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Falsodex (anti-estrogen and anti-progestin)
- Thread starter LT3
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LT3
New member
dont know about sides or anything. i just found what i pasted above. but i swore off nandrolones untill there was something that significantly helped combating P sides. so this seems to be it. and ye 1 shot per month is awesome. for the avarage cycle you only need 4 shots. AG guys would be smart to make some, coz this shit would sell.
LT3
New member
Taken from PubMed.
This paper reviews the recent Twenty-third Annual San Antonio Breast Cancer Symposium. A total of 580 studies were presented either orally or as posters. Two phase III multi-centre clinical trials found that fulvestrant (Falsodex), given as a once-monthly intramuscular injection (250 mg), was well-tolerated and at least as good as anastrozole (1 mg) in postmenopausal women with advanced breast cancer that had progressed or recurred on prior endocrine therapy. Another phase III randomised trial found that letrozole (2.5 mg daily) was superior to tamoxifen as a neoadjuvant therapy in postmenopausal women with ER- and/or PgR-positive breast cancer unsuitable for breast-conserving surgery. In a phase III study, capecitabine (Xeloda) was found to be well-tolerated and able to improve survival by three months when added to Taxotere. Cutting edge data on microarray gene profiling in breast cancer were presented. The potential role of this new technology in predicting outcome and selecting therapy was discussed. Furthermore, its limitations and the need for validation were highlighted. The role of new diagnostic tools, such as fibre-optic ductoscopy (FDS) and microcatheters to obtain ductal cells, was discussed. Finally, the worldwide overview was presented.
This paper reviews the recent Twenty-third Annual San Antonio Breast Cancer Symposium. A total of 580 studies were presented either orally or as posters. Two phase III multi-centre clinical trials found that fulvestrant (Falsodex), given as a once-monthly intramuscular injection (250 mg), was well-tolerated and at least as good as anastrozole (1 mg) in postmenopausal women with advanced breast cancer that had progressed or recurred on prior endocrine therapy. Another phase III randomised trial found that letrozole (2.5 mg daily) was superior to tamoxifen as a neoadjuvant therapy in postmenopausal women with ER- and/or PgR-positive breast cancer unsuitable for breast-conserving surgery. In a phase III study, capecitabine (Xeloda) was found to be well-tolerated and able to improve survival by three months when added to Taxotere. Cutting edge data on microarray gene profiling in breast cancer were presented. The potential role of this new technology in predicting outcome and selecting therapy was discussed. Furthermore, its limitations and the need for validation were highlighted. The role of new diagnostic tools, such as fibre-optic ductoscopy (FDS) and microcatheters to obtain ductal cells, was discussed. Finally, the worldwide overview was presented.
macrophage69alpha
New member
just to be clear aromatase inhibitors also reduce progesterone receptor expression (the absence of oestrogen or complete blocking without activity in the case of faslodex have the same effect in that respect)
there are likely going to be issue with complete lack of agonism. Though have not looked thoroughly at this drug.
there are likely going to be issue with complete lack of agonism. Though have not looked thoroughly at this drug.
LT3
New member
Fulvestrant ('Faslodex'): Current and future role in breast cancer management.
Howell A.
Cancer Research UK Department of Medical Oncology, University of Manchester, Christie Hospital NHS Trust, Wilmslow Road, Withington, Manchester M20 4BX, UK.
Fulvestrant ('Faslodex') is a new type of estrogen receptor antagonist with no agonist effects, that reduces cellular levels of both estrogen and progesterone receptors. Results from two Phase III trials showed that fulvestrant is at least as effective as the third-generation selective aromatase inhibitor anastrozole in postmenopausal women with advanced breast cancer following progression on antiestrogen therapy, indicating the potential for second-line fulvestrant in this setting. In clinical practice, fulvestrant is well tolerated, with good rates of clinical benefit observed as first-line therapy and following progression on prior endocrine agents. Other endocrine agents have been shown to have good clinical activity when resistance to fulvestrant has developed, showing that fulvestrant lacks cross-resistance with other treatments. Ongoing trials are investigating the efficacy of fulvestrant after failure on aromatase inhibitors and evaluating its use in combination with therapies that target growth factor receptor signaling pathways.
