COUR Pharmaceuticals has published details of a study with the Miller Lab at Northwestern University, in which treatment with the COUR NanoParticle Platform (CNP) prevented beta cell destruction in the pancreas, stopping the progression of Type 1 diabetes in non-obese diabetics (NOD).
COUR’s immune-modifying nanoparticles are designed to reprogram the immune system in treating autoimmune disorders. The CNPs’ mechanism of action is induction of regulatory T cells which inhibit the infiltration of inflammatory autoreactive T cells into the pancreas, where they would otherwise destroy insulin producing beta cells.
The findings provide proof of principle for a potential paradigm shift in the treatment of Type 1 diabetes to move patients away from life-long patient-driven management by halting the progression of disease and delaying the need for insulin.
“This is the first time a therapy has held normal glycemic levels in the NOD model, one of the most challenging models for Type 1 diabetes and autoimmunity,” said Stephen Miller, professor of microbiology-immunology. “The results of this preclinical study are very exciting and the team at COUR are passionate to bring the COUR NanoParticle Platform encapsulating human disease relevant antigens (CNP-103) into the clinic to provide a potential life changing therapy.”
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