Evidence map›Paper›PMID 19897019›Full record

ArticleBrain research bulletin2010

The effects of nepafenac and amfenac on retinal angiogenesis.

Susan E Yanni, Monika L Clark, Rong Yang, David P Bingaman, John S Penn

Open access · greenAbstract read
In one paragraph

Article in Brain research bulletin, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. PGFEMBO molecular medicine · 2023
    Article
  7. Lipid Signaling in Ocular Neovascularization.International journal of molecular sciences · 2020
    Review
  8. Article
  9. Article
  10. A Critical Analysis of the AvailableJournal of ophthalmology · 2017
    Review
  11. The role of cytochrome P450 epoxygenases in retinal angiogenesis.Investigative ophthalmology & visual science · 2014
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

5 authors at 3 institutions in 1 country.

Susan E YanniDepartment of Cell and Developmental Biology, Vanderbilt University School of Medicine, 8000 Medical Center East, Nashville, TN 37232-8808, USA. susan.e.yanni@vanderbilt.edu
Monika L Clark
Rong Yang
David P Bingaman
John S Penn
Vanderbilt University Medical Center · USAlcon (United States) · USVanderbilt University · US

Funding

RETINOPATHY OF PREMATURITY--UNDERSTAND ITS PATHOGENESISR01EY007533 · NEI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PENN, JOHN S. · 1993 to 2018
$7.0M
ANIMAL MODEL FOR RETINOPATHY OF PREMATURITYR29EY007533 · NEI · UNIVERSITY OF ARKANSAS MED SCIS LTL ROCK · PI PENN, JOHN S. · 1988 to 1992
–
NEI NIH HHS EY01826NEI NIH HHS EY07533NEI NIH HHS R01 EY007533
6 · The paper itself

Abstract

purposeNepafenac is a potent NSAID that rapidly penetrates the eye following topical ocular administration. In the eye, nepafenac is converted to amfenac, which has unique time-dependent inhibitory properties for COX-1 and COX-2. The purpose of the present study was to investigate the capacity of amfenac to inhibit discrete aspects of the angiogenic cascade in vitro, and to test the efficacy of amfenac and nepafenac in vivo, using the rat OIR model.

methodsMüller cells were treated with amfenac, celecoxib (COX-2), or SC-560 (COX-1), and hypoxia-induced VEGF and PGE(2) assessed. Endothelial cells were treated with amfenac, celecoxib, or SC-560, and VEGF-induced proliferation and tube formation assessed. Rat pups were subjected to OIR, received intravitreal injections of amfenac, celecoxib, or SC-560, and neovascularization (NV), prostanoid production, and VEGF assessed. Other OIR-exposed pups were treated with topical nepafenac, ketorolac, or diclofenac, and inhibition of NV assessed.

resultsAmfenac treatment failed to inhibit hypoxia-induced VEGF production. Amfenac treatment significantly inhibited VEGF-induced tube formation and proliferation by EC. Amfenac treatment significantly reduced retinal prostanoid production and NV in OIR. Nepafenac treatment significantly reduced retinal NV in OIR; ketorolac and diclofenac had no effect.

conclusionsNepafenac and amfenac inhibit OIR more effectively than the commercially available topical and injectable NSAIDs used in this study. Our data suggests there are COX-dependent and COX-independent mechanisms by which amfenac inhibits OIR. Because it is bioavailable to the posterior segment following topical delivery, nepafenac appears to be a promising advancement in the development of therapies for neovascular eye diseases.

Indexed as

Analysis of VarianceAnimalsAnimals, NewbornAnti-Inflammatory Agents, Non-SteroidalBenzeneacetamidesCelecoxibCell ProliferationCyclooxygenase InhibitorsDinoprostoneDisease Models, AnimalDose-Response Relationship, DrugEpithelial CellsGene Expression RegulationHumansNeurogliaOxygenamfenacAnti-Inflammatory Agents, Non-SteroidalBenzeneacetamidesCelecoxibCyclooxygenase InhibitorsDinoprostonenepafenacOxygenPhenylacetatesProstaglandinsPyrazolesSC 560SulfonamidesVascular Endothelial Growth Factor A

Identifiers

PMID19897019
PMCPMC2815002
OpenAlexW1980156445

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.