SEATTLE, April 2, 2013 /PRNewswire/ -- Omeros Corporation (NASDAQ: OMER) today announced positive data using OMS721, the lead human monoclonal antibody in Omeros' mannan-binding lectin-associated serine protease-2 (MASP-2) program, in a well-established animal model of thrombotic microangiopathy (TMA), a disorder that occurs in the microcirculation (e.g., venules and capillaries) of the body's organs, most commonly the kidney and brain. Omeros expects to submit a European Clinical Trial Application (CTA) this quarter to initiate clinical trials evaluating OMS721. The lead indication planned for OMS721 clinical trials is atypical hemolytic uremic syndrome (aHUS), a rare but life-threatening form of TMA. Omeros controls the worldwide rights to MASP-2 and all therapeutics targeting MASP-2, a novel pro-inflammatory protein involved in activation of the complement system – an important component of the immune system. The complement system plays a role in the inflammatory response to tissue damage or microbial infection. OMS721 selectively inhibits MASP-2, blocking the lectin pathway of the complement system while leaving intact the classical pathway, or the acquired immune response to infection. The Company has conducted a series of preclinical studies that suggest that MASP-2 inhibition may have a preventive or therapeutic effect in the treatment of aHUS, HUS, wet age-related macular degeneration (AMD), paroxysmal nocturnal hemoglobinuria (PNH), transplant-related complications, ischemia-reperfusion injury, and other immune-related disorders. The studies reported today were conducted to support the planned initial indication for OMS721 – aHUS. In this well-established model, thrombus (blood clot) formation is induced in microvessels following phototoxic injury of the vessel wall. Using intravital microscopy, a high-resolution imaging technique that allows direct visualization of dynamic biological processes in the microcirculation in live animals, the effects of OMS721 on thrombus formation were assessed. Specifically, the study evaluated OMS721's ability to delay the time to onset of thrombus formation and to complete occlusion of the blood vessel. 100 percent of isotype-antibody control animals versus 71 percent of OMS721-treated animals showed thrombus formation, with the initiation of thrombus formation delayed approximately three-fold in the OMS721-treated group relative to control (a median of 19.0 vs. 6.8 minutes; p=0.0097). Eighty percent of control-treated animals showed complete occlusion within the observation period while only 43 percent of those treated with OMS721 occluded completely. Median time to complete occlusion was 18.0 minutes for control and 38.0 minutes for the OMS721-treated animals (p=0.0036).