Formestane vs Erase

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  1. Formestane vs Erase


    Which do you prefer?
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  2. CEL Formestane is one of the best supplements I have ever used.
    I'm Back...

  3. Quote Originally Posted by Clickster View Post
    CEL Formestane is one of the best supplements I have ever used.
    have you tried PP's LV Formestane?
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  4. I have never used Formestane so don't have a personal opinion on the topic I am afraid fightback.
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  5. Quote Originally Posted by fightbackhxc View Post
    have you tried PP's LV Formestane?
    No, I have not.
    I'm Back...

  6. Quote Originally Posted by Clickster View Post
    No, I have not.
    I have a couple bottles and I was just wondering.
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  7. I have used transdermal Formastanzol which is known for having an excellent carrier and other goodies in the dermal besides the Form. Great product. I have also used Erase on a Test cycle and enjoyed it. Both are good.

    I saw more drying out and hardening up on the Formastanzol but probably because I was using it with Natty estrogen levels.

  8. Id vote for Form. if i recall correctly, it was use injectably long ago by bbers
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  9. Better for what?

    They aren't really comparable IMO.

    As for formestane via oral route...no point unless youre taking 500mg per day
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  10. Quote Originally Posted by GeekPoop View Post
    Id vote for Form. if i recall correctly, it was use injectably long ago by bbers
    It was injected as an acetate ester in cancer research but quickly went away when much better oral options came to the market
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  11. Erase is definitely cheaper and effective.Just wanting to know because I have a bottle of Formestane and I am unsure if I want to take it or not.
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  12. ive got the fastest heartbeating in my live after taking formestane (LV version).. never never again...

  13. Quote Originally Posted by kev4me View Post
    ive got the fastest heartbeating in my live after taking formestane (LV version).. never never again...
    interesting, I wonder why
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  14. Quote Originally Posted by fightbackhxc View Post
    interesting, I wonder why
    yeah, dont really know why.

    my sleep shedule is ****ed up too... got nightsweat and all that ****...

  15. Quote Originally Posted by kev4me View Post
    ive got the fastest heartbeating in my live after taking formestane (LV version).. never never again...
    hmm I found after talking it I would get some high blood pressure symptoms.


    I like Formestane for the aggression, but if I dose over 4 pumps a day it gets so high I get a bit of anxiety, drys me yo good too. I havn't tried Formastanzol but I have a bottle waiting for me in the future.

    Erase gives a much smaller aggression boost for me, no anxiety issues, at 3 caps a day drys me out more then formestane, I noticed an increase in Vascularity as well, something I never saw from Form. Overall and body comp changes I give to Erase, aggression boost I give props to Formestane.
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  16. Sounds like everything I am wanting is coming from Erase. Ill stick to that.
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  17. I like both but they are two different products. Ive used two different types of form used the transdermal and oral. Trans works much better in my opinion. Erase is a great product though and i use it frequently when i have done natty testbooster runs, helps with cortisol levels for sure in me. But you can't go wrong with both products.

  18. Quote Originally Posted by PrepNwa23 View Post
    I like both but they are two different products. Ive used two different types of form used the transdermal and oral. Trans works much better in my opinion. Erase is a great product though and i use it frequently when i have done natty testbooster runs, helps with cortisol levels for sure in me. But you can't go wrong with both products.
    I like the fact that it lowers cortisol, its a great addition to the estrogen lowering effects.
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  19. Quote Originally Posted by nattydisaster View Post
    It was injected as an acetate ester in cancer research but quickly went away when much better oral options came to the market
    ah gotcha! i remember reading it somewhere thanks
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  20. I prefer Erase over formestane for a number of reasons. Formestane requires transdermal application to have any decent bio-availability, which can be a nuisance. Formestane has decent affinity for the 5a reductase enzyme as well due androgenic metabolite conversion. Since it has the ability to competitively inhibit the 5a-r enzyme it can produce lower DHT levels depending on dose, of course. DHT not only directly antagonizes the estrogen receptor, but its also found to inhibit aromatase.

    It seems counter-intuitive to administer an AI and have gyno problems, but depending on the formestane dose i feel the potential is there.

    Erase doesnt have any androgenic metabolites, so the aforementioned problems would be of no concern. Since its a metabolite of 7-oxo, and since 11b-hsd is required to metabolize 7-keto and 7-hydroxy groupings, it acts as a competitive inhibitor of this enzyme. This means more inactive cortisone and less active cortisol.
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  21. The 5AR inhibiting effect is made up for with the androgenic metabolite conversion if you are considering gyno. Formestane also lowers SHBG which will cause more active androgenic effects in the body and again makes gyno highly unlikely. And of course it lowers estrogen. I don't think gyno is of any concern with Formestane whatsoever.

