Targeting big potassium (BK+) channels for therapeutic treatment
This technology is a modified big potassium (BK+) channel agonist that selectively activates lysosome channels to reduce extracellular deposit formation as a treatment for dry age-related macular degeneration (AMD), exfoliation glaucoma, and Danon disease.
Unmet Need: Lack of effective treatments for AMD
Current FDA-approved therapies for dry age-related macular degeneration (AMD) provide limited efficacy and do not address the underlying cellular dysfunction driving retinal degeneration. As AMD progresses, it can lead to irreversible retinal damage and decreased quality of life in patients. Consequently, there is a critical need to identify disease-modifying therapies for the treatment of AMD and related eye disease.
The Technology: Maxi-K channel agonist that restores lysosomal degradation
This technology is a metabolically stable, modified BK+ agonist that selectively activates lysosomal big potassium (BK+) channels. Increasing channel activity promotes the degradation of misfolded protein aggregates and extracellular deposits, which are major contributors to acute macular degeneration (AMD). It is both metabolically and kinetically stable, with no apparent toxicity in vivo. As such, this technology can be an effective treatment for AMD and other diseases with impaired cellular autophagy.
This technology has been validated in mouse models.
Applications:
- Enhancing lysosomal trafficking
- Promoting degradation of extracellular deposits
- Prevention and treatment of dry acute macular degeneration (AMD)
- Prevention and treatment of exfoliation glaucoma
- Treatment of disease involving autophagic and phagocytic defects
Advantages:
- Specifically targets lysosomal maxi-K channel
- Increases maxi-K channel current by 20-fold
- Restores autophagy and phagocytosis in vivo
- Metabolic and kinetic stability
Lead Inventor:
Patent Information:
Patent Pending
Related Publications:
Tech Ventures Reference:
IR CU25219
Licensing Contact: Kristin Neuman