Introduction PHARMACOLOGICAL therapy must be based on a therapeutic aim coupled with an understanding of relevant normal physiology. As reviewed elsewhere in this issue, pituitary gonadotropes exposed to GnRH pulses outside the physiological range of 0.5–1 pulses/h fail to sustain gonadotropin output. Consequently, clinical applications of GnRH are designed to stimulate gonadal function when endogenous GnRH pulsatility is deficient (hypogonadism, delayed puberty) by mimicking physiological patterns using exogenous GnRH pulse frequencies of 0.5–1 pulses/h (1). Conversely, GnRH analog (superactive agonists or pure antagonists) treatment is intended to suppress gonadal function via pituitary desensitization as a result of sustained pituitary overexposure to GnRH effects by continuous or quasi-continuous administration (2, 3). Thus treatment regimens with GnRH or the analogs will have different optimal modes of application based on the pharmacokinetics of the compound and pharmacodynamics of the target physiological systems. This article will review the pharmacokinetics of GnRH and its analogs and the relevance to regimens designed to stimulate or suppress gonadal function.