Toremifene (fareston) - for Dr.D and others
- Thread starter turkish
- Start date
max-rot98
Board Supporter
Unfortunately bigcat hasn't used it so I am not going to dismiss it that easily. It is proven far safer than tamoxifen in long term use in women(tam. has caused moderate to severe vision problems, hair and teeth loss etc.). Dr. D loves it and of the studies I read on it it sounds very promising. If you want register at the ibe forums web page and ask in the product suggestions forum. I have a thread going right now and the more people asking for it the better.
DR.D
Well-known member
turkish said:
What can I say. BC and I don't see eye to eye on a lot of things! He also thinks SD is a weak, second rate steroid. I've been at it with him for weeks now over on some BB.com threads concerning this. I've been trying to educate him otherwise and point to the fact that 90% of users are making serious gains, but he just won't hear it. Oh well. I posted about 10 Pub-Med studies in a thread here not too long ago comparing Nolva to Fareston. The toxicity data alone condemns Nolva. Just start writing sponsors and tell them you want toremifene citrate. That’s what I did. As soon as someone takes this seriously, we are all in for a new age in SERM treatment! It would probably be the only SERM I’d ever use if I could get some. Gyno, PCT, whatever, it covers everything with the least toxicity.
judge-mental
Board Supporter
man... you are saying nolva caused my floaters and mad tracers...? I thought clomid was bad for the eyes...
:frustrate
now that I can imaginaly get toremifene I would like to know its effect on the eyes...
:frustrate
now that I can imaginaly get toremifene I would like to know its effect on the eyes...
max-rot98
Board Supporter
judge-mental said:
I have read before but I have no studies to paste so take it as you may but nolva can cause blurred vision and tracers as well. It takes longer but still happens. If you have a chance run a google search on tamoxifen and check out some of the medical forum boards and see what some of the side effects these women have after just six months of use. I remember one in particular a woman said she would read before she went to sleep every night and no longer could because her vision was so blurred. And it didn't go away after she stopped using.
DR.D
Well-known member
judge-mental said:
Yeah, just like Max said, it can do it. People use larger doses of Clomid so they notice it more but Nolva will do it too. Phosphonic acid formation is the culprit if I remember correctly. Toremifene may do it too at large doses, but it didn't to me at 120mg/d for 2-3 wks. Clomid does if I go over 200mg for a wk or two.
max-rot98
Board Supporter
Some studies on toremifene
Ok when raloxiphene came out people wanted to know a couple of things. Effects on lipids compared to nolva, bone density effects and toxicity. Well I have found some studies in regards to these issues. It is safer toxicity wise than nolva, and better on lipids and bone density than tamoxifen. So here you go:
Bone Mineral Density and Lipid Changes During 5 Years of Follow-up in a Study of Prevention of Breast Cancer with Toremifene in Healthy, High-risk Pre- and Post-menopausal Women.
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Department of Obstetrics and Gynaecology, Turku University Central Hospital, Turku, Finland.
A double-blind, randomised, placebo-controlled pilot study was initiated to evaluate the feasibility of chemoprevention with toremifene 60 mg/day in healthy women at high risk for breast cancer. Enrolment in the study was terminated earlier than planned because of slow patient accrual, although 13% of patients continued for 5 years. The revised efficacy outcomes were change in bone mineral density (BMD) from baseline at four skeletal sites, plus effects on serum lipids. In premenopausal women there was a trend for sustained increase in BMD during toremifene therapy after year 1 in lumbar spine. In postmenopausal women, toremifene had little or no effect on BMD trends. Levels of total and low-density lipoprotein (LDL) cholesterol were largely unchanged from baseline in premenopausal women treated with toremifene but were often slightly lower than in the placebo group during follow-up. Total and LDL cholesterol levels declined slightly from baseline in the postmenopausal women and were, at several points during the first 3 years, significantly lower than in the corresponding placebo group (p < 0.01). We conclude that: (a) assessment of toremifene 60 mg/day in chemoprevention will require further clinical trials; (b) toremifene 60 mg/day has no substantive negative effects on BMD in pre- or postmenopausal women and may exert a minor favourable influence (in particular, the effects of toremifene 60 mg/day on BMD in premenopausal women may make the drug an attractive alternative to tamoxifen 20 mg/day for that patient subset); (c) lipid effects of toremifene 60 mg/day are, at minimum, neutral and may be modestly favourable for reducing cardiovascular risk.
