Overview
Glaucoma is usually linked to high pressure in the eye. All current treatments for glaucoma aim to lower eye pressure to prevent more damage to the optic nerve. This is true even for drugs to treat ‘normal pressure’ glaucoma.
But glaucoma treatments don’t always work well enough; they don’t reduce pressure enough to prevent ongoing optic nerve damage in some patients. In others, lowering pressure doesn’t stop the damage from getting worse. So we need to develop some alternatives.
In this project the research team is aiming to identify new substances that work well both at lowering eye pressure and at preventing nerve damage. Their results should give us proof-of-concept data that can be used to plan clinical trials.
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Scientific summary
Characterisation of the mechanism of a potential new glaucoma drug.
New drugs for glaucoma are required, particularly to treat the on-going neurodegenerative aspects of the disease which do not respond to current IOP lowering therapies such as latanoprost. The research team has identified new highly-selective activators of an ion channel. The drugs can address disease pathology in three ways: 1) neuronal (retinal ganglion cell) protection, 2) improving vascular blood flow and 3) targeting the trabecular meshwork and Schlemm’s canal endothelium to improve outflow and lower IOP.
In this project they aim to characterise the activities of their molecules in three different models of ocular conditions, testing IOP outflow mechanisms (ex vivo), neurodegeneration induced by raised pressure and neurodegeneration induced by inflammation (optic neuritis). They will define their neuroprotective effect and mechanism of action at the cellular and systems level, with the goal of IOP reduction and retinal neuroprotection.
The results will provide crucial proof of concept data in vivo for the molecules which can then be developed (with further funding) as new drugs. Intellectual property will be managed by UCL.