Overview

The detrimental effects of neuroinflammation, especially neuromyelitis optica spectrum disorder (NMOSD), on cognitive performance can include severe vision loss, motor deficits, and cognitive decline. We have invented a method that targets the detrimental effects of neuroinflammation on cognitive performance by using a CRTH2 (chemoattractant receptor-homologous molecule expressed on Th2 cells) antagonist as an CHI3L1 inhibitor.

Market Opportunity

The neurological disorder NMOSD is characterized by inflammation of the optic nerves and spinal cord. One type of NMOSD, the result of primary astrocytopathy caused by autoantibodies targeting the astroglial protein aquaporin 4 (AQP4), causes severe vision loss, motor deficits, and cognitive decline. Considering this, there is a need for effective therapies to treat the cognitive deficits in NMOSD and other central nervous system disorders.

Innovation and Meaningful Advantages

We have invented a method that targets the detrimental effects of neuroinflammation, including NMOSD, on cognitive performance. Our invention blocks the interaction of CHI3L1 with the CRTH2 receptor by administering a CRTH2 antagonist. The CHI3L1 inhibitor may consist of a small molecule, an antibody molecule, a nucleic acid, or a polypeptide. The treatment can promote neural stem cell proliferation and differentiation. In addition to NMOSD, it can be used to treat Alzheimer’s disease, glioblastoma, and autoimmune disorders such as multiple sclerosis.

Collaboration Opportunity

We are interested in exploring 1) research collaborations with leading pharmaceutical companies to develop this method of treatment; and 2) licensing opportunities with pharmaceutical companies.

Principal Investigator

IP Information

PCT/CN2023/083374, Filed March 23, 2023

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