Aflibercept and Faricimab Equipotently Restore Endothelial Barrier Function.
T, S., M, R., F, P., J, T., R, L., J, M., R, T., C, L., & L, B. (2026). Aflibercept and Faricimab Equipotently Restore Endothelial Barrier Function.. Investigative ophthalmology & visual science. https://doi.org/10.1167/iovs.67.8.5
T S, M R, F P, J T, R L, J M, et al. Aflibercept and Faricimab Equipotently Restore Endothelial Barrier Function.. Investigative ophthalmology & visual science. 2026; doi: 10.1167/iovs.67.8.5
T S, M R, F P, et al. Aflibercept and Faricimab Equipotently Restore Endothelial Barrier Function.[J]. Investigative ophthalmology & visual science. 2026. DOI: 10.1167/iovs.67.8.5.
@article{t2026,
author = {Strunz T and Rao M and Prinz F and Toedling J and Lesche R and Mielke J and Tetzner R and Lange C and Brunck L},
title = {Aflibercept and Faricimab Equipotently Restore Endothelial Barrier Function.},
journal = {Investigative ophthalmology & visual science},
year = {2026},
doi = {10.1167/iovs.67.8.5},
note = {PMID: 42390173},
}
TY - JOUR AU - Strunz T AU - Rao M AU - Prinz F AU - Toedling J AU - Lesche R AU - Mielke J AU - Tetzner R AU - Lange C AU - Brunck L TI - Aflibercept and Faricimab Equipotently Restore Endothelial Barrier Function. T2 - Investigative ophthalmology & visual science PY - 2026 DO - 10.1167/iovs.67.8.5 AN - PMID:42390173 ER -
PURPOSE: To study the biological effects of aflibercept and faricimab on vascular endothelial growth factor (VEGF)-A165-induced vascular permeability in an in vitro head-to-head comparison using human-derived endothelial cells. METHODS: This in vitro study used a human umbilical vein endothelial cell (HUVEC)-based model, in which cells were exposed to VEGF-A165, followed by the addition of aflibercept (1.7 nM) or faricimab (2.0 nM) either simultaneously (preventive) or 24 hours later (therapeutic/rescue). Cell-layer permeability was measured on the xCELLigence platform, global transcriptomic changes by RNA sequencing, and VEGF-A165-induced release of angiogenesis-related proteins by electrochemiluminescence immunoassay. RESULTS: Concurrent addition of aflibercept or faricimab prevented VEGF-A165-triggered increase of HUVEC cell-layer permeability (P = 0.0005). In the therapeutic/rescue setting, either drug temporally improved the cell-layer integrity (P = 0.0001). Aflibercept was non-inferior to faricimab in both the preventive (P < 0.0001) and therapeutic/rescue (P < 0.0001) settings. Aflibercept and faricimab comparably downregulated VEGF-A165-induced angiogenesis-related genes. Aflibercept and faricimab equipotently suppressed or reversed VEGF-A165 upregulation of ANGPT2 gene expression and angiopoietin-2 (ANG2) protein in culture supernatant. VEGF-A165-driven TEK gene expression and soluble Tie2 increase in culture supernatant was reversed with aflibercept and faricimab in both settings. CONCLUSIONS: In this in vitro model of VEGF-A165-driven vascular permeability, additional blockade of ANG2 with faricimab did not improve endothelial barrier integrity beyond VEGF-A165 blockade alone with aflibercept, despite significant upregulation of ANG2 expression after VEGF-A165 stimulation. Aflibercept and faricimab were comparable in maintaining or restoring endothelial barrier function and thereby vascular integrity, mainly attributable to inhibition of VEGF-A165 binding to its receptor.