Complement C3

Class

Complement C3 inhibitor (cyclic peptide)

Complement C3 sits at the center of the complement system, a network of blood proteins that helps the innate immune system detect and destroy pathogens and clear damaged cells. Three separate triggers—the classical, lectin, and alternative pathways—all converge on C3, where it is cleaved into fragments that tag microbes for destruction (opsonization), recruit inflammatory cells, and assemble the membrane attack complex that ruptures target cell membranes. Because C3 is this convergence point, inhibiting it blocks the entire cascade far upstream, rather than only its terminal steps. This broad shutdown is useful in diseases where complement is chronically or inappropriately activated, such as geographic atrophy (a form of age-related macular degeneration), paroxysmal nocturnal hemoglobinuria, and various complement-mediated kidney and blood disorders. A cyclic peptide inhibitor binds C3 directly, preventing its cleavage and thereby limiting both fragment generation and downstream membrane damage. The rationale for a C3-level block, compared to intervening further downstream, is comprehensiveness: it dampens inflammatory signaling and opsonization together, not just the lytic endpoint. This comes with a corresponding trade-off, since C3 is also essential for clearing common bacterial infections, so its suppression carries meaningful infection risk.