    Formestane raises IGF-1 which is another bonus

  22. Quote Originally Posted by kevinhy View Post
    I prefer Erase over formestane for a number of reasons. Formestane requires transdermal application to have any decent bio-availability, which can be a nuisance. Formestane has decent affinity for the 5a reductase enzyme as well due androgenic metabolite conversion. Since it has the ability to competitively inhibit the 5a-r enzyme it can produce lower DHT levels depending on dose, of course. DHT not only directly antagonizes the estrogen receptor, but its also found to inhibit aromatase.

    .
    formestane is a very poor 5ar inhibitor. you should specify the places it inhibits 5ar as well. prostate and cancer tissue. never heard of it inhibiting 5ar in skeletal muscle, cardiac muscle, liver etc. etc.
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  23. Quote Originally Posted by chocolatemilk View Post
    The 5AR inhibiting effect is made up for with the androgenic metabolite conversion if you are considering gyno. Formestane also lowers SHBG which will cause more active androgenic effects in the body and again makes gyno highly unlikely. I don't think gyno is of any concern with Formestane whatsoever. And not to mention Formestane raises IGF-1 which is another bonus.
    The main metabolite of formestane is 4-hydroxytestosterone, which is significantly less androgenic than DHT. It's sort of like saying nandrolones hogging of the 5-ar is made up for with DHN. I'm not saying it's a gyno recipe, but stranger things have happened, and I believe I've heard anecdotal reports suggesting that very thing. I haven't seen any studies suggesting it increases igf 1 levels, perhaps you could PM me the study?

  24. Quote Originally Posted by kevinhy View Post
    The main metabolite of formestane is 4-hydroxytestosterone, which is significantly less androgenic than DHT. It's sort of like saying nandrolones hogging of the 5-ar is made up for with DHN. I'm not saying it's a gyno recipe, but stranger things have happened, and I believe I've heard anecdotal reports suggesting that very thing. I haven't seen any studies suggesting it increases igf 1 levels, perhaps you could PM me the study?
    in vitro it's the major metabolite. in vivo, it is not. less than 1% IIRC
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  25. Quote Originally Posted by Bry17 View Post
    in vitro it's the major metabolite. in vivo, it is not. less than 1% IIRC
    Lol, I don't believe I've seen that data, I'll attempt to find later on. If I have trouble finding would it be any trouble to PM me the study?

  26. 4OHT being mildly androgenic was just one of the reasons. It was in retrospect with everything else I mentioned which makes gyno extremely unlikely. And if it is a poor 5AR inhibitor and site-specific then I really don't think gyno and Formestane are anything worth discussing.

    I will PM you when I'm out of work on the IGF-1 kevinhy.

  27. In rat:

    The metabolism of the aromatase inhibitor-4-hydroxyandrostenedione (4-OHA) was studied in vitro and in vivo in the rat. To accomplish this, deuterium- and tritium-labeled 4-OHA were prepared from 4-hydroxyandrosta-4, 6-dione-3,17-dione. The latter was synthesized from 4-androstene-3,17-dione. Using deuterated 4-OHA in in vitro incubations of rat ovarian microsomes, 4-hydroxytesterone (4-OHT) was identified by gas chromatography/mass spectroscopy as the major metabolite. 4-OHT constituted approximately 20% of the total radioactivity from [6,7-3H]-4-OHA in the ovarian microsomal incubations. Conversion of [6,7-3H]-4-OHA to 4-hydroxyesterone was approximately 0.1%. The major metabolite of [6, 7-3H]-4-OHA in vivo identified in the free, neutral fraction of rat blood was 3 beta-hydroxyandrostane-4,17-dione. The metabolite accounted for approximately 5% of the total radio-activity in the blood, Whereas 4-OHT accounted for only 0.1%, 4-OHT inhibited in vitro ovarian aromatization by 59%, but 3 beta-hydroxyandrostane-4-17-dione had little effect. It was concluded that the in vivo effects of 4-OHA previously reported are largely due to its own activity although additional effects of its metabolic products cannot be excluded.

