DHEA + Formestane = ???

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  1. Question DHEA + Formestane = ???

    If one were to take large amounts of DHEA and some formestane at the same time, would this result in a large amount of free testosterone in the body with little to no other (unwanted) hormone levels being raised at the same time?

    Formestane is an aromatase enzyme inhibitor. Are there other pathways to estrogen? Are there other conversions to unwanted hormones than estrogen? Can those be blocked?


  2. Good question, I am thinking of doing a E-Form (formastane) and DHEA stack. I too would like to know the results of these two.

  3. the only thing in this stack to raise t-levels would be Formestane,due to its receptor binding activity and anti e properities.
    DHEA does nothing with xour test levels until you´re over 50 or so.
    Side effects of too little estrogen is a bad blood lipid profile,leaving you with cardio-vascular risks.

  4. Are you quite sure? Isn't Formestane a suicide aromatase inhibitor, meaning that it binds to the aromatase enzyme and deactivates it?

    Isn't the very reason why DHEA is of no use before 50 that it generates increased test, but also estrogen in parallel, taking you to higher test, but much higher estrogen?

    That's the info that I got, of course I'm still trying to piece it all together.

  5. Formestane does inhibit aromatase and it does stimulate the HPTA.

    DHEA is proven to do nothing significant with the hormones of a healthy young
    man(slightly higher esrtogens but not significant),nor does it improve any sporting efforts.

    But when DHEA levels decline with age below a threshold where even testosterone production
    will suffer,a suplementation will do significant improvements.

    With a DHEA supplementation u will keep the cortisol/DHEAS ratio high and boost your immune functions,
    and maybe your recoverytime from great exertion since with them,DHEA is greatly depleted to DHEAS.

    Plus DHEA supplemetation seems to hold bodyweight.It has itself an androgenic activity,without converting to any
    other hormone.

  6. Formestane = Aromatase inhibitor

    Breast Cancer Res Treat. 1994;30(1):81-7. Related Articles, Links
    Second generation aromatase inhibitor--4-hydroxyandrostenedione.

    Dowsett M, Coombes RC.

    Academic Dept of Biochemistry, Royal Marsden Hospital, London, UK.

    4-hydroxyandrostenedione is a steroidal, suicide substrate inhibitor of aromatase, which has been widely tested in postmenopausal breast cancer patients. It is highly specific with the only notable endocrine changes other than oestrogen suppression being a dose-related suppression of sex-hormone binding globulin when the drug is given orally (a reflection of the drug's minor androgenic activity). Intramuscular administration of 250 mg every second week is the schedule of choice. This achieves peripheral aromatase inhibition of about 85% and oestradiol suppression of about 65%. The drug is usually used second-line, after tamoxifen, with an overall response rate in unselected patients of 26%. Side-effects are minimal and consist almost entirely of local reactions at the site of injection. 4-hydroxyandrostenedione is therefore a useful new treatment option as the first selective aromatase inhibitor to have wide clinical availability.

    Publication Types:

    • Review
    • Review, Tutorial
    PMID: 7949207 [PubMed - indexed for MEDLINE]


    Cancer Chemother Pharmacol. 1990;27(1):67-71. Related Articles, Links
    Comparison of the pharmacokinetics and pharmacodynamics of unformulated and formulated 4-hydroxyandrostenedione taken orally by healthy men.

    Dowsett M, Lloyd P.

    Department of Biochemical Endocrinology, Royal Marsden Hospital, London, U.K.

    A study of the aromatase inhibitor 4-hydroxy-androstenedione (4-OHA) was conducted in normal healthy men to compare the oral administration of two preparations of the drug: an unformulated, micronized powder and a formulated microcrystalline material (CGP 32349). The formulated material achieved a significantly higher mean peak concentration (88% greater than that obtained using the unformulated powder) and a higher mean AUC (not significant). The median time to peak was 1.5 h for both preparations and the elimination rate constants were similar (0.31 for micronized 4-OHA and 0.36 h-1 for formulated 4-OHA). Plasma concentrations of 4-OHA in this group were markedly lower than those previously observed in postmenopausal breast cancer patients. Significant biological activity was demonstrated with the formulated material in its suppression of plasma oestradiol levels, whereas no significant suppression was obtained using the micronized powder. An increase in androgen levels was observed that may have been due to competitive inhibition of enzymes involved in metabolic clearance of androgens and/or to decreased feedback inhibition of gonadotrophin secretion by oestradiol.

