SunRegen is pioneering a novel class of orally bioavailable lipid therapeutics that halt neuronal apoptosis at the molecular level.
The pharmaceutical industry has failed to solve neurodegeneration, not for lack of investment, but because of a fundamental strategic error: targeting a single protein in a multi-protein disease. Every approved anti-amyloid antibody targets one protein; none address tau, α-synuclein, or other co-occurring neurotoxic aggregates. Our lead candidate, SBC003, takes a fundamentally different approach: a rare natural lipid discovered through phenotype-first reverse engineering that fortifies the neuron's own survival machinery, regardless of which upstream insult is occurring.
SBC003, our lead platform molecule, has been validated across multiple mammalian species, including non-human primates, 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 lipid therapeutic. Its discovery represents a landmark in phenotype-first drug development: SunRegen identified the compound's exceptional neuroprotective activity in validated animal models, then reverse-engineered the complete molecular mechanism through advanced genomic screening and yeast-model validation.
SBC003 works via two synergistic, precisely characterized molecular pathways. First, it modulates p-bodies, cytoplasmic processing bodies that act as crucial regulators of messenger RNA stability, to significantly upregulate the expression of neuroglobin in mammalian neurons. Neuroglobin is a potent intracellular scavenger and anti-apoptotic protein that directly mitigates the toxicity of aggregating proteins and protects neurons from oxidative stress. Second, SBC003 enhances the expression of specific chaperone genes that actively maintain cellular proteostasis, preventing the toxic aggregation of misfolded proteins and clearing existing lipofuscin deposits, the hallmark pathology driving geographic atrophy in macular degeneration.
The compound has demonstrated remarkable neuroprotective, neuro-rescuing, and neurotrophic effects in vitro, with both mouse primary neurons and human neurons derived from iPSCs (induced pluripotent stem cells).
First-in-class orally bioavailable lipid therapeutic; 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 four animal models with non-human primate confirmation
In rigorous evaluations using N-nitroso-N-methylurea (NMU)-induced photoreceptor degeneration murine models, oral administration of SBC003 exhibited a highly potent, dose-dependent neuroprotective effect. Optical Coherence Tomography (OCT) imaging confirmed a statistically significant preservation of photoreceptor and neuroretinal layer thickness across peripheral, mid-peripheral, and central retinal regions compared to vehicle controls.
In rd10 genetic models characterized by rapid photoreceptor degeneration, SBC003 demonstrated profound neuro-rescuing effects, preserving critical visual infrastructure even when administration was delayed until 21 days after birth. This late-stage efficacy is clinically significant, indicating that SBC003 can rescue neurons already committed to the apoptotic pathway, not merely prevent damage.
To bridge the translational gap to human clinical trials, SBC003 was evaluated in Rhesus monkeys (Macaca mulatta) presenting with spontaneous optic atrophy and retinal disease. Following oral dosing at 5–50 mg/kg, subjects exhibited statistically significant recovery in Retinal Nerve Fiber Layer (RNFL) thickness and a distinct restoration of the interdigitation zone and photoreceptor structure in the macular area. Together with the murine and stroke models, this robust efficacy across four animal models strongly supports the transition to Phase I/II clinical trials.
In the transient middle cerebral artery occlusion (tMCAO) rodent model of ischemic stroke, oral SBC003 significantly reduced infarct volume and improved neurological function scores versus vehicle controls. Presented at the American Academy of Neurology (AAN) Annual Meeting, these data extend SBC003's neuroprotective signature beyond the retina into central nervous system injury, supporting platform expansion into stroke and broader neurodegeneration.
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 modulates p-bodies (cytoplasmic mRNA processing bodies), which act as key regulators of messenger RNA stability. This modulation significantly upregulates the expression of neuroglobin in mammalian neurons. Neuroglobin (orthologous to the yeast nitric oxide oxidoreductase Yhb1) is a potent intracellular scavenger that actively prevents the formation of toxic amyloid oligomer aggregates and exerts powerful anti-apoptotic effects.
SBC003 simultaneously upregulates a panel of molecular chaperone genes responsible for maintaining cellular proteostasis. These chaperones actively prevent the initial toxic aggregation of misfolded proteins and enhance lysosomal scavenger function to clear existing lipofuscin deposits, the pathological hallmark of Dry AMD geographic atrophy.
SBC003 preserves mitochondrial integrity and bioenergetic function in stressed neurons, stabilizing membrane potential and limiting the cytochrome-c release that triggers intrinsic apoptosis. This third pillar reinforces the upstream neuroglobin and proteostasis pathways by safeguarding the energetic core of every neuron, a critical determinant of survival under chronic neurodegenerative stress.
By synergistically acting across neuroglobin-mediated apoptosis inhibition, chaperone-mediated proteostasis restoration, and mitochondria 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 lipid therapeutics to halt neurodegeneration and restore vision. Clinical-stage. Basel, Switzerland.
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