Analysis Affinity and Kinetics of IFN-α2A with Sifalimumab by KinExA (CAT#: STEM-MB-0054-CJ)

Introduction

nterferons (IFNs) belong to the “4-helical cytokines” superfamily and can be grouped into types I, II, and III. whereas type I IFNs constitute a family of cytokines expressed from more than 15 genes. Most notably, these include IFN-α, IFN-β, IFN-τ, IFN-κ, IFN-ϵ, IFN-δ and IFN-ω. The critical role of IFNs in modulating the host mammalian responses to infections has been well documented. More recently, IFNs have also been shown to be key immunoregulatory cytokines. As such, they play a central role in the onset of various autoimmune diseases. The autoimmune-predisposed mice deficient in the IFN-α/-β receptor will exhibit significantly reduced disease manifestations such as the presence of anti-erythrocyte autoantibodies, hemolytic anemia, anti-DNA autoantibodies, and kidney disease. In particular, systemic lupus erythematosus, type I diabetes, and Sjögren syndrome, as well as thyroid diseases, have now been linked to the action of IFN-α. To contribute to the treatment of autoimmune diseases, AstraZeneca/MedImmune has developed sifalimumab, a fully human monoclonal antibody that binds to, and inhibits the actions of multiple IFN-α subtypes.