New data in a mouse model of spontaneous choroidal neovascularisation support the role of angiopoietin‐2 inhibition in driving sustained vascular stabilisation and reduced fibrosis progression

Purpose To explore the vessel stabilisation potential of dual angiopoietin‐2 (Ang‐2)/vascular endothelial growth factor‐A (VEGF‐A) inhibition in a mouse model of spontaneous choroidal neovascularisation (sCNV) in the context of phase 2 clinical data on faricimab, a bispecific antibody that binds to and neutralises both Ang‐2 and VEGF‐A. Methods Seven‐week‐old JR5558 mice, developing sCNV in both eyes, were treated intraperitoneally with mouse cross‐reactive tool antibodies against Ang‐2, VEGF‐A, or both (bispecific antibody VA2); n = 7–15 mice per group. Fluorescein angiography (FA)‐evaluated CNV leakage and fibronectin (fibrosis marker) deposition on the retinal pigment epithelium (RPE)/choroid and around CNV lesions were assessed at baseline and 1 (PT1), 3 (PT2) and 5 weeks (PT3) post treatment to assess the effects on CNV lesion activity relative to untreated/IgG‐exposed mice. Results Anti‐Ang‐2‐, anti‐VEGF‐A‐ and VA2‐treated mice showed a significant reduction in CNV leakage (p