Evidence map›Paper›PMID 20824139›Full record

ArticlePloS one2010

Broad spectrum antiangiogenic treatment for ocular neovascular diseases.

Ofra Benny, Kei Nakai, Takeru Yoshimura, Lauren Bazinet, James D Akula, Shintaro Nakao, Ali Hafezi-Moghadam, Dipak Panigrahy, Pouya Pakneshan, Robert J D'Amato

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

13 citing papers in PubMed, 32 citations in OpenAlex.

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  12. Inhibitory effects of TNP-470 in combination with BCNU on tumor growth of human glioblastoma xenografts.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2010
    Article
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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

10 authors at 3 institutions in 1 country.

Ofra BennyVascular Biology Program and Department of Surgery, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, United States of America. ofra.bennyratsaby@childrens.harvard.edu
Kei Nakai
Takeru Yoshimura
Lauren Bazinet
James D Akula
Shintaro Nakao
Ali Hafezi-Moghadam
Dipak Panigrahy
Pouya Pakneshan
Robert J D'Amato
Harvard University · USBoston Children's Hospital · USMassachusetts Eye and Ear Infirmary · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledPathological neovascularization is a hallmark of late stage neovascular (wet) age-related macular degeneration (AMD) and the leading cause of blindness in people over the age of 50 in the western world. The treatments focus on suppression of choroidal neovascularization (CNV), while current approved therapies are limited to inhibiting vascular endothelial growth factor (VEGF) exclusively. However, this treatment does not address the underlying cause of AMD, and the loss of VEGF's neuroprotective can be a potential side effect. Therapy which targets the key processes in AMD, the pathological neovascularization, vessel leakage and inflammation could bring a major shift in the approach to disease treatment and prevention. In this study we have demonstrated the efficacy of such broad spectrum antiangiogenic therapy on mouse model of AMD. METHODS AND

findingsLodamin, a polymeric formulation of TNP-470, is a potent broad-spectrum antiangiogenic drug. Lodamin significantly reduced key processes involved in AMD progression as demonstrated in mice and rats. Its suppressive effects on angiogenesis, vascular leakage and inflammation were studied in a wide array of assays including; a Matrigel, delayed-type hypersensitivity (DTH), Miles assay, laser-induced CNV and corneal micropocket assay. Lodamin significantly suppressed the secretion of various pro-inflammatory cytokines in the CNV lesion including monocyte chemotactic protein-1 (MCP-1/Ccl2). Importantly, Lodamin was found to regress established CNV lesions, unlike soluble fms-like tyrosine kinase-1 (sFlk-1). The drug was found to be safe in mice and have little toxicity as demonstrated by electroretinography (ERG) assessing retinal and by histology.

conclusionsLodamin, a polymer formulation of TNP-470, was identified as a first in its class, broad-spectrum antiangiogenic drug that can be administered orally or locally to treat corneal and retinal neovascularization. Several unique properties make Lodamin especially beneficial for ophthalmic use. Our results support the concept that broad spectrum antiangiogenic drugs are promising agents for AMD treatment and prevention.

Indexed as

Angiogenesis InhibitorsAnimalsCyclohexanesCytokinesDisease Models, AnimalDrug Evaluation, PreclinicalHumansMacular DegenerationMiceMice, Inbred C57BLNeovascularization, PathologicO-(Chloroacetylcarbamoyl)fumagillolRatsRats, Inbred LewSesquiterpenesAngiogenesis InhibitorsCyclohexanesCytokinesO-(Chloroacetylcarbamoyl)fumagillolSesquiterpenes

Identifiers

PMID20824139
PMCPMC2931703
OpenAlexW2095637752

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.