The progression of neurodegeneration during experimental glaucoma is tied to the early degradation of anterograde transport along retinal ganglion cells to central brain targets, which is followed by frank optic nerve degeneration.
Previous findings had shown that injecting pepatin-1 prevented the death of retinal ganglion cells (RGCs) in rats with ocular hypertension. Additionally, transcriptomic analysis in RGCs revealed cAMP response element-binding protein (CREB) signaling to be activated by peptain-1 conjugated with a cell-penetrating peptide, named P1-CPP.
Kiora Pharmaceuticals Inc.’s development and commercialization deal with Théa Open Innovation (TOI), a sister company of Laboratoires Théa, for KIO-301 in degenerative retinal diseases “takes a bit of an industry-standard type of approach” in terms of structure, said CEO Brian Strem.
Traumatic optic neuropathy (TON) is a serious complication combining craniocerebral, orbital and facial injuries. While there is currently no reliable animal model of this condition, it has been previously demonstrated that TON can cause the loss of retinal ganglion cells (RGC). In the current study, researchers from Shanghai Jiaotong University developed a novel mouse model of distal TON, with the aim of assessing the cascade reactions of RGCs in this disease.