    PMID: 2123133 [PubMed - indexed for MEDLINE]


    Drugs. 1993 Jan;45(1):66-84. Related Articles, Links
    Formestane. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic potential in the management of breast cancer and prostatic cancer.

    Wiseman LR, McTavish D.

    Adis International Limited, Auckland, New Zealand.

    Formestane (4-hydroxyandrostenedione) is an effective and competitive inhibitor of aromatase, the enzyme responsible for the conversion of androgens to estrone and estradiol. Significant reductions in plasma estradiol levels are observed following intramuscular administration of formestane to postmenopausal women with advanced metastatic breast cancer. Overall response rates to intramuscular formestane in these patients are approximately 25 to 30% and a further 20 to 30% of patients experience disease stabilisation during treatment. Response rates are improved in patients with hormone responsive tumours and in those who have responded to previous endocrine therapy. Soft tissue metastases generally show the best response to formestane treatment while visceral metastases (in particular liver) show a poor response. The median duration of response is usually between 7 months and 1 year. Formestane has been generally well tolerated in the relatively small clinical trials conducted to date with adverse effects reported in approximately 13% of patients following intramuscular administration. The most frequent adverse effects are local reactions at the injection site and systemic effects mainly related to the effect of the drug on the hormonal milieu. Thus, formestane is effective as a second-line endocrine treatment for advanced metastatic breast cancer in women with natural or artificially induced menopause, with apparent tolerability advantages over older agents such as aminoglutethimide; with wider study and experience it may yet challenge tamoxifen as a first-line endocrine therapy in metastatic breast cancer.

    Publication Types:
    • Review
    • Review, Tutorial
    PMID: 7680986 [PubMed - indexed for MEDLINE]


    J Enzyme Inhib. 1997 Dec;12(4):241-54. Related Articles, Links
    Inhibition and inactivation of equine aromatase by steroidal and non-steroidal compounds. A comparison with human aromatase inhibition.

    Moslemi S, Seralini GE.

    Laboratoire de Biochimie et Biologie Moleculaire, EP CNRS 9, IBBA, Universite de Caen, France.

    In order to approach the detailed structure-function relationships of aromatase, we studied the inhibitory and inactivatory potencies of several steroidal androstenedione analogues (1: 4-hydroxyandrostenedione, 2: 4-acetoxyandrostenedione and 3: 7 alpha-(4'-amino)phenylthio-4-androstene-3, 17-dione) and non-steroidal imidazole derivatives (4: ketoconazole, 5: miconazole and 6: fadrozole) on equine aromatase in placental microsomes, a well established mammalian model. Human placental microsomes and the purified enzyme from equine testis were also used to compare inhibition by 1 and 2. In equine microsomes, all compounds tested exhibited a competitive inhibition, with Ki values of 4.1, 26 and 1.8 nM for 1, 2 and 3, and of 2400, 1.4 and 4 nM for 4, 5, and 6, respectively. The Km for androstenedione, the substrate mainly used in these studies, was 1.8 +/- 0.13 nM. The three non-steroidal derivatives did not inactivate equine aromatase, but 1 and 2 acted as comparable inactivators to a much higher degree than 3. Compound 1 inhibited in a similar manner (89-94%) purified or equine and human microsomal aromatases, whereas 2 inhibited microsomal aromatase more efficiently in the horse than in man (92% and 33% inhibition, respectively). There was only a 40% inhibition with 2 on the purified equine enzyme, which is no more in the natural membrane environment. The comparisons between equine and human microsomal aromatases allow precise functional and structural differences to be observed with these enzymes.

    PMID: 9502046 [PubMed - indexed for MEDLINE]


    Br J Cancer. 1993 Aug;68(2):393-8. Related Articles, Links
    Erratum in:

    • Br J Cancer 1994 Mar;69(3):626.
    Plasma and urinary oestrogens in breast cancer patients on treatment with 4-hydroxyandrostenedione.

