Anti-Müllerian hormone (AMH) is a transforming growth factor-beta superfamily peptide that plays critical roles in reproductive and non-reproductive physiology. Produced by Sertoli cells during male fetal development and by granulosa cells of preantral and small antral follicles in females, AMH functions as a negative regulator of follicle development 1. AMH binds its type-II receptor (AMHR2) and heterodimerizes with type-I receptors to activate SMAD-mediated signaling pathways that inhibit the primordial-to-primary follicle transition and decrease FSH sensitivity of growing follicles 2. In males, AMH induces Müllerian duct regression during fetal sexual differentiation. Circulating AMH levels reflect the ovarian reserve and follicle pool size, exhibiting peak levels in the early 20s before declining toward menopause 1. In polycystic ovary syndrome (PCOS), markedly elevated AMH levels contribute to anovulation through excessive pre-antral follicle growth and impaired antral follicle maturation 2. AMH positively correlates with the LH/FSH ratio in lean PCOS patients, indicating direct involvement in neuroendocrine dysfunction 3. Beyond reproduction, AMH promotes osteoblast differentiation and bone mineralization 4 and exhibits protective effects through BRCA1 downregulation in ovarian tissue 5. Given AMH's ability to inhibit apoptosis and regulate cell proliferation, it has emerged as a therapeutic target in oncology and bone metabolism research.