Anti-complement component C5 therapy (Eculizumab) utilizes a humanized monoclonal antibody that is a terminal complement inhibitor. Eculizumab was developed and was approved by the United States Food and Drug Administration (FDA) in 2007 for the treatment of paroxysmal nocturnal hemoglobinuria (PNH) and in 2011 for the treatment of atypical hemolytic uremic syndrome (aHUS). Eculizumab inhibits the cleavage of C5 to C5a and C5b by the C5 convertase, which prevents the generation of the terminal complement complex C5b-9 (and also exhibits prothrombotic and proinflammatory effects). Both C5a and C5b-9 cause the terminal complementmediated events that are characteristic of aHUS. By inhibiting the complement cascade at this point, the normal, disease-preventing functions of the proximal complement system are largely preserved, while the properties of C5 that promote inflammation and cell destruction are impeded. We present a review of the role of anti-complement component C5 therapy (Eculizumab) in aHUS patients.
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