Experiments with transdermal hormones
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@yeyo12 No lol, it's safe.
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Thank you, not sure if I notice any different anyway, been doing transdermal T with different formulas in a while.
Now doing forearms and back of knees. I was doing shoulders but I think alcohol irritated the skin there so I changed to forearms.
I just got DMSO so this is the first batch with DMSO. We'll see how it goes
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@brightside Sorry for the bump but how did you purify exemestane from pills?
I got my hands on some and am eager to try transdermal to not waste it taking orally. -
@PissBoy the bioavailabilty of exemestane is around 50% if I rememember correctly, and if you take it with a fatty meal, it increases by around 30%, giving you around 80% absorption.
It is a modified version of 1,4-androstenedione that is designed to have high oral bioavailability, long half life and no hepatoxcity. It converts into a drug very similar to boldenone inside the body.
You will likely loose more exemestane trying to extract it in a solvent. Furthermore, it likely contains silicon dioxide and titanium dioxide which might be soluble in the solvents.
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@alfredoolivas Also, given how little the effective dosage is (2.5-7.5 mg), there is virtually no point in administering it in a way that gives higher bioavailability.
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@alfredoolivas the Pfizer exesmastane 25mg pills or whatever they are are insanely hard to slice up ime
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@alfredoolivas According to the wiki page on exemestane, exemestane succeeds as an aromatase inhibitor because its metabolites competitively bind to aromatase (in place of aromatase's 'natural' substrate 4-androstenedione), rendering the aromatase enzyme inactive.
That description makes it seem as though testosterone cannot aromatize without converting to androstenedione first. If that is true, it is notable.
Second, the oral bioavailability of exemestane is high - the wiki page claims 60%. I'm not sure if that means 60% of oral exemestane survives first pass metabolism OR that 60% of the oral exemestane is converted to active metabolites after first pass metabolism. I strongly believe the latter is the correct interpretation.
Finally, the structure of exemestane and its lack of hepatotoxicity makes it blaringly obvious how easy it is to develop a non-17a alkylated orally active AAS. You just need a tiny bit of thinking to figure it out.
In time there is life but no knowledge; outside time there is knowledge but no life
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@eduardo-crispino Use a pill cutter, I have cut them succesfully using one
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@jamezb46
There is some confusion here I think, due to the wikipedia page@jamezb46 said in Experiments with transdermal hormones:
According to the wiki page on exemestane, exemestane succeeds as an aromatase inhibitor because its metabolites competitively bind to aromatase (in place of aromatase's 'natural' substrate 4-androstenedione), rendering the aromatase enzyme inactive.
Okay so the 17-beta hydroxy metabolite of 6-methylene-androsta-1,4-dien-3-one binds to the aromatase enzymes and inactivates it?
@jamezb46 said in Experiments with transdermal hormones:
That description makes it seem as though testosterone cannot aromatize without converting to androstenedione first. If that is true, it is notable.
But this suggests that testosterone, the 17-beta-hydroxy metabolite of androstenedione cannot bind to the aromatase enzyme?
These statements are contradictory to my understanding, please feel free to explain them further.
Exemestane doesn't have to metabolise to inhibit aromatase:
Exemestane showed a higher aromatase affinity than 10 (Ki=26 and 92 nM, respectively) and a faster enzyme inactivation@jamezb46 said in Experiments with transdermal hormones:
Second, the oral bioavailability of exemestane is high - the wiki page claims 60%. I'm not sure if that means 60% of oral exemestane survives first pass metabolism OR that 60% of the oral exemestane is converted to active metabolites after first pass metabolism. I strongly believe the latter is the correct interpretation.
Exemestane's bioavailability is 60%.
"Exemestane is extensively metabolized, with levels of the unchanged drug in plasma accounting for less than 10% of the total radioactivity after administration of radiolabeled exemestane to healthy postmenopausal women (CExemestane is extensively metabolized, with levels of the unchanged drug in plasma accounting for less than 10% of the total radioactivity after administration of radiolabeled exemestane to healthy postmenopausal women (Clemett and Lamb, 2000). P)"
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@jamezb46 said in Experiments with transdermal hormones:
Finally, the structure of exemestane and its lack of hepatotoxicity makes it blaringly obvious how easy it is to develop a non-17a alkylated orally active AAS. You just need a tiny bit of thinking to figure it out.
Given it converts into 6-methylene-boldenone which has a strong affinity to the androgen receptor, with a 24 hour half life I believe, I would love to see if it has anabolic effects. It has been shown to have anabolic effects in bones.
Currently, I am taking 50mg of exemestane powder a day, so I should be getting some 6-methylene-boldenone
The addition of the methyl group onto position 17 of androgens makes them much more anabolic and activators of the AR, if I rememember correctly, so perhaps the 17-alkylation of steroids has more effects than increasing it's half life and bioavailability
