1 in every 200 people in the US with eye-related irritation are suffering from uveitis. Prolonged use of drugs that help treat chronic uveitis can cause serious side effects such as glaucoma. Having an alternative treatment for uveitis available is imperative.

NIH inventors have proposed targeting the transcription-3(STAT3) pathway required for the differentiation and expansion of Th17 cells as a potential therapy for mitigating uveitis, as genetically modified mice incapable of inducing Th17 cells are resistant to developing uveitis. However, there was not currently a way to deliver inhibitors inside tricellular proteins such as STAT3.

NIH inventors have discovered a novel STAT3-nanobody (SBT-100) that can cross the blood-retina-barrier (BRB), inhibit pathogenic Th17 lymphocytes, and suppress experimental autoimmune uveitis (EAU). The antibody’s small size, rapid clearance from the blood, and sequence similarity with mammalian STAT3 render SBT-100 non-immunogenic. These factors provide important advantages for its therapeutic use, not only for chronic uveitis, but also for inflammatory diseases like multiple sclerosis. 
 

The NIH National Eye Institute is seeking a licensee and/or collaborator for this potential therapeutic for uveitis. If you are interested in learning more or contacting the licensing manager, please view the abstract: Suppression of Uveitis by a STAT3 Single Domain Antibody