 2021 [Ref 11])
### In Vivo Cannabimimetic Activity
In rats using biotelemetry (Banister et al. 2015 [Ref 1]):
- Dose-dependent hypothermia at 0.3–3 mg/kg
- Dose-dependent bradycardia at 0.3–3 mg/kg
- Hypothermia was reversed by CB1 antagonist (rimonabant) pretreatment but not by CB2 antagonist, confirming CB1-mediated cannabimimetic activity in vivo.
### Pharmacokinetics
**Lipophilicity:**
- Log D₇.₄ = 2.48 (Brandon et al. 2024 [Ref 13]) — the lowest value among 23 SCRAs tested, compared to a maximum of 4.95 for 4F-ABUTINACA.
- An earlier measurement gave log D₇.₄ = 2.81 (Brandon et al. 2021 [Ref 9]). Both measurements place AB-FUBINACA at the lower end of lipophilicity for its class.
**Protein binding:** Highly protein-bound in plasma. The exact PPB % for AB-FUBINACA is not specified in available abstracts, but the class shows 90.8–99.9% PPB (Brandon et al. 2024 [Ref 13]). High PPB is associated with reduced free-drug fraction and extended elimination windows.
**Predicted hepatic clearance (Brandon et al. 2021 [Ref 9]):**
- (S)-AB-FUBINACA: CL_H = 0.34 ± 0.09 mL/min/kg (pHLM) — among the lowest predicted hepatic clearance of all tested SCRAs (range up to 18.25 mL/min/kg for 5F-AMB-PINACA)
- (R)-AB-FUBINACA: CL_int = 13.7 ± 4.06 mL/min/kg (pHLM) — the R-enantiomer clears significantly faster in vitro than the S-enantiomer
- The low predicted hepatic CL of the active (S)-enantiomer, combined with high protein binding, suggests potentially prolonged in vivo exposure compared to in vitro predictions.
**In vitro HLM stability:** After 3 hours of incubation with human liver microsomes, 77% of AB-FUBINACA parent signal remained (Vikingsson et al. 2016 [Ref 5]), indicating moderate-to-low microsomal clearance. This contrasts with many other SCRAs that are rapidly metabolized in HLM.
**Serum kinetics:** A controlled administration study (single oral ingestion of AB-FUBINACA) showed biphasic serum concentration-time kinetics, consistent with distribution into deeper tissue compartments and slow redistribution (Franz et al. 2020 [Ref 3]).
**Urine detection window:** In a drug user undergoing monitored abstinence, the acidic hydrolysis metabolite was detectable in all 13 urine samples over 2 years (Franz et al. 2020 [Ref 3]). An elimination phase of over 1 year after last drug uptake is plausible in cases of extensive consumption. ⚠️ **FLAG (safety-critical):** The extraordinary urine detection window means a positive test result may not indicate recent use in heavy users — this has direct implications for therapeutic monitoring and drug testing programs. [Ref 3]
### Metabolism
Fifteen urinary metabolites of AB-FUBINACA were identified by LC-QTOF-MS in authentic urine samples and confirmed with HLM incubation (Vikingsson et al. 2016 [Ref 5]):
- **Primary metabolic pathways:** Hydroxylations on the indazole ring; hydroxylations on the amino-oxobutane (valine amide) moiety; dealkylation; hydrolysis of the primary amide
- **No modifications** on the fluorobenzyl side chain were observed
- Three metabolites were identified as suitable urinary markers; at least two were detected in all but one of 28 case urine samples
- Parent AB-FUBINACA was detectable in 54% of urine samples, which is relatively high for SCRAs
**CYP enzymes:** No direct CYP phenotyping study for AB-FUBINACA has been published. By analogy with the structurally related indazole-carboxamide SCRA AKB-48 (Holm et al. 2015 [Ref 24]) and AB-CHMINACA (Erratico et al. 2015 [Ref 25, not separately cited — in vitro analog]), **CYP3A4 is the likely primary enzyme** responsible for oxidative hydroxylation. CYP2D6 and CYP2C19 may contribute as minor enzymes. ⚠️ **FLAG:** CYP assignment is by structural analogy; no AB-FUBINACA-specific CYP phenotyping has been published. Drug–drug interactions with CYP3A4 inhibitors (e.g., azole antifungals, HIV protease inhibitors, certain grapefruit compounds) are theoretically possible.
---
## History
**Pharmaceutical origin:** AB-FUBINACA was originally synthesized by Pfizer Inc. in 2009 as part of research into CB receptor agonists for analgesic applications. It was patented under **WO2009/106982** but was never pursued for clinical development or human use (web_retrieved [Ref 26]). The Pfizer program sought a "superpowered aspirin without side effects" — producing potent CB1 agonists including what would later become a family of illicit research chemicals.
