generation run 2026-05-11
96 min completedmodel pipeline-v5plan not recordedrun/946da842…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
- sparse_evidence
Reproduce
- inputs
- 29 source keys (listed under Sources)
- plan
- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
- streams
- none — agent transcripts are persisted from 2026-09 onward
19 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed | quinolin-8-yl indole carboxylate synthetic cannabinoid forensic case report | 2 | 2 | Fatality data and novel metabolite in forensic context |
| 2 | PubMed | PB-22 5F-PB-22 carboxylesterase ester hydrolysis human liver microsome | 1 | 1 | Direct metabolic pathway data for 5F-PB-22 - CES1 identified as primary metabolizing enzyme |
| 3 | OpenAlex | 5F-PB-22 synthetic cannabinoid pharmacology receptor | 10 | 3 | High-citation papers providing pharmacology, toxicology, and epidemiology context |
| 4 | PubChem | 5F-PB-22 | 1 | 1 | Primary chemical identity data; confirms formula/MW absent from seed data |
| 5 | ClinicalTrials.gov · absence | 5F-PB-22 synthetic cannabinoid | 0 | — | No relevant trials found - expected for an unscheduled research chemical |
| 6 | OpenAlex | 5F-PB-22 PB-22 QUPIC metabolism biotransformation | 10 | 3 | Metabolism and pharmacology data directly relevant to 5F-PB-22 |
| 7 | PubMed | 5F-PB-22 pharmacology receptor binding cannabinoid CB1 | 2 | 2 | Primary receptor binding and functional activity data for 5F-PB-22 |
| 8 | PubMed | 5F-PB-22 synthetic cannabinoid | 15 | 6 | Selected for pharmacology, toxicology, forensic identification, and metabolism relevance |
| 9 | PubMed | PMID 28455676 - Watanabe 2017 fungal model metabolism | 1 | 1 | Detailed metabolic pathway data for 5F-PB-22 |
| 10 | PubMed | PMID 27632803 - DEA final rule Schedule I placement 2016 | 1 | 1 | Definitive US legal status documentation |
| 11 | Web (Google Search) | 5F-PB-22 5F-QUPIC controlled substance Japan Canada Australia UK legal status | 10 | 2 | Legal status data for major jurisdictions |
| 12 | PubMed | PMID 24518903 - Wohlfarth 2014 5F-PB-22 metabolism | 1 | 1 | Primary metabolism data for 5F-PB-22 |
| 13 | Web (Google Search) | 5F-PB-22 legal status scheduling DEA Schedule I UK Misuse of Drugs Act | 10 | 3 | Legal scheduling history for US, UK, China - key jurisdictions |
| 14 | Web (Google Search) | Banister 2015 5F-PB-22 CB1 CB2 EC50 FLIPR ACS Chemical Neuroscience | 10 | 1 | Specific receptor potency values for CB1 and CB2 |
| 15 | PubChem REST API | CID 72710774 properties JSON | 1 | 1 | Physical property data for lipophilicity assessment |
| 16 | PubMed | PMID 25586398, 41423817, 30552295, 27074934, 30811628 - toxicology and dependence papers | 5 | 5 | Toxicology, dependence, withdrawal, and severe outcomes - needed for safety section |
| 17 | Web (Google Search) | UK Psychoactive Substances Act 2016 synthetic cannabinoids 5F-PB-22 | 10 | 2 | UK legal history for 5F-PB-22 |
| 18 | Web (Google Search) | 5F-PB-22 metabolism hepatocyte metabolites urine 3-carboxyindole Wohlfarth 2014 | 10 | 2 | Key metabolism data for urinary detection and metabolite identification |
| 19 | Crossref DOI verification | DOI 10.1007/s11419-017-0395-4 | 1 | 1 | Confirming this key metabolism paper |
93 claims by section — every cited sentence, checked against its source
safety26 · 22 ok
Three decedents experienced abrupt sudden death; one had a rapidly deteriorating hospital course.supported
Three decedents experienced abrupt sudden death. bku048
Claim in safety — inconclusiveinconclusiveworking →
Cause of death was certified as combined alcohol and synthetic cannabinoid toxicity.supported
Cause of death: combined alcohol and synthetic cannabinoids. j.jflm.2018.07.012
Blood concentrations in impaired but surviving drivers (0.10-5.0 ng/mL) overlap substantially with those found in fatal cases (0.37-1.5 ng/mL)supported
Blood concentrations 0.10-5.0 ng/mL in DUI specimens. j.forsciint.2019.110106
Blood concentrations in impaired but surviving drivers (0.10-5.0 ng/mL) overlap substantially with those found in fatal cases (0.37-1.5 ng/mL)partially supported
