Evidence map›Paper›PMID 42130720›Full record

ArticleACS pharmacology & translational science2026

Bemarituzumab Suppresses Choroidal Neovascularization in Mice by Downregulating Melanoma Cell Adhesion Molecule and Yes-Associated Protein 1.

Liujun Ding, Bintao Xie, Jineng Lv, Zhonglou Zhou, Xin Zhou, Kunchao Wu, Qin Zhang, Fan Lu, Cong Wang, Jia Qu and 2 more

Abstract read
In one paragraph

Article in ACS pharmacology & translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Liujun DingState Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Bintao XieState Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Jineng LvState Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Zhonglou ZhouState Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Xin ZhouState Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Kunchao WuState Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Qin ZhangState Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Fan LuState Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Cong WangSchool of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou 325027, China.ORCID https://orcid.org/0000-0002-2184-6879
Jia QuState Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Lue XiangState Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.
Qi ChenState Key Laboratory of Eye Health, Eye Hospital, Wenzhou Medical University, Wenzhou 325027, China.ORCID https://orcid.org/0000-0003-3773-4641

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years, some fibroblast growth factors (FGFs) have been reported to be promising therapeutic targets for neovascular age-related macular degeneration (nAMD). Interestingly, we found that the FGFR2b inhibitor bemarituzumab (FPA144) exerts a beneficial effect in a mouse choroidal neovascularization (CNV) model. Our current study aims to uncover the potential molecular mechanism by which FPA144 alleviates CNV. The effect of FPA144 was evaluated in a laser-induced CNV mouse model. Fundus fluorescein angiography (FFA), optical coherence tomography (OCT), and choroidal flat mounts were carried out for the quantitative assessment of CNV. Label-free quantitative proteomics analysis was performed to assess changes in molecular pathways. Primary cultured human umbilical vein endothelial cells (HUVECs) were used for further confirmation of the target pathway in vitro. FFA, OCT, and choroidal flat mounts demonstrate the protective effect of FPA144 in a mouse CNV model. Compared to the control group, the treated group has smaller vascular leakage areas or smaller CNV lesions. Proteomic analyses indicate that the melanoma cell adhesion molecule (MCAM, CD146)-Yes-associated protein 1 (Yap1) pathway may be involved in the effect of FPA144. Immunostaining of choroidal flat mounts and cryosections reveals decreased expression of CD146 and Yap1 in the vascular endothelial cells of the treated animals. Experiments on HUVECs further verify the inhibitory effect of FPA144 on vascular endothelial cells. Our findings demonstrate that FPA144 can efficiently inhibit the development of choroidal neovascularization in mice by downregulating CD146 and Yap1.

Indexed as

CD146Choroidal neovascularizationFGFR2Neovascular age-related macular degenerationYap1

Identifiers

PMID42130720
PMCPMC13162049

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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.