Which do you prefer?
have you tried PP's LV Formestane?CEL Formestane is one of the best supplements I have ever used.
No, I have not.have you tried PP's LV Formestane?
I have a couple bottles and I was just wondering.No, I have not.
It was injected as an acetate ester in cancer research but quickly went away when much better oral options came to the marketId vote for Form. if i recall correctly, it was use injectably long ago by bbers
interesting, I wonder whyive got the fastest heartbeating in my live after taking formestane (LV version).. never never again...
yeah, dont really know why.interesting, I wonder why
hmm I found after talking it I would get some high blood pressure symptoms.ive got the fastest heartbeating in my live after taking formestane (LV version).. never never again...
I like the fact that it lowers cortisol, its a great addition to the estrogen lowering effects.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.
ah gotcha! i remember reading it somewhere thanksIt was injected as an acetate ester in cancer research but quickly went away when much better oral options came to the market
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.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.
.
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?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.
in vitro it's the major metabolite. in vivo, it is not. less than 1% IIRCThe 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?
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?in vitro it's the major metabolite. in vivo, it is not. less than 1% IIRC
sure.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?
Thats because you forgot to bold itIn 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.
nvm. thats right. i thought 4-oht was tested seperate there.Thats because you forgot to bold it
No worries B1 (i officially approve you as B1 of 3 on the CEL team)ok, not identified in rats much, but in humans yes. my mistake.
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