PMID: 16172794 [PubMed - in process]
Ok when raloxiphene came out people wanted to know a couple of things. Effects on lipids compared to nolva, bone density effects and toxicity. Well I have found some studies in regards to these issues. It is safer toxicity wise than nolva, and better on lipids and bone density than tamoxifen. So here you go:
Bone Mineral Density and Lipid Changes During 5 Years of Follow-up in a Study of Prevention of Breast Cancer with Toremifene in Healthy, High-risk Pre- and Post-menopausal Women.
Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.
Department of Obstetrics and Gynaecology, Turku University Central Hospital, Turku, Finland.
A double-blind, randomised, placebo-controlled pilot study was initiated to evaluate the feasibility of chemoprevention with toremifene 60 mg/day in healthy women at high risk for breast cancer. Enrolment in the study was terminated earlier than planned because of slow patient accrual, although 13% of patients continued for 5 years. The revised efficacy outcomes were change in bone mineral density (BMD) from baseline at four skeletal sites, plus effects on serum lipids. In premenopausal women there was a trend for sustained increase in BMD during toremifene therapy after year 1 in lumbar spine. In postmenopausal women, toremifene had little or no effect on BMD trends. Levels of total and low-density lipoprotein (LDL) cholesterol were largely unchanged from baseline in premenopausal women treated with toremifene but were often slightly lower than in the placebo group during follow-up. Total and LDL cholesterol levels declined slightly from baseline in the postmenopausal women and were, at several points during the first 3 years, significantly lower than in the corresponding placebo group (p < 0.01). We conclude that: (a) assessment of toremifene 60 mg/day in chemoprevention will require further clinical trials; (b) toremifene 60 mg/day has no substantive negative effects on BMD in pre- or postmenopausal women and may exert a minor favourable influence (in particular, the effects of toremifene 60 mg/day on BMD in premenopausal women may make the drug an attractive alternative to tamoxifen 20 mg/day for that patient subset); (c) lipid effects of toremifene 60 mg/day are, at minimum, neutral and may be modestly favourable for reducing cardiovascular risk.
PMID: 16172794 [PubMed - in process]
Last edited:
max-rot98
Board Supporter
Initiating activity of the anti-estrogen tamoxifen, but not toremifene in rat liver.
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American Health Foundation, Valhalla, New York, USA.
A striking difference between two structurally related anti-estrogen medicines is that tamoxifen is strongly hepatocarcinogenic in the rat, whereas toremifene lacks such activity. To study the basis for this difference, the initiating potential of tamoxifen and toremifene were studied by measurement of rapid induction of hepatocellular altered foci (HAF) that express placental-type glutathione S-transferase in the livers of female Sprague-Dawley (S-D) rats and female Fischer 344 (F344) rats. Both agents were administered by gavage at equimolar doses up to a dose that produced marked weight gain suppression. In rats given the high dose of 40 mg/kg per day tamoxifen continuously for 36 weeks, 75% of S-D rats developed liver neoplasms, in contrast to only 10% of F344 rats. In the S-D strain, tamoxifen produced a tendency to increased HAF at 2 weeks at the dose of 40 mg/kg per day and by 12 weeks, a dose-related increase was evident. In contrast, toremifene induced no HAF even at the equimolar high dose of 42.4 mg/kg per day for 12 weeks. The induction of HAF by tamoxifen was less in the F344 rats. Neither agent elicited increases in hepatocellular proliferation in S-D or F344 rats. When phenobarbital was administered for 24 weeks as a promoting agent after the anti-estrogens, S-D rats given tamoxifen at 20 mg/kg per day for 12 weeks, developed liver neoplasms, but not F344 rats or rats of either strain given even a higher dose (42.4 mg/kg) of toremifene. Thus, tamoxifen has initiating activity in these rat strains whereas toremifene does not.
