Omeros (OMER) Announces Significant OMS721 Data as MASP-2-Targeting Antibody

September 8, 2016 7:04 AM EDT

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Omeros Corporation (Nasdaq: OMER) announced results from its OMS721 complement program. OMS721 is Omeros’ lead antibody targeting mannan-binding lectin-associated serine protease-2 (MASP-2). In well-established animal models of ischemic brain injury or stroke, MASP-2 deficiency or inhibition significantly limited brain infarct size and protected against functional loss. The results of the studies were recently published in the Journal of Neuroinflammation (Orsini et al., Mannan binding lectin-associated serine protease-2 (MASP-2) critically contributes to post-ischemic brain injury independent of MASP-1, J. Neuroinflammation 2016, 13:213) and can be accessed online at

The studies were conducted collaboratively in the laboratories of Prof. Wilhelm Schwaeble at the University of Leicester and of Dr. Maria-Grazia De Simoni, head of the Laboratory of Inflammation and Nervous System Diseases, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri. Focal brain ischemia was induced in wild-type (WT) mice and in mice deficient for MASP-2 by transient middle cerebral artery occlusion (tMCAO). Forty-eight hours after ischemia, histopathologic damage to brain tissue and functional neurological deficits were assessed. All surgical procedures and assessments were performed by investigators blinded to the experimental conditions. MASP-2-deficient mice, compared to WT mice, had significantly reduced infarct volumes (19 percent reduction, p < 0.05) and significantly lower neurological deficits (44 percent [p < 0.05] and 39 percent [p < 0.01] reductions for general and focal functional deficits, respectively). Consistent results were seen with a derivative of Omeros’ lead human MASP-2 antibody OMS721 modified for improved activity in mice and administered in three doses, two prior to and the third following ischemia. Compared to an isotype control antibody, the OMS721 derivative decreased infarct volume by 20 percent (p < 0.05) and reduced general (46 percent, p < 0.01) and focal (45 percent, p < 0.01) neurological deficits. In an additional model of stroke in which brain ischemia is induced by three-vessel occlusion, MASP-2-deficient mice were again protected against ischemic brain damage as evidenced by a 31 percent reduction (p < 0.01) in infarct volume. Immunohistochemical and morphologic analyses further demonstrated the protective effects of MASP-2 inhibition on brain tissue during stroke. Additional studies are planned to define further the therapeutic window for OMS721 in stroke.

“The data clearly identify MASP-2, the effector enzyme of the lectin pathway, as a primary driver in ischemic brain tissue injury,” said Prof. Dr. Eberhard Weihe, director of the Institute of Anatomy and Cell Biology and head of the department of molecular neuroscience at Philipps-University, Marburg. “The strength and consistency of the data in these studies across infarct size, functional outcomes and other histopathological assessments suggest an important role for OMS721, a highly selective MASP-2 inhibitor, in protecting the brain, heart, kidney and other organs from the damage of ischemic injury. Certainly the ability to preserve both cerebral tissue and associated neurological function would represent a major advance in the acute management of stroke patients.”

Omeros currently is conducting a Phase 3 clinical program evaluating OMS721 in atypical hemolytic uremic syndrome as well as Phase 2 programs assessing the drug in hematopoietic stem cell transplant-associated thrombotic microangiopathy, in thrombotic thrombocytopenic purpura and in IgA nephropathy and other complement-related renal diseases.

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