SEATTLE, July 31, 2012 /PRNewswire/ -- Omeros Corporation (NASDAQ: OMER) today reported that it believes it has identified the proteins that activate the alternative pathway of the complement system, an important part of the immune system. The work was led by the Company's collaborator, Professor Wilhelm Schwaeble of the University of Leicester, and Omeros controls the worldwide exclusive rights to this discovery. The complement system plays an important role in the inflammatory response and becomes activated as a result of tissue damage or microbial infection. The discovery announced today further expands Omeros' mannan-binding lectin associated serine protease-2 (MASP-2) program and may permit the development of new antibodies to treat disorders that involve alternative pathway activation. The complement system can be activated through the following three distinct pathways: the classical, lectin and alternative. The classical pathway is part of the acquired immune system while the lectin and alternative pathways are part of the innate immune system. In contrast to the classical and lectin pathways, no specific recognition molecules had previously been identified to drive complement activation via the alternative pathway. In connection with his research for the MASP-2 program, Omeros collaborator Professor Schwaeble has now identified the proteins that drive activation of the alternative pathway. In addition to advancing Omeros' MASP-2 program, this discovery is expected to lead to new therapeutics targeting disorders linked to the alternative pathway. Omeros has recently filed a series of patent applications that claim a broad intellectual property position related to this new discovery, potential therapeutics targeting this protein alone or in conjunction with MASP-2, and a host of inflammatory disease indications linked to the inhibition of this protein and/or MASP-2. "The discovery of the mechanism that directs alternative pathway activation has recharted our understanding of the complement system and answered one of the remaining questions about its role in the inflammatory response," said Dr. Wilhelm Schwaeble, Professor of Immunology at the University of Leicester and Royal Society-Wolfson Research Merit Award Holder. "This new paradigm could lead to improved therapies to treat complement-mediated disorders." Omeros' MASP-2 program has been focused on the development of antibodies that target MASP-2 and its unique role in the activation of the lectin pathway. The Company has conducted a series of in vivo studies that suggest that MASP-2 inhibition may have a preventive or therapeutic effect in the treatment of hemolytic uremic syndrome (HUS), atypical HUS (aHUS), paroxysmal nocturnal hemoglobinuria (PNH), wet age-related macular degeneration (AMD), ischemia-reperfusion injury, transplant-related complications and other immune-related disorders. "In parallel with our MASP-2 program initially targeting aHUS, Omeros is now advancing the development of antibodies that would block activation of the lectin and alternative pathways to treat inflammatory disorders linked to both," said Gregory A. Demopulos, M.D., chairman and chief executive officer of Omeros. "These antibodies are expected to be delivered by a single subcutaneous or intramuscular injection and, equally important, to not interfere with the classical pathway – a critical component of the acquired immune response to infection. We expect the same advantages with our MASP-2 antibody, and our team is working hard to move that product into the clinic in the first part of 2013." About Omeros' MASP-2 Program MASP-2 is a novel pro-inflammatory protein target involved in activation of the complement system, which is an important component of the immune system. The complement system plays a role in the inflammatory response and becomes activated as a result of tissue damage or microbial infection. MASP-2 appears to be unique to, and required for the function of, one of the principal complement activation pathways, known as the lectin pathway. Importantly, inhibition of MASP-2 does not appear to interfere with the antibody-dependent classical complement activation pathway, which is a critical component of the acquired immune response to infection, and its abnormal function is associated with a wide range of autoimmune disorders. MASP-2 is generated by the liver and is then released into the circulation. Adult humans who are genetically deficient in one of the proteins that activate MASP-2 do not appear to be detrimentally affected by the deficiency. Therefore, Omeros believes that it may be possible to deliver MASP-2 antibodies systemically.