The University of Alabama at Birmingham startup TIXiMED, Inc., has obtained clearance from the United States Food and Drug Administration to proceed to clinical trials under an Investigational New Drug for TIX100, its novel oral Type 1 diabetes drug. This represents a major milestone in the development of this new approach to T1D treatment and gives TIXiMED the green light to start human studies with TIX100.
The development of TIX100 is based on decades of research by Anath Shalev, M.D., the Nancy R. and Eugene C. Gwaltney Family Endowed Chair in Juvenile Diabetes Research in the UAB Division of Endocrinology, Diabetes and Metabolism in the Department of Medicine and the director of the UAB Comprehensive Diabetes Center.
“Since TIX100 is available orally, it promises to ease the burden of the multiple daily insulin injections or insulin infusions people with T1D depend on,” Shalev said. “We are so excited to see our work being translated into a better diabetes treatment that may impact so many people and provide a breakthrough for T1D.”
Prior to first use in humans, every new drug must be rigorously safety tested. To get IND approval, TIX100 underwent extensive safety pharmacology and toxicokinetics testing as well as elaborate chemistry, manufacturing and control development to ensure an extremely pure, medical-grade drug product for the upcoming clinical trial.
Shalev noted that TIX100 is a potent, effective and specific TXNIP inhibitor and as such functions differently from any approved diabetes drug. By promoting proper islet cell function, it further targets a key underlying cause of the disease.
In diabetes, TXNIP, a protein involved in oxidative stress, is elevated in pancreatic islets and causes beta cell death and dysfunction. Shalev’s research has shown that inhibiting TXNIP protects beta cells and promotes beta cell health and function.
Shalev first identified TXNIP in 2002 in human islets exposed to high glucose and went on to show that it played an important role in glucose toxicity and diabetic beta cell loss.