At Galimedix, we aim to stop neurodegeneration at its source and develop game-changing neuroprotective therapies for the treatment of serious eye and brain diseases impacting millions of people.

Normal amyloid beta (Aβ) monomers are important to neuronal function, but misfolding of these monomers can lead to the development of toxic forms of Aβ – oligomers and protofibrils – that can be highly damaging to the retina and brain cells, and, according to a large number of studies, the underlying cause of neurodegenerative diseases of the eye, such as dry age-related macular degeneration (dAMD), glaucoma. Recent approvals and Phase 3 results of anti-Aβ drugs also have validated them as a key target in Alzheimer’s disease.

To tackle this, we are developing orally and topically administered small molecules that target the beginning of the Aβ peptide aggregation cascade and, prevent the formation of the toxic species. GAL-101/201 have a unique mode of action, through which they only remove already formed toxic species, potentially impacting disease progression without disturbing normal neuronal function.