    Johannessen DC, Adlercreutz H, Fotsis T, Lonning PE.

    Department of Oncology, University Hospital of Bergen, Haukeland sykehus, Norway.

    Plasma and urinary oestrogens were measured in nine breast cancer patients (eight postmenopausal women and one man) before and during treatment with the aromatase inhibitor 4-hydroxyandrostenedione. Urinary oestrogens were measured by using a highly specific GC-MS method. Plasma levels of oestrone, oestradiol and oestrone sulphate were suppressed by 66.6% (+/- 3.6%), 57.7% (+/- 5.1%) and 51.8% (+/- 6.4%) respectively (P < 0.005 for all). Twenty-four hour urinary excretion of total oestrogens, oestradiol, oestriol, 2-hydroxyoestrone, 16 alpha-hydroxyoestrone and the minor metabolites 16 beta- and 15 alpha-hydroxyoestrone were all suppressed by mean values ranging from 60% to 82%, (oestradiol: P < 0.025, otherwise P < 0.005). There were no significant changes in the ratios between the different plasma oestrogens. The finding of sustained plasma and urinary oestrogens at 20-40% compared to their control levels indirectly support a hypothesis of alternative oestrogen sources in postmenopausal breast cancer patients on treatment with 4-hydroxyandrostenedione.

    PMID: 8135918 [PubMed - indexed for MEDLINE]


    J Steroid Biochem. 1986 Nov;25(5B):867-76. Related Articles, Links
    Aromatase inhibitors and benign prostatic hyperplasia.

    Henderson D, Habenicht UF, Nishino Y, Kerb U, el Etreby MF.

    A growing amount of evidence implies that estrogens may play a role together with androgens in the genesis of benign prostatic hyperplasia (BPH) in man. We review here some of this evidence together with advances made in characterizing inhibitors of estrogen biosynthesis (aromatase inhibitors). It is proposed that aromatase inhibitors may find application in non-surgical treatment of BPH.

    PMID: 2433507 [PubMed - indexed for MEDLINE]


    J Steroid Biochem. 1983 Apr;18(4):391-6. Related Articles, Links
    Effects of testosterone, estradiol, aromatase inhibitor, gonadotropin and prolactin on the response of mouse testes to acute gonadotropin stimulation.

    Dalterio S, Bartke A, Brodie A, Mayfield D.

    These studies determined the local acute responsiveness of the testis to intratesticular administration of human chorionic gonadotropin (hCG) under basal, stimulated (systemic hCG pre-treated), hypogonadotropic (steroid pre-treatment) and hyperprolactinemic conditions in male mice. In addition, testicular testosterone (T) levels were determined after intratesticular administration of the aromatase inhibitor, 4-hydroxyandrostenedione (4-OHA) or progesterone under basal or hCG-stimulated conditions. Intratesticular administration of 0.025, 0.25, 2.5 or 25 mIU hCG resulted in a dose-dependent (3- to 14-fold) increase in testicular T concentrations in hCG compared to vehicle-injected testes. Systemic (i.p.) pre-treatment with 5 IU hCG 24 h before prevented any further increases in the already elevated (10-fold basal) T levels after direct intratesticular hCG injection. Pretreatment with 250 micrograms testosterone propionate (TP) reduced basal testicular T concentrations, but resulted in increased responsiveness to intratesticular hCG administration. In contrast, estradiol benzoate (EB) pretreatment, which also reduced basal testicular T concentrations, did not affect the testicular responsiveness to hCG. Hyperprolactinemia reduced testicular responsiveness to intratesticular administration of 0.025, 0.25 or 2.5 mIU hCG, but basal levels of testicular T were elevated. One hour after intratesticular injections of an aromatase inhibitor, 4-OHA; (0.25 micrograms) testis, T levels were increased in males pre-treated with 5 IU hCG (i.p.) 24 h earlier. Higher doses of 4-OHA (2.5, 25 or 250 micrograms) resulted in significant, dose-related increases in basal testicular T levels which were attenuated by hCG-pre-treatment. Intratesticular administration of 20 micrograms progesterone increased testicular T concentrations 2.7-fold, but this effect was attenuated (1.5-fold) in hCG-pre-treated mice, suggesting that enzymatic lesions beyond progesterone may be involved in hCG-induced testicular desensitization. These results indicate that testicular responsiveness to hCG depends on the existing levels of gonadotropic stimulation. However, it is evident that estrogens and prolactin also influence the sensitivity of the testis to gonadotropin.

