Complement component C1q (C1q) and classical complement pathway components (C1q/CP)

Complement component C1q is the primary recognition molecule of the classical complement pathway, forming the C1 complex alongside the serine proteases C1r and C1s (UniProt P02745). It initiates the cascade by binding to the Fc regions of IgM or IgG antibodies within immune complexes, or directly to pathogens and apoptotic cells (Gaboriaud et al., 2004). Beyond its traditional role in innate immunity and opsonization, C1q is recognized for its non-complement functions, such as mediating synaptic pruning in the brain and maintaining peripheral self-tolerance (Stevens et al., 2007). Pathological overactivation of the classical pathway is a key driver in autoimmune conditions like cold agglutinin disease and neurodegenerative disorders where C1q-mediated synapse loss occurs (Ricklin et al., 2010). Therapeutic targeting of C1q or its downstream components, such as C1s, aims to selectively inhibit classical pathway-driven inflammation and tissue damage while preserving the alternative and lectin pathways for host defense (FDA Label: Enjaymo).

Other names

C1 complexC1qrs complexClassical complement cascadeComplement C1

Selective inhibition of the C1 complex (specifically C1q binding or C1s enzymatic activity) to prevent the cleavage of C4 and C2, thereby halting the classical complement cascade and preventing the formation of C3 convertase and the membrane attack complex (Ricklin et al., 2010; FDA Label: Enjaymo).