Abstract

We have developed a partial peptide of RANKL (receptor activator of NF-κB ligand) that suppresses TLR (toll-like receptor)-related inflammation via RANKL/RANK (receptor activator of nuclear factor-κB) signals in the acute phase of ischemic stroke. This peptide has been found to be a therapeutic agent for ischemic stroke that can be used in combination with tPA in a mouse model. Based on the findings, we are working on translational research to aim for clinical application of this peptide through collaboration with pharmacy companies. However, the problem is that the need for development of medication in the acute stage of ischemic stroke is currently low in pharmaceutical companies due to the failure of many investigational drugs in the past. To overcome the problem, we are examining the effects of this peptide in other diseases included in the company's priority areas and explaining the environmental changes in the clinical trials due to the development of endovascular treatment in the acute stage of ischemic stroke.

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