Endometriosis is a gynecological disorder characterized by the presence of tissue that is morphologically and functionally similar to the endometrium, but located outside the uterine cavity. The disease is chronic and prone to recurrence. According to recent estimates, endometriosis affects over 190 million women worldwide. Fibrosis plays a central role in the pathogenesis and progression of the disease, as well as in the development of its clinical manifestations. The fibrotic process is initiated by an inflammatory response marked by the release of pro-inflammatory and pro-fibrotic mediators, particularly TGF-β1, IL-17, and other cytokines. These signaling molecules stimulate the proliferation of fibroblasts and their differentiation into myofibroblasts. Myofibroblasts, in turn, excessively produce collagen, hyaluronic acid, and other extracellular matrix components, driving the formation of fibrotic tissue and adhesions. This mechanism underlies the advancement of fibrosis and adhesion formation associated with endometriosis, contributing to persistent pelvic pain, poor response to medical therapy, infertility, and ultimately a decline in patients’ quality of life. In this study, we evaluated the efficacy of bovhyaluronidase azoximer — a conjugated enzyme compound consisting of hyaluronidase linked to a high-molecular-weight carrier (azoximer), which enhances the enzyme’s pharmacokinetics by increasing its stability and duration of action — in the treatment of endometriosis and endometriosis-associated fibrosis. Using an established animal model developed by Adamyan et al., bovhyaluronidase azoximer was shown to suppress key pro-fibrotic mechanisms, thereby confirming its anti-fibrotic potential. These findings highlight the promise of innovative non-hormonal therapeutic approaches to endometriosis and associated fibrosis, offering new opportunities for comprehensive disease management, improved treatment of infertility, and enhanced quality of life for affected patients.