This technology is an oral, small-molecule therapeutic that selectively inhibits the transcription factor FOXO1 to reprogram intestinal cells into insulin-producing cells, providing a non-invasive treatment option for Type 2 Diabetes.
Type 2 diabetes affects over 23 million people in the U.S. and is a leading cause of morbidity and mortality worldwide. Current treatment strategies, such as injectable insulin and GLP-1 analogs, are invasive and often fail to address the underlying loss of functional beta cells. Widely prescribed oral drugs like metformin can have gastrointestinal and metabolic side effects, and do not restore insulin production capacity. There remains a strong clinical need for non-invasive, durable therapies that restore or replace beta cell function to maintain glycemic control without daily injections.
This technology describes a novel class of pyrazole-based small molecules that selectively inhibit the FOXO1 transcription factor in the gastrointestinal tract. FOXO1 inhibition triggers conversion of enteroendocrine cells into insulin-producing cells, functionally replacing damaged or deficient pancreatic beta cells. This platform represents a promising oral therapeutic approach for insulin-dependent diabetes, combining ease of administration with potential long-term restoration of endogenous insulin production.
The compounds have been synthesized and tested in vitro, demonstrating selective inhibition of FOXO1 and induction of insulin expression in gut-derived cells.
Patent Pending (US 20220185797)
IR CU19186
Licensing Contact: Cynthia Lang
