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Toremifene: Usually dosed around 60 mgs, some dose it up to 240 mgs. Its androgenicity:estrogenicity ratio is 5x that of Nolvadex. It is prescribed to female patients for breast cancer and has shown a high affinity for bonding to the Estrogen receptors in the breast tissue. Male patients treated with toremifene citrate 80 mg compared to placebo demonstrated statistically significant increases in bone mineral density in the lumbar spine, hip, and femur skeletal sites. It decreased the risk by up to 50%. Toremifene citrate 80 mg treatment compared to placebo also resulted in a decrease in total cholesterol, LDL, and triglycerides, and an increase in HDL. There were also statistically significant improvements in gynecomastia. This data are from an ongoing study of men receiving treatment for ADT (androgen depravation therapy). These men are receiving ADT for advanced prostate cancer. ADT removes much of the testosterone and estrogen in the body which helps the prostatic cancer cells grow. So these men were suffering from side effects from reduced estrogen and testosterone in the body. Some studies have even suggested that Torm doesn't regulate progesterone receptors and we may see in the future the possibility of using it with 19-nors.
I have never tried this as I use tamoxifen. But will have to give it a go as it sounds extremely useful :)
I've been told that Toremifene drops your nuts and enlarges them after administration much like hcg and gives a dramatic sex drive increase.
Yeah from the sounds of things it is better in every department. Tamoxifen has always been great for me though so no complaints at all (I should add they are very different). But I will try this out so I can compare :)
Toremifene/Fareston differs from Nolvadex in several ways, however- even though its very similar to it in others. Firstly, the risk of certain side effects (although relatively rare with Nolvadex) is actually quite a bit lower with Fareston.However unlikely these risks are in the first place, the risk of stroke, pulmonary embolism, and cataract is probably lower with Fareston than with Nolvadex. This is going to be of interest to people who have issues with floaters in their vision, which is sometimes caused by Nolvadex and Clomid, as this product may represent significantly less occular toxicity. It also differs slightly from Nolvadex in its potent with regards to improving lipid (cholesterol) profiles. In terms of improving bone mineral density, Fareston is roughly equal to Nolvadex.
Randomized controlled trial of toremifene 120 mg compared with exemestane 25 mg after prior treatment with a non-steroidal aromatase inhibitor in postmenopausal women with hormone receptor-positive metastatic breast cancer.
AuthorsYamamoto Y, et al. Show all Journal
BMC Cancer. 2013 May 16;13(1):239. [Epub ahead of print]
BACKGROUND: After the failure of a non-steroidal aromatase inhibitor (nsAI) for postmenopausal patients with metastatic breast cancer (mBC), it is unclear which of various kinds of endocrine therapy is the most appropriate. A randomized controlled trial was performed to compare the efficacy and safety of daily toremifene 120 mg (TOR120), a selective estrogen receptor modulator, and exemestane 25 mg (EXE), a steroidal aromatase inhibitor. The primary end point was the clinical benefit rate (CBR). The secondary end points were objective response rate (ORR), progression-free survival (PFS), overall survival (OS) and toxicity.
METHODS: Initially, a total of 91 women was registered in the study and randomly assigned to either TOR120 (n = 46) or EXE (n = 45) from October 2008 to November 2011. Three of the 46 patients in the TOR120 arm were not received treatment, 2 patients having withdrawn from the trial by their preference and one having been dropped due to administration of another SERM.
RESULTS: When analyzed after a median observation period of 16.9 months, the intention-to-treat analysis showed that there were no statistical difference between TOR120 (N = 46) and EXE (n = 45) in terms of CBR (41.3% vs. 26.7%; P = 0.14), ORR (10.8% vs. 2.2%; P = 0.083), and OS (Hazard ratio, 0.60; P = 0.22). The PFS of TOR120 was longer than that of EXE, the difference being statistically significant (Hazard ratio, 0.61, P = 0.045). The results in treatment-received cohort (N = 88) were similar to those in ITT cohort. Both treatments were well-tolerated with no severe adverse events, although the treatment of 3 of 43 women administered TOR120 was stopped after a few days because of nausea, general fatigue, hot flush and night sweating.
CONCLUSIONS: TOR120, as a subsequent endocrine therapy for mBC patients who failed non-steroidal AI treatment, could potentially be more beneficial than EXE.
Toremifene improves lipid profiles in men receiving androgen-deprivation therapy for prostate cancer: interim analysis of a multicenter phase III study.
AuthorsSmith MR, et al. Show all Journal
J Clin Oncol. 2008 Apr 10;26(11):1824-9. doi: 10.1200/JCO.2007.13.5517.
Eur Urol. 2008 Nov;54(5):1202-3.
