This exposure was sufficient to achieve optimal blockade of C5a-induced CD11b upregulation, as well as C5a-induced degranulation, reactive oxygen intermediate production, and C5a-directed migration of neutrophils ex vivo, forming the basis for the dose selected for avacopan in subsequent clinical studies of ANCA-associated vasculitis. This evidence concerns the gene C5AR1 and anti-neutrophil cytoplasmic antibody-associated vasculitis.