Complement fragment 3b and Complement fragment 4b (C3b and C4b)

Complement fragments C3b and C4b are the primary activation products of the complement system, a critical component of the innate immune response (NIH, 2024). C4b is generated by the cleavage of C4 by the C1 complex or MASP-2, while C3b is produced by the cleavage of C3 by C3 convertases (Wikipedia, 2018). Both fragments contain a highly reactive internal thioester bond that enables them to covalently attach to the surfaces of pathogens and immune complexes, marking them for destruction by phagocytes—a process known as opsonization (ASM, 2024). Beyond their role as opsonins, C3b and C4b serve as essential structural subunits of the C3 and C5 convertase enzymes, which amplify the complement cascade and initiate the formation of the membrane attack complex (Creative Biolabs, 2024). Dysregulation or excessive deposition of these fragments is a key driver in the pathogenesis of various autoimmune and inflammatory conditions, including systemic lupus erythematosus, C3 glomerulopathy, and age-related macular degeneration (NIH, 2024). Therapeutic agents targeting these fragments, such as soluble complement receptor 1 (sCR1) and membrane-targeted regulators like Mirococept, aim to neutralize their activity, accelerate the decay of convertases, and promote the proteolytic inactivation of the fragments to prevent tissue damage (JST, 2019; NIH, 2023).

Other names

C3bC4bComplement component 3bComplement component 4bOpsonins C3b and C4bComplement activation fragments

Inhibition of C3 and C5 convertase formation, acceleration of convertase decay, and acting as a cofactor for Factor I-mediated inactivation of C3b and C4b.