PURPOSE: Androgen-deprivation therapy (ADT) is associated with greater risk of incident coronary heart disease and hospital admission for myocardial infarction; treatment-related increases in serum lipids may contribute to greater cardiovascular disease risk. We evaluated the effects of toremifene, a selective estrogen-receptor modulator, on fasting serum lipid levels in men receiving ADT for prostate cancer.
PATIENTS AND METHODS: In an ongoing, multicenter, double-blind, placebo-controlled phase III fracture-prevention study, 1,389 men receiving ADT for prostate cancer were randomly assigned to receive toremifene (80 mg/d) or placebo. In this interim analysis of 188 patients, changes in fasting serum lipids from baseline to month 12 were compared between the placebo and toremifene groups.
RESULTS: Changes in serum lipids differed significantly between the groups. Mean (+/- SE) total cholesterol decreased by 1.0% +/- 1.7% from baseline to month 12 in the placebo group and decreased by 8.1% +/- 1.4% in the toremifene group (P = .001 for between group comparison). Low-density lipoprotein (LDL) cholesterol increased by 0.8% +/- 2.5% in the placebo group and decreased by 8.2% +/- 2.5% in the toremifene group (P = .003). In contrast, high-density lipoprotein (HDL) cholesterol decreased by 4.9% +/- 1.2% in the placebo group and increased by 0.5% +/- 2.2% in the toremifene group (P = .018). Triglycerides increased by 6.9% +/- 4.2% in the placebo group and decreased by 13.2% +/- 3.6% in the toremifene group (P = .003).
CONCLUSION: Toremifene significantly decreased total cholesterol, LDL cholesterol, and triglycerides, and increased HDL cholesterol in men receiving ADT for prostate cancer.
A two-year dietary carcinogenicity study of the antiestrogen toremifene in Sprague-Dawley rats.
AuthorsKarlsson S, et al. Show all Journal
Drug Chem Toxicol. 1996 Nov;19(4):245-66.
The carcinogenic potential of the nonsteroidal triphenylethylene antiestrogen toremifene (Fareston) was evaluated in a standard 104-week rat dietary carcinogenicity study. The doses were 0, 0.12, 1.2, 5.0 and 12 mg/kg/day and the number of animals 50/sex/dose group. The body weight gain and food consumption were monitored once weekly (study weeks 1-16) or once every four weeks thereafter (study weeks 17-104). Blood samples were taken at weeks 34, 52 and 104 and the plasma concentrations of toremifene, as well as the two main metabolites (deaminohydroxy)toremifene and N-demethyltoremifene, were measured. All doses of toremifene reduced food intake and body weight gain. Toremifene caused a significant reduction in mortality, which was mainly due to reduced incidences of pituitary tumors. This was evident in all dose groups. Drug-related decrease of mammary tumors in females (at all doses) and testicular tumors in male rats (doses > or = 1.2 mg/kg/day) were also evident. The incidence of the preneoplastic foci of basophilic hepatocytes were significantly decreased in treated female groups. Toremifene induced no preneoplastic or neoplastic lesions. Based on histopathology, no obvious toxicity could be observed. Drug-related changes were observed in the genital organs, thyroid, spleen, mammary gland, adrenal, kidney, stomach and lung. These changes were due to hormonal disturbances or as a result of reduced food consumption or reduced incidences of pituitary, mammary or testicular tumors. This study indicates that toremifene is an efficient antiestrogen in long-term treatment, is well tolerated and has no tumorigenic potential in rats.
Toremifene Improves Lipid Profiles in Men Receiving Androgen-Deprivation Therapy for Prostate Cancer: Interim Analysis of a Multicenter Phase III Study
Matthew R. Smith, S. Bruce Malkowicz, Franklin Chu, John Forrest, Paul Sieber, K. Gary Barnette, Domingo Rodriquez, and Mitchell S. Steiner
Author information ► Copyright and License information ►
The publisher's final edited version of this article is available at J Clin Oncol
See other articles in PMC that cite the published article.
Androgen-deprivation therapy (ADT) is associated with greater risk of incident coronary heart disease and hospital admission for myocardial infarction; treatment-related increases in serum lipids may contribute to greater cardiovascular disease risk. We evaluated the effects of toremifene, a selective estrogen-receptor modulator, on fasting serum lipid levels in men receiving ADT for prostate cancer.
Patients and Methods
In an ongoing, multicenter, double-blind, placebo-controlled phase III fracture-prevention study, 1,389 men receiving ADT for prostate cancer were randomly assigned to receive toremifene (80 mg/d) or placebo. In this interim analysis of 188 patients, changes in fasting serum lipids from baseline to month 12 were compared between the placebo and toremifene groups.
