Evidence map›Paper›PMID 19639277›Full record

ReviewHandbook of experimental pharmacology2009

Introduction to adenosine receptors as therapeutic targets.

Kenneth A Jacobson

Open access · greenAbstract readReview
In one paragraph

Review in Handbook of experimental pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
7.7field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 117 citations in OpenAlex.

  1. Article
  2. Guideline on Stress Echocardiography - 2026.Arquivos brasileiros de cardiologia · 2026
    Article
  3. Article
  4. Selected Medicines That Can Cause Cardiac Arrest with Asystole.Current issues in molecular biology · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Quantitation of the APharmaceuticals (Basel, Switzerland) · 2022
    Article
  12. Vasodilators and myocardial blood flow by CZT cameras: Make us see further.Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2022
    Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. CD73 (Cluster of Differentiation 73) and the Differences Between Mice and Humans.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Review
  18. Review
  19. Article
  20. Review
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

1 author at 1 institution in 1 country.

Kenneth A JacobsonMolecular Recognition Section, Laboratory of Biooorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0810, USA. kajacobs@helix.nih.gov
National Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Development Of Drugs Acting At Adenosine ReceptorsZIADK031117 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JACOBSON, KENNETH ALAN · 2009 to 2025
$10.4M
Drugs that Act at Adenosine ReceptorsZ01DK031117 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI JACOBSON, KENNETH ALAN · 1991 to 2008
$854k
Intramural NIH HHS Z01 DK031117Intramural NIH HHS Z99 DA999999Intramural NIH HHS Z99 DK999999Intramural NIH HHS Z99 OD999999
6 · The paper itself

Abstract

Adenosine acts as a cytoprotective modulator in response to stress to an organ or tissue. Although short-lived in the circulation, it can activate four subtypes of G protein-coupled adenosine receptors (ARs): A(1), A(2A), A(2B), and A(3). The alkylxanthines caffeine and theophylline are the prototypical antagonists of ARs, and their stimulant actions occur primarily through this mechanism. For each of the four AR subtypes, selective agonists and antagonists have been introduced and used to develop new therapeutic drug concepts. ARs are notable among the GPCR family in the number and variety of agonist therapeutic candidates that have been proposed. The selective and potent synthetic AR agonists, which are typically much longer lasting in the body than adenosine, have potential therapeutic applications based on their anti-inflammatory (A(2A) and A(3)), cardioprotective (preconditioning by A(1) and A(3) and postconditioning by A(2B)), cerebroprotective (A(1) and A(3)), and antinociceptive (A(1)) properties. Potent and selective AR antagonists display therapeutic potential as kidney protective (A(1)), antifibrotic (A(2A)), neuroprotective (A(2A)), and antiglaucoma (A(3)) agents. AR agonists for cardiac imaging and positron-emitting AR antagonists are in development for diagnostic applications. Allosteric modulators of A(1) and A(3) ARs have been described. In addition to the use of selective agonists/antagonists as pharmacological tools, mouse strains in which an AR has been genetically deleted have aided in developing novel drug concepts based on the modulation of ARs.

Indexed as

AdenosineAllosteric RegulationAnimalsClinical Trials as TopicGene DeletionHumansPurinergic P1 Receptor AgonistsPurinergic P1 Receptor AntagonistsRadioligand AssayReceptors, Purinergic P1AdenosinePurinergic P1 Receptor AgonistsPurinergic P1 Receptor AntagonistsReceptors, Purinergic P1

Identifiers

PMID19639277
PMCPMC3415694
OpenAlexW1601888527

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.