Evidence map›Paper›PMID 25866875›Full record

ReviewMolecular endocrinology (Baltimore, Md.)2015

Minireview: From the bench, toward the clinic: therapeutic opportunities for cannabinoid receptor modulation.

Robert P Picone, Debra A Kendall

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular endocrinology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Endocannabinoid-Binding Receptors as Drug Targets.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Indole compounds withMedChemComm · 2019
    Article
  11. Article
  12. A patent update on cannabinoid receptor 1 antagonists (2015-2018).Expert opinion on therapeutic patents · 2019
    Review
  13. Article
  14. CBScientific reports · 2017
    Article
  15. β-Cell Inactivation ofDiabetes · 2017
    Article
  16. Review
  17. Article
  18. Assessing Allosteric Modulation of CBMethods in enzymology · 2017
    Article
  19. Review
  20. 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

2 authors at 2 institutions in 1 country.

Robert P PiconeClinical Development (R.P.P.), Medical and Regulatory Affairs, Novo Nordisk Inc, Plainsboro, New Jersey 08536; and Department of Pharmaceutical Sciences (D.A.K.), University of Connecticut, Storrs, Connecticut 06269-3092.
Debra A KendallClinical Development (R.P.P.), Medical and Regulatory Affairs, Novo Nordisk Inc, Plainsboro, New Jersey 08536; and Department of Pharmaceutical Sciences (D.A.K.), University of Connecticut, Storrs, Connecticut 06269-3092.
Novo Nordisk (United States) · USUniversity of Connecticut · US

Funding

Determinants of the Cannabinoid Receptor Life CycleR01DA020763 · NIDA · UNIVERSITY OF CONNECTICUT STORRS · PI KENDALL, DEBRA A · 2007 to 2011
$1.5M
NIDA NIH HHS DA020763NIDA NIH HHS R01 DA020763
6 · The paper itself

Abstract

The effects of cannabinoids have been known for centuries and over the past several decades two G protein-coupled receptors, CB1 and CB2, that are responsible for their activity have been identified. Endogenous lipid-derived cannabinergic agents have been found, biosynthetic and catabolic machinery has been characterized, and synthetic agents have been designed to modulate these receptors. Selective agents including agonists, antagonists, inverse agonists, and novel allosteric modulators targeting either CB1 or CB2 have been developed to inhibit or augment their basal tone. As a result, the role these receptors play in human physiology and their potential therapeutic applications in disease states are being elucidated. The CB1 receptor, although ubiquitous, is densely expressed in the brain, and CB2 is largely found on cells of immune origin. This minireview highlights the role of CB1 in excitotoxic assaults in the brain and its potential to limit addiction liability. In addition, it will examine the relationship between receptor activity and stimulation of insulin release from pancreatic β-cells, insulin resistance, and feeding behavior leading toward obesity. The roles of CB2 in the neuropathology of amyotrophic lateral sclerosis and in the central manifestations of chronic HIV infection potentially converge at inflammatory cell activation, thereby providing an opportunity for intervention. Last, CB2 modulation is discussed in the context of an experimental model of postmenopausal osteoporosis. Achieving exquisite receptor selectivity and elucidating the mechanisms underlying receptor inhibition and activation will be essential for the development of the next generation of cannabinergic-based therapeutic agents.

Indexed as

Translational Research, BiomedicalCannabinoid Receptor ModulatorsDiseaseHumansNeuroprotectionReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2Cannabinoid Receptor ModulatorsReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2

Identifiers

PMID25866875
PMCPMC4447638
OpenAlexW2049960720

What OpenQuestion holds

Textmetadata
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.