Evidence map›Paper›PMID 36652070›Full record

ArticleForensic toxicology2023

Characterisation of AMB-FUBINACA metabolism and CB

Hunter D J Webb, David B Finlay, Shuli Chen, Andrea J Vernall, Eric Sparkes, Samuel D Banister, Rhonda J Rosengren, Michelle Glass

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Forensic toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 33% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Enzymatic hydrolysis of ∆Forensic toxicology · 2025
    Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Hunter D J WebbDepartment of Pharmacology and Toxicology, University of Otago, Dunedin, 9016, New Zealand.
David B FinlayDepartment of Pharmacology and Toxicology, University of Otago, Dunedin, 9016, New Zealand.
Shuli ChenDepartment of Pharmacology and Toxicology, University of Otago, Dunedin, 9016, New Zealand.
Andrea J VernallDepartment of Chemistry, University of Otago, Dunedin, 9016, New Zealand.
Eric SparkesLambert Initiative for Cannabinoid Therapeutics, Brain and Mind Centre, The University of Sydney, Sydney, NSW, 2050, Australia.
Samuel D BanisterLambert Initiative for Cannabinoid Therapeutics, Brain and Mind Centre, The University of Sydney, Sydney, NSW, 2050, Australia.
Rhonda J RosengrenDepartment of Pharmacology and Toxicology, University of Otago, Dunedin, 9016, New Zealand.
Michelle GlassDepartment of Pharmacology and Toxicology, University of Otago, Dunedin, 9016, New Zealand. michelle.glass@otago.ac.nz.ORCID 0000-0002-5997-6898
University of Otago · NZThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAMB-FUBINACA is a synthetic cannabinoid receptor agonist (SCRA) which is primarily metabolised by hepatic enzymes producing AMB-FUBINACA carboxylic acid. The metabolising enzymes associated with this biotransformation remain unknown. This study aimed to determine if AMB-FUBINACA metabolism could be reduced in the presence of carboxylesterase (CES) inhibitors and recreational drugs commonly consumed with it. The affinity and activity of the AMB-FUBINACA acid metabolite at the cannabinoid type-1 receptor (CB

methodsThe effect of CES1 and CES2 inhibitors, and delta-9-tetrahydrocannabinol (Δ

resultsAMB-FUBINACA was rapidly metabolised by HLM in the presence and absence of NADPH. Additionally, CES1 and CES2 inhibitors both significantly reduced AMB-FUBINACA metabolism. Furthermore, digitonin (100 µM) significantly inhibited CES1-mediated metabolism of AMB-FUBINACA by ~ 56%, while the effects elicited by Δ

conclusionsCES1A1 was identified as the main hepatic enzyme responsible for the metabolism of AMB-FUBINACA to its less potent carboxylic acid metabolite. This biotransformation was significantly inhibited by digitonin. Since other xenobiotics may also inhibit similar SCRA metabolic pathways, understanding these interactions may elucidate why some users experience high levels of harm following SCRA use.

Indexed as

CannabinoidsCannabinoid Receptor AgonistsDigitoninDronabinolHEK293 CellsHumansIndazolesValineCannabinoid Receptor AgonistsCannabinoidsDigitoninDronabinolIndazolesmethyl 2-(1-(4-fluorobenzyl)-1H-indazole-3-carboxamido)-3-methylbutanoateValineAMB-FUBINACACannabinoid receptorCarboxylesterase 1Carboxylic acid metaboliteHuman liver microsomesSynthetic cannabinoid receptor agonist

Identifiers

PMID36652070
PMCPMC9849163
OpenAlexW4307511667

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.