In addition to reducing IOP, activation of the A1 receptor is also associated with protecting nervous system tissue (neuroprotection). In preclinical models, A1 receptor activation at the onset of neuronal injury has been shown to attenuate brain damage, whereas its blockade exacerbates damage*. Therefore, we believe trabodenson may also have the potential to protect retinal ganglion cells (RGCs) and directly interfere with the process leading to irreversible blindness in glaucoma patients.

In a preclinical model of retinal ischemia secondary to acute ocular hypertension, trabodenoson treatment in an eye drop formulation was able to protect ~100% of RGCs from death secondary to the high pressure ischemic insult.