PMID: 9395228 [PubMed - indexed for MEDLINE]
Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.
American Health Foundation, Valhalla, New York, USA.
A striking difference between two structurally related anti-estrogen medicines is that tamoxifen is strongly hepatocarcinogenic in the rat, whereas toremifene lacks such activity. To study the basis for this difference, the initiating potential of tamoxifen and toremifene were studied by measurement of rapid induction of hepatocellular altered foci (HAF) that express placental-type glutathione S-transferase in the livers of female Sprague-Dawley (S-D) rats and female Fischer 344 (F344) rats. Both agents were administered by gavage at equimolar doses up to a dose that produced marked weight gain suppression. In rats given the high dose of 40 mg/kg per day tamoxifen continuously for 36 weeks, 75% of S-D rats developed liver neoplasms, in contrast to only 10% of F344 rats. In the S-D strain, tamoxifen produced a tendency to increased HAF at 2 weeks at the dose of 40 mg/kg per day and by 12 weeks, a dose-related increase was evident. In contrast, toremifene induced no HAF even at the equimolar high dose of 42.4 mg/kg per day for 12 weeks. The induction of HAF by tamoxifen was less in the F344 rats. Neither agent elicited increases in hepatocellular proliferation in S-D or F344 rats. When phenobarbital was administered for 24 weeks as a promoting agent after the anti-estrogens, S-D rats given tamoxifen at 20 mg/kg per day for 12 weeks, developed liver neoplasms, but not F344 rats or rats of either strain given even a higher dose (42.4 mg/kg) of toremifene. Thus, tamoxifen has initiating activity in these rat strains whereas toremifene does not.
PMID: 9395228 [PubMed - indexed for MEDLINE]
max-rot98
Board Supporter
[SIZE=+1]Comparison of DNA reactivity of the polyphenylethylene hormonal agents diethylstilbestrol, tamoxifen and toremifene in rat and hamster liver.[/SIZE]
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American Health Foundation, Valhalla, NY 10595.
The polyphenylethylene estrogenic drug diethylstilbestrol and a structural analogue tamoxifen have been found to be hepatocarcinogenic in female rats, whereas another analogue, toremifene, did not induce liver tumors. The 32P post-labelling technique for detection of DNA adducts was used to investigate the DNA reactivity of these three hormonal agents in the livers of female Sprague-Dawley rats and Syrian hamsters. Adducts were quantified using a radioanalytic imaging system in comparison with the standard Cerenkov assay. With administration of the chemicals at several doses by daily gavage to rats for 10 days and to hamsters for 7 days, tamoxifen was found to produce five adducts in rat liver and six adducts in hamster liver. The amounts of adducts were dose related from 10 to 90 mumol/kg per day in rats and from 17 to 160 mumol/kg per day in hamsters. The two methods of quantification yielded comparable results. Under these conditions, neither toremifene nor diethylstilbestrol produced adducts in rats and diethylstilbestrol produced none in hamsters. We conclude that tamoxifen is highly DNA reactive in the species studied and that this is likely to be involved in its strong carcinogenicity in rat liver.
PMID: 8067901 [PubMed - indexed for MEDLINE]
Invalid Link Removed, Invalid Link Removed.
American Health Foundation, Valhalla, NY 10595.
