Objective To study the inhibitory effect and mechanism of flavoxate on prostatic fibrosis induced by bisphenol A (BPA). Methods At the animal level, the BPA exposure model was established by orally administering 10 µg·kg^-1 BPA daily to rats for 6 weeks. Then, the rat prostates were collected to evaluate tissue collagen deposition by Sirius red and Masson staining, as well as to assess epithelial-mesenchymal transition (EMT) by immunohistochemistry analysis and quantitative real-time PCR (qPCR) analysis for E-cadherin (E-cad), vimentin (VIM) and α-smooth muscle actin (α-SMA). At the cellular level, the BPA exposure model was established by incubating human prostatic epithelial RWPE-1 cells with 100 nmol·L^-1 BPA. The collagen secretion and EMT of RWPE-1 cells were evaluated by qPCR analysis for the mRNA levels of α-SMA, E-cad, Col1A1 and Col3A1. The mechanism of flavoxate was investigated by Western blot analysis for TGF-β1. Results At the animal level, daily treatment with 80 or 40 mg·kg^-1 flavoxate attenuated BPA-induced rat prostate collagen deposition and EMT. At the cellular level, compared with the model group, 50 µg·L^-1 flavoxate significantly downregulated α-SMA, VIM, Col1A1 and Col3A1 while upregulated E-cad in RWPE-1 cells, accompanied by suppression of TGF-β1. These effects were partially reversed by a TGF-β pathway agonist. Conclusion Flavoxate can improve BPA-induced prostatic fibrosis by suppressing TGF-β1 and inhibiting collagen deposition and EMT.