Dermira, Inc. announced that new scientific findings highlighting the role of interleukin-13 (IL-13) in amplifying itch and the role lebrikizumab plays in reducing itch, will be presented at the 10thWorld Congress on Itch taking place November 17-19 in Sydney, Australia. Itch is defined as an unpleasant sensation causing the desire to scratch the surface of the skin. Chronic itch affects approximately one-fifth of the global population and can have a significant impact on a person’s quality of life. Itch is often associated with sleep disorders, depression and anxiety and is cited as one of the most burdensome aspects of atopic dermatitis, as underscored during a recent Patient-Focused Drug Development meeting. IL-13 is believed to be a central pathogenic mediator that drives multiple aspects of the pathophysiology underlying the range of signs and symptoms of atopic dermatitis by promoting type 2 inflammation and mediating its effects on tissue, resulting in skin barrier dysfunction, itch, skin thickening and infection. Key Research Findings: In laboratory experiments, cultured human sensory neurons were stimulated with IL-13 and subsequently introduced to several common itch-inducing agents (pruritogens), including histamine, serotonin and BAM8-22. The experiments demonstrated that IL-13 directly interacts with human sensory neurons, enhancing the itch induced by these itch-inducing agents. When lebrikizumab was introduced, it significantly inhibited these potentiated itch signals to known pruritogens, demonstrating that lebrikizumab has the potential to block enhanced itch signals in inflammatory skin conditions such as atopic dermatitis. This finding supports the results observed in Dermira’s Phase 2b dose-ranging study evaluating lebrikizumab in patients with moderate-to-severe atopic dermatitis, who reported improvements in itch symptoms as early as day two of treatment. Lebrikizumab is a novel, investigational, monoclonal antibody designed to bind IL-13 with very high affinity, specifically preventing the formation of the IL-13Ra1/IL-4Ra heterodimer complex and subsequent signaling, thereby inhibiting the biological effects of IL-13 in a targeted and efficient fashion.