Remigromig (EYE-103; MK-3000) is a humanized dual-target monoclonal antibody that targets LRP5 and FZD4. Remigromig activates the Wnt/β-catenin signaling pathway by mimicking the natural ligand Norrin, induces tight junction formation and restores blood-retinal barrier function. Administered via intravitreal injection, Remigromig reduces retinal vascular leakage, and demonstrates improvements in best-corrected visual acuity and reductions in retinal thickness in studies of diabetic macular edema. Remigromig can be used for research related to macular degeneration [1].
In Vivo, Intravitreally administered Remigromig demonstrates effects of reducing retinal vascular leakage, improving best-corrected visual acuity, and decreasing retinal thickness in studies of diabetic macular edema and neovascular age-related macular degeneration[1].
In Vitro, Remigromig activates the Wnt/β-catenin signaling pathway by mimicking the natural ligand Norrin, induces tight junction formation in endothelial cells, and enhances the function of the blood-retinal barrier[1].
References:
[1]. Shirian JD, et al. Exploring new horizons in neovascular age-related macular degeneration: novel mechanisms of action and future therapeutic avenues. Eye (London, England). 2025 Jan;39(1):40-44.
In Vivo, Intravitreally administered Remigromig demonstrates effects of reducing retinal vascular leakage, improving best-corrected visual acuity, and decreasing retinal thickness in studies of diabetic macular edema and neovascular age-related macular degeneration[1].
In Vitro, Remigromig activates the Wnt/β-catenin signaling pathway by mimicking the natural ligand Norrin, induces tight junction formation in endothelial cells, and enhances the function of the blood-retinal barrier[1].
References:
[1]. Shirian JD, et al. Exploring new horizons in neovascular age-related macular degeneration: novel mechanisms of action and future therapeutic avenues. Eye (London, England). 2025 Jan;39(1):40-44.