In vitro experiments demonstratedits ability to inhibit complement activation through binding of complementfactors C3 and C5, while in vivo studies confirmed reduced levelsof the pro-inflammatory mediator C5a, resulting in impaired leukocytechemotaxis., Structure–activity relationshipshave also been explored, and dPGS has demonstrated therapeutic potentialin various disease models, including neurological disorders, cancer, and arthritis. These findings underscore its promise as a multivalent,polymeric antiinflammatory agent. The gene discussed is C5; the disease is Arthritis.