Omeros Corporation (NASDAQ: OMER) today announced pharmacokinetic and pharmacodynamic data from the evaluation of OMS906 in non-human primates. OMS906 inhibits mannan-binding lectin-associated serine protease-3 (MASP-3), the protein critical to activation of the alternative pathway of complement (APC), a key component of the immune system. MASP-3 is responsible for the conversion of pro-factor D to factor D. Converted factor D is necessary for the activation of the APC. The APC is involved in a wide range of diseases, including paroxysmal nocturnal hemoglobinuria (PNH), atypical hemolytic uremic syndrome, age-related macular degeneration, arthritis, asthma and traumatic brain injury. Single-dose administration of OMS906 to cynomolgus monkeys resulted in sustained ablation of systemic APC activity for approximately 16 days. The extent of APC ablation was comparable to that achieved by complete inhibition of factor D in vitro, indicating that OMS906 fully blocked the conversion of pro-factor D to factor D. Similar results were obtained with a number of the company's other antibodies targeting MASP-3. No safety concerns were identified. The primate data are consistent with recently reported results from well-established animal models in which OMS906 reduced the incidence and severity of arthritis by 86 percent (p < 0.005) and 90 percent (p < 0.01), respectively, and significantly improved the survival of PNH-like red blood cells approximately four-fold better (p = 0.029) than did a complement factor 5 (C5) inhibitor. "The OMS906 primate data bode well for the antibody's long-acting inhibition of MASP-3 in patients, and the unique mechanism of action of MASP-3 inhibition likely has significant clinical advantages over many other alternative pathway inhibitors," said Sir Peter Lachmann, ScD FRCP FRCPath FRS FMedSci, Emeritus Sheila Joan Smith Professor of Immunology, University of Cambridge. "In PNH, the MASP-3 inhibitor OMS906 blocks not only intravascular hemolysis, as do C5 inhibitors, but also prevents extravascular hemolysis, a problem that C5 inhibition cannot address. Other alternative pathway targets, such as factor D or factor B, turn over at extremely high rates, making them difficult to drug. In contrast, MASP-3 circulates in the body at a relatively low concentration with a slow rate of turnover, enabling sustained inhibition by either MASP-3-targeting antibodies or small molecules."