Complement component 3 fragments C3b and iC3b (C3b/iC3b)

Complement fragments C3b and iC3b are central effector molecules of the complement system, generated through the proteolytic cleavage of complement component 3 (C3) [2.1.2]. C3b is a potent opsonin that covalently attaches to pathogen surfaces, facilitating phagocytosis and serving as a critical subunit for C3 and C5 convertases, which amplify the complement cascade [2.3.4]. Subsequent cleavage of C3b by Factor I produces iC3b (inactivated C3b), which loses convertase activity but remains a powerful opsonin recognized by complement receptors CR3 and CR4 on leukocytes [2.3.1, 2.3.5]. Dysregulation of these fragments is implicated in various diseases, including paroxysmal nocturnal hemoglobinuria (PNH), where C3b deposition on red blood cells leads to extravascular hemolysis, and C3 glomerulopathy [2.4.3, 3.4.4]. Therapeutic strategies include C3 inhibitors like pegcetacoplan, which prevent fragment generation, and novel agents like CG001 and TT30 that specifically target deposited C3b/iC3b to block downstream immune activation or accelerate their decay [3.4.1, 3.5.1].

Other names

C3biC3bInactivated C3bOpsoninsC3 cleavage products

Inhibition of C3/C5 convertase formation, blockade of opsonization, prevention of receptor binding (CR1, CR3, CR4), and promotion of C3b degradation via cofactor activity for Factor I [2.1.2, 3.5.1].