Therapeutic administration of pirfenidone reverses fibrosis in cGVHD BO model. B10.BR mice were conditioned with cytoxan (120 mg/kg/day, intraperitoneally [IP], day-3 and day-2) and TBI (8.3 Gy, day-1), followed by infusion of 10⁷ B6 T cell–depleted bone marrow only as healthy control, or plus 75 000 purified splenic T cells to induce cGVHD (day 0). In the treatment group, cGVHD mice received pirfenidone (400 mg/kg) from day 28 to day 56. (A) Pulmonary function tests on day 56 post-transplantation showed that pirfenidone restored lung function of cGVHD mice. Data are representative of 3 experiments with similar results. (B) Hydroxyproline assay of the right lungs harvested on day 56 indicated that pirfenidone significantly reduced hydroxyproline content. Five to 6 mice from each group were analyzed. Data are representative of 2 experiments with similar results. (C) Representative images of Masson’s trichrome staining images of lung (upper) and liver (lower). Collagen (blue stain) was quantified in (D) and (E). (F-G) Representative lung immunoglobulin deposition images and quantification. Data are representative of 2 experiments with similar results. *P ≤ .05, **P < .01, ***P < .001; data are shown as the mean ± standard error of the mean (SEM).