With Stanford University and Johns Hopkins University’s recent breakthroughs into potential neuroprotective strategies for Parkinson’s and Alzheimer’s, the topic of neuroprotection and how it might be applied to glaucoma is currently witnessing quite a resurgence of interest.
Given this renewed interest in the field, it is perhaps telling that Glaucoma 360, upcoming in San Francisco (January 29-31, 2026), is featuring the distinguished retina specialist (yes, retina!) and professor of ophthalmology at the University of California, San Francisco (UCSF), Dr. Eugene de Juan, Jr., as its keynote speaker.
De Juan’s speech, “Neuroprotection: The Need, The Opportunity, The Path,” will center around the “need” for glaucoma neuroprotection (i.e., to create a drug that can address the well-known issues of patient compliance currently associated with glaucoma and daily drops), as well as his own research into the field.
As Chief Strategy Officer at Perceive Pharma (a spin-out company of Perceive Biotherapeutics concentrated on developing novel small molecule neuroprotective therapeutics), de Juan is building on the previous works of researchers like Dr. Donald Zack (ophthalmologist and geneticist at Johns Hopkins, and co-director of the Center for Stem Cells and Ocular Regenerative Medicine (STORM)) and Dr. Derek Welsbie (Principal Investigator at the Welsbie Lab) in hopes of developing neuroprotective therapeutics for glaucoma.
Earlier this week, and ahead of his impending Glaucoma 360 keynote, I spoke with de Juan to learn more about this research. “One of [the] pathways we’re particularly focused on is the DLK/LZK (Dual Leucine Zipper Kinase/Leucine Zipper Kinase) pathway,” he explained. “In glaucoma, this is one of the first signaling pathways that are activated when you have axonal damage, like in glaucoma at the optic nerve. The research from Johns Hopkins determined that this pathway was the primary, earliest, and strongest pathway identified with axonal damage.”
De Juan went on to discuss how Perceive Pharma is currently developing a drug – PBI-671 – aimed at inhibiting the DLK/LZK pathway to directly prevent the vision loss associated with glaucoma. “[We have already done] animal experiments that show almost complete protection of retinal ganglion cells in the presence of this drug [and] we're now trying to develop it for sustained release,” he said.
And while de Juan concedes that the research is not quite ready to be put into clinical translation just yet, with glaucoma treatments – as well as other ophthalmic conditions such as geographic atrophy (GA) and diabetic retinopathy – being explored by a number of different companies, at various stages of clinical development, it is certainly an exciting time to be involved in neuroprotection research.
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