Using both allergy and transplantation model systems, it has been demonstrated that activation of the Notch signaling pathway in immune cells results in an antigen-specific immune suppression selective for the co-administered antigen. This finding may have significant commercial potential for the development of novel classes of therapeutics, and is the basis for our preclinical development program directed at type I (insulin-dependent) autoimmune diabetes and its complications.
Our CDX-S03 product candidate (based on the Notch binding protein Delta) is designed to be administered with a disease specific antigen to selectively and actively suppress the undesired immune response that causes destruction of insulin-producing cells in the pancreas and thus causes the dysregulated glucose metabolism observed in diabetic patients. CDX-S03 triggers antigen-specific suppression of the immune system, resulting in inhibition of the pathological immune response without affecting other immune responses. CDX-S03 is currently a preclinical program with proof of concept efficacy and dose optimization studies in progress. By combining CDX-S03 with other disease-specific antigens, CDX-S03 may also be developed as an immunotherapy for other autoimmune diseases such as multiple sclerosis, systemic lupus erythematosus and rheumatoid arthritis.
In addition to CDX-S03, we are also exploiting our APC-targeting technology to develop therapeutic approaches for autoimmune and allergic disorders in which disease-specific antigens and/or immunomodulatory molecules are delivered selectively to dendritic cells to induce antigen-specific immune suppression.