Clomifene C is a non-steroidal selective estrogen receptor modulator (SERM) of the triphenylethylene group. Clomiphene was developed and approved for use in the early 1970s for the treatment of female infertility and later on subsequently expanded to treating male infertility as well.
In most all cases, this SERM is used for post-cycle therapy (PCT) purposes, by-which use is intended to stimulate natural testosterone production that has been suppressed through the use of anabolic steroids. Clomiphene stimulates the hypothalamus which stimulates the anterior pituitary gland to release gonadotrophic hormones. The gonadotrophic hormones are follicle stimulating hormone (FSH) and luteinizing hormone (LH). FSH stimulates (in males) the spermatogenesis and LH stimulates the leydig cells of testicles to secrete more testosterone. This feedback mechanism is known as the hypothalamic-pituitary-testes axis (HPTA), and results in an increase of the body’s own testosterone production. Blood levels rise, as to compensate for the diminishing levels of exogenous steroids. This is vital to minimize post cycle muscle losses.
Clomiphene as well as all of the triphenylethylene compounds under the SERM family (tamoxifen, clomiphene and toremifene) also exhibit estrogen agonistic effects. Clomiphene, being a SERM, does not reduce circulating estradiol levels in the blood, but instead serves to occupy the receptor sites so that estrogen itself cannot bind to these receptors due to clomiphene’s stronger binding strength to them. So, clomiphene binds to estrogen receptors on cells blocking them to estrogen in the blood. However, it should be noted that clomiphene actually operates at a much poorer efficiency compared to tamoxifen in regards to its estrogen antagonistic activity in breast tissue.