Pharmacology: Pharmacodynamics: The action of Chorionic Gonadotropin (Pubergen) is virtually identical to that of pituitary LH, although hCG appears to have a small degree of FSH activity as well. It stimulates production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testes to produce androgens and the corpus luteum of the ovary to produce progesterone. The biologic action of hCG is similar to that of LH. It causes leutinisation of ovarian follicular and interstitial cells. Induction of ovulation of a mature follicle stimulation of Leydig cells. and augmentation of progesterone (ovary) and testosterone (testis) biosynthesis, hCG exerts it biologic effect (increasing steroid biosynthesis by augmenting the conversion of cholesterol to pregnenolone) via activation of adenylate cyclase and increase of adenosine cyclic 3'-5'-monophosphate (cyclic AMP, CAMP). Besides its role of maintain and stimulating steroid production by the corpus luteum, hCG also appears to promote fetoplacental-unit steroidogenesis, hCG has been shown to enhance placental conversion of cholesterol to pregnenolone and progesterone in vitro. Also, hCG has been found to stimulate fetal adrenal dehydroepiandrosterone sulphate (DHEA-S) synthesis. The fetal testis has specific binding sites of hCG, and the hormone stimulates testosterone production in the fetal testis during early pregnancy. Fetal serum testosterone levels and Leydig cell proliferation reach peak around 15 to 17 weeks of gestation; that is after serum hCG concentrations have peaked. The action of CG on the testis can hardly be regarded as physiological, for the hormone gains access to the male only in utero, when it does cause minimal gonadal stimulation; CG stimulates the interstitial cells of the testis to secrete androgen. Activation of somniferous epithelium is minimal and may be mediated entirely by the androgen of Leydig-cell origin.