Diabetic macular edema (DME), a prevalent complication of diabetic retinopathy, is a leading cause of vision loss among working-age individuals worldwide. It is characterized by chronic vascular leakage, inflammation, and disruption of the blood–retinal barrier, resulting in macular fluid accumulation. Anti-vascular endothelial growth factor A (VEGF-A) therapies, such as ranibizumab and aflibercept, have significantly improved visual outcomes; however, limitations such as frequent injections, persistent edema, and suboptimal responses continue to pose challenges in clinical practice. Faricimab is the first bispecific monoclonal antibody designed to concurrently inhibit VEGF-A and angiopoietin-2 (Ang-2), two key regulators of vascular permeability and inflammation. Through its dual-targeting mechanism, faricimab enhances vascular stability, reduces leakage, and enables extended treatment intervals. Phase III clinical trials (YOSEMITE and RHINE) have demonstrated its noninferior efficacy compared to aflibercept, with a substantial proportion of patients achieving dosing intervals up to 16 weeks. Emerging real-world data further support its effectiveness and durability, particularly in individuals refractory to conventional anti-VEGF agents. This review summarizes the current evidence regarding faricimab’s molecular mechanisms, pharmacokinetic profile, clinical efficacy, real-world applications, and safety. By alleviating treatment burden and supporting individualized management, faricimab represents a promising advancement in the long-term care of DME. Future research should focus on its long-term safety, identification of response biomarkers, and integration with imaging-guided algorithms to refine personalized treatment strategies.
Gao et al. (2025) studied this question.