The polyphenylethylene estrogenic drug diethylstilbestrol and a structural analogue tamoxifen have been found to be hepatocarcinogenic in female rats, whereas another analogue, toremifene, did not induce liver tumors. The 32P post-labelling technique for detection of DNA adducts was used to investigate the DNA reactivity of these three hormonal agents in the livers of female Sprague-Dawley rats and Syrian hamsters. Adducts were quantified using a radioanalytic imaging system in comparison with the standard Cerenkov assay. With administration of the chemicals at several doses by daily gavage to rats for 10 days and to hamsters for 7 days, tamoxifen was found to produce five adducts in rat liver and six adducts in hamster liver. The amounts of adducts were dose related from 10 to 90 mumol/kg per day in rats and from 17 to 160 mumol/kg per day in hamsters. The two methods of quantification yielded comparable results. Under these conditions, neither toremifene nor diethylstilbestrol produced adducts in rats and diethylstilbestrol produced none in hamsters. We conclude that tamoxifen is highly DNA reactive in the species studied and that this is likely to be involved in its strong carcinogenicity in rat liver.
PMID: 8067901 [PubMed - indexed for MEDLINE]
max-rot98
Board Supporter
Breast Cancer Res Treat. 2004 Nov;88(1):9-16.Related Articles, Links
[SIZE=+1]Crossover trial for lipid abnormality in postmenopausal breast cancer patients during selective estrogen receptor modulators (SERMs) administrations.[/SIZE]
Kusama M, Kaise H, Nakayama S, Ota D, Misaka T, Aoki T.
The Third Department of Surgery, Tokyo Medical University, Tokyo, Japan. [email protected]
The objective of this study was to evaluate the different profiles of serum lipids resulting from the administration of selective estrogen receptor modulators (SERMs). Postmenopausal primary breast cancer patients (n = 197) with node-negative, hormone receptor-positive who were treated at our department or in other related medical institutions from April 1997 through March 2001 were given adjuvant therapy. The adjuvant therapy included 1 year's administration of tamoxifen (TAM) 20 mg or toremifene (TOR) 40 mg. The profiles of serum lipids such as total cholesterol (TC), high-density lipoprotein cholesterol (HDL) and triglyceride (TG) were observed. After 1 year administration TC had significantly decreased (p < 0.001) both in the TAM group and the TOR group, but no significant difference was found between these groups (p = 0.249). HDL had significantly decreased in the TAM group (p < 0.001), while it had significantly increased in the TOR group (p < 0.001), and a significant difference was found between the groups (p < 0.001). TG had significantly increased in the TAM group (p < 0.001) but significantly decreased in the TOR group (p < 0.001). The medication was switched in those who still had abnormal lipid metabolism and given to them for another year. After 1 year from the crossover TC and HDL had increased to the levels of before administration (p < 0.001) and TG had decreased in those (n = 57) whose medication was switched from TAM to TOR. While TC had decreased and TG had increased in those (n = 23) whose medication was switched from TOR to TAM (p < 0.001). The above findings have suggested that TOR provides better profiles of lipid metabolism than TAM.
Publication Types:
[SIZE=+1]Crossover trial for lipid abnormality in postmenopausal breast cancer patients during selective estrogen receptor modulators (SERMs) administrations.[/SIZE]
Kusama M, Kaise H, Nakayama S, Ota D, Misaka T, Aoki T.
The Third Department of Surgery, Tokyo Medical University, Tokyo, Japan. [email protected]
The objective of this study was to evaluate the different profiles of serum lipids resulting from the administration of selective estrogen receptor modulators (SERMs). Postmenopausal primary breast cancer patients (n = 197) with node-negative, hormone receptor-positive who were treated at our department or in other related medical institutions from April 1997 through March 2001 were given adjuvant therapy. The adjuvant therapy included 1 year's administration of tamoxifen (TAM) 20 mg or toremifene (TOR) 40 mg. The profiles of serum lipids such as total cholesterol (TC), high-density lipoprotein cholesterol (HDL) and triglyceride (TG) were observed. After 1 year administration TC had significantly decreased (p < 0.001) both in the TAM group and the TOR group, but no significant difference was found between these groups (p = 0.249). HDL had significantly decreased in the TAM group (p < 0.001), while it had significantly increased in the TOR group (p < 0.001), and a significant difference was found between the groups (p < 0.001). TG had significantly increased in the TAM group (p < 0.001) but significantly decreased in the TOR group (p < 0.001). The medication was switched in those who still had abnormal lipid metabolism and given to them for another year. After 1 year from the crossover TC and HDL had increased to the levels of before administration (p < 0.001) and TG had decreased in those (n = 57) whose medication was switched from TAM to TOR. While TC had decreased and TG had increased in those (n = 23) whose medication was switched from TOR to TAM (p < 0.001). The above findings have suggested that TOR provides better profiles of lipid metabolism than TAM.
