Stenbolone acetate discussion

[asaly]

Why not just use compounds that don’t enlarge liver in rats or humans? You can still get the same anabolic effect from a well researched and know compound.

many compounds have some very bad effects on animals, especially rats, which are very different from humans,

Currently, vial DHB costs me $21, if I discover in multiple tests that it does not affect my health parameters, I will probably use it instead of a compound that is several times more expensive

 

[Pinnacle Elements]

Well so far it seems difficult to source. I'm hoping Axle pulls through and gets some. All the raw suppliers I reached out to so far, Haven't had it.

I’ve already gone down this path bro trust me lol but let me know

 

[Pinnacle Elements]

many compounds have some very bad effects on animals, especially rats, which are very different from humans,

Currently, vial DHB costs me $21, if I discover in multiple tests that it does not affect my health parameters, I will probably use it instead of a compound that is several times more expensive

But many compounds have human trials and were marketed for human use. Why take the risk? They all more or less do the same thing. Nitrogen retention, increase protein synthesis, etc.

I just don’t get why you’d risk it.

View attachment IMG_1204.webp


“Milligram for milligram, DHB was shown to induce less muscle growth than Testosterone, while stimulating the prostate and seminal vesicle just as much”

 

[asaly]

But many compounds have human trials and were marketed for human use. Why take the risk? They all more or less do the same thing. Nitrogen retention, increase protein synthesis, etc.

I just don’t get why you’d risk it.

View attachment 275637


“Milligram for milligram, DHB was shown to induce less muscle growth than Testosterone, while stimulating the prostate and seminal vesicle just as much”

I have no idea where you got the theory that testosterone is twice as anabolic as DHB. We have no studies on humans, and studies on rats have shown that in theory its twice as anabolic as testosterone. Apart from the fact that this rat test is flawed, of course

We also know that stenbolone reacts with 3alpha HSD like DHT, masterone and primo, which neutralizes the strength of the compound in the muscles, but I dont have data to what extent it does it. For comparison, it seems to me that DHB also reacts with 3alpha HSD, but it does so to a much lesser extent than the three above-mentioned compounds

maybe an expert @Type-IIx will tell us something more

 

[Bronzino]

It’s not like either. The anabolic:androgen ratio is like 80:30. It’s not that impressive.

It should be andro:ana 115:300, more interesting
If it act like primo with this ratio, could be an interesting product.

 

[Pinnacle Elements]

I have no idea where you got the theory that testosterone is twice as anabolic as DHB. We have no studies on humans, and studies on rats have shown that in theory its twice as anabolic as testosterone. Apart from the fact that this rat test is flawed, of course

We also know that stenbolone reacts with 3alpha HSD like DHT, masterone and primo, which neutralizes the strength of the compound in the muscles, but I dont have data to what extent it does it. For comparison, it seems to me that DHB also reacts with 3alpha HSD, but it does so to a much lesser extent than the three above-mentioned compounds

maybe an expert @Type-IIx will tell us something more

I’ve had @Type-IIx chime in on this same topic before. He agrees with what I’ve said.

I never said twice as anabolic, but a study on rats, mg for mg, showed:

1. Approx 20% more LBM increase from Test P vs DHB

2. Increase in liver weight in the DHB group.

View attachment IMG_1206.webp

 

[asaly]

I’ve had @Type-IIx chime in on this same topic before. He agrees with what I’ve said.

and he also thought it was 3x more anabolic than testosterone? and according to what you say, 6x more anabolic than DHB?

 

[Pinnacle Elements]

and he also thought it was 3x more anabolic than testosterone? and according to what you say, 6x more anabolic than DHB?

I’m only talking about the DHB topic. I’m not even sure what you’re talking about?

 

[Type-IIx]

I have no idea where you got the theory that testosterone is twice as anabolic as DHB. We have no studies on humans, and studies on rats have shown that in theory its twice as anabolic as testosterone. Apart from the fact that this rat test is flawed, of course

We also know that stenbolone reacts with 3alpha HSD like DHT, masterone and primo, which neutralizes the strength of the compound in the muscles, but I dont have data to what extent it does it. For comparison, it seems to me that DHB also reacts with 3alpha HSD, but it does so to a much lesser extent than the three above-mentioned compounds

maybe an expert @Type-IIx will tell us something more

Everything you state here is correct.

