SBC003 Development Pipeline

A single oral compound advancing across four indications: retinal degeneration first, CNS neurodegeneration next.

The mechanism: SBC003 induces neuroglobin expression via p-body modulation — a mutation-agnostic, endogenous pathway that protects neurons regardless of the upstream trigger. One molecule, multiple indications, no injections.

Development Overview

Four programs, one oral pill — no intravitreal injections.

IND-EnablingPreclinical Development
SBC003IND-Enabling

Retinitis Pigmentosa

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

Development Stage

IND-Enabling
Preclinical Development
Research Stage
Discovery
SBC003Preclinical Development

Dry AMD

Indication: Dry Age-Related Macular Degeneration (DAMD)Route: Oral Administration
  • Prevents and repairs photoreceptor apoptosis through anti-neuronal apoptotic mechanism
  • Improves visual function by enhancing lysosomal scavenger protein aggregation
  • Reduces age-related cellular debris accumulation
  • Recovery of interdigitation zone/photoreceptor structure in the macular area

Development Stage

IND-Enabling
Preclinical Development
Research Stage
Discovery
SBC003Preclinical Development

Optic Atrophy

Indication: Primary and Secondary Optic Atrophy (POA, GOA)Route: Oral Administration
  • Following oral administration, Rhesus monkeys with spontaneous optic atrophy showed recovery in RNFL thickness
  • Improvement in both RNFL and macular structure suggests broad utility

Development Stage

IND-Enabling
Preclinical Development
Research Stage
Discovery
SBC003Preclinical Development

CNS Neurodegeneration

Indication: CNS Neurodegeneration (Alzheimer's, Parkinson's, ALS)Route: Oral Administration
  • Excellent blood-brain barrier penetrance as a low-molecular-weight, orally bioavailable compound
  • Anti-apoptotic and proteostasis mechanisms validated in retinal models translate directly to CNS proteinopathies
  • Endogenous neuroprotective pathway activation relevant across multiple CNS neurodegenerative targets defined by toxic protein aggregation
  • Strong scientific rationale for target expansion into Alzheimer's disease, Parkinson's disease, and ALS following RP clinical validation

Development Stage

IND-Enabling
Preclinical Development
Research Stage
Discovery

Market Opportunity

SBC003's four lead indications span retinal degeneration and CNS neurodegeneration. The neurodegenerative therapeutics market is growing at 5.7–7.2% CAGR, driven by aging demographics and the structural shortcomings of the one-target drug paradigm.

Retinitis Pigmentosa

Market Size

Significant unmet need

Growth

12.1% CAGR

Patients

2M globally

Unmet need: 99% have no disease-modifying treatment

Dry AMD

Market Size

Significant unmet need

Growth

9.3% CAGR

Patients

200M globally

Unmet need: No approved oral treatment; EMA rejected both approved injectables

Optic Atrophy

Market Size

Significant unmet need

Growth

8.8% CAGR

Patients

~2M in US/EU/China/Japan

Unmet need: No approved neuroprotective treatment

CNS Neurodegeneration

Market Size

Significant unmet need

Growth

5.7–7.2% CAGR

Patients

32–38M Alzheimer's, 10M Parkinson's, globally

Unmet need: No approved disease-modifying therapy across all major CNS indications.

Why SBC003 Is Different

No other compound in development combines oral bioavailability, broad-spectrum neuroprotection, and retinal + CNS potential in a single molecule.

Oral Administration

SBC003 is a simple, daily pill.

Mutation-agnostic

Targets the universal neuronal apoptosis pathway downstream of any mutation. Applicable to 100% of RP patients vs. <1% eligible for gene therapies like Luxturna.

Five-protein shield

Published evidence of protection against all five major neurotoxic proteins, amyloid-β, α-synuclein, tau, prion, and amylin, in a single peer-reviewed Aging Cell paper.

Validated in primates

Significant RNFL recovery in rhesus monkeys with naturally occurring optic atrophy at oral doses of 5–50 mg/kg. Plasma concentrations of 47.6–86.4 ng/mL confirmed.

01 / 04
Next: Mutation-agnostic

Explore the Science Behind the Pipeline

Understand the mechanism of action, preclinical data, and the peer-reviewed evidence supporting SBC003.

SBC003 is investigational and has not been approved by any regulatory authority. This page presents scientific and development-stage information only.