Glaucoma focus

AAV‑IKV‑Decorin for fibrotic outflow biology.

The glaucoma program focuses on the TGFβ2 / decorin axis at the trabecular meshwork, where extracellular matrix remodeling can impair aqueous humor outflow and elevate intraocular pressure.

IOP
Trabecular meshwork fibrosis
TGFβ2 signaling
AAV‑IKV‑Decorin

Disease biology

Glaucoma can be viewed through outflow tissue remodeling.

Elevated intraocular pressure is the principal modifiable risk factor in glaucoma. Visiogene’s program is organized around upstream tissue biology that can contribute to pressure elevation: fibrosis and extracellular matrix deposition at the trabecular meshwork.

Outflow tissue

Trabecular meshwork

Fibrotic remodeling can compromise aqueous humor drainage and increase outflow resistance.

Molecular driver

TGFβ2 / EMT

TGFβ2 is implicated in epithelial-to-mesenchymal transition and extracellular matrix remodeling relevant to glaucoma.

Counter-regulator

Decorin

Decorin is a proteoglycan regulator of TGFβ biology and the therapeutic payload in the AAV‑IKV glaucoma program.

Visiogene approach

Local expression of decorin in anterior segment tissues.

The program uses AAV‑IKV as the delivery layer and human decorin as the expressed transgene. Preclinical work is focused on fibrosis, intraocular pressure, retinal ganglion cell integrity, and ocular tolerability.

AAV‑IKV+intracameral delivery
Decorin+TGFβ2 counter-regulation
Measured outcomesfibrosis, IOP, RGCs

Evidence package

Preclinical study components.

The public data package links AAV‑IKV delivery, a TGFβ2-driven disease model, AAV‑IKV‑Decorin intervention, and initial non-human primate tolerability observations.

01

Anterior chamber transduction

AAV‑IKV transduction was evaluated in murine anterior chamber tissues including trabecular meshwork, cornea, and ciliary body.

02

Fibrosis model

AAV‑IKV‑TGFβ2CS was used to model trabecular meshwork fibrosis, IOP elevation, and retinal ganglion cell degeneration.

03

Decorin intervention

AAV‑IKV‑Decorin attenuated fibrosis, elevated IOP, and retinal ganglion cell loss in the model.

04

NHP observation

Intracameral AAV‑IKV‑GFP plus Nuc1 in a non‑human primate study showed corneal expression without a discernible toxicity signal in the reported observations.