Masteron as a growth promoter

You know, a few members on Propeciahelp have a great deal of experience with DHT, proviron and masteron, and were able to compare them first-hand.

I had a chat with those people.
Call it broscience if you will, but I won't wait for a randomized double-blind study on DHT vs masteron that will never see the light.
Dht and proviron get inactivated in the muscles by the 3hsd enzyme where masteron doesn't. William Llewallyn has discussed it
 

What is the Difference Between Proviron and Masteron?
April 23, 2010 By William Llewellyn

What is the Difference Between Proviron and Masteron?
Q: What is the difference between Proviron and Masteron? I heard they are both DHT derivates and one was really just an oral form of the other. Could I use Proviron instead of Masteron for contest prep? I lost my source for British Dragon Mastabol.

A: Proviron (oral 1-methyl-dihydrotestosterone) and Masteron (an injectable form of 2-methyl-dihydrotestosterne) are indeed structurally very similar. Both are DHT hormones with a minor modification (methylation) on each. This similarity, however, doesn’t carry over extremely closely when it comes to function. Both steroids are DHT derivatives, yes, and because of this there is no estrogen conversion possible with either drug. They lack a structural trait necessary for their conversion to estrogen. This characteristic may also allow both steroids to offer some level of anti-estrogenic activity, as the non-aromatizable steroid may compete with other aromatizable steroids (like your own endogenous testosterone) for binding to the aromatase enzyme. This should lower estrogen levels and heighten the ratio of relative androgenic to estrogenic activity in the body. As such, both steroids could be used to some extent for cutting or contest preparations. The main value in this regard is that both may help, instead of hinder, the visible retention of fat and subcutaneous water. With less water retained, muscle definition can increase provided body fat is low enough. But this is about where the functional similarities between the two agents end.

The main difference between Proviron and Masteron is their relative level of anabolic activity in skeletal muscle. Both steroids are capable of attaching to and activating the androgen receptor in muscle tissue. As such, both are theoretically capable of supporting muscle growth. But there is one major problem with Proviron. Like the base steroid dihydrotestosterone, Proviron has a high affinity for the 3-alpha hydroxysteroid dehydrogenase (3HSD) enzyme. Why is this important? It is important because 3HSD produces a weaker steroid by removing the highly important 3-keto group on the active steroid molecule. It this case it produces what are known as weak steroid “diols”. 3HSD is present in high amounts in muscle tissue, and represents a sort of blocking wall for the steroid to get through before it is able to find its corresponding receptor in the cytosol of the cell. Proviron and DHT will be actively looking for 3HSD if you will, and as a result very little will find the receptor before being converted to weakly active steroids. This is why people do not gain a lot of muscle mass while taking DHT or Proviron. The 1-methlation may result in improving the oral bioavailability of Proviron, hence the fact that it is an oral drug, but it doesn’t do much to protect it from 3HSD.

Masteron contains a 2-methylated derivative of DHT. Unlike the 1-methylation of Proviron, this alteration doesn’t effectively protect the steroid during oral dosing. This is why we only see Masteron as an injectable medication. However, shifting the methyl group from the 1 to the 2 position on the steroid backbone very effectively prevents conversion by 3HSD. As a result, the steroid is well equipped to enter the cell and break through the defensive line of 3HSD enzymes. It will reach the cytosolic androgen receptor in high concentrations, and because of this may impart a measurable tissue-building effect.

So the bottom line is that while both may help improve the look of hardness to the muscles during contest preparations, only Masteron is actually going to offer a strong effect in muscle tissue itself. This means the potential for much more muscle size and strength gains during building phases of training, and at the very least a greater level of muscle preservation during cutting phases of training (the latter due to anabolic action in muscle helping to counter the catabolic effects of calorie restriction).

These two drugs illustrate well the fact that categorizing the actions of steroids based on the three derivative bases (testosterone, nandrolone, and dihydrotestosterone) is not a highly accurate practice. So the next time someone tells you “This is a DHT derivative… so”, you can tell them “So what? I want to know what THIS steroid does, not DHT!”
 
So you are better off not contributing



Why do you even comment then ?



You don't decide when it ends. I was the one reviving this thread to have @Type-IIx input, not yours.
Neither do you, it's not your yard and you're not really something special here or something apart from existing here for 10 years.