Changes in serum lipids differed significantly between the groups. Mean (± SE) total cholesterol decreased by 1.0% ± 1.7% from baseline to month 12 in the placebo group and decreased by 8.1% ± 1.4% in the toremifene group (P = .001 for between group comparison). Low-density lipoprotein (LDL) cholesterol increased by 0.8% ± 2.5% in the placebo group and decreased by 8.2% ± 2.5% in the toremifene group (P = .003). In contrast, high-density lipoprotein (HDL) cholesterol decreased by 4.9% ± 1.2% in the placebo group and increased by 0.5% ± 2.2% in the toremifene group (P = .018). Triglycerides increased by 6.9% ± 4.2% in the placebo group and decreased by 13.2% ± 3.6% in the toremifene group (P = .003).
Toremifene significantly decreased total cholesterol, LDL cholesterol, and triglycerides, and increased HDL cholesterol in men receiving ADT for prostate cancer.
Toremifene for the prevention of prostate cancer in men with high grade prostatic intraepithelial neoplasia: results of a double-blind, placebo controlled, phase IIB clinical trial.
AuthorsPrice D, et al. Show all Journal
J Urol. 2006 Sep;176(3):965-70; discussion 970-1.
PURPOSE: A randomized, double-blind, dose finding, placebo controlled, parallel group clinical study was done to determine the incidence of prostate cancer in men with high grade prostatic intraepithelial neoplasia treated with toremifene.
MATERIALS AND METHODS: A total of 514 patients with high grade prostatic intraepithelial neoplasia and no evidence of prostate cancer on screening biopsy were randomized to 20, 40 or 60 mg toremifene, or placebo daily for 12 months. Patients underwent re-biopsy at 6 and 12 months.
RESULTS: The number of evaluable patients, that is those with 1 on study biopsy who were compliant, was 447. The cumulative risk of prostate cancer was decreased in patients on 20 mg toremifene compared with placebo (24.4% vs 31.2%, p <0.05). The annualized rate of prevention was 6.8 cancers per 100 men treated. In patients with no biopsy evidence of cancer at baseline and 6 months, the 12-month incidence of prostate cancer was decreased by 48.2% with 20 mg toremifene compared with placebo (9.1% vs 17.4%, p <0.05). The 20 mg dose was most effective but cumulative and 12-month incidences of prostate cancer were lower for each toremifene dose vs placebo with a cumulative risk of 29.2% and 28.1%, and a 12-month incidence of 14.3% and 13.0% for 40 and 60 mg, respectively. Gleason scores were similar across treatments. The overall incidence of drug related and serious adverse events did not differ between any of the toremifene groups and the placebo group.
CONCLUSIONS: Toremifene decreased the incidence of prostate cancer by 1 year and had a tolerability profile comparable to that of placebo in a high risk population.
Toremifene increases bone mineral density in men receiving androgen deprivation therapy for prostate cancer: interim analysis of a multicenter phase 3 clinical study.
AuthorsSmith MR, et al. Show all Journal
J Urol. 2008 Jan;179(1):152-5. Epub 2007 Nov 14.
PURPOSE: We evaluated the effects of toremifene on bone mineral density, a surrogate for fracture risk, in men receiving androgen deprivation therapy for prostate cancer.
MATERIALS AND METHODS: In an ongoing, multicenter, phase 3 fracture prevention study 1,392 men 50 years or older with prostate cancer receiving androgen deprivation therapy were randomized to 80 mg toremifene per day or placebo. Bone mineral density of the lumbar spine, total hip and femoral neck was assessed using dual energy x-ray absorptiometry. In this planned interim analysis of the first 197 subjects we compared bone mineral density changes from baseline to month 12 between the placebo and toremifene groups.
RESULTS: Compared with the placebo group men in the toremifene group had significant increases in bone mineral density at each evaluated skeletal site. Lumbar spine bone mineral density decreased 0.7% in the placebo group and increased 1.6% in the toremifene group (between group comparison p <0.001). Total hip bone mineral density decreased 1.3% in the placebo group and increased 0.7% in the toremifene group (p = 0.001). Femoral neck bone mineral density decreased 1.3% in the placebo group and increased 0.2% in the toremifene group (p = 0.009). Between group differences in the change in bone mineral density from baseline to month 12 were 2.3%, 2.0% and 1.5% for the lumbar spine, total hip and femoral neck, respectively.
CONCLUSIONS: Toremifene significantly increased hip and spine bone mineral density in men receiving androgen deprivation therapy for prostate cancer. The effect of toremifene on the fracture risk is being assessed in the ongoing randomized, controlled trial.
The beneficial effects of toremifene administration on the hypothalamic-pituitary-testicular axis and sperm parameters in men with idiopathic oligozoospermia
To evaluate whether toremifene, a selective estrogen receptor modulator (SERM), has a beneficiary effect on all three main sperm parameters.
