How did the myth start that Primobolan was an AI?

[BigDadd7]

...

 

[Bobik]

Ridiculous and do not believe. This isn’t even possible with masteron at that dose, which was developed for this purpose.

Masteron does not reduce E2, it only blocks receptors in breast tissue etc.

For me the ideal ratio Test 1050mg + 700mg Primo = ideal E2 in the range without AI

 

[Tbaz192]

It’s not in the toothpaste the government puts it in the drinking water.

Whoa. We’re screwed

 

[Tbaz192]

Atamestane is not a metabolite of methenolone in human metabolism due to differences in their chemical structures, metabolic pathways, and the specific enzymatic processes involved in their breakdown. Below is a detailed explanation:

1. Chemical Structure Differences
• Atamestane: Atamestane (1-methylandrosta-1,4-diene-3,17-dione) has the molecular formula C20H26O2 and a molar weight of 298.4 g/mol. It is a steroidal aromatase inhibitor with a characteristic 1-methyl group and a 3,17-dione structure, featuring two ketone groups at positions 3 and 17, and double bonds at positions 1 and 4 in the steroid A-ring.
• Methenolone: Methenolone exists as Methenolone Acetate (C22H32O3, 344.49 g/mol) or Methenolone Enanthate (C27H42O3, 414.62 g/mol). It is a 17β-hydroxy-1-methyl-5α-androst-1-en-3-one, meaning it has a hydroxyl group at position 17 (in the acetate or enanthate ester form) and a single double bond at position 1, with a 3-keto group. The key structural differences include:
• Methenolone has a 17β-hydroxyl group (or esterified hydroxyl), whereas atamestane has a 17-keto group.
• Atamestane has an additional double bond at position 4 (making it a 1,4-diene), which methenolone lacks.
• The ester groups in methenolone (acetate or enanthate) are cleaved during metabolism, but the resulting core structure (methenolone base) is still distinct from atamestane.

These structural differences mean that transforming methenolone into atamestane would require specific enzymatic modifications (e.g., oxidation of the 17β-hydroxyl to a ketone and introduction of a double bond at position 4) that are not typically part of human metabolic pathways for anabolic steroids like methenolone.


2. Human Metabolic Pathways


• Methenolone Metabolism: In humans, methenolone (as acetate or enanthate) undergoes metabolism primarily through:
• Ester hydrolysis: The acetate or enanthate ester is cleaved by esterases, yielding the parent compound, methenolone (17β-hydroxy-1-methyl-5α-androst-1-en-3-one).
• Phase I metabolism: This involves reduction, oxidation, or hydroxylation, primarily at the 3-keto or 17β-hydroxy groups, and reduction of the 1,2-double bond. Common metabolites include 3α-hydroxy-1-methylen-5α-androstan-17-one and other hydroxylated derivatives, as identified in urinary excretion studies.
• Phase II metabolism: Conjugation with glucuronides or sulfates for excretion.
• The primary metabolites of methenolone retain the 1-methyl and 5α-reduced structure, with modifications mainly at the 3- or 17-positions. None of these transformations produce a 1,4-diene-3,17-dione structure like atamestane.
• Atamestane: Atamestane is a synthetic compound not naturally produced in the body or derived from other steroids in human metabolism. Its metabolism involves:
• Hydroxylation of the 1-methyl group.
• 5β-reduction and C-6 hydroxylation.
• Action of 17β-hydroxysteroid dehydrogenase, which can reduce the 17-keto group to a hydroxyl group in some metabolites. These pathways are distinct from those of methenolone, and there is no evidence that methenolone’s metabolic transformations in humans (e.g., via cytochrome P450 enzymes or steroid dehydrogenases) yield atamestane’s specific structure.


3. Fungal Biotransformation vs. Human Metabolism
• While atamestane has been identified as a metabolite (metabolite 12) of methenolone acetate in biotransformation studies using the fungus Fusarium lini, this is not relevant to human metabolism. Fungal biotransformation involves unique microbial enzymes that perform specific reactions, such as:
• Dehydrogenation to introduce a double bond at position 4.
• Oxidative cleavage of the acetate ester and oxidation of the 17β-hydroxyl to a 17-keto group
• These enzymatic capabilities are not present in human liver or other tissues. Human steroid metabolism primarily involves cytochrome P450 enzymes, reductases, and hydroxylases that do not catalyze the precise combination of reactions needed to convert methenolone’s 17β-hydroxy-1-methyl-5α-androst-1-en-3-one structure into atamestane’s 1-methylandrosta-1,4-diene-3,17-dione structure.


