This page contains Forward Looking Statements made as of October 19, 2016.*

Vepoloxamer for Stroke

Stroke is the fourth leading cause of death in the U.S. and a leading cause of long-term disability.  Over 85% of all strokes are ischemic strokes, meaning they occur when a blood vessel that supplies blood to the brain is occluded, or blocked, by a clot. Timely restoration of blood flow is critical for stroke patients as brain damage is a rapid, progressive process.  In a typical large-vessel acute ischemic stroke, 1.9 million neurons may be lost each minute. Recombinant tissue plasminogen activator, or tPA, is approved for treatment of acute ischemic stroke. However, in stroke patients, due to bleeding risks, tPA should not be administered until intracranial hemorrhage has been excluded by a cranial computerized tomography, or CT, scan, which can delay treatment. At the same time, tPA has not demonstrated improved outcomes for stroke patients if administered more than three hours after onset of stroke symptoms.

There is a significant need for a pharmacologic agent that enhances the breakdown of blood clots, or thrombolysis. The mechanistic activities of vepoloxamer facilitate thrombolysis and suggest potential to shorten the time to clot lysis or attain similar thrombolysis at a reduced dosage of thrombolytic, such as tPA. In addition, vepoloxamer’s cytoprotective properties may reduce reperfusion injury, with the potential to limit tissue necrosis. Further, improving microvascular flow and distal tissue reperfusion should also reduce untoward events from the no-reflow phenomenon, relieving persistent tissue ischemia despite restoration of large vessel patency. Additionally, because the risk of hemorrhagic complications from thrombolytics is associated with the dose and duration of infusion, more rapid thrombolysis and/or lower dosage of thrombolytic agent has the potential to decrease the risk of bleeding.

Development Status

We are currently evaluating partnership opportunities for vepoloxamer in ischemic stroke (phase 2-ready).

Based on our nonclinical data, as well as published data from third party studies of poloxamer 188, we believe, and several medical experts in the field have agreed, that sufficient data now exists to support clinical development of vepoloxamer in ischemic stroke. Nonclinical studies have demonstrated that vepoloxamer in combination with fibrinolytic agents can shorten time to thrombolysis and improve post-lysis perfusion. Vepoloxamer also expanded the treatment window for t-PA in a nonclinical animal model.  Additionally, in clinical studies, vepoloxamer was well-tolerated in healthy volunteers and individuals with sickle cell disease at similar or higher doses than are anticipated for use in stroke.

In August of 2016, we received a Small Business Innovation Research (SBIR) grant from the National Institute Of Neurological Disorders And Stroke (NINDS) of the National Institutes of Health (NIH).  The grant will support investigation of vepoloxamer in combination with tissue plasminogen activator (tPA) in experimental models of embolic stroke.  Mast will collaborate on the grant with leading stroke researchers at the Neuroscience Institute at Henry Ford Health System for this study, which is expected to be completed July 2017.

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