Neurimmune Announces Publication in Nature Communications of its Experimental Therapy Depleting Pathologic IAPP Aggregates to Protect Beta Cell Health
Neurimmune announced today that preclinical data relating to its human antibody NI203 targeting pathologic aggregates of the beta cell peptide hormone islet amyloid polypeptide (IAPP) have been published in the current issue of Nature Communications. The paper “A human antibody against pathologic IAPP aggregates protects beta cells in type 2 diabetes models” describes a monoclonal antibody that binds selectively to IAPP oligomers and protects from IAPP toxicity.
NI203 was discovered by Neurimmune’s Reverse Translational MedicineTM (RTMTM ) technology through comprehensive analyses of memory B cell repertoires derived from healthy elderly subjects. The antibody efficiently neutralized IAPP aggregate toxicity by preventing membrane disruption and apoptosis in vitro. NI203 treatment of transgenic or human islet-engrafted rodent type 2 diabetes models triggered the clearance of IAPP oligomers, resulting in beta cell protection and improved glucose control.
“We are excited about these results which provide the scientific basis for the development of NI203 as a potential disease-modifying treatment for patients with type 2 diabetes and progressive beta cell loss”, said Jan Grimm, CSO of Neurimmune. “Depleting pathologic IAPP oligomers from the pancreas is a novel therapeutic strategy anticipated to translate into durable control of beta cell health.”
Type 2 diabetes is a chronic metabolic disorder characterized by insulin resistance and progressive dysfunction and loss of insulin-producing pancreatic beta cells, resulting in insulin deficiency and elevated blood glucose. While the primary cause of beta cell failure in type 2 diabetes is unknown, the accumulation of aggregated forms of IAPP in pancreatic islets is a key contributor to decreased beta cell function and mass.