The role of C5a in chronic inflammation has become increasingly clear in recent years, making C5a an attractive target for chronic and autoimmune inflammatory diseases. This is largely because of its ability to skew T-cell responses, causing a substantial imbalance and shift towards pro-inflammatory T-cell responses. In line with this finding, many chronic inflammatory diseases are burdened by flare phases with intensified inflammation causing tissue damage, which is often promoted by auto-activation of neutrophils.
Blocking C5a delivers various potentially beneficial effects in chronic inflammatory diseases. Blocking the C5a / C5aR signaling axis has been shown to re-establish T-cell balance by increasing regulatory T-cells and decreasing pro-inflammatory Th-17 and Th-1 responses. C5a blockade also offers a strong potential to control neutrophil activation in addition to its other important anti-inflammatory mechanisms.
Vilobelimab, the company's first-in-class anti-human C5a monoclonal antibody is currently being developed in several chronic inflammatory diseases with high unmet medical need. These indications include: