SunRegen is pioneering a novel class of orally bioavailable compounds that halt neuronal apoptosis at the molecular level.
The pharmaceutical industry has struggled to solve neurodegeneration, not for lack of investment, but because of a fundamental strategic gap: most approved approaches act on a single pathway in a multi-pathway disease. Our lead candidate, SBC003, takes a fundamentally different approach: a proprietary compound discovered through phenotype-first development that fortifies the neuron's own survival machinery, regardless of which upstream insult is occurring.
SBC003, our lead platform molecule, has been validated across a broad preclinical program spanning multiple species, and is currently advancing through IND-enabling Chemistry, Manufacturing and Controls (CMC) and GLP toxicology studies in preparation for Phase I/II clinical trials in Retinitis Pigmentosa.
The fundamental pathology underlying retinal neurodegenerative diseases, including Retinitis Pigmentosa, Dry Age-Related Macular Degeneration, and Optic Atrophy, is the breakdown of protein homeostasis (proteostasis) and the irreversible loss of photoreceptor and retinal ganglion cells. Current standards of care are largely palliative, with approved disease-modifying options restricted to minuscule genetic subsets. SunRegen is engineered to fundamentally change this therapeutic paradigm by targeting the molecular mechanisms of neuronal apoptosis.
The first sign of RP is usually a loss of night vision, which becomes apparent in childhood. Problems with night vision can make it difficult to navigate in low light. Later, the disease causes blind spots to develop in the side (peripheral) vision. Over time, these blind spots merge to produce tunnel vision. The disease progresses over years or decades to affect central vision, which is needed for detailed tasks such as reading, driving, and recognizing faces. In adulthood, many people with retinitis pigmentosa become legally blind.
Prevalence & Market: Currently, there are approximately 2 million RP patients worldwide. The typical clinical phenomenon of RP indication is apoptosis of photoreceptor cells, which leads to visual impairment and blindness.
DAMD is a common eye disorder among people over 50. It causes blurred or reduced central vision due to the breaking down of the inner layers of the macula. The macula is the part of the retina that gives the eye clear vision in the direct line of sight. DAMD is a slow deterioration of the cells of the macula, often over many years, as the retinal cells die off and are not renewed. The term 'dry' does not mean the person has dry eyes, just that the condition is not wet AMD.
Prevalence & Market: As of 2024, approximately 200 million people worldwide are affected by Age-related Macular Degeneration (AMD). This number is projected to increase to 288 million by 2040 due to aging populations, and 85-90% of AMD patients are DAMD. There is no effective treatment for DAMD.
Optic atrophy is a disease that affects the function of the optic nerve, resulting in lesions of retinal ganglion cells and their axons, and clinically classified into two main categories: primary and secondary optic atrophy. Primary Optic Atrophy (POA) is an optic neuropathy that primarily affects the ganglion cells and their axons between the retina and the lateral geniculate body. Secondary Optic Atrophy (SOA) is a manifestation of optic nerve damage, which unlike primary optic atrophy, is usually caused by other eye diseases or lesions. Clinically, it is commonly seen in secondary optic atrophy caused by diseases such as glaucoma and diabetic retinopathy. Glaucoma Optic Atrophy (GOA) is very common among later stage glaucoma.
Prevalence & Market: According to Globaldata, there are currently nearly 2 million patients in the United States, China, Japan and 5 Western Europe countries.
SBC003 is an orally bioavailable, first-in-class small-molecule compound. Its discovery represents a landmark in phenotype-first drug development: SunRegen identified the compound's exceptional neuroprotective activity in validated preclinical models, then characterized its mechanism through proprietary mechanistic studies.
SBC003 acts through synergistic, precisely characterized molecular pathways that fortify the neuron's endogenous survival machinery and restore cellular proteostasis. The result is a multi-pathway, mutation-agnostic intervention that addresses the upstream drivers of neurodegeneration rather than any single downstream protein.
The compound has demonstrated neuroprotective, neuro-rescuing, and neurotrophic effects across diverse preclinical systems, including translationally relevant human neuronal models.
First-in-class orally bioavailable compound; no intravitreal injections required
Unique neuro-rescuing effects targeting the root cause of neuronal apoptosis
Mutation-agnostic mechanism effective across all genetic subtypes of RP
Excellent safety & tolerability profile
Validated brain and retinal exposure of SBC003
SBC003 preclinical data has been presented at the ARVO Annual Meeting and published in peer-reviewed journals.
Converging data across a broad preclinical program with non-human primate confirmation
In rigorous evaluations using a validated murine photoreceptor-degeneration system, oral administration of SBC003 exhibited a potent, dose-dependent neuroprotective effect. Optical Coherence Tomography (OCT) imaging confirmed statistically significant preservation of photoreceptor and neuroretinal layer thickness across peripheral, mid-peripheral, and central retinal regions compared to vehicle controls.
In a genetic murine model of rapid photoreceptor degeneration, SBC003 demonstrated neuro-rescuing effects, preserving critical visual infrastructure even when administration was initiated at an advanced disease stage. This late-stage efficacy is clinically significant: SBC003 can rescue neurons already committed to apoptosis, not merely prevent damage.
To bridge the translational gap to human clinical trials, SBC003 was evaluated in non-human primates presenting with spontaneous optic atrophy and retinal disease. Following oral dosing, subjects exhibited statistically significant recovery in Retinal Nerve Fiber Layer (RNFL) thickness and restoration of macular photoreceptor structure. Together with the rodent retinal and CNS programs, this efficacy across multiple species supports the transition to Phase I/II clinical trials.
In a rodent model of CNS ischemic injury, oral SBC003 significantly reduced damage and improved neurological function scores versus vehicle controls. These data extend SBC003's neuroprotective signature beyond the retina into broader CNS injury, supporting platform expansion into stroke and other neurodegenerative indications.
The SBC003 mechanism of action was elucidated through cutting-edge genomic technology, including advanced yeast-model genetic screens and mammalian validation studies, and confirmed through clean (knockout) genetic experiments. SBC003 exerts its neuroprotective effects through three synergistic, precisely defined pathways:
SBC003 activates an endogenous neuroprotective pathway that fortifies neurons against oxidative stress and toxic protein aggregation. The result is potent anti-apoptotic activity that arises from the neuron's own survival machinery, rather than from suppression of any single upstream protein.
SBC003 reinforces the cell's proteostasis machinery, helping to prevent toxic aggregation of misfolded proteins and supporting clearance of disease-associated cellular debris. This addresses a core pathological process shared across retinal and CNS neurodegeneration.
SBC003 preserves mitochondrial integrity and bioenergetic function in stressed neurons, stabilizing membrane potential and limiting the cascade that triggers intrinsic apoptosis. This third pillar reinforces the other neuroprotective pathways by safeguarding the energetic core of every neuron — a critical determinant of survival under chronic neurodegenerative stress.
By synergistically acting across endogenous neuroprotection, proteostasis restoration, and mitochondrial protection, SBC003 addresses the full pathological cascade of photoreceptor and retinal ganglion cell degeneration with a single, orally bioavailable compound.
Development Plan
An expedited regulatory path through Retinitis Pigmentosa to validate the mechanism in humans, then expand into multi-billion-dollar indications.
Indication
Retinitis Pigmentosa (RP)
Route
Oral Administration
Unique neuro-rescuing effects against neuronal apoptosis
Strong neuroprotective effects against multiple neurotoxins
Strong neurite outgrowth promoting effects
Predicted with favourable safety and tolerability profile
With a good uptake by the brain and retina
Recovery of interdigitation zone/photoreceptor structure in the macular area
Take the next step
SBC003 has cleared the bar of mechanism, model, and species. The next chapter is the clinic. Explore the investor case, dig into the published evidence, or reach out directly.
Pioneering first-in-class orally bioavailable compounds to halt neurodegeneration and restore vision. Clinical-stage. Basel, Switzerland.
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