Trabecular meshwork
Fibrotic remodeling can compromise aqueous humor drainage and increase outflow resistance.
Glaucoma focus
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.
Disease biology
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.
Fibrotic remodeling can compromise aqueous humor drainage and increase outflow resistance.
TGFβ2 is implicated in epithelial-to-mesenchymal transition and extracellular matrix remodeling relevant to glaucoma.
Decorin is a proteoglycan regulator of TGFβ biology and the therapeutic payload in the AAV‑IKV glaucoma program.
Visiogene approach
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.
Evidence package
The public data package links AAV‑IKV delivery, a TGFβ2-driven disease model, AAV‑IKV‑Decorin intervention, and initial non-human primate tolerability observations.
AAV‑IKV transduction was evaluated in murine anterior chamber tissues including trabecular meshwork, cornea, and ciliary body.
AAV‑IKV‑TGFβ2CS was used to model trabecular meshwork fibrosis, IOP elevation, and retinal ganglion cell degeneration.
AAV‑IKV‑Decorin attenuated fibrosis, elevated IOP, and retinal ganglion cell loss in the model.
Intracameral AAV‑IKV‑GFP plus Nuc1 in a non‑human primate study showed corneal expression without a discernible toxicity signal in the reported observations.