Inhibition of Memapsin 1 Cleavage in the Treatment of Diabetes
Lead compounds that inhibit the memapsin 1 enzyme are developed to increase pancreatic beta cell mass, offering a therapeutic approach for diabetes treatment and improved glucose control.
Diabetes is a widely prevalent disease that currently affects 25.8 million people in the United States. The predominant form of diabetes is characterized by hyperglycemia resulting from a combination of reduction in pancreatic beta cell activity and mass, which leads to insufficient insulin production. An enzyme called memapsin 1 is known to be part of the biochemical pathway that leads to the problems with pancreatic beta cells and ultimately causes insulin deficiency. Memapsin 1 deactivates a transmembrane protein shown to increase beta cell proliferation and improve glucose stimulated insulin secretion. The transmembrane protein is deactivated when it undergoes ectodomain cleavage in a process triggered by memapsin 1.
Researchers at Purdue University in collaboration with Oklahoma Medical Research Foundation have developed and assayed a series of lead compounds that act as memapsin 1 inhibitors and increase pancreatic beta cell mass. Treatment with these compounds may also be complimented by other therapeutics that increase insulin production, improve glucose homeostasis, or inhibit hyperglucagonemia.
Advantages:
-Improved glucose homeostasis
-Specific enzyme pathway regulation
Potential Applications:
-Medical/Healthcare
-Pharmaceuticals
TRL: 4
Intellectual Property:
Provisional-Patent, 2012-03-29, United States | Utility Patent, 2013-03-11, United States | PCT-Patent, 2013-03-11, WO | Provisional-Patent, 2013-09-13, United States | Utility Patent, 2014-09-12, United States
Keywords: Diabetes, hyperglycemia, memapsin 1 inhibitors, pancreatic beta cell mass, insulin deficiency, glucose homeostasis, enzyme pathway regulation, pharmaceuticals, medical healthcare, ectodomain cleavage