Trabodenoson found to prevent retinal ganglion cell death, the cause
of vision loss in glaucoma patients, in preclinical animal model
This preclinical neuroprotection study was designed to compare the protective effects of trabodenoson and brimonidine in a rat model of ischemia-induced retinal ganglion cell (RGC) death. Trabodenoson was delivered as an eye drop at a clinically relevant dose. Results of the study showed that trabodenoson provided 100% protection against the thinning of the ganglion cell layer (p=0.001 compared to vehicle-treated eyes).
“These data are both encouraging and consistent with the known effects of naturally occurring or endogenous adenosine in central nervous system tissue where it is well known to be neuroprotective”, said
The study was completed in the laboratory of
About Trabodenoson for Glaucoma
Trabodenoson is an eye drop therapy in clinical development for the treatment of glaucoma, a leading cause of blindness globally. In a clinical Phase 2b trial, trabodenoson was found to be safe and well tolerated as a single agent, with intraocular pressure (IOP) lowering efficacy in the range of the prostaglandin analogs. Another Phase 2b clinical study of trabodenoson, in combination with the most widely-prescribed glaucoma drug, the prostaglandin analog latanoprost (LAT), is ongoing. Patients admitted to the trial must have elevated intraocular pressure (IOP) that remains uncontrolled despite ongoing treatment with latanoprost. The study will measure the additive or synergistic IOP-lowering effect of trabodenoson when combined with LAT, and will also evaluate the safety and tolerability of the combined treatment regimen. Top line data is expected in the 4th quarter of 2014.
When trabodenoson stimulates adenosine A1 receptors, fluid outflow is increased via the trabecular meshwork, the eye’s main drainage pathway, and the ocular pressure is reduced. This novel mechanism of action is significantly differentiated from currently approved products, as well as those in development.
Current products for glaucoma, such as prostaglandins, lower IOP by either reducing the inflow of fluid in the eye or by increasing its drainage through a secondary outflow pathway in the eye — the uveoscleral pathway. However, none of these drugs safely and effectively target the trabecular meshwork, the primary outflow pathway where the majority of aqueous fluid exits the eye. The trabecular meshwork comprises a pressure-sensitive mechanism through which healthy eyes maintain a normal, safe ocular pressure (IOP). As the eye ages and glaucoma advances, flow through the eye’s trabecular meshwork grows increasingly difficult. Trabodenoson has been shown to target an endogenous pathway that increase the natural metabolic activity of the trabecular meshwork tissue, by up-regulating proteases found in the eye. These proteases are responsible for clearing out hydrolyzed proteins, which block outflow, thus restoring the eye to a more normal, healthy state.
For additional information on
William McVicar, 781-676-2122