From metabolism studies, it is extensively 3α-reduced, its primary metabolites including 3 alpha-hydroxy-2-methyl-5 alpha-androst-1-en-17-one & 3 alpha-hydroxy-2 xi-methyl-5 alpha-androst-17-one.

Where it does claw back some theoretical potency is by its 2α-methylation, that ↓androgenic & ↑anabolic activity, slowing the rate of ring A reductions... in 5α-andostan-3-one steroids, this would be confirmed by greater number of metabolic steroid products retaining the 5α-andostan-3-one system... and in actuality it does do a fairly good job at this:

Firstly, its primary metabolite is itself, reflecting some resistance to metabolism.

Secondly, stenbolone's intermediary metabolites 16ξ-hydroxy-stenbolone & 16ξ-hydroxy-2-methyl-5α-androst-1-ene-3,17-dione do maintain the 5α-andostan-3-one steroidal core that provides the 3-keto group whose lone pair of electrons serve to accept H-bonds permitting it to form a strong bond with the AR's N-terminus/amino-group & aydrophobic backbone with good flatness (less bulky than T) to fit into the hydrophobic cavity of the binding site on the AR.

Practically, stenbolone is a good AAS, that is patented for human use, being
originally introduced by Schering AG in Germany in 1961, then by Syntex UK in 1963. Duchaine referred to stenbolone as his "sentimental favorite," referring to the (no longer commercially available) Farmacologio Latino 25 mg/mL. As of July 3, 1991, records indicate that Merck holds the registration for producing stenbolone, if it so chooses.

It is practically equivalent to metenolone ("Primo") & drostanolone ("Mast"). It is, like those counterparts, an androst-1-ene-3-one, that Duchaine refers to as being applied commonly at 100 - 200 mg weekly doses, and remarked that it is "reat for cutting, especially for women (low androgenicity)," & augments RBC/HCT/Hb on par with oxymetholone, which is, also, consistent with its counterparts.

I’ve had @Type-IIx chime in on this same topic before. He agrees with what I’ve said.

I never said twice as anabolic, but a study on rats, mg for mg, showed:

1. Approx 20% more LBM increase from Test P vs DHB

2. Increase in liver weight in the DHB group.

View attachment 275642

Don't take anything I said out of context please.

Rodent (Hershberger) Assays are not at all reflective of human biological effects, in no small part because the vastus lateralis in rat is in fact the dorsal bulbocaverous, a sex organ, therefore, both anabolic & androgenic ratings derived from it do not actually distinguish between androgenic vs. anabolic activity. The assay is useless. I am certain that I also qualified the "liver size increases" as almost certainly inapplicable to man, but interesting on a background of liver changes by AAS in rodent being quite unusual.

I don't accuse anyone of intentionally misreprestening my statements, but I always am misquoted it seems when my posts are not referred to explicitly by quote (copy & paste from original thread) & links to the relevant portions of a thread. Please, I only ask that you use this good practice for citing my writing in the future.

 

[nightprowler7]

Everything you state here is correct.

From metabolism studies, it is extensively 3α-reduced, its primary metabolites including 3 alpha-hydroxy-2-methyl-5 alpha-androst-1-en-17-one & 3 alpha-hydroxy-2 xi-methyl-5 alpha-androst-17-one.

Where it does claw back some theoretical potency is by its 2α-methylation, that ↓androgenic & ↑anabolic activity, slowing the rate of ring A reductions... in 5α-andostan-3-one steroids, this would be confirmed by greater number of metabolic steroid products retaining the 5α-andostan-3-one system... and in actuality it does do a fairly good job at this:

Firstly, its primary metabolite is itself, reflecting some resistance to metabolism.

Secondly, stenbolone's intermediary metabolites 16ξ-hydroxy-stenbolone & 16ξ-hydroxy-2-methyl-5α-androst-1-ene-3,17-dione do maintain the 5α-andostan-3-one steroidal core that provides the 3-keto group whose lone pair of electrons serve to accept H-bonds permitting it to form a strong bond with the AR's N-terminus/amino-group & aydrophobic backbone with good flatness (less bulky than T) to fit into the hydrophobic cavity of the binding site on the AR.

