Complement C1q / neutrophil effectors (myeloperoxidase, NETosis)

Class

Complement/neutrophil inhibitor

Complement C1q and neutrophil effector mechanisms (myeloperoxidase and NETosis) represent two arms of the innate immune system that, while essential for defending against infection, can each cause collateral tissue damage when excessively activated. C1q is the recognition component that initiates the classical complement pathway, a proteolytic cascade that tags pathogens and damaged cells for destruction and generates potent inflammatory signals. Neutrophils, recruited by these signals, kill pathogens using myeloperoxidase, an enzyme that generates reactive oxidants, and through NETosis, a process in which neutrophils release extracellular webs of DNA and antimicrobial proteins to trap microbes. Both pathways amplify each other and, in settings of severe tissue injury such as ischemia, hypoxia, or sepsis, can drive excessive inflammation that worsens organ damage rather than resolving it. An agent that inhibits both C1q-initiated complement activation and neutrophil effector functions addresses two converging, mutually reinforcing sources of tissue injury simultaneously, offering a broader dampening of acute inflammatory damage than targeting either pathway in isolation, while aiming to preserve enough residual immune function to avoid compromising host defense.