Blood concentrations 1.1-1.5 ng/mL. bku048
A systematic review of approximately 4,000 synthetic cannabinoid presentations reports the following class-level adverse event profile:supported
Systematic review of ~4000 SC cases including ~26 deaths. Major complications: cardiovascular events (MI, stroke), AKI, generalized tonic-clonic seizures, psychosis, hyperemesis. 15563650.2015.1110590
Claim in safety — inconclusiveinconclusiveworking →
CB1R-mediated enhancement of neuronal differentiation at biologically relevant concentrations (<=1 uM) in vitro raises concern for prenatal and early developmental exposuresupported
Both 5F-PB22 and THJ-2201 enhanced differentiation ratios and neurite length ~2-fold in NG108-15 cells via CB1R activation (blocked by SR141718). SCs increased mitochondrial TMRE accumulation at <=1 uM. ijms21176277
Full CB1 agonism without co-present CBD substantially increases psychosis-inducing risk compared to cannabissupported
SCRAs are full CB1 agonists more potent than THC; higher psychosis-inducing potential than cannabis due to full agonism and absence of CBD. 0269881114565142
Class-level data identify first-episode psychosis, paranoia, and acute agitation as recognized psychiatric complications of synthetic cannabinoid usesupported
Major complications: cardiovascular events (MI, stroke), AKI, generalized tonic-clonic seizures, psychosis, hyperemesis. Most common: tachycardia 37-77%, agitation 16-41% 15563650.2015.1110590
Regular synthetic cannabinoid users meeting cannabis dependence criteria have been described, and synthetic cannabinoid use has been reported to alleviate cannabis withdrawal symptoms, confirming cross-dependencesupported
Case series of SC users meeting cannabis dependence criteria; SC use alleviated cannabis withdrawal; potential for dependence documented. j.1521-0391.2012.00240.x
Claim in safety — inconclusiveinconclusiveworking →
Treatment approaches include benzodiazepines for symptom relief, with quetiapine (an atypical antipsychotic) showing utility in some cases.supported
Withdrawal symptom relief reported with benzodiazepines and quetiapine. s11920-016-0694-1
Claim in safety — inconclusiveinconclusiveworking →
Pharmacokinetic: CES enzymes catalyze transesterification of 5F-PB-22 with ethanol, producing 5F-PB-22 ethyl ester - a novel bioactive metabolite detected in postmortem blood at 0.4 ug/L. In vitro data confirm this CES-mediated reaction.supported
5F-PB22 and ethanol co-consumption producing 5F-PB22 ethyl ester transesterification product detected in postmortem blood at 0.4 ug/L. bkaa030
Pharmacokinetic: CES enzymes catalyze transesterification of 5F-PB-22 with ethanol, producing 5F-PB-22 ethyl ester - a novel bioactive metabolite detected in postmortem blood at 0.4 ug/L. In vitro data confirm this CES-mediated reaction.partially supported
CES enzyme mediates transesterification to produce SC ethyl esters with reduced CB receptor activity. s11419-019-00491-0
Fatality data: The UK fatality involved blood alcohol of 311 mg/100 mL; the German fatality involved ethanol co-detection.supported
Post-mortem blood samples detected both SCs plus 311 mg/100mL alcohol. j.jflm.2018.07.012
Fatality data: The UK fatality involved blood alcohol of 311 mg/100 mL; the German fatality involved ethanol co-detection.supported
Relevant ethanol co-consumption in one case. j.forsciint.2017.10.042
No published data are specific to 5F-PB-22, but the polypharmacy risk is underscored by fatality case series in which multiple CNS-active substances were co-detected.supported
Male decedents aged 25-41 with known drug use history. Relevant ethanol co-consumption in one case. j.forsciint.2017.10.042
Cardiovascular disease (absolute): Full CB1 agonism produces tachycardia and may precipitate myocardial infarction or arrhythmia. Fatalities with cardiac involvement have been reported for synthetic cannabinoids as a class.supported
Major complications: cardiovascular events (MI, stroke), AKI, generalized tonic-clonic seizures, psychosis, hyperemesis. Most common: tachycardia 37-77% 15563650.2015.1110590