And you're not even OP, so back off. I wasn't even talking to you in the first place. I decide when I stop talking to you. Over.
 
@Type-IIx

What is it with the methyl group added to regular DHT that makes Masteron so much more available to muscle tissues and other tissues where pure DHT is usually not that active ?

Does methylation prevent break down ? How ?
The 2α-methyl group of drostanolone (Mast) protects the Δ⁴-3-ketone moieity (and ↑anabolic and markedly ↓androgenic activity), but does not prevent metabolism by 3α-HSD (this is obvious due to its metabolism. Per Schanzer: "The parent steroid is excreted as a conjugate that can be hydrolysed with β-glucuronidase. The main metabolite is the 17-keto-oxidized 3α-hydroxy-reduced product 3α-hydroxy-2α-methyl-5α-androstan-17-on, which in comparison with T metabolism, is the 2α-methyl androsterone analog."). You can think of this attachment as serving to protect the "core" of the steroid from breakdown. And yet, it doesn't do this particularly well in the case of Masteron; unlike Superdrol (essentially Methyl Masteron), where the presence of both the 2α- & 17α- methyl groups result in substantial resistance to metabolism (i.e., 1/6th of Superdrol consumed remains unmetabolized as the parent drug reflecting its resistance to hepatic breakdown).
 

What is the Difference Between Proviron and Masteron?
April 23, 2010 By William Llewellyn

What is the Difference Between Proviron and Masteron?
Q: What is the difference between Proviron and Masteron? I heard they are both DHT derivates and one was really just an oral form of the other. Could I use Proviron instead of Masteron for contest prep? I lost my source for British Dragon Mastabol.

A: Proviron (oral 1-methyl-dihydrotestosterone) and Masteron (an injectable form of 2-methyl-dihydrotestosterne) are indeed structurally very similar. Both are DHT hormones with a minor modification (methylation) on each. This similarity, however, doesn’t carry over extremely closely when it comes to function. Both steroids are DHT derivatives, yes, and because of this there is no estrogen conversion possible with either drug. They lack a structural trait necessary for their conversion to estrogen. This characteristic may also allow both steroids to offer some level of anti-estrogenic activity, as the non-aromatizable steroid may compete with other aromatizable steroids (like your own endogenous testosterone) for binding to the aromatase enzyme. This should lower estrogen levels and heighten the ratio of relative androgenic to estrogenic activity in the body. As such, both steroids could be used to some extent for cutting or contest preparations. The main value in this regard is that both may help, instead of hinder, the visible retention of fat and subcutaneous water. With less water retained, muscle definition can increase provided body fat is low enough. But this is about where the functional similarities between the two agents end.

The main difference between Proviron and Masteron is their relative level of anabolic activity in skeletal muscle. Both steroids are capable of attaching to and activating the androgen receptor in muscle tissue. As such, both are theoretically capable of supporting muscle growth. But there is one major problem with Proviron. Like the base steroid dihydrotestosterone, Proviron has a high affinity for the 3-alpha hydroxysteroid dehydrogenase (3HSD) enzyme. Why is this important? It is important because 3HSD produces a weaker steroid by removing the highly important 3-keto group on the active steroid molecule. It this case it produces what are known as weak steroid “diols”. 3HSD is present in high amounts in muscle tissue, and represents a sort of blocking wall for the steroid to get through before it is able to find its corresponding receptor in the cytosol of the cell. Proviron and DHT will be actively looking for 3HSD if you will, and as a result very little will find the receptor before being converted to weakly active steroids. This is why people do not gain a lot of muscle mass while taking DHT or Proviron. The 1-methlation may result in improving the oral bioavailability of Proviron, hence the fact that it is an oral drug, but it doesn’t do much to protect it from 3HSD.

Masteron contains a 2-methylated derivative of DHT. Unlike the 1-methylation of Proviron, this alteration doesn’t effectively protect the steroid during oral dosing. This is why we only see Masteron as an injectable medication. However, shifting the methyl group from the 1 to the 2 position on the steroid backbone very effectively prevents conversion by 3HSD. As a result, the steroid is well equipped to enter the cell and break through the defensive line of 3HSD enzymes. It will reach the cytosolic androgen receptor in high concentrations, and because of this may impart a measurable tissue-building effect.

