The potential utility for drugs that inhibit complement dependent acute inflammatory events in diseases such as rheumatoid arthritiq2 lupus erythemato~ us,~ and glomerulonephritis4 has been well documented. Although many chemicals, including several antiinflammatory agents, have been reported to be inhibitory of the complement cascade in~ itro,~ none has been shown to display clinical efficacy via this mechanism. Thus, with clear relevance to ...
