Retinitis Pigmentosa (RP) NHP Model

Retinal degenerative diseases such as Retinitis Pigmentosa (RP) and dry Age-related Macular Degeneration (AMD) represent major causes of irreversible vision loss worldwide. Despite significant advances in molecular and gene therapies, translational gaps between rodent models and human retinal pathology remain a major obstacle for preclinical drug evaluation.

At Prisys Biotechnologies, we have established a nonhuman primate (NHP) model of RP induced by intravitreal sodium iodate (NaIO₃) to bridge this translational divide. Leveraging the structural and functional similarity of the primate retina to humans, this model provides a reliable and clinically relevant platform for assessing novel therapies targeting retinal degeneration, RPE dysfunction, and inflammation-mediated vision loss.

Sodium iodate selectively damages retinal pigment epithelial (RPE) cells, leading to secondary photoreceptor degeneration and progressive retinal thinning. When applied to cynomolgus monkeys (Macaca fascicularis), the induced pathology closely recapitulates key features of human retinal degenerative diseases:

Key Advantages:

• Structural disruption: Optical coherence tomography (OCT) reveals ellipsoid zone (EZ) loss, punctate hyperreflective deposits above the RPE layer, and marked retinal thinning within 14 days post-induction.

• Functional impairment: Flash electroretinogram (ERG) responses demonstrate irreversible decline, indicating severe photoreceptor dysfunction.

  Fundus alterations: Fluorescein angiography (FFA) identifies localized hyperfluorescent lesions corresponding to RPE damage.

• Histopathology: RPE cell clustering, pigment deposition, and photoreceptor disorganization confirm the degeneration process.

• Molecular responses: Upregulation of complement components (C3, CFB) and chemokines (CCL-2) indicates activation of inflammatory and immune pathways associated with RPE stress and retinal atrophy

• High translational relevance: The primate retina shares macular structure, cone density, and immune microenvironment with humans, offering superior predictive value over rodent systems.

• Multi-modal evaluation: Integration of OCT, FFA, ERG, and histopathological assessment allows comprehensive, human-clinical–style readouts.

  Stable and reproducible pathology: Retinal degeneration and visual function loss are consistent across subjects and time points, supporting robust efficacy assessments.

• Customizable design: Depending on therapeutic mechanisms-antioxidant, anti-inflammatory, neuroprotective, or regenerative-we provide tailored study designs and multi-timepoint evaluations.

Prisys' NHP RP model provides a versatile platform for:

• Preclinical testing of novel therapeutics for RP, dry AMD, and RPE-protective strategies;
• Mechanistic studies on oxidative stress, complement activation, and retinal immune responses;
• Evaluation of ocular drug delivery and pharmacokinetics in a physiologically relevant system;
• Validation of imaging biomarkers translatable to human clinical endpoints.

By combining AAALAC-accredited NHP facilities with advanced ophthalmic imaging and electrophysiological technologies, Prisys Biotechnologies delivers scientifically rigorous and customizable in vivo studies for retinal degenerative disease research.

We welcome collaborations with academic investigators and biopharmaceutical partners interested in translational ophthalmology and NHP pharmacology.

Contact us to discuss how our RP model can accelerate your discovery pipeline toward clinical success.

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