    In human:

    4-Hydroxyandrost-4-ene-3,17-dione is a second generation, irreversible aromatase inhibitor and commonly used as anti breast cancer medication for postmenopausal women. 4-Hydroxytestosterone is advertised as anabolic steroid and does not have any therapeutic indication. Both substances are prohibited in sports by the World Anti-Doping Agency, and, due to a considerable increase of structurally related steroids with anabolic effects offered via the internet, the metabolism of two representative candidates was investigated. Excretion studies were conducted with oral applications of 100mg of 4-hydroxyandrostenedione or 200mg of 4-hydroxytestosterone to healthy male volunteers. Urine samples were analyzed for metabolic products using conventional gas chromatography-mass spectrometry approaches, and the identification of urinary metabolites was based on reference substances, which were synthesized and structurally characterized by nuclear magnetic resonance spectroscopy and high resolution/high accuracy mass spectrometry. Identified phase-I as well as phase-II metabolites were identical for both substances. Regarding phase-I metabolism 4-hydroxyandrostenedione (1) and its reduction products 3beta-hydroxy-5alpha-androstane-4,17-dione (2) and 3alpha-hydroxy-5beta-androstane-4,17-dione (3) were detected. Further reductive conversion led to all possible isomers of 3xi,4xi-dihydroxy-5xi-androstan-17-one (4, 6-11) except 3alpha,4alpha-dihydroxy-5beta-androstan-17-one (5). Out of the 17beta-hydroxylated analogs 4-hydroxytestosterone (18), 3beta,17beta-dihydroxy-5alpha-androstan-4-one (19), 3alpha,17beta-dihydroxy-5beta-androstan-4-one (20), 5alpha-androstane-3beta,4beta,17beta-triol (21), 5alpha-androstane-3alpha,4beta,17beta-triol (26) and 5alpha-androstane-3alpha,4alpha,17beta-triol (28) were identified in the post administration urine specimens. Furthermore 4-hydroxyandrosta-4,6-diene-3,17-dione (29) and 4-hydroxyandrosta-1,4-diene-3,17-dione (30) were determined as oxidation products. Conjugation was diverse and included glucuronidation and sulfatation.

    ^don't see any mention of 4-oht in bolded.
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  28. I did not know that Bry... nice!

  29. It appears as though the bolded still contains 5-ar metabolites, which would lead to lowered overall DHT levels. It may actually be beneficial if it is actually site specific (prostate, scalp) vs skeletal muscle. Is there a study that suggests this?

  30. Quote Originally Posted by kevinhy View Post
    It appears as though the bolded still contains 5-ar metabolites, which would lead to lowered overall DHT levels. It may actually be beneficial if it is actually site specific (prostate, scalp) vs skeletal muscle. Is there a study that suggests this?
    sure.



    Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore.
    Estrogens have an important role in the growth of breast and other hormone-sensitive cancers. We have shown that 4-hydroxyandrostenedione (4-OHA) selectively blocks estrogen synthesis by inhibiting aromatase activity in ovarian and peripheral tissues and reduces plasma estrogen levels in rat and non-human primate species. In postmenopausal men and women, estrogens are mainly of peripheral origin. When postmenopausal breast cancer patients were administered either by daily oral or parenteral weekly treatment with 4-OHA, plasma estrogen concentrations were significantly reduced. Complete or partial response to treatment occurred in 34% of 100 patients with advanced breast cancer, while the disease was stabilized in 12%. We recently studied the effects of 4-OHA and other aromatase inhibitors, 10-propargylestr-4-ene-3,17-dione (PED) and imidazo[1,5-alpha]3,4,5,6-tetrahydropyrin-6-yl-(4-benzonitrile) (CGS 16949A) as well as 5 alpha-reductase inhibitors, N,N-diethyl-4-methyl-3-oxo-4-aza-5 alpha-androstane-17 beta-carboxyamide (4-MA) and 17 beta-hydroxy-4-aza-4-methyl-19norandrost-5-en-3-one (L651190) in prostatic tissue from 11 patients with prostatic cancer and six patients with benign prostatic hypertrophy (BPH), and from normal men at autopsy. We attempted to measure aromatase activity in tissue incubation by quantitating 3H2O released during aromatization of androstenedione or testosterone labeled at the C-1 position. The amount of 3H2O released from all samples was at least twice that of the heat inactivated tissue samples. The 3H2O release was significantly inhibited by 4-OHA and 4-MA, but not by the other aromatase inhibitors. However, when HPLC and TLC were used to isolate steroid products, no estrone or estradiol was detected in the incubates. Furthermore, no aromatase mRNA was detected following amplification by PCR. The 4-OHA was found to inhibit 5 alpha-reductase in both BPH and cancer tissue, although to a lesser extent than 4-MA. The other aromatase inhibitors were without effect. Although a mechanism involving intraprostatic aromatase is not likely, inhibitors may act to reduce peripherally-formed estrogens. In postmenopausal breast cancer, the results indicate that 4-OHA is of significant benefit.