So the bottom line is that while both may help improve the look of hardness to the muscles during contest preparations, only Masteron is actually going to offer a strong effect in muscle tissue itself. This means the potential for much more muscle size and strength gains during building phases of training, and at the very least a greater level of muscle preservation during cutting phases of training (the latter due to anabolic action in muscle helping to counter the catabolic effects of calorie restriction).

These two drugs illustrate well the fact that categorizing the actions of steroids based on the three derivative bases (testosterone, nandrolone, and dihydrotestosterone) is not a highly accurate practice. So the next time someone tells you “This is a DHT derivative… so”, you can tell them “So what? I want to know what THIS steroid does, not DHT!”
Llewellyn makes a lot of mistakes in his writings; this is one of them. Put simply, 2α-methylation doesn't confer resistance to 3α-HSD.
 
Llewellyn makes a lot of mistakes in his writings; this is one of them. Put simply, 2α-methylation doesn't confer resistance to 3α-HSD.
how would primo compare to masteron in terms of anabolism.

Would you think its still effective as an anabolic?

Where would you rate it in regards to others?


EDIT: nvm found your post
Primo is virtually interchangeable functionally with Mast. Both are relatively modest in their potency to transactivate mammalian AR, but Mast > Primo actually in this potency (33.2% the potency of DHT [Mast] vs. 28.75% the potency of DHT [Primo] per Houtman). Both are unfortunately subject to metabolism (breakdown in human skeletal muscle) by 3α-HSD, resulting in dramatically reduced skeletal muscle anabolism in human vs. rodent. Indeed, this similarity is shared by Proviron, and as such it is not unreasonable to mention Proviron (a far more potent AR agonist on paper than Mast or Primo) in the same discussion.

Where the two seem to differ functionally, is that Mast has been shown to prevent the uptake of estrogens into, e.g. breast cells, and is therefore a tissue-specific modulator of estrogenic activity (not unlike epitiostanol, the non-methylated counterpart of Epistane that is used clinically in Japan to treat gynecomastia). Primo may serve to reduce circulating estrogens by 17β-HSD1 inhibition (DHT has been shown to be a good ligand for this enzyme), and metenolone's more saturated/estrogen-like A-ring may confer some inhibitory potency for 17β-HSD1 [resulting in decreased E2]), and/or aromatase inhibition. There is insufficient evidence to state either with confidence presently. What matters is that both have good efficacy and attenuated androgenicity particularly in treatment-resistant advanced cancer of the breast. Mast fell out of favor because of its significantly greater androgenicity to Primo in women, however; hence the actual reason why it's not available commercially as a pharmaceutical preparation.

It's great that you are a student of medicine, I wish you all the best brother. Do be aware that bold confidence on this forum, as a practical AAS neophyte, will require that you do more than make appeals to authority of ongoing education, however. And do avoid the perils (I am not saying you have done so, but I think I see a tendency) of conflating absence of evidence with evidence of absence, a common logical pitfall or fallacy.

I disagree that Primo iS iNcOmPrEnSiBlY nOnCoMpArAbLe to Mast in practice. They are remarkably similar. While I think most do prefer Primo, as I do; this is largely because it's appealing to me that it has known advantageous cardiovascular effects versus testosterone (but absence of evidence for Mast is not evidence of absence for these effects), and that it is still commercially available in some markets as a pharmaceutical product. It does not follow that Primo is superior per se to Mast, however.

Indeed, if you investigate Primo (metenolone enanthate)'s safety profile using a tool like FAFDrugs4tool, you may be surprised to learn that it fails to comply with the GlaxoSmithKline 4/400 Rule, Lilly Med Chem Rules, in addition to Pfizer's 3/75 Rule on logP, and is thus regarded as an unsafe and therefore unapproved medicine under many international and national standards.
 
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Llewellyn makes a lot of mistakes in his writings; this is one of them. Put simply, 2α-methylation doesn't confer resistance to 3α-HSD.
So are you saying that Masteron doesn’t confer any more anabolism on the muscle than proviron or DHT? Or is it somewhat more resistant to enzymatic breakdown?
 
how would primo compare to masteron in terms of anabolism.

Would you think its still effective as an anabolic?

Where would you rate it in regards to others?


EDIT: nvm found your post
Primo vs. Mast with respect to muscle anabolism are virtually interchangeable. Mast is ever so slightly more potent at the AR and slightly more androgenic as well (e.g., more virilizing in women), and Primo is evidenced to have relatively reduced cardiac harms (but absence of evidence for Mast does not imply evidence of absence). The two are really functionally equivalent, practically.
 