Publication Types:
- Clinical Trial
max-rot98
Board Supporter
ok two more
Estrogenic effects of toremifene and tamoxifen in postmenopausal breast cancer patients.
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Clinical Development, Orion Corporation, Orion Pharma, Turku, Finland. [email protected]
Intrinsic estrogenicities of the selective estrogen receptor modulators (SERMs) toremifene 60 mg daily or 200 mg daily and tamoxifen 20 mg daily (TOR60, TOR200 and TAM20) were compared in a randomized clinical study in postmenopausal women with advanced breast cancer. The study was open label in three parallel groups. Variables for analysis were serum follicle stimulating hormone (FSH), luteinizing hormone (LH), sex hormone binding globulin (SHBG), estradiol (E2), antithrombin III (AT III), aspartate aminotransferase (ASAT) and vaginal cytology. Clinical efficacy and safety have been reported earlier. A total of 648 patients were randomized (221 to TOR60, 212 to TOR200 and 215 to TAM20). Sera were available for the analysis from 148, 165 and 156 and for vaginal cytology from 98, 93 and 86 patients, respectively. All treatment regimens showed tissue-specific and dose-dependent estrogen agonist effect. In the primary measure of in vivo estrogenicity, effect on hypothalamus-pituitary-axis, all three treatment regimens decreased serum FSH (p < 0.001). TOR200 was more potent than the two other treatments (p < 0.05), but surprisingly, TAM20 was more estrogenic than TOR60 (p < 0.001). As could be expected in postmenopausal women, the treatments had no effect on mean serum E2 concentrations and decrease of serum LH was similar to that of FSH. Estrogenic effect on the liver was seen as dose-dependent increase of SHBG with statistically significant differences between the treatment groups (p < 0.001). Trends of transient ASAT elevations in TOR200 group (p = 0.07) and in all treatment groups AT III decrease (p = 0.1) were seen in the beginning of the treatment. TOR60 or TAM20 did not have an effect on mean ASAT values, and AT III decreased in TAM20 group more than in the two other groups (p = 0.1 compared to TOR60 and p < 0.05 compared to TOR200). Estrogenic effects on vaginal superficial cells were higher in TOR60 and TOR200 groups when compared to TAM20 (p < 0.05). Toremifene and tamoxifen had tissue-specific and partially dose-dependent estrogenic effects in hypothalamus-pituitary-axis, in the liver and in the vaginal epithelium of postmenopausal women. In some tissues tamoxifen 20 may be more estrogenic than toremifene 60 mg/day.
Estrogenic effects of toremifene and tamoxifen in postmenopausal breast cancer patients.
Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.