Psychotic disorders or family history of psychosis (absolute): Full CB1 agonism without CBD substantially elevates psychosis risk.supported
SCRAs are full CB1 agonists more potent than THC; higher psychosis-inducing potential than cannabis due to full agonism and absence of CBD. 0269881114565142
Concurrent ethanol use (absolute): Documented fatalities and a unique pharmacokinetic interaction (transesterification) establish this as a high-risk combination.supported
5F-PB22 and ethanol co-consumption producing 5F-PB22 ethyl ester transesterification product detected in postmortem blood at 0.4 ug/L. bkaa030
Concurrent ethanol use (absolute): Documented fatalities and a unique pharmacokinetic interaction (transesterification) establish this as a high-risk combination.supported
Cause of death: combined alcohol and synthetic cannabinoids. j.jflm.2018.07.012
Pregnancy (absolute): In vitro evidence of CB1-mediated enhancement of neuronal differentiation at biologically relevant concentrations raises developmental concern.supported
Both 5F-PB22 and THJ-2201 enhanced differentiation ratios and neurite length ~2-fold in NG108-15 cells via CB1R activation (blocked by SR141718). ijms21176277
Renal impairment (relative): Acute kidney injury is reported in class-level synthetic cannabinoid data.supported
Major complications: cardiovascular events (MI, stroke), AKI, generalized tonic-clonic seizures, psychosis, hyperemesis. 15563650.2015.1110590
Seizure disorders (relative): Generalized tonic-clonic seizures are reported in synthetic cannabinoid presentations.supported
Major complications: cardiovascular events (MI, stroke), AKI, generalized tonic-clonic seizures, psychosis, hyperemesis. 15563650.2015.1110590
pharmacology23 · 14 ok
Parent compound is detectable in urine only at trace levels (5.1-470 pg/mL) using sensitive LC-MS/MS methods.supported
Urinary 5F-PB-22: 5.1-470 pg/mL s11419-017-0395-4
Claim in pharmacology — inconclusiveinconclusiveworking →
At CB1, the compound displays a binding affinity of Ki = 0.13 nM in native rat cerebral cortex membrane preparations (competition with [3H]CP55940)supported
5F-PB-22 showed the lowest Ki of binding to CB1 receptors (0.11 and 0.13 nM) j.neuropharm.2015.11.017
Functional potency, measured by GTPgammaS accumulation, yields an EC50 of 3.7 nM with an Emax of 203% relative to basal - confirming full agonist status with supramaximal efficacysupported
potency (EC50, 2.9 and 3.7 nM, respectively) and efficacy (Emax, 217% and 203%, respectively) as CB1 agonists higher than JWH-018 j.neuropharm.2015.11.017
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
As a potent full CB1 agonist, 5F-PB-22 may also engage non-cannabinoid targets shared across the synthetic cannabinoid class, including orphan receptors GPR55 and GPR18, peroxisome proliferator-activated receptors (PPARs), and TRPV1 channelssupported
Review of SC health risks: activation of CB1R, CB2R, GPR55, GPR18, PPARs, TRPV1. s40001-023-01443-6
Claim in pharmacology — inconclusiveinconclusiveworking →
The compound's high lipophilicity (logP 5.80-6.74) predicts extensive tissue distribution, high protein binding, and efficient CNS penetrationsupported
5F-PB-22 has logP 5.80-6.74 (Class 2 SC). j.forsciint.2019.110106
Blood concentrations in impaired drivers range from 0.10 to 5.0 ng/mLsupported
Blood concentrations 0.10-5.0 ng/mL in DUI specimens. j.forsciint.2019.110106
The primary metabolic pathway is ester hydrolysis catalyzed by carboxylesterase 1 (CES1), the major human hepatic and pulmonary enzyme for this reaction, as determined in human liver microsomes and recombinant enzyme preparationssupported
CES1 identified as the major human hepatic and pulmonary enzyme responsible for ester hydrolysis of PB-22, 5F-PB-22, and BB-22. dta.1731
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
5F-PB-22 3-carboxyindole - the major urinary marker resulting from ester hydrolysis (urinary concentrations 8.25-880 ng/mL)supported
5F-PB-22 3-carboxyindole: 8.25-880 ng/mL s11419-017-0395-4
