Our goal is to develop compounds that are active within an extended time-window post-stroke and are administered intravenously. AGY has carried out a comprehensive functional and chemical genomics approach and derived novel molecular pathways of post-ischemic damage. Drug targets within these pathways have been selected and characterized and compounds that modulate these targets were identified.

AGY-221 is an enzyme target. Potent, selective inhibitors of this enzyme provide strong neuroprotective activity in vivo when administered six hours after occlusion in the middle cerebral artery occlusion model.

AGY-220 is a protein kinase involved in the regulation of ischemia-induced cell death. We have shown that the activity of this kinase is regulated by ischemic conditions in vivo and in vitro. AGY has assembled a compound library of potential kinase inhibitory scaffolds with predicted CNS activity during. A high-throughput screen for AGY-220 has been completed.

AGY-218 is a cysteine protease involved in regulation of inflammatory processes after stroke. Selective inhibitors of this protease are highly neuroprotective against ischemia-induced cell death.

AGY-207 is a novel target involved in post-stroke protein aggregation. Inhibition of the enzymatic function of AGY-207 represents a conceptually new approach towards neuroprotection. Inhibitors of AGY-207 were identified by high-throughput screening and characterized in neuroprotection assays.
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