4. Enzymatic Feasibility
• To convert methenolone to atamestane in humans, the following would be required:
• Oxidation of the 17β-hydroxyl to a 17-keto group: This is possible via 17β-hydroxysteroid dehydrogenase, but it is not a dominant pathway for methenolone, which is more likely to undergo conjugation or reduction.
• Introduction of a double bond at position 4: This requires a specific dehydrogenase or desaturase enzyme, which is not typically involved in human metabolism of 5α-reduced steroids like methenolone. The 1,4-diene structure is characteristic of certain synthetic steroids (e.g., boldenone derivatives) but not a natural metabolite of methenolone.
• Retention of the 1-methyl group and 3-keto group: While these are preserved, the additional double bond and 17-keto formation are not consistent with methenolone’s known metabolic fate.
• Human enzymes involved in steroid metabolism (e.g., 3α/3β-hydroxysteroid dehydrogenases, 5α/5β-reductases, or cytochrome P450 enzymes) do not facilitate this specific transformation. In contrast, Fusarium lini possesses unique microbial enzymes capable of these reactions, which explains why atamestane can be produced in fungal biotransformation but not in humans.


5. Literature and Evidence
• Studies on methenolone metabolism in humans, such as those using gas chromatography-mass spectrometry (GC-MS) to detect urinary metabolites, identify compounds like 3α-hydroxy-1-methylen-5α-androstan-17-one and other hydroxylated or conjugated derivatives, but not atamestane.
• Atamestane is described as a synthetic compound designed as an aromatase inhibitor, not a naturally occurring metabolite of other steroids in human physiology.
• The fungal biotransformation study with Fusarium lini explicitly notes atamestane as a product of microbial metabolism, not human metabolism, reinforcing that this transformation is specific to the fungal enzymatic system.


Conclusion

Atamestane cannot be a metabolite of methenolone in human metabolism because the structural transformations required (17β-hydroxyl oxidation to a ketone and introduction of a 4,5-double bond) are not catalyzed by human enzymes involved in methenolone metabolism. The production of atamestane from methenolone acetate in Fusarium lini is due to unique microbial enzymes absent in humans. Thus, in the context of human pharmacokinetics, atamestane is not a metabolite of methenolone or its esters.

Yeah no one is gonna read that hahaha

 

[Tbaz192]

Countless labs and proof that primo and EQ do indeed lower /crash estrogen.

My labs included. Never had worse panic attacks on EQ with crashed e2. Dbol and test prop saved me.

 

[eryximachus]

Yeah no one is gonna read that hahaha

There's no reason for bro science to persist unquestionably when we have such fantastic artificial intelligence models that will do all the research for you.

 

[Spaceman Spiff]

do you also believe fluoride in toothpaste is the governments mind control drug?

It's telling us primo keeps the e2 down

 

[eryximachus]

Countless labs and proof that primo and EQ do indeed lower /crash estrogen.

My labs included. Never had worse panic attacks on EQ with crashed e2. Dbol and test prop saved me.

I keep reading this. But no one is doing a cycle log with posted bloodwork so far as I can tell.

But no one can explain to me why I have never read it until the 3rd decade of the 21st century. This is a drug that has been out since 1961. Why was this not reported in the 1960s? Or 1970s? Or 1980s? or 1990s? or 2000s? Or 2010s?

Why can't anyone explain the chemistry? We've got one decent explanation here that I consider plausible, but it still wouldn't explain what people are claiming here. They are basically claiming it is as strong or stronger than letrozole, which is absurd. And we have one explanation that was proven false. The rest are "trust me bro".

Why didn't the manufacturer notice this property and apply for a breast cancer indication to compete with Masteron?

Is it possible poly pharmacy is the issue? People run a lot of compounds now. Hell, even I run a lot of compounds versus 10 years ago, but I'm an old fuck.

Another possibility: is gear being intentionally contaminated with aromatase inhibitors? This is not something tested for.

 

[Spaceman Spiff]

Countless labs and proof that primo and EQ do indeed lower /crash estrogen.

My labs included. Never had worse panic attacks on EQ with crashed e2. Dbol and test prop saved me.