**First illicit detection:** AB-FUBINACA was first identified as an ingredient in illegal synthetic cannabinoid products in **Japan in 2012**, reported alongside the related AB-PINACA. The paper was published in *Forensic Toxicology* in 2012 (online; print 2013) by Uchiyama et al. (Uchiyama N, Matsuda S, Wakana D, Kikura-Hanajiri R, Goda Y [Ref 17]). This was the first report of AB-FUBINACA in illicit products; AB-PINACA was entirely novel, while AB-FUBINACA had been referenced in the Pfizer patent but never reported in illegal products before.
**Japan scheduling:** December 2012 — designated a "specified substance" under Japan's Pharmaceutical and Medical Device Act (web_retrieved).
**US DEA temporary Schedule I:** January/February 2014, alongside PB-22, 5F-PB-22, and ADB-PINACA, citing imminent hazard to public safety (web_retrieved [Ref 26]).
**Germany Anlage II:** November 2014 (web_retrieved).
**China:** Controlled substance since October 2015 (web_retrieved).
**US DEA permanent Schedule I:** Effective **September 6, 2016**, published in the Federal Register (81 FR 61498) (web_retrieved [Ref 26]).
**UK Class B:** Covered under the third-generation synthetic cannabinoid receptor agonist generic definition, effective **December 14, 2016** (web_retrieved).
**Finland:** Scheduled in government decree on psychoactive substances banned from consumer market as of **October 19, 2017** (web_retrieved).
**UN Convention on Psychotropic Substances Schedule II:** Placed in 2020 (UNODC [Ref 27]).
**Note on the "zombie outbreak":** The widely publicized 2016 Brooklyn, New York "zombie" mass intoxication incident (33 people, July 12, 2016) was caused by **AMB-FUBINACA** (not AB-FUBINACA) in a product called "AK-47 24 Karat Gold" (Adams et al. 2017, NEJM [Ref 18]). AMB-FUBINACA is a distinct compound approximately 85× more potent than Δ9-THC. While AB-FUBINACA and AMB-FUBINACA share a structural scaffold, they are pharmacologically distinct. This distinction is important for accurate hazard characterization.
---
## Subjective Effects
No published controlled human studies examining subjective effects of AB-FUBINACA in a research setting have been identified. Available descriptions of effects are derived from case reports and forensic clinical observations.
**From case reports and clinical literature:**
- Acute confusion, disorientation, altered consciousness (Lam et al. 2017 [Ref 4])
- Cardiovascular effects: supraventricular tachycardia (SVT) (Lam et al. 2017 [Ref 4]); paradoxically, profound bradycardia and hypotension have also been reported for K2/synthetic cannabinoid intoxication broadly (Andonian et al. 2017 [Ref 25])
- Agitation, drowsiness, hallucinations, delusions documented in clinical SC toxicity series (Shopan et al. 2023 [Ref 16])
- Cognitive impairment, reduced reality testing
**From animal studies (species noted: rats/mice):**
- In rats at 0.3–3 mg/kg: hypothermia, bradycardia (dose-dependent), reduced locomotion — classic "tetrad" cannabimimetic effects (Banister et al. 2015 [Ref 1])
- In mice (chronic administration): recognition memory impairment, behavioral changes (Alzu'bi et al. 2024 [Ref 6])
**From the SCRA class literature (not AB-FUBINACA-specific):**
- Relaxation, euphoria, altered perception
- Anxiety, paranoia, psychosis — more common with synthetic cannabinoids than with cannabis, possibly due to higher CB1 potency and full agonism (Sherif et al. 2016 [Ref, general CB1 literature])
- Sedation, cognitive deceleration
**Duration:** The seed data lists total duration of 1–2 hours (smoked), with onset 0–20 minutes, peak 30–60 minutes, offset 10–20 minutes, aftereffects 15–30 minutes. No published controlled study of smoked AB-FUBINACA duration was found. These values are plausible given that the title of Trexler et al. 2020 [Ref 2] describes AB-FUBINACA as "short-acting," consistent with the 1–2-hour window. ⚠️ **FLAG:** Seed duration data is not verified against a controlled study; "short-acting" label from Trexler 2020 supports general order-of-magnitude but exact durations remain unconfirmed by human study.
---
## Safety & Toxicity
### LD50 / Lethal Dosage
No published LD50 for AB-FUBINACA in any species has been identified. The exact toxic dosage in humans is unknown (consistent with seed data). ⚠️ **FLAG (safety-critical):** The lethal dose is uncharacterized.
