Fareston (toremifene citrate) is a selective estrogen receptor modulator (SERM) derived from triphenylethylene. Toremifene was patented and approved in Europe in the mid-1990s to treat metastatic ER+ breast cancer in postmenopausal women. Men in bodybuilding use toremifene as a drug for post-cycle therapy (PCT) and/or block some of the effects of excessive estradiol in the body resulting from the aromatization of various steroids. Toremifene inhibits the negative feedback of estrogen at the hypothalamus and pituitary gland, allowing the anterior pituitary gland to release gonadotrophic hormones, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). FSH stimulates (in males) spermatogenesis, and LH stimulates the Leydig cells of the testicles to secrete more testosterone. This is vital to minimize post-cycle muscle losses. Toremifene affects the activity of estrogen in various other tissues by competing with or binding more strongly than estradiol at target receptor sites (hence the term SERM); it is used particularly to restore levels of endogenous testosterone as well as to prevent estrogen-induced gynecomastia. 

It is important to note that toremifene does not lower overall total circulating blood plasma levels of estradiol in the body; it merely inhibits estrogen activity in certain tissues. This is the main difference between aromatase inhibitors (AI) and SERMs. An AI binds to the aromatase enzyme responsible for the conversion of androgens into estradiol (aromatization) and reduces the total circulating levels of estradiol in the body. Toremifene, being a SERM, is a true estrogen blocker that binds to the receptor site and remains inert (does not activate the receptors), resulting in the inability of estradiol to bind to these receptors, as they have already been occupied by toremifene. 

The chemical structure of toremifene is very similar to that of tamoxifen. However, toremifene is a new-generation drug that is much more desirable because it has fewer toxic side effects than tamoxifen (it has been determined that tamoxifen may be carcinogenic). Nonetheless, toremifene has some negative properties as well. Firstly, and perhaps most importantly, is the effect it has on Sex Hormone Binding Globulin (SHBG) levels in the body; clinical research has demonstrated that while toremifene can and does stimulate natural endogenous production of testosterone, it raises SHBG levels in the blood. 

WARNING: Toremifene increases sex hormone-binding globulin (SHBG) levels in the blood; as such, it may decrease the efficiency of a cycle when taken within a cycle as a drug to combat gynecomastia symptoms. 

Also, it has been determined that toremifene is not as potent as an equivalent dose of tamoxifen in regards to the restoration of HPTA and endogenous testosterone production in males. Studies have demonstrated that toremifene, when administered at doses of 60 mg daily, raised testosterone levels in test subjects by a significant increase of 42%, but in the same study, a standard 20 mg daily dose of tamoxifen increased testosterone levels by 71%. 

Therefore, toremifene dosage, for a more effective boost in testosterone production, should be in the range of up to 120 mg per day. This dose can be maintained for the first week of PCT, 100 mg/day for the second week of PCT, and then 60 mg/day for the remaining 3–4 weeks of PCT. Of course, exact dosages should be determined individually based on blood work results. 

ADVICE: The correct time to commence post-cycle therapy (PCT) depends completely on the type and half-lives of steroids you have been using. Toremifene taken while androgen levels in the blood are still high will be a waste. It is crucial to wait for androgen levels to fall before implementing PCT. However, if taken too late, there is a risk that quality mass, which has been put on through hard work, could possibly be lost. 

Post-cycle therapy (PCT)