Overview
- Peer-reviewed results show the compound prevented RAGE–DIAPH1 binding, reducing inflammation, cell death, and organ injury in diabetes models.
- In human blood–derived cells from people with type 1 diabetes, RAGE406R lowered levels of the proinflammatory chemokine CCL2.
- Topical treatment accelerated wound closure in obese mice with type 2 diabetes while dampening inflammatory responses.
- The candidate was redesigned to remove a structural feature that caused the prior lead, RAGE229, to fail a standard genotoxicity screen.
- The study appears as a Cell Chemical Biology cover story with supporting grants and patent filings, and the team plans structural and biomarker studies to advance toward clinical testing.