PB-22 N-5-hydroxypentyl - hydroxylation of the alkyl chainsupported
B-22 N-5-hydroxypentyl s11419-017-0395-4
PB-22 N-pentanoic acid - omega-oxidation product (urinary concentrations 12.0-2090 pg/mL)supported
PB-22 N-pentanoic acid: 12.0-2090 pg/mL s11419-017-0395-4
Claim in pharmacology — inconclusiveinconclusiveworking →
Oxidative defluorination products (including the corresponding carboxylic acid)supported
5F-PB-22 metabolized by dihydroxylation, oxidative defluorination, ester hydrolysis, and glucosidation via C. elegans fungal model. s12248-017-0078-4
This has been demonstrated in human liver microsomes in vitro and confirmed in postmortem blood at 0.4 ug/Lpartially supported
In vitro metabolism of PB-22, NPB-22, 5F-PB-22, and 5F-NPB-22 with ethanol using human liver microsomes. CES enzyme mediates transesterification to produce SC ethyl esters with reduced CB receptor activity. s11419-019-00491-0
This has been demonstrated in human liver microsomes in vitro and confirmed in postmortem blood at 0.4 ug/Lsupported
5F-PB22 and ethanol co-consumption producing 5F-PB22 ethyl ester transesterification product detected in postmortem blood at 0.4 ug/L. bkaa030
Hydroxypentyl metabolites of structurally related synthetic cannabinoids retain full efficacy at human CB1 and CB2, albeit with reduced affinity and potencysupported
Hydroxypentyl metabolites of synthetic cannabinoids retain full efficacy at hCB1 and hCB2 with reduced affinity. jpet.118.254425
summary11 · 8 ok
It functions as a high-potency full agonist at the cannabinoid CB1 receptor (Ki = 0.13 nM), approximately 26-fold more potent than JWH-018 at the same targetsupported
BB-22 and 5F-PB-22 showed the lowest Ki of binding to CB1 receptors (0.11 and 0.13 nM), i.e., 30 and 26 times lower respectively than that of JWH-018 (3.38 nM) j.neuropharm.2015.11.017
Duration of action is approximately 90 minutes via inhalation and 2-3 hours orally, consistent with rapid ester hydrolysis by carboxylesterase 1.partially supported
CES1 identified as the major human hepatic and pulmonary enzyme responsible for ester hydrolysis of PB-22, 5F-PB-22, and BB-22. dta.1731
5F-PB-22 emerged on recreational drug markets in 2012-2013 as a component of herbal Spice blends, representing the first synthetic cannabinoid class to combine an ester bond linkage with a quinoline substructurepartially supported
PB-22 and 5F-PB-22 are the first marketed synthetic cannabinoids with an ester bond linkage and a quinoline substructure. s00216-014-7668-0
The compound was permanently placed in United States Schedule I in 2016 and United Nations Schedule II in 2018partially supported
Final rule permanently placing quinolin-8-yl 1-(5-fluoropentyl)-1H-indole-3-carboxylate (5F-PB-22) into Schedule I of the Controlled Substances Act. pmid:27632803
Claim in summary — inconclusiveinconclusiveworking →
Functional potency is high at both CB1 (EC50 = 2.8-3.7 nM, Emax = 203%) and CB2 (EC50 = 11 nM)partially supported
potency (EC50, 2.9 and 3.7 nM, respectively) and efficacy (Emax, 217% and 203%, respectively) as CB1 agonists higher than JWH-018 j.neuropharm.2015.11.017
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
Multiple fatalities have been attributed to 5F-PB-22, with postmortem blood concentrations (0.37-1.5 ng/mL) overlapping those observed in impaired but surviving individuals (0.10-5.0 ng/mL)partially supported
Quantitative detection in four postmortem cases (July-October 2013). Blood concentrations 1.1-1.5 ng/mL. bku048
Multiple fatalities have been attributed to 5F-PB-22, with postmortem blood concentrations (0.37-1.5 ng/mL) overlapping those observed in impaired but surviving individuals (0.10-5.0 ng/mL)supported
Blood concentrations 0.10-5.0 ng/mL in DUI specimens. j.forsciint.2019.110106
Dependence liability is moderate at the class level, with cross-tolerance to other cannabinoidssupported
Case series of SC users meeting cannabis dependence criteria; SC use alleviated cannabis withdrawal; potential for dependence documented. j.1521-0391.2012.00240.x
pharmacokinetic-detail7 · 5 ok
