ArticleEBioMedicine2026
The therapeutic effects of the VEGF decoy receptor fusion protein VEGF-Grab in chronic inflammatory diseases.
Article in EBioMedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPlacental growth factor (PlGF) plays a crucial role in the pathogenesis of autoimmune diseases, including rheumatoid arthritis (RA) and multiple sclerosis (MS), by enhancing angiogenesis, disease-aggravating features of fibroblast-like synoviocytes (FLSs), and pathogenic T helper type 17 (Th17) cells. The therapeutic potential of a VEGF decoy receptor fusion protein, VEGF-Grab, which potently binds and neutralises VEGF and PlGF, has not been studied in autoimmune diseases. Therefore, we investigated the therapeutic effects of VEGF-Grab in RA and MS by using in vitro and in vivo models.
methodsTwo forms of VEGF-Grab (PB101 and PB102) were engineered to enhance their binding affinity for VEGF and PlGF. In vitro assays-including Transwell migration and wound-healing assays of endothelial cells and FLSs, as well as Th17 cell differentiation-were employed to evaluate the effects of VEGF-Grab on angiogenesis and immune-cell function. To assess therapeutic efficacy in vivo, mouse models of inflammatory and autoimmune arthritis, as well as experimental autoimmune encephalomyelitis (EAE), were utilised.
findingsOur results indicate that VEGF-Grab exerted significant inhibitory effects across various animal models of autoimmune diseases, targeting abnormal angiogenesis, cartilage invasion, and pathogenic Th17 cells. Furthermore, combined treatment with IFN-β in the EAE model suggested enhanced efficacy of therapeutic effects.
interpretationOur findings highlight the multifaceted therapeutic potential of VEGF-Grab in RA and MS, targeting angiogenesis, the aggressiveness of FLSs, and the pathogenicity of Th17 cells, all driven by the 'angio-lymphokine', PlGF. Thus, VEGF-Grab has the potential to be a therapeutic candidate for the treatment of RA and MS, warranting further clinical exploration.
fundingThis study was supported by grants funded by the National Research Foundation of Korea (RS-2024-00442793 to W.U.K.), and Biomlogic/GenoFocus and Panolos Biosciences (to S.H.L.).
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.