Glaucoma is the number one cause of irreversible blindness worldwide. High pressure in the eye can lead to optic nerve damage, which can progress to permanent vision loss. For this reason, reduction of intraocular pressure is the main therapeutic mechanism available. Unfortunately, glaucoma can continue to progress even in patients with normalized intraocular pressure. Therefore, there is an urgent need for the development of new therapeutic approaches with distinct mechanistic targets that prevent vision loss in glaucoma patients.

Targeting glucagon-like peptide 1 receptor (GLP1-R) prevents the cellular death responsible for vision loss in glaucoma. Even in cases where intraocular pressure remains elevated, the therapeutic is able to improve the survival of cells required for vision.

Pro-inflammatory astrocytes in glaucoma contributes to the death of retinal ganglion cells, which make up the optic nerve and are required for vision. Reduction of intraocular pressure does not prevent activation of these astrocytes. Investigators identified that targeting GLP1-R in a mouse model of glaucoma reduces ocular inflammation and prevents the damaging effects of these astrocytes, thereby rescuing retinal ganglion cells.

• Reduces expression of pro-inflammatory factors in resident microglia and infiltrating macrophages (IL-1a, TNF-a, C1q)
• Improves retinal ganglion cell survival in environment of elevated intraocular pressure (~25% after 42 days in mouse model of glaucoma)