Anti-Human IL-13 (Tralokinumab) (I-2110-50mg)

IL-13 is an important mediator of allergic inflammation and disease1 that plays a role in the regulation of IgE synthesis, induction of adhesion molecules, and chemokine expression2. The functions of IL-13 overlap considerably with those of IL-41. IL-13 induces its effects through a multi-subunit receptor composed of the alpha chain of the IL-4 receptor (IL-4Rα) and an IL-13 binding subunit IL-13Rα1. IL-13 induces many features of allergic lung disease, including airway hyper-responsiveness, goblet cell metaplasia, and mucus hypersecretion, which all contribute to airway obstruction. IL-13 is also associated with the induction of chronic pulmonary eosinophilia and eosinophilic esophagitis3 and plays a key role in the pathogenesis of atopic dermatitis4. Although IL-13 is associated primarily with the induction of airway disease, it also has anti-inflammatory properties1. CAT-354 (Tralokinumab) was isolated and optimized using antibody display technologies3. Tralokinumab acts as a neutralizing antibody2 that binds specifically and with high affinity to IL- 13, preventing interaction with the IL-13 receptor4. In mice administered human IL-13, tralokinumab blocks human IL-13-induced lung eosinophilia, significantly decreases airway hyper-responsiveness, and inhibits eosinophil recruitment to the esophagus3. Tralokinumab does not affect human IL-13-induced goblet cell metaplasia in mouse lungs. Additionally, phase 3 trials produced inconsistent benefits for the treatment of asthma and clinical evaluation was discontinued for this indication4. Tralokinumab has been studied and approved for use in atopic dermatitis4.