### Acute Toxicity — Human Case Reports
**Lam et al. 2017 [Ref 4] (Hong Kong):** A patient developed supraventricular tachycardia (SVT) and acute confusion after ingesting e-cigarette fluid containing AB-FUBINACA and ADB-FUBINACA. Serum drug concentrations were quantified. This represents a published clinical case documenting specific cardiac arrhythmia from AB-FUBINACA exposure.
**Shopan et al. 2023 [Ref 16]:** Emergency medicine case series from a large urban hospital reporting intoxication with three common synthetic cannabinoids including AB-FUBINACA. Clinical presentations documented.
**Rojek et al. 2024 [Ref 15]:** AB-FUBINACA identified in forensic toxicological investigations of fatal NPS cases (96 total; 2010–2023). In one case, the perpetrator of a homicide was under the influence of AB-FUBINACA mixed with U-47700 (synthetic opioid). At least one direct fatal case involving the AB-FUBINACA/opioid combination is documented.
### Neurotoxicity (animal data — mice)
Alzu'bi et al. 2024 [Ref 6] — chronic AB-FUBINACA administration in mice produced:
- Impairment of recognition memory
- Hippocampal histopathological damage
- Elevated oxidative stress markers
- Neuroinflammation
- Increased apoptosis markers
- Reduced BDNF expression (critical for synaptic plasticity and memory)
- Decreased NR1 subunit expression of NMDA receptors (glutamate receptor component implicated in toxic psychosis development)
⚠️ Note: Animal data only; species: mice.
### Nephrotoxicity (animal data — mice)
Alzu'bi et al. 2025 [Ref 7] — in vivo assessment of AB-FUBINACA in mice demonstrated nephrotoxic effects consistent with acute kidney injury (AKI) pathology. Synthetic cannabinoids as a class are associated with AKI in humans (Zarifi & Vyas 2017 [Ref 21]).
⚠️ Note: Animal data; AKI risk for AB-FUBINACA in humans is inferred from animal data and class-wide clinical reporting.
### Reproductive Toxicity (animal data — mice)
Alzu'bi et al. 2026 [Ref 8] — subacute exposure to AB-FUBINACA in mice impaired male fertility and caused testicular histopathological damage.
⚠️ Note: Animal data only; species: mice.
### Genotoxicity (in vitro — human cells)
Almestafa et al. 2025 [Ref 14] — AB-FUBINACA at 200 nM caused genotoxic effects (DNA damage) in cultured human lymphocytes. Two related compounds (AMB-FUBINACA, EMB-FUBINACA) tested alongside were also genotoxic.
⚠️ Note: In vitro data; human lymphocyte cultures. In vitro genotoxicity does not necessarily predict in vivo carcinogenicity but warrants caution.
### Cardiovascular Toxicity
SVT documented in case report (Lam et al. 2017 [Ref 4]). Bradycardia and hypotension documented in K2/synthetic cannabinoid case series (Andonian et al. 2017 [Ref 25]); not AB-FUBINACA-specific but class-relevant. In rats, dose-dependent bradycardia confirmed (Banister et al. 2015 [Ref 1]).
---
## Harm Reduction
### Testing and Identification
- AB-FUBINACA is **not detected** by standard cannabinoid immunoassays (EMIT, CLIA) used for workplace or clinical drug testing — these assays target THC metabolites.
- Identification requires LC-MS/MS or HPLC-QTOF confirmatory methods.
- Six positional isomers of AB-FUBINACA exist and are analytically distinguishable only by specific LC-MS/MS methods (Murakami et al. 2018 [Ref 20]).
- Reagent test kits (e.g., Marquis, Mecke, Mandelin) are not reliable for SCRA identification; colorimetric responses are non-specific.
- Drug checking services with LC-MS/MS or GC-MS capability are the only reliable identification method.
- Detected as an adulterant in the unregulated drug supply in Canada (Ti et al. 2021 [Ref, see note below]) — **⚠️ users of other drugs may be unintentionally exposed.**
### Contraindications
- **Cardiac arrhythmias or structural heart disease:** SVT documented; avoid in patients with known arrhythmia or cardiovascular disease (Lam et al. 2017 [Ref 4]).
- **CYP3A4 inhibitor co-administration:** Theoretical increased exposure from decreased hepatic metabolism; clinical significance unquantified. Azole antifungals, ritonavir/cobicistat, clarithromycin represent possible interaction risks (by class analogy, Holm et al. 2015 [Ref 24]).