Clinical Development, Orion Corporation, Orion Pharma, Turku, Finland. [email protected]
Intrinsic estrogenicities of the selective estrogen receptor modulators (SERMs) toremifene 60 mg daily or 200 mg daily and tamoxifen 20 mg daily (TOR60, TOR200 and TAM20) were compared in a randomized clinical study in postmenopausal women with advanced breast cancer. The study was open label in three parallel groups. Variables for analysis were serum follicle stimulating hormone (FSH), luteinizing hormone (LH), sex hormone binding globulin (SHBG), estradiol (E2), antithrombin III (AT III), aspartate aminotransferase (ASAT) and vaginal cytology. Clinical efficacy and safety have been reported earlier. A total of 648 patients were randomized (221 to TOR60, 212 to TOR200 and 215 to TAM20). Sera were available for the analysis from 148, 165 and 156 and for vaginal cytology from 98, 93 and 86 patients, respectively. All treatment regimens showed tissue-specific and dose-dependent estrogen agonist effect. In the primary measure of in vivo estrogenicity, effect on hypothalamus-pituitary-axis, all three treatment regimens decreased serum FSH (p < 0.001). TOR200 was more potent than the two other treatments (p < 0.05), but surprisingly, TAM20 was more estrogenic than TOR60 (p < 0.001). As could be expected in postmenopausal women, the treatments had no effect on mean serum E2 concentrations and decrease of serum LH was similar to that of FSH. Estrogenic effect on the liver was seen as dose-dependent increase of SHBG with statistically significant differences between the treatment groups (p < 0.001). Trends of transient ASAT elevations in TOR200 group (p = 0.07) and in all treatment groups AT III decrease (p = 0.1) were seen in the beginning of the treatment. TOR60 or TAM20 did not have an effect on mean ASAT values, and AT III decreased in TAM20 group more than in the two other groups (p = 0.1 compared to TOR60 and p < 0.05 compared to TOR200). Estrogenic effects on vaginal superficial cells were higher in TOR60 and TOR200 groups when compared to TAM20 (p < 0.05). Toremifene and tamoxifen had tissue-specific and partially dose-dependent estrogenic effects in hypothalamus-pituitary-axis, in the liver and in the vaginal epithelium of postmenopausal women. In some tissues tamoxifen 20 may be more estrogenic than toremifene 60 mg/day.
max-rot98
Board Supporter
Endocrine mechanism of action of toremifene at the level of the central nervous system in advanced breast cancer patients.
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Clinical Research Department, National Institute of Oncology, Budapest, Hungary.
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]
Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed, Invalid Link Removed.
Clinical Research Department, National Institute of Oncology, Budapest, Hungary.
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]
meowmeow
Active member
Toremifene Citrate is available from Toronto Research Chemicals, Inc's catalog
Cat. Number: T547500 CAS Number: 89778-26-7
Chemical Name: Toremifene Citrate
Synonym: 2-[4-[(1Z)-4-Chloro-1,2-diphenyl-1-butenyl]phenoxy]-N,N-dimethylethanamine
Mol. Formula: C32H36ClNO8
Mol. Weight: 598.08
Melting Point: 108-110°C
Boiling Point:
Appearance: White-to-Off-White Solid
Application Notes:
An antiestrogen and antineoplastic. Nonsteroidal antiestrogen structurally similar to tamoxifen.
References:
Kallio, S., et al.: Cancer Chemother. Pharmacol., 17, 103 (1986), Valavaara, R., et al.: Eur. J. Cancer Clin. Oncol., 24, 785 (1988),
Category:
Pharmaceuticals, Intermediates & Fine Chemicals, Inhibitors
Keywords:
50 mg $95 USD Quantity:
500 mg $760 USD Quantity:
Cat. Number: T547500 CAS Number: 89778-26-7
Chemical Name: Toremifene Citrate
Synonym: 2-[4-[(1Z)-4-Chloro-1,2-diphenyl-1-butenyl]phenoxy]-N,N-dimethylethanamine
Mol. Formula: C32H36ClNO8
Mol. Weight: 598.08
Melting Point: 108-110°C
Boiling Point:
Appearance: White-to-Off-White Solid
Application Notes:
An antiestrogen and antineoplastic. Nonsteroidal antiestrogen structurally similar to tamoxifen.
References:
Kallio, S., et al.: Cancer Chemother. Pharmacol., 17, 103 (1986), Valavaara, R., et al.: Eur. J. Cancer Clin. Oncol., 24, 785 (1988),
Category:
Pharmaceuticals, Intermediates & Fine Chemicals, Inhibitors
Keywords:
50 mg $95 USD Quantity:
500 mg $760 USD Quantity:
Ubiquitous
Registered User
that price is ridiculous MeowMeow 
Grassroots082
Board Supporter
Think Ill have to pass on that
meowmeow
Active member
Ubiquitous said:that price is ridiculous MeowMeow
Ooops! I wasn't paying attention. Ridiculous it is. I was looking at their cabergoline which isn't priced that far out of line when compared to internet pharms so I was just assuming pricing would be okay.
