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EmtinB
Glaucoma and Our Approach with EmtinB
Glaucoma and Our Approach with EmtinB
Glaucoma is an eye disease that damages the optic nerve, which connects the eye to the brain. It is one of the leading causes of blindness worldwide, affecting more than 60 million people globally and around 300,000 Australians.
Current therapies can reduce eye pressure and slow disease progression, but glaucoma cannot be cured. Once vision is lost, it cannot be restored.
Why Glaucoma Causes Vision Loss
Glaucoma is most often linked to elevated intraocular pressure (IOP) caused by impaired drainage of the eye’s fluid (aqueous humor). Over time, this pressure damages astrocytes (nerve-supporting cells) and leads to the degeneration of retinal ganglion cells in the optic nerve, resulting in irreversible vision loss.
While today’s treatments lower IOP, this alone does not guarantee protection against further damage to the optic nerve.
The Promise of EmtinB
We believe EmtinB has the potential to protect both astrocytes and retinal ganglion cells from pressure-related injury. By directly targeting the mechanisms that lead to nerve damage, EmtinB may not only stop disease progression but also offer the possibility of reversing vision loss.
What is EmtinB?
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Origin: EmtinB is based on the beta-domain of metallothionein-II (MT-II), a naturally occurring protein involved in neuroprotection.
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Design: It is manufactured as a tetrameric dendrimer, where four short peptides are linked via a lysine backbone. This structure provides improved stability compared to single peptides, which normally degrade quickly in the body.
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Mechanism: EmtinB binds to LDLR-family cell receptors, activating intracellular pathways that promote neuron survival and reduce neuroinflammation.
Development Status
EmtinB is currently being developed for:
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Optic nerve diseases such as glaucoma
We have completed GLP toxicology studies and CMC manufacturing programs, and are preparing to begin Phase I clinical trials.
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