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
CES1 catalyzes the rate-limiting ester hydrolysis step, yielding the 3-carboxyindole metabolite as the predominant urinary speciessupported
5F-PB-22 3-carboxyindole: 8.25-880 ng/mL; PB-22 N-pentanoic acid: 12.0-2090 pg/mL s11419-017-0395-4
Secondary oxidative pathways - hydroxylation, omega-oxidation, oxidative defluorination - produce metabolites that retain pharmacological activity at CB1 and CB2, potentially extending the effective pharmacological duration beyond that of the parent compound.supported
Hydroxypentyl metabolites of synthetic cannabinoids retain full efficacy at hCB1 and hCB2 with reduced affinity. Phase I metabolites contribute to in vivo pharmacology and toxicology. jpet.118.254425
The logP-dependent urinary excretion model places 5F-PB-22 above the threshold (logP > 5) at which parent compound is no longer reliably detectable in urinesupported
Not detectable in urine due to high lipophilicity (logP boundary between detectable/non-detectable in urine is logP 4-5). j.forsciint.2019.110106
Metabolite-based assays targeting 5F-PB-22 3-carboxyindole are required for urinary confirmation.supported
Validated UHPLC-QTOF-MS method for 18 SC metabolites in urine (including 5F-PB-22 3-carboxyindole). dta.2464
CES1-mediated transesterification converts the parent compound to 5F-PB-22 ethyl ester in the presence of ethanolsupported
CES enzyme mediates transesterification to produce SC ethyl esters with reduced CB receptor activity. s11419-019-00491-0
chemistry5 · 5 ok
This architecture places 5F-PB-22 among Class 2 synthetic cannabinoids in the toxicokinetic classification of Kakehashi et al.supported
5F-PB-22 has logP 5.80-6.74 (Class 2 SC). j.forsciint.2019.110106
This bond is susceptible to hydrolysis by carboxylesterases, a property that governs the compound's metabolic fate.supported
CES1 identified as the major human hepatic and pulmonary enzyme responsible for ester hydrolysis of PB-22, 5F-PB-22, and BB-22. dta.1731
Ten positional isomers of 5F-PB-22 exist, incorporating quinolinyl and isoquinolinyl substitution variants, not all of which are scheduled under current legislation.supported
Analytical differentiation of 5F-PB-22 from 10 positional isomers using GC-EI-MS and LC-MS/MS. s11419-016-0334-9
Crystal structure has been determined by single-crystal and powder X-ray diffractionsupported
crystal structure determined by single-crystal and powder X-ray diffraction. fchem.2020.00693
The compound exhibits high lipophilicity, with measured logP values of 5.80-6.74 and a computed XLogP of 5.0partially supported
5F-PB-22 has logP 5.80-6.74 (Class 2 SC). j.forsciint.2019.110106
comparative-pharmacology5 · 4 ok
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Fluorine substitution improves CB1 potency approximately 1.8-fold and CB2 potency approximately 3.4-fold, while shifting the selectivity profile toward CB2partially supported
fluorinated analogues generally showing increased CB1 receptor potency (~2-5 times) acschemneuro.5b00107
This pattern - enhanced potency and reduced CB1 selectivity with terminal fluorination - is consistent across multiple synthetic cannabinoid series (JWH-018 to AM-2201; UR-144 to XLR-11; APICA to STS-135).supported
Effects of bioisosteric fluorine in synthetic cannabinoid designer drugs JWH-018, AM-2201, UR-144, XLR-11, PB-22, 5F-PB-22, APICA, and STS-135. acschemneuro.5b00107
Under identical assay conditions (native rat CB1, [3H]CP55940 competition), 5F-PB-22 (Ki = 0.13 nM) is approximately 26-fold more potent than JWH-018 (Ki = 3.38 nM).supported
5F-PB-22 showed the lowest Ki of binding to CB1 receptors (0.11 and 0.13 nM), i.e., 30 and 26 times lower respectively than that of JWH-018 (3.38 nM) j.neuropharm.2015.11.017
THC functions as a partial agonist at CB1, with self-limiting activation even at receptor saturation. 5F-PB-22 is a full agonist (Emax = 203% of basal), with no intrinsic ceiling on receptor activationsupported
efficacy (Emax, 217% and 203%, respectively) as CB1 agonists higher than JWH-018 j.neuropharm.2015.11.017
