Prime-editing therapy targets PRPH2 splice mutations (c.828+) for retinal dystrophies, enabling precise in-eye gene corrections.

Mutation-independent CRISPR pair replaces dominant alleles with a functional gene to treat autosomal dominant diseases.

AAV BEST1 gene therapy targets dominant BEST1 retinal mutations to restore function and potentially cure associated degeneration.

CRB1-targeted gene therapy delivers isoform-specific CRB1 to Müller glia and photoreceptors, treating CRB1-retinopathies.

Broad, gene-agnostic retinal therapy using AAV-delivered PGC1α/NRF2 or inhibitors to rebalance metabolism, reduce oxidative stress, slow degeneration.

Metabolic reprogramming to boost cellular anabolism, slowing neurodegeneration by targeted glycolytic pathway manipulation.

AI-enhanced portable OCT improves image quality and automatically detects AMD, enabling low-cost, accessible eye disease screening.

Femtosecond infrared laser noninvasively induces collagen crosslinks to strengthen cornea/cartilage, enabling vision correction and OA therapy.

Prime editing corrects CRB1 mutations in retinal dystrophy, offering isoform-independent gene therapy and research tool potential.

Inhibits neuronal NO synthase with S-methyl-L-thiocitrulline derivatives to prevent and treat myopia, via oral/topical delivery.

Berberine-based anti-myopia therapy for children and young adults; topical/systemic options aim to prevent progression with minimal side effects.

Fingolimod-based therapy targets myopia mechanisms and symptoms, offering oral, topical, or injectable prevention and treatment options.

A library of eye-development–targeting compounds treats or prevents myopia via versatile administration with minimal side effects.

Chop-Stick CRISPR therapy edits dominant ocular genes to disable mutations and replace with wild-type function for RP and related diseases.

Promotes retinal cholesterol efflux via CES1 upregulation or EGFR signaling modulation to slow or prevent macular degeneration.