    To determine the effects of 4-hydroxy-4-androstene-3,17-dione (4-OH-A) on the in vitro conversion of testosterone (T) to 5 alpha-androstan-17 beta-ol-3-one (dihydrotestosterone, DHT), 5 alpha-androstan-3 alpha, 17 beta-diol and 5 alpha-androstan-3 beta, 17 beta-diol (diols), human benign hypertrophic prostatic (BPH) tissue was incubated with 4-14C-T as substrate, in the presence of 4-OH-A (10(-8) to 10(-6) M); the amounts of the 5 alpha-reduced metabolites formed were quantitated. The effects of 4-OH-A were compared with those of 17 beta-N,N-diethylcarbamoyl-4-methyl-4-aza-5 alpha-androstan-3-one (4-MA), a known inhibitor of the 5 alpha-reductase. In the absence of 4-OH-A and 4-MA, human BPH tissue converted T to DHT and the diols readily. Both 4-OH-A and 4-MA induced significant and dose-related decreases in the formation of both DHT and the diols. The degree of inhibition induced by the different concentrations of 4-OH-A and 4-MA were 31, 41, 72% and 57, 87, 97%, respectively. The decreased formation of the diols was a consequence of the decreased availability of DHT (the immediate precursor of the diols) and was not due to direct effects of the inhibitors on the 3-hydroxysteroid dehydrogenases; both 4-OH-A and 4-MA were totally unable to modify the conversion of DHT to the diols, when 4-14C-DHT was used as substrate. Thus, 4-OH-A inhibits the process of 5 alpha-reduction of T in BPH tissue. This molecule might represent a potential new agent for the prevention and/or treatment of human BPH.




    Department of Pharmacology and Experimental Therapeutics, School of Medicine, University of Maryland, Baltimore 21201.
    The effects of 4-hydroxyandrostenedione (4-OHA) and other aromatase inhibitors, 10-propargylestr-4-ene-3,17-dione and imidazo[1,5-alpha]-3,4,5,6-tetrahydropyrin-6-yl-(4-benzonitrile), as well as 5 alpha-reductase inhibitors N,N-diethyl-4-methyl-3-oxo-4-aza-5 alpha-androstane-17 beta-carboxyamide and 4-methyl-3-oxo-4-aza-androsta-5-ene-17-ol were investigated in prostatic tissue from six patients with benign prostatic hypertrophy and seven patients with prostatic cancer, and from normal men at autopsy. We attempted to measure aromatase activity in the tissue incubations by quantitating 3H2O released from androstenedione or testosterone labeled at the C-1 position. High performance liquid chromatography and thin layer chromatography were used to isolate steroid products. Although the amount of 3H2O released was at least twice that of the heat-inactivated tissue samples, no estrone or estradiol was detected on high performance liquid chromatography. The 3H2O release was significantly inhibited by 4-OHA and N,N-diethyl-4-methyl-3-oxo-4-aza-5 alpha-androstane-17 beta-carboxyamide, but not by the other aromatase inhibitors. 4-OHA also inhibited 5 alpha-reductase in both benign prostatic hypertrophy and cancer tissue, although to a lesser extent than N,N-diethyl-4-methyl-3-oxo-4-aza-5 alpha-androstane-17 beta-carboxyamide. The other aromatase inhibitors were without effect on 5 alpha-reductase. Our results indicate that 3H2O released from [1 beta-3H]androstenedione and [1,2,6,7-3H]androstenedione does not correlate with estrogen formation and may be the result of other metabolic reactions. Although it appears that the prostate lacks aromatase, 4-OHA may be of benefit in patients with benign prostatic hypertrophy or prostatic cancer by inhibiting this enzyme in peripheral tissue.


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  31. Quote Originally Posted by Bry17 View Post
    In rat:

    The metabolism of the aromatase inhibitor-4-hydroxyandrostenedione (4-OHA) was studied in vitro and in vivo in the rat. To accomplish this, deuterium- and tritium-labeled 4-OHA were prepared from 4-hydroxyandrosta-4, 6-dione-3,17-dione. The latter was synthesized from 4-androstene-3,17-dione. Using deuterated 4-OHA in in vitro incubations of rat ovarian microsomes, 4-hydroxytesterone (4-OHT) was identified by gas chromatography/mass spectroscopy as the major metabolite. 4-OHT constituted approximately 20% of the total radioactivity from [6,7-3H]-4-OHA in the ovarian microsomal incubations. Conversion of [6,7-3H]-4-OHA to 4-hydroxyesterone was approximately 0.1%. The major metabolite of [6, 7-3H]-4-OHA in vivo identified in the free, neutral fraction of rat blood was 3 beta-hydroxyandrostane-4,17-dione. The metabolite accounted for approximately 5% of the total radio-activity in the blood, Whereas 4-OHT accounted for only 0.1%, 4-OHT inhibited in vitro ovarian aromatization by 59%, but 3 beta-hydroxyandrostane-4-17-dione had little effect. It was concluded that the in vivo effects of 4-OHA previously reported are largely due to its own activity although additional effects of its metabolic products cannot be excluded.

