Prostatic inhibin peptide (PIP) suppresses the synthesis as well as release of FSH from the rat pituitary whereas the carboxy terminal nonapeptide (86-94) of PIP elevated the release of pituitary FSH. Addition of a tyrosine residue at the NH2-terminal end of nonapeptide and blocking the sulfhydryl group of the cysteine residue at position 87 resulted in a decapeptide having the property of suppressing FSH release from rat pituitary. Human prostate has been shown to synthesize FSH in vitro. PIP, nonapeptide, and decapeptide modulate the prostatic FSH biosynthesis, the pattern of which was similar to that observed for pituitary.