neuroscience5 · 3 ok
Claim in neuroscience — inconclusiveinconclusiveworking →
In NG108-15 neuroblastoma/glioma cells, 5F-PB-22 at biologically relevant concentrations (<=1 uM) approximately doubled neuronal differentiation and neurite outgrowth via a CB1R-dependent mechanism (blocked by the CB1 antagonist SR141716)supported
Both 5F-PB22 and THJ-2201 enhanced differentiation ratios and neurite length ~2-fold in NG108-15 cells via CB1R activation (blocked by SR141718). ijms21176277
The compound also increased mitochondrial membrane potential (assessed by TMRE fluorescence accumulation)supported
SCs increased mitochondrial TMRE accumulation at <=1 uM. ijms21176277
The absence of CBD - which modulates ECS tone through negative allosteric modulation of CB1 and agonism at 5-HT1A - removes an additional regulatory mechanism present in cannabis.supported
higher psychosis-inducing potential than cannabis due to full agonism and absence of CBD. 0269881114565142
Claim in neuroscience — inconclusiveinconclusiveworking →
clinical-evidence3 · 3 ok
Published case series document acute intoxication and fatality, but no systematic study of dose-response relationships, subjective pharmacology, or therapeutic efficacy has been conductedsupported
Quantitative detection in four postmortem cases (July-October 2013). Blood concentrations 1.1-1.5 ng/mL. bku048
Published case series document acute intoxication and fatality, but no systematic study of dose-response relationships, subjective pharmacology, or therapeutic efficacy has been conductedsupported
Three death cases in Germany with 5F-PB-22 blood concentration of 0.37 ng/mL. j.forsciint.2017.10.042
Published case series document acute intoxication and fatality, but no systematic study of dose-response relationships, subjective pharmacology, or therapeutic efficacy has been conductedsupported
Fatality following ingestion of 5F-PB-22 and 5F-AKB-48. j.jflm.2018.07.012
history3 · 3 ok
Wohlfarth et al. identified PB-22 and 5F-PB-22 as the first marketed substances with an ester bond linkage among synthetic cannabinoids - a structurally novel class that expanded the chemical diversity of available synthetic cannabinoid receptor agonists.supported
PB-22 and 5F-PB-22 are the first marketed synthetic cannabinoids with an ester bond linkage and a quinoline substructure. s00216-014-7668-0
In the United States, 5F-PB-22 was detected forensically in postmortem cases during July-October 2013, found alongside AKB-48 in the herbal product marketed as Psyclonepartially supported
Quantitative detection in four postmortem cases (July-October 2013). bku048
This temporary order was extended in February 2016 and made permanent in September 2016 via DEA final rulepartially supported
Final rule permanently placing quinolin-8-yl 1-(5-fluoropentyl)-1H-indole-3-carboxylate (5F-PB-22) into Schedule I of the Controlled Substances Act. pmid:27632803
receptor-pharmacology3 · 1 ok
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
A discrepancy exists between the peer-reviewed Ki value (0.13 nM; native rat CB1, [3H]CP55940 competition) and a value reported in non-peer-reviewed web sources (0.055 nM)supported
5F-PB-22 showed the lowest Ki of binding to CB1 receptors (0.11 and 0.13 nM) j.neuropharm.2015.11.017
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
legal-status2 · 2 ok
Not all isomers are explicitly scheduled under current legislation, and analytical differentiation requires LC-MS/MS with collision-induced dissociation spectrum analysis.supported
Analytical differentiation of 5F-PB-22 from 10 positional isomers using GC-EI-MS and LC-MS/MS. LC separation achieved for all isomers; collision-induced dissociation enables mass spectrometric differentiation. s11419-016-0334-9
Not all isomers are explicitly scheduled under current legislation, and analytical differentiation requires LC-MS/MS with collision-induced dissociation spectrum analysis.supported
Fluoropentyl positional isomers of 5F-PB-22 separated and identified using GC-MS, GC-IR, and 1H/13C NMR. j.forsciint.2017.08.009