One person with experience
"Finally there is the newest comer to the post cycle therapy regiment and that is toremifene. This is my personal favorite and in comparing it to nolva which I also have experience with I will only use toremifene from now on. There is a study showing that toremifene actually lowers LH production, but my experience and the experience o pretty much everyone that has used toremifene as a post cycle therapy (pct) and posted on here will agree that toremifene is amazing for post cycle therapy (pct). It tends to bring your HPTA up almost overnight. It'll get your balls swinging in no time and there are many reports of a greatly reduced "crash" when used as the post cycle therapy (pct) SERM. It should be dosed like this
120mg days 1-3/4
90mg days 4-14
60mg days 15-21
30mg days 22-28
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And another off meso
"by Anthony Roberts - Toremifene Citrate (Fareston) is a Selective Estrogen Receptor Modulator (SERM) derived from triphenylethelyne. It is Licensed in the United States under the brand name “Fareston” and currently FDA approved for use in advanced (metastatic) breast cancer. It is currently being studies for use in prostate cancer as well.
Background
Toremifene Citrate was originally patented as Fareston by the Orion Corporation of Finland, and approved for the treatment of breast cancer in Europe in 1996. In September of 1999, Roberts Pharmaceutical Corporation was granted the rights to market the drug in the United States of America.
Action
Toremifene Citrate exerts its effects by antagonizing the estrogen receptor in some tissues, and agonizing it in others. In this way, certain estrogenic pathways are activated and others are blockaded. It seems to exert estrogenic effects on blood lipids, reducing LDL and total cholesterol, as well as estrogenic effects on bone, improving density. It would also appear to exert anti-estrogenic effects in breast tissue, displacing the traditional effects of estrogen, effectively helping prevent breast cancer in postmenopausal women.
Technical Data
Fareston is a Selective Estrogen Receptor Modulator. Other drugs in this class are Clomid and Nolvadex. SERMs act by being an estrogen agonist in certain tissues and an estrogen antagonist in others.
In men, at the hypothalamus and pituitary, estrogen acts in cooperation with the body’s negative feedback loop to send a signal to decrease the secretion of LH. When LH secretion is lowered, so are natural testosterone levels. SERMs, like Fareston, possibly act as an estrogen antagonist in the hypothalamus and pituitary, in order to increase testosterone production. Thus, although it hasn’t been studied to any great degree, it’s highly likely that Fareston is capable (or better) of increasing testosterone in the same way that Nolvadex it, as it’s androgenicity:estrogenicity ratio is 5x that of Nolvadex (1). However, in terms of improving bone mineral density, Fareston is roughly equal to Nolvadex. (2) Fareston, like other SERMS, would appear to have very beneficial effects on blood lipid levels and other health markers.
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And one last one
"PURPOSE: To differentiate the antagonistic and agonistic effect of toremifene at the level of the hypothalamus-hypophysis axis a leutinizing hormone-releasing hormone (LHRH) test was performed during a phase II clinical trial. METHODS: In 15 postmenopausal patients with advanced breast cancer, follicle-stimulating hormone (FSH) and LH release--induced by an LHRH agonist (Suprefact injection, 0.5 mg s.c.)--was monitored during a 16-week period of toremifene treatment (60 mg/day p.o.). Prolactin, estradiol, and sex hormone-binding globulin (SHBG) levels were also measured. The functional test was carried out prior to toremifene therapy and then 4, 8, 12, and 16 weeks afterward. RESULTS: The drug sensitized the pituitary to the action of the gonadotrophins; the LHRH-induced FSH and LH release showed a considerably increasing tendency during the toremifene therapy. Estradiol levels decreased statistically significantly and SHBG levels showed a statistically significant increase. A decreased level of prolactin is the sign of an antiestrogenic effect of toremifene on the hypophysis and, as a result, provides evidence for a direct influence of toremifene upon the pituitary. An increase in LH and prolactin release in response to the LHRH test was characteristic in the responders. CONCLUSION: According to the LHRH test, the antagonistic effect of toremifene seems to be more dominant than the concomitantly existing agonistic property. Neither clinical nor endocrinological side effects could be observed at the level of the CNS during a prolonged period of toremifene administration.
PMID: 9685060 [PubMed - indexed for MEDLINE]
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