Targeting key angiogenic pathways with a bispecific CrossMAb optimized for neovascular eye diseases

Abstract

Figure 1A

Revised figure. Box plots of vitreal ANG‐1 levels from newly diagnosed patients with wAMD, DR, proliferative DR and RVO compared to controls (macular hole). The interquartile range of the data is indicated by the box. A nonparametric Kruskal–Wallis analysis followed by Dunn's method for multiple comparisons was used to show significant differences of the groups to control, which are indicated by asterisks. ANG‐1 levels did not differ significantly. Source data are available online for this figure.

Figure 9B

Revised figure. Inhibition of neovascularization measured in severity grades, change of severity from baseline is shown for each treatment; all treatment significantly reduced the severity grade compared to IgG control. In addition, efficacy of RG7716 (150‐kDa molecule at 90 μg/50 μl injected IVT) was significantly better at equal molar concentration of binding sites than anti‐VEGF‐A (ranibizumab, 50‐kDa molecule at 30 μg/50 μl injected IVT) and anti‐ANG‐2. Error bars show SEM of n = 6 cynomolgus monkeys and nine spots per eye in the group; * denotes significance after one‐sided ANOVA and Tukey's multiple t‐test. IgG control is significantly different from anti‐VEGF‐A (***, P = 0.0003), anti‐ANG‐2 (*, P = 0.0325), RG7716, 30 μg (***, P = 0.0001) and RG7716, 90 μg (****, P < 0.0001). Furthermore, RG7716, 90 μg is significantly different from anti‐ANG‐2 (***, P = 0.0002) and anti‐VEGF‐A (*, P = 0.0317). Source data are available online for this figure.