Prospective interventional clinical study.
One-hundred subfertile men with idiopathic oligozospermia.
Toremifene (60 mg daily) was administered to all men for 3 months. At baseline and at the end of each month, serum concentrations of follicle-stimulating hormone (FSH), testosterone, inhibin B, and sex hormonebinding globulin (SHBG) were measured. At baseline and at the end, semen analysis was performed and sperm concentration, spermatozoal motility and normal sperm forms were determined.
Main Outcome Measure(s)
Gonadotropin, testosterone, inhibin-B levels, total sperm count, sperm morphology and motility.
Toremifene administration resulted in a significant increase in FSH, testosterone, SHBG, and inhibin B levels, as well as in sperm concentration, percentage motility and normal sperm forms. Twenty-two men's partners achieved pregnancy within 2 months of the end of treatment. At the end of the third month, serum FSH levels were significantly higher in the men whose partners did not achieve pregnancy, and total sperm count and normal sperm forms were significantly lower compared with the group of men whose partners achieved pregnancy.
Toremifene administration for a period of 3 months in men with idiopathic oligozoospermia is associated with significant improvements of sperm count, motility, and morphology, mediated by increased gonadotropin secretion and possibly a direct beneficial effect of toremifene on the testes. The above findings are also indicative of a better testicular exocrine (improved sperm parameters) response to treatment in men whose partners achieved pregnancy compared with those who did not. Further randomized, placebo-controlled trials should be conducted to determine whether this particular selective estrogen receptor modulator can be useful as an initial approach in men with oligozoospermia.
Toremifene PCT dosing schedule:
150 3 days
100 3 days
50 until PCT is over
Torem is good for pct however mot as good for gyno as tamox. Binding affinity to e recptor in brest tissue is less than thzt of tamox. The side effect profile makes it pretty attractive option for pct. One thing to keep in mind with torem and you will see this from time to time on the boards and Im not sure why it happens. Some people quite simply do not respond to it when it come to LH stimulation. I have seen posts over time with people using pharma torwm and just not getting the response they should and upon switching to tamox their new blood work indicated the desired response. It seems rare but it definitely does occur. This was recently observed over at Meso.
Toremifene citrate 80 mg treatment compared to placebo resulted in a decrease in total cholesterol, LDL, and triglycerides, and an increase in HDL.
Post from another forum...
"I used tor in last pct. 120 MG's for a WK, then 60 MG's for 2 wks overlapped by 50 MG's clomid weeks 2-4. Administration of Tor led to an noticeable increase in sex drive, very similar to a mild dose of test."
Toremifene for breast cancer: a review of 20 years of data.
AuthorsVogel CL, et al. Show all Journal
Clin Breast Cancer. 2014 Feb;14(1):1-9. doi: 10.1016/j.clbc.2013.10.014. Epub 2013 Oct 31.
Endocrine therapy is a cornerstone of medical treatment for estrogen receptor-positive breast cancer. The discovery of selective estrogen receptor modulators (SERMs) > 40 years ago represented a revolutionary advance in the treatment of breast cancer. As a therapeutic class, SERMs have either estrogenic or antiestrogenic activity, depending on the target tissue and the hormonal environment. In breast tissue, SERMs are antiestrogenic, making them a major treatment option for women with hormone-sensitive breast cancer. Toremifene citrate was developed > 20 years ago with the goal of achieving efficacy similar to that of tamoxifen and with an improved safety profile. Although studies to date have not confirmed a clear safety advantage or disadvantage for toremifene, clinical data support the efficacy and safety of toremifene for the treatment of breast cancer in postmenopausal patients. Toremifene also has a pharmacokinetic profile and metabolic pathway different from that of tamoxifen, which may provide a therapeutic advantage in certain patients. In addition, because of the selective estrogenic effects of SERMs in bone and on lipid levels along with a different side effect profile compared with the aromatase inhibitors (AIs), toremifene is a viable option to the AIs for some patients. Despite a number of clinical trials and over 500,000 patient years of use, many oncologists have limited familiarity with toremifene data. This article will examine the rationale for the use of toremifene in the treatment of women with breast cancer and review data from 20 years of clinical experience with this agent.
Is there a difference between HCG and Torem for PCT? Both get the nuts working, correct?
Originally Posted by JJB1
From posts I've seen Toremifene gets the nuts dropping ASAP and sex drive up. In the studies they say they came out with Toremifene to be a safer alternative to Nolvadex but with benefits just as good or better.
Originally Posted by MI1972
i was actually trying to figure out the same question of whether or not you can use Toremifene in place of hcg because it's very hard to find hcg unless you buy internationally.
thats exactly my problem... most of the sources show sold out.