Unique role of IL-22 in epithelial healing
Interleukin-22, or IL-22, is a unique atypical cytokine that selectively targets epithelia, promotes epithelial healing, and is not immunomodulatory. IL-22 is secreted in response to tissue damage, infection or inflammation in diseases caused by epithelial injury. Injury to the epithelium is a corner stone in the pathology of several serious human diseases with large unmet need, not least Inflammatory Bowel Disease (IBD). The beneficial effects of IL-22 on promoting epithelial repair and mediating host defense against pathogens have been demonstrated in preclinical models across a wide range of indications. Early-phase clinical studies in ulcerative colitis and other indications provide preliminary proof of clinical benefits of new IL-22 drug class.
Novel approach to directly improve mucosal healing in IBD
IL-22 provides a unique direct approach to protect and repair the intestinal (epithelial) barrier, damage to which is central to the disease pathology of inflammatory bowel disease (IBD). More than 7 million patients worldwide live with IBD, and the incidence is increasing each year. The most common types of IBD, Ulcerative Colitis and Crohn’s Disease, are currently treated with immunomodulatory medication to dampen the disease and control symptoms. In contrast, our long-acting IL-22 directly addresses the key unmet need in IBD – epithelial healing – thus representing a novel treatment paradigm for patients living with this debilitating disease.
Our long-acting lipidated IL-22 program
Cytoki Pharma’s lead program features a long-acting lipidated IL-22 with best-in-class potential for treatment of epithelial injury. It is part of a licensed full pharma program from Novo Nordisk using its commercially proven lipidation technology for turning short lived native proteins into therapeutics with long half-life. Unlike other commonly used technologies to make proteins long acting, lipidation is a minimal modification of a protein comprising attachment of a small fatty acid chain. By enabling non-covalent binding to circulating serum albumin this modification protects the protein from fast clearance and degradation. An equilibrium exists between an albumin-bound and a free fraction of the lipidated native-like IL-22, allowing the free fraction to distribute freely and engage with relevant receptors.