Anti-Human IL-4Rα (CD124) (Dupilumab) (I-1260-1.0mg)

IL-4R is a heterodimeric receptor composed of a common subunit (IL-4Rα) that pairs with distinct auxiliary subunits1 to create Type I and Type II IL-4 receptors as well as the IL-13 receptor system2. The IL-4/IL-13/IL-4R axis promotes T helper 2 (Th2) cell differentiation and mediates the pro-allergic adaptive immune response1. The IL‐4R pathway is central to allergic inflammation via its ligands IL-4 and IL-131, driving disease progression in atopic and allergic diseases3. IL‐4R activates effector pathways in target tissues where disease occurs1. Immunotherapies targeting IL-4R are being sought to interrupt the allergic inflammatory response. REGN668 (Dupilumab) selectively binds to IL-4Rα and inhibits the signaling of type 2 (Th2) cytokines IL-4 and IL-13, thereby inhibiting the release of proinflammatory cytokines, chemokines, and IgE as well as reducing key Th2-associated biomarkers3. An increase in serum levels of IL-4 and IL-13 is seen following blockade. Additionally, dupilumab inhibits IgE production by ex vivo B cells induced by IL-4 treatment 1. Since IL-4Rα is targeted, dupilumab can block both Type I and Type II receptors. However, based on clinical data, dupilumab may not equally inhibit both receptor types1. IL-4 signaling is inhibited via the Type I receptor. While both IL-4 and IL13 signaling are inhibited via the Type II receptor. Dupilumab has been approved for the treatment of atopic dermatitis and eosinophilic asthma.