More than eighty percent of all stroke cases are ischemic insults caused by blocked blood flow and oxygen deprivation to a focal brain area, typically due to a blood clot. Ischemia leads to massive cell death resulting in an irreversibly damaged infarct core with surrounding, potentially salvageable area called the penumbra. Reperfusion* with tPA is the only pharmacologic therapy. However, rapid reperfusion, although necessary for the restoration of brain metabolic activity, comes with additional health risks.The development of neuro-protection strategies is badly needed to protect brain cells from both ischemia and reperfusion injury and to increase the time window for thrombolytic treatment. A number of cellular and molecular mechanisms have been studied, but none have provided a solution. Zocere, Inc.’s drug is a derivative of the brain-specific STEP protein tyrosine phosphatase, which is an important downstream regulator of NMDAR-dependent neuronal injury. Other studies that have examined the importance of NMDAR blockade as a strategy for ischemic stroke treatment have failed. Our technology is different. By targeting downstream signaling, molecules that are activated following NMDAR stimulation may protect neurons from damage and obviate the deleterious consequences of NMDAR antagonism. This is a significant advancement. Our stroke drug candidate is a cell-permeable recombinant peptide that has been overexpressed in E. coli and purified using standard laboratory procedures. The peptide can cross the blood-brain barrier, is resistant to degradation, and can bind constitutively to its substrates. It has been demonstrated in rodent models of transient ischemic stroke that intravenous administration of the peptide will significantly reduce brain damage. This promising new tool for ischemic stroke therapy has the potential to be the first neuro-protectant drug in the market. * Tissue damage caused when blood supply returns to the tissue after a period of ischemia or lack of oxygen.
“The development of neuro-protection strategies is badly needed to shield neurons from both ischemia and reperfusion injury and widen the time window for thrombolytic treatment.” Surojit Paul, PhD Inventor & Associate Professor Department of Neurology University of New Mexico
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