Since the luteinizing hormone-releasing hormone (LH-RH) has been identified and its mode of action understood, it has become possible to envisage a therapeutic use of long-acting, non toxic analogues. Biochemical modifications of the decapeptide have resulted in the synthesis of potent LH-RH antagonists and agonists. Paradoxically, however, the agonists, devised to induce ovulation, exert an antagonistic action due to a decrease in the number of pituitary LH-RH receptors and to desensitization of the pituitary gland to the decapeptide. These inhibitory effects are associated with the prolonged activity of the analogues, in contrast with the stimulant effects of physiological LH-RH which has a short half-life and is secreted by bursts. The direct action of LH-RH analogues on gonads suggested by animal experiments has not been found in man since human gonads are devoid of specific LH-RH receptors. Alterations in steroid production are consecutive to the rise in LH initially induced by LH-RH agonists. The complete gonadotropic inhibition which follows the administration of LH-RH antagonists or agonists suggests that these compounds could be used in man, notably for the treatment of hormone-dependent carcinomas and isosexual early puberty and in the field of contraception.