Skip to content


Of the nearly 15 million individuals affected by AMD in the U.S., approximately 80-90% are the “dry” atrophic type. Dry age-related macular degeneration is characterized by deteriorating macula function caused by the formation of debris (drusen) on the retina causing the macula to degenerate overtime. Dry AMD is thought to be caused by a combination of hereditary and environmental factors. Dry AMD patients can experience some vision loss and frequently experience substantial functional limitations, including vision fluctuations, loss of peripheral vision, and reduced night vision.


The etiology of dry AMD and its advanced stages is multifactorial. Monotherapies evaluated for clinical utility in this disease have exhibited nominal or no improvement in clinical outcomes. The multiple pathogenic mechanisms in dry AMD initiation and progression include hyperinflammation, cell degeneration and atrophy, hypoxia, and dysfunctional lipid metabolism, among others. These warrant the development of therapies which can interface with these many disease mediators. Furthermore, different disease targets, which may be inside of the cell or located extracellularly, may require multiple therapeutic modalities; for example, a small molecule may be tailored for intracellular targets that are considered undruggable by antibodies. Therefore a single molecule triplet therapy enabled by our platform accommodates large and small molecules alike and facilitates, for the first time, the modulation of multiple distinct pathological processes in parallel.