ABSTRACT
Gonadotrophin-releasing hormone (GnRH), a decapeptide composed of 10 amino acids, is secreted from the hypothal hypothalamus in a pulsatile manner. Through G protein-coupled receptors located on gonadotrope cells, GnRH stimulates the synthesis and release of the gonadotrophins FSH and LH, which in turn regulate folliculogenesis and steroidogenesis
in the ovaries [1] (see Fig. 15.1). Furthermore, evidence suggests that GnRH may have a direct effect on the functions of the ovary, such as steroidogenesis, oocyte maturation and follicle rupture [2-5]. Many derivatives, known as GnRH analogs, including agonists and antagonists, were synthesized with an enhanced biological potency of binding with GnRH receptors [1]. These analogs have been used in ovarian stimulation to prevent a premature LH surge that can impair follicular development [6-7]. A GnRH agonist combined with FSH and/or human menopausal gonadotrophin (HMG), widely used in IVF centers, has some advantages in reducing the rate of cycle cancellation, improving the rate of live birth and enabling flexibility to schedule oocyte retrieval [8-10].