So are you saying that Masteron doesn’t confer any more anabolism on the muscle than proviron or DHT? Or is it somewhat more resistant to enzymatic breakdown?
No. Masteron does confer more muscle anabolism than DHT and probably Proviron (on a molar basis; per-mg, assuming that 24-hr blood levels are maintained). Proviron and DHT almost certainly have reduced muscle cell bioavailable androgen uptake given an equimolar dose of Mast. And yet this is consistent with everything that I have said here. Correct, it is still resistant to metabolism to a moderate extent given its 2α-methylation, but not because of resistance to 3α-HSD.
 
Primo vs. Mast with respect to muscle anabolism are virtually interchangeable. Mast is ever so slightly more potent at the AR and slightly more androgenic as well (e.g., more virilizing in women), and Primo is evidenced to have relatively reduced cardiac harms (but absence of evidence for Mast does not imply evidence of absence). The two are really functionally equivalent, practically.

Again, appreciate the education and input
 
The 2α-methyl group of drostanolone (Mast) protects the Δ⁴-3-ketone moieity (and ↑anabolic and markedly ↓androgenic activity), but does not prevent metabolism by 3α-HSD (this is obvious due to its metabolism. Per Schanzer: "The parent steroid is excreted as a conjugate that can be hydrolysed with β-glucuronidase. The main metabolite is the 17-keto-oxidized 3α-hydroxy-reduced product 3α-hydroxy-2α-methyl-5α-androstan-17-on, which in comparison with T metabolism, is the 2α-methyl androsterone analog."). You can think of this attachment as serving to protect the "core" of the steroid from breakdown. And yet, it doesn't do this particularly well in the case of Masteron; unlike Superdrol (essentially Methyl Masteron), where the presence of both the 2α- & 17α- methyl groups result in substantial resistance to metabolism (i.e., 1/6th of Superdrol consumed remains unmetabolized as the parent drug reflecting its resistance to hepatic breakdown).

Thanks a ton.

Would Masteron propionate raw powder be more orally bioavailable than proviron raw powder ?
 
Neither do you, it's not your yard and you're not really something special here or something apart from existing here for 10 years.

And you're not even OP, so back off. I wasn't even talking to you in the first place. I decide when I stop talking to you. Over.

When you talk I picture a midget with anger management issues.
 
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There seems to be two camps now. Masteron is just good for hard peckers and hardened look, or it’s just as good a growth promoter as test/tren/deca.

I just keep thinking of two twins in fairytale land, everything exactly the same…one running HRT plus 600 mast for 12 weeks and the other running HRT and 600mg NPP. I just can’t accept contractile tissue gains would be basically the same.

But I’ve been wrong a whole fucking lot in my life lol
 
There seems to be two camps now. Masteron is just good for hard peckers and hardened look, or it’s just as good a growth promoter as test/tren/deca.

I just keep thinking of two twins in fairytale land, everything exactly the same…one running HRT plus 600 mast for 12 weeks and the other running HRT and 600mg NPP. I just can’t accept contractile tissue gains would be basically the same.

But I’ve been wrong a whole fucking lot in my life lol
I dont think most would say it is as potent as Test/tren/deca for growth.

I would say 200mg of mast is nothing like 200mg of tren or deca.

It would be hard to say that 200mg of Deca would generate more growth than 800mg of mast.

I for damn sure know that 250mg of tren fucks up my labs more than 600mg of mast.



The thing is...

Its about if it can be used as a growth promoter. from old forums, people used to talk mad shit about primo saying it was useless unless it was 600mg. wtf changed?

People have different preferences on different anabolics, some people like test solo and do well off of it, some people dont like the water retention. Maybe Deca breaks one guys dick and tren doesnt, vice versa.


This was mainly supposed to be a discussion to review one of the many compounds that can be utilized in a cycle build. Masteron does have a better safety profile than some of the other anabolics.


I am contemplating running 300 test and and 800 mast for my next cycle now because of this discussion to prove a point.
 
Masteron does have a better safety profile than some of the other anabolics.
And this is exactly why people are considering mast, nowadays the focus seems to have changed to be more... Heath conscious, so "weaker" anabolics that don't impact health as much are being preferred.
 
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