Neovascular age-related macular degeneration (nAMD) is a leading cause of vision loss in the elderly. Despite significant advances in anti-vascular endothelial growth factor (VEGF) therapy, a substantial subset of patients exhibit suboptimal responses to conventional treatments. With the evolution of diagnostic criteria and the integration of multimodal imaging techniques, the definition of refractory nAMD has gradually expanded to encompass anatomical, functional, and therapeutic response parameters. Its pathogenesis is complex, involving adaptive upregulation of the VEGF signaling pathway, compensatory activation of alternative pro-angiogenic pathways, reprogramming of downstream endothelial signaling, development of neutralizing antibodies, elevated angiopoietin-2 (Ang-2) levels, structural remodeling of macular neovascularization, and reduced retinal microvascular density. Faricimab, the first dual-pathway inhibitor targeting both VEGF-A and Ang-2, demonstrates significant advantages by synergistically suppressing abnormal angiogenesis and vascular leakage, modulating the inflammatory microenvironment, and improving choroidal perfusion, thereby enhancing anatomical outcomes and enabling extended dosing intervals. Evidence from clinical trials and real-world studies suggests that faricimab has therapeutic potential in patients with refractory nAMD; however, long-term safety and durability of efficacy require further investigation. Future management of refractory nAMD is likely to emphasize individualized treatment strategies, leveraging dynamic assessment frameworks based on multimodal imaging and biomarkers, as well as artificial intelligence–assisted decision-making models, to transition from reactive, fixed-interval therapy toward predictive, precision-guided interventions.