    PMID: 6834825 [PubMed - indexed for MEDLINE]


    So Formestane *IS* a suicide aromatase inhibitor that indirectly causes testosterone release from the testes. Good for PCT I say.

    That still doesn't answer my question. And please, if you KNOW the answer to something, please post it. If you BELIEVE or HAVE HEARD something about something, please don't make it out as fact. It's much easier on everyone. Thanks.

  7. yes,it surely is.

    i don´t know if there´s a study ro back up wether formesrtane raises frteee test but it does seem to raise test in general.
    Along with the DHEA it should be great for PCT ´cause DHEA does attain bodyweight and promotes fatloss at the same time.
    Anecdotally DHEA is said to help with libido better than without in PCT.

  8. How does regular DHEA's anti cortisol effects compare to Lean Xtreme? Which is more potent in that area. Is formestane good for PCT or as a stand alone, seeing how it has an androgenic property?

  9. I'd say better for PCT because it is firstly an estrogen-killer.

  10. Formestane seems to be a good,smooth performance enhancer as well,as a stand alone.
    Not to grow much more muscles and I haven´t been using it for long but it definately did something the first two weeks,although I´ve gotten used to the effects or they wore off.
    don´t know,but I stopped taking it then whatsoever.

  11. Thanks for the info. What about the cortisol comparison between DHEA and Lean Xtreme do they both have the same anti cortisol effect.

  12. DHEA has affinity to the AR but I don´t know if this action is also partially competitive with the GR,as it is with so many AAS:

    but a high ratio of Cort/DHEAS is a sign of lesser fatigue and stress and,obviously,it seems to help my immune system after prolongued,excessive bouts of training.

    i dont think it´s a placebo effect,´cause I dont´really in believe in it(in anything at first),but when I forget to take it,I will take it,for it really helps.

  13. Can DHEA be taking while on cycle with something like SD or is it better in pct.

  14. I´m using it and I´m on var and dbol and it really seems to be benificial to me.

    my boys don´t seem to shrink as much as w/o,too.

  15. *** B U M P *** The question remains unanswered and there are people who do have the knowledge for answering it here... I guess they haven't seen this thread!

  16. What do you mean with "no other unwanted hormones" ?

    It´s unlikeley to have one without the other.

    DHEA leads to an weight increase in lbm without effecting the hormones significantly.

    Formestanen lowers estrogen to about 65% and raises testosterone.
    Also,with foremstane you´ll have higher IGF-1 levels.

    If it´s that what you´re looking for-go for it.

  17. Well I was wondering about prolactin, progesterone, and other similar things. There are lots of steroids in the body and DHEA is a precursor to lots of them... DHEA + tribulus + formestane seems good on paper, although I do have gyno already...

  18. B U M P

  19. Well, I can't give you any more info than you already know, my log is going to be good answer for you.

  20. You gonna get bloodwork DURING the DHEA/ATD treatment?

  21. You mean test, free test? Then no.

  22. Dmitry, can you post a link to your log. I am also thinking of running an ATD/DHEA cycle for 3-4 weeks to see what happens. Im mostly looking to decrease bf and gain a little muscle. Im thinking of dosing ATD @ 50mgED at night and DHEA @ 100mgED in the morning or pre-workout. Any thoughts on this?????

    Im still not 100% on this, I might just save it for PCT of my next cycle.

  23. http://www.anabolicminds.com/forum/s...ad.php?t=34573

    I think it's a very good idea, but I don't know how usefull my log is gonna be. I have too much **** going on in my life I'm too damn busy and tired. I started Rxt because I'm fighting with gyno I got 4 months after SD cycle and decided to throw DHEA, just because.

  24. Ive decided to start my ATD/DHEA cycle tomorrow. I'll post a log tomorrow to let you guys know how it goes.

  25. Why do you guys keep saying to use formestane for PCT when it's suppressive?


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