But Macro, i wouldnt take a AI to protect myself from nandrolone sides. IMO AIs do help in P sides but not significantly.
Howell A.
Cancer Research UK Department of Medical Oncology, University of Manchester, Christie Hospital NHS Trust, Wilmslow Road, Withington, Manchester M20 4BX, UK.
Fulvestrant ('Faslodex') is a new type of estrogen receptor antagonist with no agonist effects, that reduces cellular levels of both estrogen and progesterone receptors. Results from two Phase III trials showed that fulvestrant is at least as effective as the third-generation selective aromatase inhibitor anastrozole in postmenopausal women with advanced breast cancer following progression on antiestrogen therapy, indicating the potential for second-line fulvestrant in this setting. In clinical practice, fulvestrant is well tolerated, with good rates of clinical benefit observed as first-line therapy and following progression on prior endocrine agents. Other endocrine agents have been shown to have good clinical activity when resistance to fulvestrant has developed, showing that fulvestrant lacks cross-resistance with other treatments. Ongoing trials are investigating the efficacy of fulvestrant after failure on aromatase inhibitors and evaluating its use in combination with therapies that target growth factor receptor signaling pathways.
But Macro, i wouldnt take a AI to protect myself from nandrolone sides. IMO AIs do help in P sides but not significantly.
macrophage69alpha
New member
LT3 said:
the effects that you are describing are going to be very similar. basically because of E deprivation (either by blocking or inhibition of aromatase).
see here
Br J Cancer. 2006 Mar 14; [Epub ahead of print] Related Articles, Links
Proliferation, steroid receptors and clinical/pathological response in breast cancer treated with letrozole.
Miller WR, White S, Dixon JM, Murray J, Renshaw L, Anderson TJ.
1The Edinburgh Breast Unit, Western General Hospital, Edinburgh EH4 2XU, UK.
Sixty-three postmenopausal women with large primary breast cancers were treated with neoadjuvant letrozole (2.5 mg daily) for 3 months. Tumour samples were taken at diagnosis and after 10-14 days and 3 months treatment. Immunohistochemical staining for Ki67, oestrogen receptor (ER) and progesterone receptor (PgR) was performed and related to clinical (ClinR) and pathological responses (PathR) after 3 months treatment. ClinR was observed in 48 of 63 cases (76.2%) and PathR in 47 of 62 (75.8%). Pretreatment Ki67 scores were similar in responders (R) and non-responders (NR). Highly significant Ki67 decreases occurred in all tumour subgroups at 10-14 days (P<0.005). A significant difference in Ki67 scores at 10-14 days (P<0.007) was found between PathR and PathNR but not between ClinR and ClinNR. At 3 months, decreases from pretreatment Ki67 scores were highly significant in all tumour subgroups irrespective of response status. However, whereas Ki67 scores were significantly different between pathological R and NR (P=0.009), the corresponding comparison of ClinR status was not. Significant decreases between 10-14 days and 3 months were found only in ClinR and PathR (P=0.02 and 0.045, respectively). Treatment significantly reduced PgR expression at 14 days and 3 months (both P<0.0001), but the level of changes was not different between response status groups. In summary, letrozole produces rapid and profound decreases in expression of Ki67 and PgR but changes do not always correlate with clinical and pathological responses.British Journal of Cancer advance online publication, 14 March 2006; doi:10.1038/sj.bjc.6603001 www.bjcancer.com.
though not arguing that its not effective, just that you will see similar effects to likley rather severe oestrogen suppression (though hard to say since dosing for AAS users has not really been even experimentally addressed)
Curr Top Med Chem. 2006;6(3):195-216. Related Articles, Links
Estrogen receptors as therapeutic targets in breast cancer.
Ariazi EA, Ariazi JL, Cordera F, Jordan VC.