Practically, stenbolone is a good AAS, that is patented for human use, being
originally introduced by Schering AG in Germany in 1961, then by Syntex UK in 1963. Duchaine referred to stenbolone as his "sentimental favorite," referring to the (no longer commercially available) Farmacologio Latino 25 mg/mL. As of July 3, 1991, records indicate that Merck holds the registration for producing stenbolone, if it so chooses.

It is practically equivalent to metenolone ("Primo") & drostanolone ("Mast"). It is, like those counterparts, an androst-1-ene-3-one, that Duchaine refers to as being applied commonly at 100 - 200 mg weekly doses, and remarked that it is "reat for cutting, especially for women (low androgenicity)," & augments RBC/HCT/Hb on par with oxymetholone, which is, also, consistent with its counterparts.


Don't take anything I said out of context please.

Rodent (Hershberger) Assays are not at all reflective of human biological effects, in no small part because the vastus lateralis in rat is in fact the dorsal bulbocaverous, a sex organ, therefore, both anabolic & androgenic ratings derived from it do not actually distinguish between androgenic vs. anabolic activity. The assay is useless. I am certain that I also qualified the "liver size increases" as almost certainly inapplicable to man, but interesting on a background of liver changes by AAS in rodent being quite unusual.

I don't accuse anyone of intentionally misreprestening my statements, but I always am misquoted it seems when my posts are not referred to explicitly by quote (copy & paste from original thread) & links to the relevant portions of a thread. Please, I only ask that you use this good practice for citing my writing in the future.

I have an IQ similar to "the tren twins", can you dumb this down for me? Stenbolone is hard on the liver?

Have you ever tried it? What is your opinion on Stenbolone for bodybuilding?

 

[lonewolf54321]

Everything you state here is correct.

From metabolism studies, it is extensively 3α-reduced, its primary metabolites including 3 alpha-hydroxy-2-methyl-5 alpha-androst-1-en-17-one & 3 alpha-hydroxy-2 xi-methyl-5 alpha-androst-17-one.

Where it does claw back some theoretical potency is by its 2α-methylation, that ↓androgenic & ↑anabolic activity, slowing the rate of ring A reductions... in 5α-andostan-3-one steroids, this would be confirmed by greater number of metabolic steroid products retaining the 5α-andostan-3-one system... and in actuality it does do a fairly good job at this:

Firstly, its primary metabolite is itself, reflecting some resistance to metabolism.

Secondly, stenbolone's intermediary metabolites 16ξ-hydroxy-stenbolone & 16ξ-hydroxy-2-methyl-5α-androst-1-ene-3,17-dione do maintain the 5α-andostan-3-one steroidal core that provides the 3-keto group whose lone pair of electrons serve to accept H-bonds permitting it to form a strong bond with the AR's N-terminus/amino-group & aydrophobic backbone with good flatness (less bulky than T) to fit into the hydrophobic cavity of the binding site on the AR.

Practically, stenbolone is a good AAS, that is patented for human use, being
originally introduced by Schering AG in Germany in 1961, then by Syntex UK in 1963. Duchaine referred to stenbolone as his "sentimental favorite," referring to the (no longer commercially available) Farmacologio Latino 25 mg/mL. As of July 3, 1991, records indicate that Merck holds the registration for producing stenbolone, if it so chooses.

It is practically equivalent to metenolone ("Primo") & drostanolone ("Mast"). It is, like those counterparts, an androst-1-ene-3-one, that Duchaine refers to as being applied commonly at 100 - 200 mg weekly doses, and remarked that it is "reat for cutting, especially for women (low androgenicity)," & augments RBC/HCT/Hb on par with oxymetholone, which is, also, consistent with its counterparts.


Don't take anything I said out of context please.

Rodent (Hershberger) Assays are not at all reflective of human biological effects, in no small part because the vastus lateralis in rat is in fact the dorsal bulbocaverous, a sex organ, therefore, both anabolic & androgenic ratings derived from it do not actually distinguish between androgenic vs. anabolic activity. The assay is useless. I am certain that I also qualified the "liver size increases" as almost certainly inapplicable to man, but interesting on a background of liver changes by AAS in rodent being quite unusual.