Agreed. Moving from primo to mast shot my e2 from 39 to 142

 

[Photon]

But no one can explain to me why I have never read it until the 3rd decade of the 21st century. This is a drug that has been out since 1961. Why was this not reported in the 1960s? Or 1970s? Or 1980s? or 1990s? or 2000s? Or 2010s?

Availability and affordability of testing.
Did you think you could just walk into a lab and ask for an ultrasensitive e2 test in the 1960s without paying an arm and a leg for it?

 

[ToesOverKnees]

Lately has been found that one of methenolone's metabolites is Atamestane which actually is an aromatase inhibitor.

The fact YOU don't experience any e2 reduction doesn't prove anything. It has to do probably with your body's enzymes, that makes us unique individuals.

Some guys don't respond to exemestane, they need insane amounts of aromasin to combat estrogen while they respond well to arimidex. Based on that logic someone could make a thread and say aromasin being an AI is a myth lol

Very interesting, I didn't know the molecule had been identified.

 

[eryximachus]

Masteron does not reduce E2, it only blocks receptors in breast tissue etc.

For me the ideal ratio Test 1050mg + 700mg Primo = ideal E2 in the range without AI

All I know is Masteron had an FDA indication for breast cancer. It is the only anabolic steroid where this is true and it was used for this purpose into the 1990s.

So far as that test dose - I never in my life have run anything close to that dose. The whole reason many of these androgens were made was because testosterone aromatizes. What's the point of running primo in that case? Makes no sense. Why not just run 2 grams of testosterone along with letrozole?

 

[eryximachus]

Very interesting, I didn't know the molecule had been identified.

This is absolutely false. See the explanation I posted or study the chemical structure of each yourself. It is impossible.

 

[eryximachus]

Availability and affordability of testing.
Did you think you could just walk into a lab and ask for an ultrasensitive e2 test in the 1960s without paying an arm and a leg for it?

Schering was a huge multinational pharmaceutical company.

Bloodwork has been affordable for 20 years.

 

[dick_starbuck]

I did bloodwork on 700mg test cyp, 210mg npp, and 560mg primo last year. My e2 was in the single digits. I dont use an AI and I aromatize at a very high rate.

Primobolan is definitely an AI of some kind and I dont really know what youre getting at here. You've been watching/listening to too much Victor Black.

 

[Bandern]

There's no reason for bro science to persist unquestionably when we have such fantastic artificial intelligence models that will do all the research for you.

This is the level of main character syndrome I strive to have one day.

“Primo didn’t affect my e2. The other 99% of primo users are probably just ghey retards”

Incredible

 

[Bobik]

All I know is Masteron had an FDA indication for breast cancer. It is the only anabolic steroid where this is true and it was used for this purpose into the 1990s.

So far as that test dose - I never in my life have run anything close to that dose. The whole reason many of these androgens were made was because testosterone aromatizes. What's the point of running primo in that case? Makes no sense. Why not just run 2 grams of testosterone along with letrozole?

maybe because I feel better, fewer side effects, better appearance? And yet muscle growth is similar.

 

[IndividualMan]

There's no reason for bro science to persist unquestionably when we have such fantastic artificial intelligence models that will do all the research for you.

did you cry while talking to the AI? do you now hold the steadfast belief that AI is god? was it a deeply emotional experience for you? are you 5´6 and balding, with hints of acromegaly?
Baboon brained mental midget, you could barely pay attention to a research paper if your own mother read it to you

 

[eryximachus]

did you cry while talking to the AI? do you now hold the steadfast belief that AI is god? was it a deeply emotional experience for you? are you 5´6 and balding, with hints of acromegaly?
Baboon brained mental midget, you could barely pay attention to a research paper if your own mother read it to you

I guess Bill Roberts is also an idiot too, huh?

Primobolan Depot (Methenolone Enanthate)

Far more powerful than its oral form Primobolan Depot is rumored to be Arnold’s favorite steroid. Very expensive Primobolan Depot is commonly counterfeited

thinksteroids.com

 

[Eddie.]

In this point I guess there’s nothing else to discuss. Case closed, you re convinced 100% that primo doesn’t lower estradiol and that won’t change no matter what.

Let us all who do bloodwork and confirm that primo reduces e2 to live in our fantasy world and keep doing what you’re doing.