C5a is a powerful inflammatory mediator, and seems to be a key factor in the development of pathology of many inflammatory diseases involving the complement system such as sepsis, rheumatoid arthritis, inflammatory bowel disease, systemic lupus erythemotosis, psoriasis. The inhibitor of C5a that can block its effects would be helpful in medical applications. 
Another candidate is PMX53 or PMX205 that is highly specific for CD88 and effectively reduces inflammatory response. C5a has been identified as a key mediator of neutrophil dysfunction in sepsis, with antibody blockade of C5a improving outcomes in experimental models.  This has also been shown in humans, with C5a-mediated neutrophil dysfunction predicting subsequent nosocomial infection and death from sepsis.  Recent data demonstrates that C5a not only impairs phagocytosis by neutrophils but also impairs phagosomal maturation, inducing a marked alteration in the neutrophil phosphoproteomic response to bacterial targets. C5a binding to C5aR1 and C5aR2 (C5L2) mediates the formation of neutrophil extracellular traps and release of cytotoxic histones to the extracellular space, which is believed to act as a pathogenetic process of acute respiratory distress syndrome (ARDS) and promote tumor growth and metastasis.