Evidence map›Paper›PMID 31454678›Full record

ArticleMolecular therapy. Nucleic acids2019

Anti-Angiogenic and Anti-Scarring Dual Action of an Anti-Fibroblast Growth Factor 2 Aptamer in Animal Models of Retinal Disease.

Yusaku Matsuda, Yosuke Nonaka, Satoshi Futakawa, Hirotaka Imai, Kazumasa Akita, Toshiaki Nishihata, Masatoshi Fujiwara, Yusuf Ali, Robert B Bhisitkul, Yoshikazu Nakamura

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
8.3field-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

36 citing papers in PubMed, 79 citations in OpenAlex.

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  3. Management of fibrosis in neovascular age-related macular degeneration.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026
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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 2 institutions in 2 countries.

Yusaku MatsudaRIBOMIC, Inc., 3-16-13 Shirokanedai, Minato-ku, Tokyo 108-0071, Japan.
Yosuke NonakaRIBOMIC, Inc., 3-16-13 Shirokanedai, Minato-ku, Tokyo 108-0071, Japan.
Satoshi FutakawaRIBOMIC, Inc., 3-16-13 Shirokanedai, Minato-ku, Tokyo 108-0071, Japan.
Hirotaka ImaiRIBOMIC, Inc., 3-16-13 Shirokanedai, Minato-ku, Tokyo 108-0071, Japan.
Kazumasa AkitaRIBOMIC, Inc., 3-16-13 Shirokanedai, Minato-ku, Tokyo 108-0071, Japan.
Toshiaki NishihataRIBOMIC, Inc., 3-16-13 Shirokanedai, Minato-ku, Tokyo 108-0071, Japan.
Masatoshi FujiwaraRIBOMIC, Inc., 3-16-13 Shirokanedai, Minato-ku, Tokyo 108-0071, Japan.
Yusuf AliRIBOMIC, Inc., 3-16-13 Shirokanedai, Minato-ku, Tokyo 108-0071, Japan.
Robert B BhisitkulDepartment of Ophthalmology, University of California, San Francisco, San Francisco, CA, USA.
Yoshikazu NakamuraRIBOMIC, Inc., 3-16-13 Shirokanedai, Minato-ku, Tokyo 108-0071, Japan; Institute of Medical Science, The University of Tokyo, Minato-ku, Tokyo 108-8639, Japan. Electronic address: nak@ims.u-tokyo.ac.jp.
The University of Tokyo · JPUniversity of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Currently approved therapies for age-related macular degeneration (AMD) are inhibitors against vascular endothelial growth factor (VEGF), which is a major contributor to the pathogenesis of neovascular AMD (nAMD). Intravitreal injections of anti-VEGF drugs have shown dramatic visual benefits for AMD patients. However, a significant portion of AMD patients exhibit an incomplete response to therapy and, over the extended management course, can lose vision, with the formation of submacular fibrosis as one risk factor. We investigated a novel target for AMD treatments, fibroblast growth factor 2 (FGF2), which has been implicated in the pathophysiology of both angiogenesis and fibrosis in a variety of tissue and organ systems. The anti-FGF2 aptamer, RBM-007, was examined for treatment of nAMD in animal models. In in vivo studies conducted in mice and rats, RBM-007 was able to inhibit FGF2-induced angiogenesis, laser-induced choroidal neovascularization (CNV), and CNV with fibrosis. Pharmacokinetic studies of RBM-007 in the rabbit vitreous revealed high and relatively long-lasting profiles that are superior to other approved anti-VEGF drugs. The anti-angiogenic and anti-scarring dual action of RBM-007 holds promise as an additive or alternative therapy to anti-VEGF treatments for nAMD.

Indexed as

AMDangiogenesisaptamerFGF2fibrosisVEGF inhibitors

Identifiers

PMID31454678
PMCPMC6716068
OpenAlexW2965124530

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.