“…FRP is believed to (a) inhibit microsomal aromatase activity and microsomal 3B-hydroxysteroid dehydrogenase activity in vitro (12)(13), (b) inhibit thecal aromatase activity from large and medium-sized follicles of pigs (16,17), (c) alter the production and secretion of progesterone from granulosa cells in vitro (14 -15), (d) inhibit the increase in ovarian weight and serum estradiol levels in hypopophsectomized, immature, diethylstilbestrol-treated female rats (2), (e) inhibit granulosa cell and placental microsomal aromatase activity (3-7), (f) delay follicular maturation in spontaneously cycling monkeys (8), (g) inhibit FSH induction of LH/hCG receptors in porcine granulosa cells (9), (h) associate with perifollicular neovascularization during folliculogenesis (10,11), (i) inhibit spermatogonial transformation from type A into type B in vivo (18), (j) disrupt seminiferous epithelial function and reduce sperm production after injection of FRP into rats (19 -21), (k) alter follicular steroid secretion and thecal morphology (24), (l) fluctuate during the menstrual cycle (25,26), (m) increase in persons with reproductive disorders (23), and finally, using the monoclonal antibody 1A8D5, FRP was suggested as a novel marker for granulosa cell cancer patients (27) and inhibit ovarian cancer cell proliferation (22). In addition monoclonal antibody 1A8D5 was also used to localize FRP in the granulosa cells of porcine follicles (28,29) and testes (30). We now report the isolation of an antigen recog-nized by monoclonal antibody 1A8D5 that appears to be a plasminogen protein.…”