    In human:

    4-Hydroxyandrost-4-ene-3,17-dione is a second generation, irreversible aromatase inhibitor and commonly used as anti breast cancer medication for postmenopausal women. 4-Hydroxytestosterone is advertised as anabolic steroid and does not have any therapeutic indication. Both substances are prohibited in sports by the World Anti-Doping Agency, and, due to a considerable increase of structurally related steroids with anabolic effects offered via the internet, the metabolism of two representative candidates was investigated. Excretion studies were conducted with oral applications of 100mg of 4-hydroxyandrostenedione or 200mg of 4-hydroxytestosterone to healthy male volunteers. Urine samples were analyzed for metabolic products using conventional gas chromatography-mass spectrometry approaches, and the identification of urinary metabolites was based on reference substances, which were synthesized and structurally characterized by nuclear magnetic resonance spectroscopy and high resolution/high accuracy mass spectrometry. Identified phase-I as well as phase-II metabolites were identical for both substances. Regarding phase-I metabolism 4-hydroxyandrostenedione (1) and its reduction products 3beta-hydroxy-5alpha-androstane-4,17-dione (2) and 3alpha-hydroxy-5beta-androstane-4,17-dione (3) were detected. Further reductive conversion led to all possible isomers of 3xi,4xi-dihydroxy-5xi-androstan-17-one (4, 6-11) except 3alpha,4alpha-dihydroxy-5beta-androstan-17-one (5). Out of the 17beta-hydroxylated analogs 4-hydroxytestosterone (18), 3beta,17beta-dihydroxy-5alpha-androstan-4-one (19), 3alpha,17beta-dihydroxy-5beta-androstan-4-one (20), 5alpha-androstane-3beta,4beta,17beta-triol (21), 5alpha-androstane-3alpha,4beta,17beta-triol (26) and 5alpha-androstane-3alpha,4alpha,17beta-triol (28) were identified in the post administration urine specimens. Furthermore 4-hydroxyandrosta-4,6-diene-3,17-dione (29) and 4-hydroxyandrosta-1,4-diene-3,17-dione (30) were determined as oxidation products. Conjugation was diverse and included glucuronidation and sulfatation.

    ^don't see any mention of 4-oht in bolded.
    Thats because you forgot to bold it
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  32. Quote Originally Posted by nattydisaster View Post
    Thats because you forgot to bold it
    nvm. thats right. i thought 4-oht was tested seperate there.
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  33. ok, not identified in rats much, but in humans yes. my mistake.
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  34. I dont really know what the argument is here...formestane may or may not convert to 4-OHT, So what if it does or doesnt? That doesnt change its effects as an AI

    The other claims by Formestane need to be examined by application. For instance I have seen formestane transdermal products claim it will lower SHBG. Studies show that oral formestane lowers SHBG but not injection, which leads me to believe the metabolites are very different when taken through each route and transdermal as well.

    Which makes sense considering how many enzymes are in the skin. Not really any way to know...but transdermal is probably more close to injection that oral...which is why form is supplied this way
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  35. What needs to happen is someone needs to release sterile formestane acetate...
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  36. Quote Originally Posted by Bry17 View Post
    ok, not identified in rats much, but in humans yes. my mistake.
    No worries B1 (i officially approve you as B1 of 3 on the CEL team)
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  37. Erase is strong for an oral, maybe the strongest oral out there. I like both, I think Formestane might have a slight edge when used on cycle but I can't really say that for sure. I thnk Formestane has a greater risk for estro rebound and you need to taper off on dosing... When you take cost into consideration erase is going to be the less expensive choice.
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  38. I like both to be honest. I wish I had more Formestane. That said I have a number of Erase bottles so I will be using that for my next stackaholics meeting.

  39. Good ref.
    shows oral forma 125mg once a day is 72% effective. I wouldnt want much more than that

    http://www.ncbi.nlm.nih.gov/pmc/arti...99/table/tbl1/
  

  
 

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