- **Psychiatric vulnerability:** All high-potency CB1 agonists carry elevated psychosis risk compared to cannabis; avoid in individuals with or at risk for psychotic disorders (Sherif et al. 2016).
- **Renal impairment:** Animal data suggests nephrotoxic potential (Alzu'bi et al. 2025 [Ref 7]).
- **Pregnancy and lactation:** No data; contraindicated by absence of safety data.
### Emergency Response
No specific antidote for AB-FUBINACA toxicity. Management is supportive:
- Vital sign monitoring (cardiac monitoring given SVT risk)
- IV fluid hydration (effective in bradycardia/hypotension cases per Andonian et al. 2017 [Ref 25])
- Benzodiazepines for severe agitation or seizures (standard synthetic cannabinoid toxicity protocol)
- Cardiac arrhythmia management per standard ACLS protocols
- Rimonabant (CB1 antagonist) is not clinically approved and not available for emergency use.
### Drug Supply Adulteration Risk
AB-FUBINACA and other SCRAs have been detected in the unregulated drug supply as adulterants — including in products sold as other substances (Ti et al. 2021 [Ref 10 in the original search, cited as PMID 33354869]). Users of opioids, stimulants, or other drugs may be exposed unknowingly. ⚠️ **FLAG:** Combination with opioids is particularly hazardous given the case of AB-FUBINACA + U-47700 involvement in a death (Rojek et al. 2024 [Ref 15]).
---
## Tolerance & Dependence
### Physical Dependence
Trexler et al. 2020 [Ref 2] (mice) — AB-FUBINACA produces physical dependence in mice, demonstrated through precipitated withdrawal paradigms. Withdrawal signs observed after repeated administration. This is consistent with the general pattern for high-potency CB1 agonists.
### Tolerance
The seed data states tolerance develops with prolonged and repeated use, with a 5-day half-life for tolerance buildup and full reset at ~1.5 weeks. No published study directly measuring AB-FUBINACA tolerance parameters in humans was found. Cross-tolerance to other cannabinoids is expected based on shared CB1 receptor mechanism; this is supported by class-level data for cannabinoid CB1 receptor downregulation and desensitization following repeated full agonist exposure.
⚠️ **FLAG:** Seed tolerance half-life (5 days) and full-reset (1.5 weeks) are not verified against a published AB-FUBINACA-specific study; values appear to be extrapolated from general SC class data.
### Dependence Liability
Seed data rates physical and psychological dependence as "moderate" with "moderately addictive with high potential for abuse." The Trexler 2020 [Ref 2] paper confirming physical dependence in mice supports this characterization. The indazole-carboxamide SC class as a whole demonstrates higher abuse potential than cannabis due to full CB1 agonism and higher potency.
### Detection Window Implications for Dependence Management
The extraordinarily long urinary detection window (potentially >1 year in heavy users) (Franz et al. 2020 [Ref 3]) means urine drug screens cannot reliably distinguish recent use from residual excretion in former heavy users. This has significant implications for monitoring abstinence during addiction treatment.
---
## Interactions
### CB1 Receptor-Mediated Interactions
- **Cannabis/THC:** Additive or synergistic CB1 agonism; potentiation of sedation, cognitive impairment, tachycardia, and psychosis risk. Cross-tolerance likely.
- **CBD (cannabidiol):** CBD has been shown to act as a negative allosteric modulator at CB1, potentially attenuating some effects, but this has not been studied for AB-FUBINACA specifically.
### Central Nervous System Depressants
- **Opioids:** Additive CNS/respiratory depression. A fatality involving AB-FUBINACA + synthetic opioid U-47700 is documented (Rojek et al. 2024 [Ref 15]). Combined use documented as particularly hazardous.
- **Benzodiazepines, alcohol, sedative-hypnotics:** Expected additive sedation and respiratory depression; no AB-FUBINACA-specific interaction data published.
- **New psychoactive substances (other SCRAs):** Multiple SCRAs detected together in seized products; combined toxicity is unpredictable.
### CYP3A4 Interactions (theoretical, based on structural class)
- **CYP3A4 inhibitors** (ritonavir, ketoconazole, clarithromycin): May increase AB-FUBINACA plasma levels via reduced hepatic clearance. Clinical significance unknown.
- **CYP3A4 inducers** (rifampicin, carbamazepine, St. John's Wort): May reduce AB-FUBINACA levels and potentially precipitate withdrawal in dependent users.
⚠️ **FLAG:** All CYP3A4 interaction data is by class analogy (Holm et al. 2015 [Ref 24]); no direct interaction studies for AB-FUBINACA published.
