Evidence map›Paper›PMID 24084047›Full record

ReviewLife sciences2014

Distinct pharmacology and metabolism of K2 synthetic cannabinoids compared to Δ(9)-THC: mechanism underlying greater toxicity?

William E Fantegrossi, Jeffery H Moran, Anna Radominska-Pandya, Paul L Prather

Abstract readComparative StudyReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Life sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed, 2 pooled it
22.0field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 2 syntheses or guidelines pooled it, 256 citations in OpenAlex.

  1. Pooled it
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  13. Observational
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  19. Article
  20. Effects of Δ9-Tetrahydrocannibinol (THC) on Obesity at Different Stages of Life: A Literature Review.International journal of environmental research and public health · 2022
    Review

21 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

William E FantegrossiDepartment of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Jeffery H MoranDepartment of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA; Arkansas Department of Public Health, Public Health Laboratory, Little Rock, AR 72205, USA.
Anna Radominska-PandyaDepartment of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.
Paul L PratherDepartment of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. Electronic address: pratherpaull@uams.edu.
University of Arkansas for Medical Sciences · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR029884 · NCRR · UNIV OF ARKANSAS FOR MED SCIS · PI LOWERY, CURTIS L · 2009 to 2011
$11.4M
NCRR NIH HHS 1 UL 1RR029884NCRR NIH HHS UL1 RR029884PHS HHS 200-2007-21729
6 · The paper itself

Abstract

K2 or Spice products are emerging drugs of abuse that contain synthetic cannabinoids (SCBs). Although assumed by many teens and first time drug users to be a "safe" and "legal" alternative to marijuana, many recent reports indicate that SCBs present in K2 produce toxicity not associated with the primary psychoactive component of marijuana, ∆(9)-tetrahydrocannabinol (Δ(9)-THC). This mini-review will summarize recent evidence that use of K2 products poses greater health risks relative to marijuana, and suggest that distinct pharmacological properties and metabolism of SCBs relative to Δ(9)-THC may contribute to the observed toxicity. Studies reviewed will indicate that in contrast to partial agonist properties of Δ(9)-THC typically observed in vitro, SCBs in K2 products act as full cannabinoid receptor type 1 (CB1R) and type 2 (CB2R) agonists in both cellular assays and animal studies. Furthermore, unlike Δ(9)-THC metabolism, several SCB metabolites retain high affinity for, and exhibit a range of intrinsic activities at, CB1 and CB2Rs. Finally, several reports indicate that although quasi-legal SCBs initially evaded detection and legal consequences, these presumed "advantages" have been limited by new legislation and development of product and human testing capabilities. Collectively, evidence reported in this mini-review suggests that K2 products are neither safe nor legal alternatives to marijuana. Instead, enhanced toxicity of K2 products relative to marijuana, perhaps resulting from the combined actions of a complex mixture of different SCBs present and their active metabolites that retain high affinity for CB1 and CB2Rs, highlights the inherent danger that may accompany use of these substances.

Indexed as

AnimalsCannabinoid Receptor AgonistsCannabinoidsDesigner DrugsDronabinolHumansIllicit DrugsReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2Cannabinoid Receptor AgonistsCannabinoidsDesigner DrugsDronabinolIllicit DrugsReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2∆(9)-TetrahydrocannabinolCB1 receptorsCB2 receptorsDrug abuseDrug metabolismK2/SpiceSynthetic cannabis

Identifiers

PMID24084047
PMCPMC3945037
OpenAlexW2041841378

What OpenQuestion holds

Textmetadata
LicenceTDM
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.