Biomaterial-induced complement activation byproducts C3a and C5a are major mediators of the thromboinflammatory response. The anaphylatoxins C3a and C5a, released during complement activation, induce a wide range of proinflammatory and procoagulant effects, mediated primarily by binding to their cognate receptors. Representative biological effects on platelets, endothelial cells, neutrophils, and monocytes are shown. P-selectin is a receptor for C3b and, when induced by C3a or C5a on platelets and endothelial cells, complement activation is reinforced by assembly of the AP. C1q-r, receptor for C1q; CSA, chondroitin sulfate A; ROS, reactive oxygen species.