Fox Chase Cancer Center, Philadelphia, PA 19111-2497 USA. [email protected].
The estrogen receptor alpha (ERalpha) has proven to be the single most important target in breast cancer over the last 30 years. The use of the selective ER modulator (SERM) tamoxifen for the treatment and prevention of breast cancer has changed therapeutics. The SERM raloxifene, approved for the treatment of osteoporosis, lacks tamoxifen's increased risk for endometrial cancer and is being evaluated for the prevention of breast cancer. Other SERMs approved or under development for use against breast cancer or osteoporosis include toremifene, GW5638, GW7604 (the active metabolite of GW5638), idoxifene, lasofoxifene, arzoxifene, bazedoxifene, EM-800 and acolbifene (the active metabolite of EM-800). Aromatase inhibitors (AIs) have recently proven to be more efficacious than tamoxifen as first-line therapy, efficacious for second-line therapy (e.g. against tamoxifen-resistant disease), and useful for extended adjuvant therapy after tamoxifen. The AIs include the non-steroidal agents letrozole and anastrole, and the steroidal agent exemestane. The pure antiestrogen fulvestrant has proven to be just as effective as AIs. Other pure antiestrogens, ZK-703, ZK-253, RU 58668 and TAS-108 show great promise. The development of resistance to endocrine therapy remains a clinically important problem, and laboratory models based on human breast cancer cells grown as tumors in immune-compromised mice have led to important insights into this problem. Progesterone receptor-negative status of ER-positive breast cancers may reflect altered growth factor receptor signaling, and helps to explain why this subclass of tumors exhibits lower response rates to tamoxifen compared to cancers typed progesterone receptor-positive. Crosstalk among plasma membrane-localized ER, growth factor receptor signaling, and nuclear-localized ER provide further insights into antihormonal-resistant breast cancer.
macrophage69alpha
New member
LT3 said:
YES.... EXCEPT in cases where you have a promiscuous ligand. For instance like a progestin that binds to the ER. though aspect of many AAS has not been explored (so it would just be a guess which ones did-- IF ANY)
there are also probably other limited cases, perhaps with ultra, ultra high doses where you have receptor cross reactivity, where it might be quite different.
macrophage69alpha
New member
LT3 said:
in truth, completely unknown.
likely yes, but for the above reason (promiscuos ligand) faslodex might be better. though if better, likely only slightly.
as a point of reference the ER binding of MENT 7alpha-methyl-19-nortestosterone is 1/200 of estradiol.
macrophage69alpha
New member
LT3 said:
hey,
searching and discussion are how new methods and ideas are found.
and there may be benefits to it when used with progestins (its just not clear how much- from the MENT not much, but other progestins may have much higher binding potentials)
macrophage69alpha
New member
cboogsrun said:
this is a bit more basic
btw- basically they both cut off Estrogen Receptor activation wholesale one by blocking and one by stopping conversion. its probably most comparable to letrozole for that reason. (stopping estrogen receptor activation decreases expression of the progesterone receptor)
the issue of difference would mainly arise when an offending hormone or chemical did not convert but was itself estrogenic (so it did not require aromatase to make it that way)
so if you were exposed to DDT or other potent xenoestrogens (or even just estrogen- say you popped a birth control pill) an AI is going to do nothing about their activity... now faslodex will (as long as the offending hormone/chemical does not have a greater binding affinity)
A
Anthony Roberts
Guest
I wrote that about 3 years ago...
SpeedFreak5
New member
Ok in ediot terms are you guys saying that all AI's are capable of prevent Erectile Dysfunction like Faslodex. Becuase thats what I'm concerned about as I think of starting a Tren cycle.
Ok can someone simplify this for me. my main concern would be running deca and having progesterone sides ie. gyno from nandro. what is best to have on hand? I have heard caber and bromo? but then have also read they don't really work on progesterone but on prolactin. so if one were to run deca for the first time what is reccomended to have? letro adex? I appologize for my newbieness
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