However they do manufacture a lot of different complex organic chemicals for biomedical research so their catalog might be worth a look.
mywetnightmares
Kyra Gracie= my future wife
IBE is adding it to their catalog along with ralox and some other goodies.
Ubiquitous
Registered User
That is great news.
thanatopsis
Member
*bump*
Great thread, I want to try Toremifene when I finally get back into the swing of working out again and start my H50 cycle.
Great thread, I want to try Toremifene when I finally get back into the swing of working out again and start my H50 cycle.
darius
Guest
Fareston is no cheap candy. I work at a pharmacy. I looked up the price today at work. A 90 count bottle costs us $540 (yes US dollars, I live in Texas lol).
:jaw:
:jaw:
max-rot98
Board Supporter
darius said:
Like I said in previous post bro. In PILL form the average price for toremifene is 105$ for 1800mg. I spent alot of time trying to price fareston after meowmeows shocking post. After spending time searching this is what I found to be the average cost. Come on you think IBE would even consider carrying something that would cost 500$ A PCT. Thats ridiculous.
DR.D
Well-known member
Don't worry guys. Of course it may be expensive at first, even for liquid products and bulk powders. After a year or two, it'll be much cheaper after it becomes more widely popular and more suppliers carry it.
Years from now, people will be like "Nolva... what's that? I think my grandpa used that stuff for PCT or something..."
Years from now, people will be like "Nolva... what's that? I think my grandpa used that stuff for PCT or something..."
Ubiquitous
Registered User
yes.. don't worry guys.. all you have to do is look hard enough... or wait..
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bioman
Well-known member
Doesn't seem to be a hard and fast rule yet. I used 120 mg for the first 3 days (then realized how quickly I would run out at that level), dropped it to 90 mg for 5 days then tapered to 60 mg. I'll drop it to 30 mgs after several more days and keep it at that level until the bottle runs out. Seems to be working fine so far at that level, but I'd almost bet you could use lower doses and have it be effective.
DR.D
Well-known member
bioman said:
Amen BIO! That's usually the way I did it. You may not need 120mg the whole first wk, but for the first 2-3 days, it's really a fast turn on to kick in PCT! The effect and recovery rate is strongly dose dependant though, so keep that in mind. You may not even "feel" 30-60mg until it's built up in your system over a few weeks (depending on your level of shutdown). Try to do at least 60mg the first 2 wks. You can drop below 60 and taper off after wk 2 with good residual.
bioman
Well-known member
..my research subject was not too badly suppressed as he used HCG throughout the cycle. I'm going to start tapering the dose down from 60 mg by 1-2 mg per day. I'll just barely have enough to run another 2 weeks it seems. Subject is also currently using Oratropin both for PCT purposes as well as to heal a myropractic back procedure.
There's still some residual estrogen lfloating around after 8 days of Torm. Adding Letro at .20 mg every other day to keep it from building up.
Definitely is a fast acting PCT agent though, I am sold.
There's still some residual estrogen lfloating around after 8 days of Torm. Adding Letro at .20 mg every other day to keep it from building up.
Definitely is a fast acting PCT agent though, I am sold.
bioman
Well-known member
So far..yes, but it is kinda early to tell. The boys are back to normal..even before the Oratropin use and I am not loosing much of my gains for a change (knock on wood!), Tmaox wrecks my skin..this seems pretty benign so far. A little acne but not bad and no blotchiness.
I feel fully recovered already..good mood, don't feel suppressed at all. Nicest PCT ever to compliment the nicest cycle ever.
I feel fully recovered already..good mood, don't feel suppressed at all. Nicest PCT ever to compliment the nicest cycle ever.