CR2-fH, A Targeted Inhibitor of Alternative Complement Pathway Reduces Dry AMD-Like Phenotype in AMD Patient iPSC-derived RPE Cells

The AP inhibitor CR2-fH delivered either as a soluble protein or via gene therapy is efficacious in preventing serum-induced complement activation that led to monolayer disruption and AMD-like pathology in iPSC-RPE cells. These results contribute to existing data highlighting the importance of the AP of complement in dry AMD pathology and its potential role in AMD treatment.