Clomiphene is a non-steroidal fertility medicine, a triphenyl ethylene stilbene derivative which is an estrogen agonist or antagonist depending on the target tissue. It causes the pituitary gland to release hormones needed to stimulate ovulation (the release of an egg from the ovary).
Clomiphene is used to cause ovulation in women with certain medical conditions - infertility due to anovulation - (such as polycystic ovary syndrome) that prevent naturally occurring ovulation.
Clomiphene may also be used for purposes not listed in this medication guide.
Clomifene (previously clomiphene) is an orally administered, non steroidal, ovulatory stimulant that acts as a selective estrogen receptor modulator (SERM). Clomifene can lead to multiple ovulation, and hence increase the risk of conceiving twins. In comparison to purified FSH, the rate of ovarian hyperstimulation syndrome is low.
There may be an increased risk of ovarian cancer and weight gain. Clomifene is capable of interacting with estrogen-receptor-containing tissues, including the hypothalamus, pituitary, ovary, endometrium, vagina, and cervix. It may compete with estrogen for estrogen-receptor-binding sites and may delay replenishment of intracellular estrogen receptors. Clomifene initiates a series of endocrine events culminating in a preovulatory gonadotropin surge and subsequent follicular rupture.
The first endocrine event, in response to a course of clomifene therapy, is an increase in the release of pituitary gonadotropins. This initiates steroidogenesis and folliculogenesis resulting in growth of the ovarian follicle and an increase in the circulating level of estradiol. Following ovulation, plasma progesterone and estradiol rise and fall as they would in a normal ovulatory cycle.
Clomifene has both estrogenic and anti-estrogenic properties, but its precise mechanism of action has not been determined. Clomifene appears to stumulate the release of gonadotropins, follicle-stimulating hormone (FSH), and leuteinizing hormone (LH), which leads to the development and maturation of ovarian follicle, ovulation, and subsequent development and function of the coprus luteum, thus resulting in pregnancy.
Gonadotropin release may result from direct stimulation of the hypothalamic-pituitary axis or from a decreased inhibitory influence of estrogens on the hypothalamic-pituitary axis by competing with the endogenous estrogens of the uterus, pituitary, or hypothalamus. Clomifene has no apparent progestational, androgenic, or antrandrogenic effects and does not appear to interfere with pituitary-adrenal or pituitary-thyroid function.
Metabolism: Hepatic
Absorption: Based on early studies with 14 C-labeled clomifene, the drug was shown to be readily absorbed orally in humans.
Route of elimination: Based on early studies with 14C-labeled clomiphene citrate, the drug was shown to be readily absorbed orally in humans and excreted principally in the feces. Mean urinary excretion was approximately 8% with fecal excretion of about 42%.
Half life: 5-7 days
All medicines may cause side effects, but many people have no, or minor, side effects.Some medical conditions may interact with Clomiphene.
Tell your doctor or pharmacist if you have any medical conditions.
Common clomiphene side effects may include: flushing (warmth, redness, or tingly feeling), breast pain or tenderness, headache or breakthrough bleeding or spotting.
This is not a complete list of all side effects that may occur. If you have questions about side effects, contact your health care provider.
