<unk>  specifically binds to the terminal complement component 5, or C5, which acts at a late stage in the complement cascade. When activated, C5 is involved in activating host cells, thereby attracting pro-inflammatory immune cells, while also destroying cells by triggering pore formation. By inhibiting the complement cascade at this point, the normal, disease-preventing functions of proximal complement system are largely preserved, while the properties of C5 that promote inflammation and cell destruction are impeded.<unk>  inhibits the cleavage of C5 by the C5 convertase into C5a a potent anaphylatoxin with prothrombotic and proinflammatory properties, and C5b, which then forms the terminal complement complex C5b-9 which also has prothrombotic and proinflammatory effects. Both C5a and C5b-9 cause the complement-mediated events that are characteristic of PNH and aHUS. The metabolism of<unk>  is thought to occur via lysosomal enzymes that cleave the antibody to generate small peptides and amino acids. The volume of distribution of<unk>  in humans approximates that of plasma. Chemistry<unk>  is a recombinant humanized monoclonal antibody against the complement protein C5. It is an immunoglobulin G-kappa (IgGκ) consisting of human constant regions and murine complementarity-determining regions grafted onto human framework light and heavy chain variable regions. The compound contains two 448-amino acid heavy chains and two 214-amino acid light chains, and has a molecular weight of approximately 148 kilodaltons (kDa).
Eculizumab
Brolucizumab
Emicizumab
Satralizumab
Natalizumab
Ixekizumab
Theralizumab
Tocilizumab