Anti-Complement

Catalyst has developed and optimized a propriety method to create novel proteases that include anti-C3 protease assets such as CB 2782 for ischemia-reperfusion injury such as delayed graft function (DGF) after kidney transplantation and the preclinical leads in the dry age-related macular degeneration (AMD) program. In September 2016, Catalyst discontinued internal anti-complement program discovery activities to focus resources on its two clinical hemophilia programs. These assets are available for partnering. Please contact Business Development for further information.

The complement cascade is a series of molecular processes that plays a central role in the body’s inflammatory and immune responses and helps to localize specific immune system cells at the site of infection or inflammation. Drugs that target the complement cascade could potentially be used in several indications, including the prevention of transplant rejection, age-related macular degeneration, cardiovascular disease, pulmonary diseases, and autoimmune disease.

CB 2782 is a novel protease derived from human membrane type serine protease 1 (MTSP-1) that cleaves complement factor 3 (C3) and may be developed to prevent ischemia-reperfusion injury driven delayed graft function (DGF) following kidney transplant. Other opportunities might include coronary artery bypass graft (CABG), acute myocardial infarction (AMI), and stroke.

Catalyst also has earlier stage, distinct anti-complement lead molecules for dry age-related macular degeneration (dry AMD) which may have significant benefits (i.e. superior efficacy and less frequent dosing) over existing anti-complement programs in development for dry AMD.