Evidence map›Paper›PMID 18600493›Full record

ArticleCurrent eye research2008

Toxicity and intraocular properties of a novel long-acting anti-proliferative and anti-angiogenic compound IMS2186.

Iryna A Falkenstein, Lingyun Cheng, Flossie Wong-Staal, Ajay M Tammewar, Erin C Barron, Gabriel A Silva, Qi-Xiang Li, Dehua Yu, Michelle Hysell, Guohong Liu and 3 more

Open access · greenAbstract read
In one paragraph

Article in Current eye research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Intravitreal inhibition of complement C5a reduces choroidal neovascularization in mice.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2015
    Article
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  6. [Pharmacological approach to treatment of proliferative vitreoretinopathy].Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft · 2013
    Review
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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

13 authors at 1 institution in 1 country.

Iryna A FalkensteinJoan and Irwin Jacobs Retina Center, Department of Ophthalmology, Shiley Eye Center, University of California, San Diego, California, USA.
Lingyun Cheng
Flossie Wong-Staal
Ajay M Tammewar
Erin C Barron
Gabriel A Silva
Qi-Xiang Li
Dehua Yu
Michelle Hysell
Guohong Liu
Ning Ke
James E Macdonald
William R Freeman
University of California, San Diego · US

Funding

TREATMENT OF RETINOPATHY ASSOCIATED WITH AIDSR01EY007366 · NEI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FREEMAN, WILLIAM R. · 1988 to 2013
$7.6M
High Throughput Mapping of Neuronal and Glial NetworksR01NS054736 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SILVA, GABRIEL A · 2006 to 2010
$1.4M
NEI NIH HHS R01 EY007366NINDS NIH HHS R01 NS054736
6 · The paper itself

Abstract

purposeTo investigate the intraocular properties and toxicity of IMS2186, a small molecule developed as an anti-choroidal neovascularization (anti-CNV) drug. MATERIALS AND

methodsCellular toxicity and mechanism of action was tested on cell lines in vitro. Intraocular studies used rabbits for drug dissolution as well as toxicity and rats for the treatment study as well as the toxicity confirmation study. Rabbits' eyes were injected with 2.5 mg of IMS2186 and observed for 36 weeks. Laser-induced CNV in rats was treated with IMS2186, Kenalog, or phosphate-buffered saline (pBS). Fluorescein angiography (FA) and immunohistochemical processing of the globes was performed.

resultsThe anti-proliferative IC(50) of IMS2186 for human fibroblast cells was 1.0-3.0 microM and 0.3-3.0 microM for human cancer cells; the IC(50) of IMS2186 to inhibit endothelial tube formation was 0.1-0.3 microM. The IC(50) of IMS2186 for inhibiting the production of pro-inflammatory cytokines was 0.3-1 microM. The IC(50) of IMS2186 for inhibiting macrophage migration was 1 micrM. These biological properties were not species specific. IMS2186 can be formulated as a suspension for long-lasting release and when delivered intraocularly, no intraocular toxicity was observed by slit lamp exam, fundus exam, intraocular pressure measurements, or by electroretinography. FA showed a reduction in the leakage in eyes treated with IMS2186 and triamcinolone acetonide; DAPI staining also showed significantly less cellularity in IMS2186-treated lesions as compared to PBS (p = 0.0025).

conclusionIMS2186 may be a safe intraocular therapeutic agent for intraocular proliferation and angiogenesis.

Indexed as

Angiogenesis InhibitorsAnimalsCell LineCell MovementCell ProliferationChoroidal NeovascularizationChromonesDinoprostoneDisease Models, AnimalElectroretinographyEndothelium, VascularFibroblastsFluorescein AngiographyHumansMiceNIH 3T3 Cells3-(1-(3-hydroxy-4-methoxyphenyl)methylidene)-6-methylchroman-4-oneAngiogenesis InhibitorsChromonesDinoprostone

Identifiers

PMID18600493
PMCPMC2664073
OpenAlexW2047598196

What OpenQuestion holds

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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.