C5a is a proinflammatory peptide generated through activation of the complement system, and is more potent than the other anaphylatoxins, C4a and C3a, in activating peripheral blood leukocytes (Gerard & Gerard, 1994). It can actively participate in the regulation of local cytokine network by stimulating production of proinflammatory cytokines (Buchner et al., 1995; Hsu, et al., 1999). The proinflammatory effects of C5a are mediated through binding to a specific 7-TM chemoattractant receptor, C5aR (CD88). Binding of C5a to phagocyte C5aR induces chemotaxis, production of superoxide anions, and release of degradative enzymes. Pharmacologic or genetic disruption of C5a/C5aR interaction reduces sepsis (Riedemann et al., 2003), immune complex-induced lung disease (Shushakova et al., 2002), and Arthrogen-induced arthritis (Grant et al., 2002) in experimental models. Chemicon's cloned human C5a receptor membrane preparations are ideal tools for screening for antagonists of C5a/C5aR interactions. The C5aR Membrane Preps bind specifically to 125I-labeled ligand C5a, with Kd of 0.59 nM. With 5 μg membrane per well and 0.1 nM 125I-labeled C5a, more than 15-fold signal:background was obtained.