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Interleukin-1β (IL-1β) is a potent multipotent cytokine that affects the function of almost all cell types. IL-1β is a major mediator of inflammatory responses by inducing the growth and differentiation of immunoactive lymphocytes. In this function, IL-1β plays a central role in the prevention of microbial pathogens and tissue damage repair. The expression level and function of IL-1β are strictly regulated by the complex system of IL-1 family members and their receptors. Overexpression of IL-1β is the main cause of increased erythrocyte sedimentation rate (ESR) , peripheral neutrophilia, thrombocytosis, pain and allergy, and anemia. These diseases include systemic juvenile idiopathic arthritis (sJIA) , neonatal multisystemic inflammatory disease (NOMID) , Muckle-Wells syndrome (MWS) , suppurative arthritis, pyoderma gangrena and acne syndrome (PAPA syndrome) , familial Mediterranean fever (FMF) , and others. Excess IL-1β also causes bone degeneration in the joints of patients with rheumatoid arthritis (RA) and affects beta cells in the pancreas, disrupting insulin production in models of type 2 diabetes. Blocking IL-1β has been shown to improve blood glucose control and beta cell function in clinical trials in patients with type 2 diabetes.
XOMA052 is a high affinity, IL-1β-specific therapeutic antibody, also known as gevokizumab. Designed specifically for high potency and infrequent dosing, the antibody is generated from a synthetic mouse antibody sequence and constructed through rational design using XOMA's antibody technology platform. XMA005 is the parent of XOMA052.