T helper type 2 (Th2) cells play an important role in the initiation, progression and persistence of protective immune responses within the body. These same cells also contribute to chronic inflammatory diseases including asthma and atopic dermatitis. During an allergic response, large numbers of Th2 cells are recruited to the airways (asthma) or skin (dermatitis), which subsequently release cytokines (IL-4, IL-5 and IL-13). In patients with allergic asthma or atopic dermatitis, these cytokines cause chronic disease – either inflammation of the airways or a severe itchy rash on the skin.
By blocking the recruitment of Th2 cells to the inflamed tissue, it may be possible to reduce or eliminate these chronic diseases. We have taken a comprehensive approach to targeting Th2 cells, with our lead compound FLX193 advancing through preclinical development. FLX193 blocks a receptor called CCR4 found on all Th2 cells. CCR4 binds to secreted factors that recruit Th2 cells to the inflamed tissue. By blocking the secreted factors from binding to CCR4, we believe FLX193 will reduce or eliminate chronic inflammatory diseases such as asthma and atopic dermatitis.
In patients with allergic asthma and atopic dermatitis, Th2 cells are recruited en masse to the site of inflamed tissue – the lungs and skin, respectively. FLX193 acts by blocking the recruitment Th2 cells therefore stopping a major cause of these chronic disorders.