The purpose of this study was to investigate how to enroll the optimal animal model for the studies on HCC therapy. The VX2 tumor is a highly malignant anaplastic squamous cell carcinoma. It is a fast-growing tumor with strong invasion, early hematogenous and lymphatic metastases and high lethality. It was reported that the VX2 tumor followed the same metastatic pattern with HCC, therefore, the VX2 tumor was also used as a metastatic model of HCC.Its antifibrotic activity has been demonstrated in various organs including the lung, kidney, and liver. In the eye, pirfenidone was shown to inhibit migration of orbital fibroblasts, prevent post-operative scarring following glaucoma surgery, and significantly inhibit TGF b induced fibrogenesis in retinal pigmented epithelial cells. The possible role of pirfenidone in preventing corneal scarring has not yet been explored. Thus the present study was designed to assess the biological effects of pirfenidone in cultured corneal fibroblasts and evaluate its effect on corneal wound healing and scarring following alkali injury. Like many other ophthalmic formulations, pirfenidone exhibits short half-life following topical application and necessitates a formulation design to prolong its action. Therefore, to avoid multiple daily doses, we prepared pirfenidone encapsulating biodegradable nanoparticles, and compared their effect with the free drug. A favorable outcome following alkali burn is restoration of normal anatomy and function of the cornea. Delayed corneal reepithelialization and stromal haze are key impediments in restoring corneal function. Corneal ECM is a highly organized structure and in adult cornea, keratocytes remain quiescent and maintain the transparency. The physiological response of cornea to injury involves the downward migration of the loosened epithelial cells AbMole Hexyl Chloroformate towards the exposed stroma. The active keratocytes in the wound area start dividing to form a hypercellular zone. These cells get converted into wound fibroblasts and behave like keratocytes of a developing cornea and produce essential components of the normal extracellular matrix ie collagen, keratocan, lumican with keratin sulfate chains to restore the highly organized ECM and normal transparency of the cornea. On the other hand under the influence of TGF beta these cells transform into myofibroblasts and produce high levels of other ECM components ie collagen, hyaluronan, and biglycan but low levels of keratin sulfate proteogylcans which results into a disorganized ECM and leads to corneal opacity. Therefore, formation of myofibroblast in the wound area is the key determinant of corneal scaring that causes blindness. Our results demonstrate that pirfenidone reduced a-SMA expression in TGF beta induced corneal fibroblasts, indicating prevention of myofibroblast formation. This further resulted in reduced collagen I expression, resulting in favorable healing process. Pirfenidone was previously shown to reduce TGF b secretion, expression of a-SMA and collagen contraction in cardiac fibroblasts and collagen I expression induced by TGF b in human alveolar epithelial cell line.