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Complement component 3b (C3b) and complement component 4b (C4b) are proteolytic fragments generated during activation of the complement system, a central part of innate immunity[2][4][6]. Both are covalently deposited on pathogen or altered self surfaces: C4b mainly via the classical and lectin pathways, and C3b by all three pathways[4][6]. Once deposited, C3b and C4b act as **opsonins**—molecules that tag targets for phagocytosis—and serve as scaffold proteins for assembly of the C3 convertase (C4bC2a in classical/lectin pathways; C3bBb in alternative pathway), which amplifies complement activation and contributes to immune complex clearance and cell lysis[1][2][3][4][5][6]. C4b and C3b fragments are critical in linking innate defense, inflammation, and removal of immune complexes; their dysregulation is implicated in infection susceptibility, autoimmune diseases, and inflammatory disorders. Deficiency or dysfunction of these complement fragments is associated with increased risk of infections, autoimmunity, and abnormal inflammation[2][5][6].
Inhibition of complement activation via blockade of C1s, C3, or C5, preventing downstream C3b and C4b formation or function Blockade of convertase assembly (e.g., C4bC2a, C3bBb) Neutralization of opsonization and complement-mediated cell lysis
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