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WHAT IS THE CURRENT KNOWLEDGE ON THE TOPIC? Riliprubart, a second-generation humanized immunoglobulin G4 that inhibits only the activated form of the C1s component of the proximal classical complement pathway, is currently in clinical development for complement-mediated diseases. WHAT QUESTION DID THIS STUDY ADDRESS? Model-informed drug development (MIDD) approaches were used to propose a dose regimen utilizing available clinical data.
Dysregulation or deficiency of the complement alternative pathway (AP) is implicated in several rare blood disorders and renal diseases,1,2 and more broadly plays a role in the progression of inflammatory conditions.3 Nascently-generated C3b molecules (from any of the 3 initiation pathways) bind factor B (FB) to form the proconvertase C3bB, which is cleaved by factor D (FD) to form the active convertase alternative pathway C3 convertase (C3bBb).
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