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Omeros Announces Publication of Data From Antifibrinolytic Program
Date:2/10/2011

PI-2, referred to as KD1, inhibits plasmin but, like Trasylol®, also inhibits kallikrein and Factor XIa. Dr. Bajaj and her colleagues demonstrate that a minimal change to the sequence of the KD1 protein increases its activity against plasmin approximately 6-fold while dramatically reducing its inhibition of kallikrein and Factor XIa by more than 100-fold. Because the variant KD1 proteins developed by the authors and exclusively licensed to Omeros are more selective than Trasylol®, they could provide more effective bleeding control with fewer side effects. Additionally, as a human protein derivative, these agents are expected to reduce the potential for immunological side effects.

The paper shows the variant KD1 reduced blood loss in a rodent model of surgical bleeding by 85 percent relative to saline treatment, demonstrating an antifibrinolytic effect at least equal to Trasylol®. Similar antifibrinolytic activity of a related variant KD1 also controlled by Omeros was confirmed by other researchers using human plasma evaluated by thromboelastography. Thromboelastograms are used clinically to assess the level of fibrinolysis in patients during surgical procedures at risk for extensive blood loss.

Importantly, the authors also found that the variant KD1 does not slow blood clotting as measured by the partial thromboplastin time (aPTT), a standard indicator of blood's ability to coagulate.  Conversely, Trasylol® increased aPTT by 60 percent, which could significantly prolong bleeding in trauma and surgical patients.  

Omeros believes the efficacy and improved selectivity of the variant KD1 provides a novel approach to the control of bleeding from surgery and trauma. Omeros has initiated scale-up activities of its lead antifibrinolytic compound in preparation for clinical trials.  

About Omeros' Antifibrinolytic Program

Omeros is developing a series of novel antifibrinolytic agents for the cont
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SOURCE Omeros Corporation
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