Complement component C3b and complement component C4b (C3b and C4b)

Complement component C3b and C4b are **major functional fragments of the complement proteins C3 and C4**, generated during activation of the innate immune complement system. Both fragments alkylate nearby surfaces via a reactive thioester, opsonizing pathogens or altered self-tissues for phagocytosis or lysis. C4b is the backbone of the classical/lectin pathway C3 convertase (C4b2a), while C3b forms the alternative pathway convertase (C3bBb) and contributes to the alternative and classical C5 convertases. Their deposition is strictly regulated by host proteins to avoid damage to self-tissues. Pathologic or excessive deposition is implicated in autoimmune, infectious, and inflammatory diseases, and their breakdown products, especially C4d, serve as clinical biomarkers. Therapeutically, both C3b and C4b are considered targets for complement inhibition strategies, with drugs in use and in development aiming to ameliorate diseases resulting from aberrant complement activation[1][3][4][5][6][9].

Other names

Complement fragment 3bComplement C3bComplement fragment 4bComplement C4b

Blockade of complement activation (prevents cleavage of C3/C5 or deposition of C3b/C4b); Inhibition of convertase activity (interrupting C3/C5 cleavage cascade at the convertase assembly stage); Prevention of opsonization (stopping marking of cells for phagocytic removal)