Scientists Discover New Compound Blocking Root Cause of Diabetic Complications
A novel experimental drug, RAGE406R, has shown promise in preventing damage to the heart, kidneys, and tissues caused by diabetes by inhibiting a harmful protein interaction.
Study Findings
Researchers at NYU Langone Health tested RAGE406R on mice, demonstrating that it blocks the interaction between two proteins, RAGE and DIAPH1. This interaction is linked to complications such as organ damage and delayed wound healing in diabetes.
“There are currently no treatments that address the root causes of diabetic complications, and our work shows that RAGE406R can – not by lowering the high blood sugar, but instead by blocking the intracellular action of RAGE,” said Ann Marie Schmidt, MD, co-senior study author and Dr. Iven Young Professor of Endocrinology at NYU Grossman School of Medicine.
Mechanism and Impact
RAGE406R is a small molecule designed to target the RAGE protein specifically. By preventing DIAPH1 from binding to RAGE, the compound reduced tissue swelling and accelerated recovery in both human cells and mice models.
The treatment lowered both immediate and long-term complications related to types 1 and 2 diabetes, addressing issues current drugs do not fully cover.
Potential Clinical Significance
If future human trials confirm these results, RAGE406R could offer a new therapeutic approach that targets the underlying cause of diabetic damage rather than just controlling blood sugar levels. This would fill existing treatment gaps, especially since most current medications focus on type 2 diabetes.
“If confirmed by further testing in human trials, the compound could potentially fill gaps in treatment, including that most current drugs work only against Type 2 diabetes," said Dr. Schmidt.
Published Source
The study appeared as a cover story in Cell Chemical Biology.
Summary: RAGE406R blocks a key protein interaction causing diabetic tissue damage, promising a novel treatment targeting the root causes of complications beyond blood sugar control.
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