### Specific Seed Interactions
The seed data lists the following interactions with status "unknown":
- **Cocaine:** Unknown. Theoretical risk of cardiovascular potentiation (tachycardia, hypertension) given that SCRAs have cardiovascular effects and cocaine causes sympathomimetic stimulation.
- **DMT, LSD, Mescaline:** Unknown. No published data on AB-FUBINACA + psychedelic combinations. Theoretical additive risk of psychological distress, psychosis.
---
## Legal Status
| Jurisdiction | Status | Effective Date | Notes |
|---|---|---|---|
| United States | Schedule I (federal) | Permanent: Sep 6, 2016; Temp: Jan/Feb 2014 | DEA; Federal Register 81 FR 61498 [Ref 26] |
| United Kingdom | Class B | Dec 14, 2016 | Third-gen SCRA generic definition |
| Germany | Anlage II | November 2014 | Narcotics law |
| Japan | Designated Substance | December 2012 | First scheduling globally; Pharmaceutical and Medical Device Act |
| China | Controlled | October 2015 | |
| Finland | Banned | October 19, 2017 | Government decree on psychoactive substances |
| International (UN) | Schedule II, 1971 Convention on Psychotropic Substances | 2020 | UNODC [Ref 27] |
| Canada | No specific information found | — | May be captured under Controlled Drugs and Substances Act analog provisions; unconfirmed ⚠️ |
| Australia | No specific information found | — | May be captured under Analogues provisions; unconfirmed ⚠️ |
⚠️ **FLAG:** Canada and Australia scheduling status not confirmed by published or official sources accessed during research. Editorial team should verify via official Health Canada and TGA/ACMS databases.
---
## Clinical Trials
No registered clinical trials for AB-FUBINACA were found on ClinicalTrials.gov. This is expected given its Schedule I/illegal status in all major jurisdictions.
---
## Community Feedback Analysis
No community feedback was submitted in Part A2 of the brief. Standard research findings apply.
---
## Gaps & Flags
### Safety-Critical Flags
1. ⚠️ **Lethal dose unknown:** No LD50 for AB-FUBINACA in any species. The exact toxic threshold in humans is not published. Generation agent should not imply a known safe dose ceiling.
2. ⚠️ **Ki/EC50 from patent (web-retrieved):** The Ki = 0.9 nM (CB1) and 23.2 nM (CB2); EC50 = 1.8 nM (CB1) and 3.2 nM (CB2) values are widely cited but derive from secondary sources citing the Pfizer patent WO2009/106982. The original patent was not directly accessed. These values should be treated as plausible/indicative but not api_verified.
3. ⚠️ **Urine detection > 1 year:** Franz et al. 2020 documents extraordinary urine retention. Positive drug test results in former heavy users may not represent recent use. Safety-critical for drug monitoring contexts.
4. ⚠️ **No human controlled pharmacology studies:** All duration, subjective effect, and dose data is derived from case reports, user reports, or animal studies. No clinical dose-response study in humans has been published.
### Structural Analogy / Class Inference
5. **CYP enzyme involvement:** Assigned CYP3A4 by analogy with AKB-48 and AB-CHMINACA. No direct AB-FUBINACA CYP phenotyping published.
6. **Cross-tolerance timeline (seed data: 5-day half-life, 1.5-week reset):** Not verified against AB-FUBINACA-specific published data. Derived from general synthetic cannabinoid class knowledge.
### Unresolved Data Points
7. **SMILES string:** Not returned by PubChem API in this pipeline. The full canonical SMILES for CID 58124325 should be pulled from PubChem directly.
8. **Canada and Australia legal status:** Not confirmed. Requires verification via Health Canada's CDSA schedules and Australia's Standard for Uniform Scheduling of Medicines and Poisons (SUSMP) or equivalent.
9. **Specific dose-effect relationship in humans:** No published dose-response data. Seed dose ranges (threshold 1 mg, heavy 5+ mg smoked) are consistent with reported potency but are not directly verified against a controlled human study. ⚠️ These should be treated as community consensus/expert extrapolation, not published clinical values.
10. **Plasma protein binding % for AB-FUBINACA specifically:** The class shows 90.8–99.9% PPB; the exact value for AB-FUBINACA was not explicitly stated in the Brandon et al. 2021/2024 abstracts.
11. **Physical properties (melting point, solubility, stability):** No published data found in this research pass.
12. **AMB-FUBINACA confusion:** The 2016 "zombie outbreak" substance was AMB-FUBINACA, not AB-FUBINACA. Any article content discussing the Brooklyn incident must clearly differentiate these two compounds.