Dry AMD / GA
Dry AMD is a chronic, progressive eye disease affecting the macula, the central part of the retina responsible for sharp, detailed vision. It is the most common cause of vision loss in people over 60 in developed countries, affecting an estimated 170–200 million people worldwide.
Dry AMD occurs when the light-sensitive cells (photoreceptors) in the macula slowly break down over time. The “dry” form accounts for approximately 80–90% of AMD cases and typically progresses more slowly than the wet form.
A hallmark of dry AMD is the accumulation of drusen, small yellow deposits of fatty proteins, beneath the retina. Another key feature is lipofuscin accumulation in the retinal pigment epithelium (RPE), which contributes to photoreceptor degeneration.
In its most advanced form, dry AMD progresses to geographic atrophy (GA), patches of retinal degeneration where the photoreceptors and RPE cells have died, creating regions of complete vision loss that grow over time.
GA affects approximately 8–12 million people globally and is responsible for significant permanent central vision loss. Unlike wet AMD, GA does not involve abnormal blood vessel growth and cannot be treated with anti-VEGF injections.
Early Stage
Intermediate Stage
Advanced (Geographic Atrophy) Stage
Despite significant investment, approved treatments for dry AMD and geographic atrophy remain limited and controversial.
Apellis Pharmaceuticals
Shows modest reduction in GA lesion growth rate but no demonstrated improvement in visual function. Rejected by the EMA and MHRA. ~$587M in 2025 revenue but ~75% of GA patients remain untreated.
Astellas Pharma
Similarly slows lesion growth but has not demonstrated meaningful visual acuity benefit. Also rejected by the EMA and MHRA. Requires repeated intravitreal injections.
Various
Reduces risk of progression to advanced AMD in some patients but has no effect on early dry AMD and does not reverse existing damage.
The gap in treatment
Both approved GA treatments require frequent intravitreal injections, have been rejected by European regulators, and do not restore lost vision. There is no approved oral treatment for dry AMD. For many patients and clinicians, the balance of benefit and burden remains unsatisfactory.
SunRegen is investigating whether SBC003's neuroglobin-induction mechanism can address the photoreceptor apoptosis underlying dry AMD through a fundamentally different pathway than complement inhibition.
Mechanism relevance
SBC003 induces neuroglobin expression, which protects photoreceptors against apoptosis and prevents protein aggregate formation, including lipofuscin-related toxicity implicated in RPE dysfunction in dry AMD.
Oral administration advantage
An orally administered neuroprotective agent would offer a major patient convenience and compliance advantage over the monthly or bi-monthly intravitreal injections required by current GA treatments.
Pioneering first-in-class orally bioavailable lipid therapeutics to halt neurodegeneration and restore vision. Clinical-stage. Basel, Switzerland.
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