In the case of glaucoma, increased levels of TGF-β2 have been observed in the anterior chamber of glaucomatous eyes and have been associated with trabecular meshwork transformation and direct optic nerve damage.

To target this, ISTH0036, a synthetic antisense oligodeoxynucleotide selectively targeting TGF-β2, has been tested in a phase I dose escalation study.

The study found that after a single intravitreal administration of ISTH0036, decreased TGF-β2 mRNA and protein levels in ocular tissues were observed for up to eight weeks in rabbit eyes, with favorable pharmacokinetic and pharmacodynamic properties and safety results when administered in patients with primary open-angle glaucoma undergoing trabeculectomy.

In corneal wound healing, TGF-β signaling is necessary for maintaining corneal epithelial homeostasis.

However, overactivation of TGF-β signaling can lead to corneal scarring and fibrosis. Blocking TGF-β activity has been suggested as a treatment option to promote corneal wound healing.

In vivo gene transfer of a soluble TGF-β type II receptor has been shown to accelerate tissue repair in injured corneas in rats, inhibiting corneal opacification, edema, and angiogenesis.

Monoclonal antibodies such as TGF-β1 and β2 antibodies have been shown to inhibit the formation of cutaneous scars in rodent wounds, making them potential treatments for corneal scarring. Tranilast, a TGF-β inhibitor, reduced the re-occurrence of corneal fibrosis, or primary pterygium, a degenerative ocular surface disorder with fibrovascular growth of the bulbar conjunctiva onto the cornea.

Inflammatory corneal diseases like Stevens-Johnson's syndrome or chemical burns are also believed to be affected by TGF-β signaling.

Elevated tear TGF-β1 profiling of patients with Stevens–Johnson’s suggests that TGF-β1 plays an inflammatory role in the pathogenesis. Inhibition of TGF-β activity via the over-expression of regulatory SMAD7 following corneal injury has been shown to be associated with scar formation. Tissue repair has been observed in damaged corneas after blocking TGF-β activity by systemic expression of the soluble TGF-β receptor by transfer of adenoviral genes.

So, targeting TGF-β signaling with ALK5 inhibitor, Vactosertib, will show potential as a therapeutic option for various eye diseases like glaucoma and corneal scarring.