I don't accuse anyone of intentionally misreprestening my statements, but I always am misquoted it seems when my posts are not referred to explicitly by quote (copy & paste from original thread) & links to the relevant portions of a thread. Please, I only ask that you use this good practice for citing my writing in the future.

Apparently I took an extra dose of stupid today lol. In retard talk, are you saying DHB is good or bad? Weak or strong?

 

[trtbuilder]

God I love @Type-IIx

I just wish I was smart enough to understand any of his posts.

 

[Type-IIx]

Apparently I took an extra dose of stupid today lol. In retard talk, are you saying DHB is good or bad? Weak or strong?

It's maybe a little more potent than Primo or Mast, in the same class, and functionally equivalent, serving in the same category of relatively antiestrogenic AAS that combine in the same way as these.

It's not particularly exotic, it's so similar to Primo or Mast that it's basically redundant. This is probably the main reason why it's not produced anymore.

There's no inherently bad or good AAS, just different tradeoffs, particular use cases. It's pretty weak bro. It's well tolerated at 100 - 200 mg weekly for women cutting per Duchaine. That alone pretty much tells you, it is basically Primo or Mast.

 

[Type-IIx]

I’m only talking about the DHB topic. I’m not even sure what you’re talking about?

I recall also basically opining that IMO 1-Test ("DHB") doesn't have any particular use case since it's just another androst-1-ene-3-one like Primo, Mast, and Sten, and given the tie-breaker – this unfavorable rodent data as well as associations with increased C-reactive protein – vs. its counterparts, I'd never use it as a result. So we agree in our opinion, but I cannot convince people that cardiovascular/hepatic risks are important. I cannot stand in their shoes and weigh their tradeoff balancing for them. If their AAS adventurism (desire to experiment with exotic compounds due to curiosity) or price sensitivity (assuming 1-Testo is relatively cheap) are weighed heavily by them, then those factors might rationally outweigh these risks.

 

[RomanMVP]

Olympia Solutions........Stenbolone (Stenbolone Acetate) 10ml 100mg $50

 

[asaly]

so

stenbolone:
stronger than primo/mast
no rare toxicity
approved for use in humans
probably very expensive, rare and probably often counterfeited

dhb:
stronger than primo/mast
liver toxicity in rats, anecdotal reports of problems with inflammatory markers in humans
no tests
cheaper, my source has it for less than 60% of the price of primbolan
increasing DHT levels

 

[lonewolf54321]

It's maybe a little more potent than Primo or Mast, in the same class, and functionally equivalent, serving in the same category of relatively antiestrogenic AAS that combine in the same way as these.

It's not particularly exotic, it's so similar to Primo or Mast that it's basically redundant. This is probably the main reason why it's not produced anymore.

There's no inherently bad or good AAS, just different tradeoffs, particular use cases. It's pretty weak bro. It's well tolerated at 100 - 200 mg weekly for women cutting per Duchaine. That alone pretty much tells you, it is basically Primo or Mast.

Thanks, I know it's probably a pain in the ass having to dumb info down sometimes for us lol.

 

[boophomet]

Goodlyfe mentioned being curious about Stenbolone after a user asked about it, if he ends up offering it I'd 100% try it.

 

[asaly]

btw, apart from stenbolone, is there any other not 17AA AAS that is very rarely available?

 

[Type-IIx]

so

stenbolone:
stronger than primo/mast

You lost me here.

Theoretically, it is (mildly) resistant to metabolism & maintains its 5α-androstan-3-ketone core reasonably well which gives it some potency... versus an AAS that does neither but not necessarily versus Primo or Mast.

Primo maintains its 5α-androstan-3-one core reasonably well too & is slightly resistant to metabolism due to its 1-methylation & Mast also due to its 2α-methylation.

This is theory.

In practice, I am so certain that you couldn't detect a difference per-mg between any of these drugs because they are functionally equivalent.

All I said was "it's maybe a bit stronger," because... maybe it is, maybe it's weaker too. They're functionally equivalent, practically identical, including in muscle anabolic potency per-mg.

no rare toxicity
approved for use in humans

Yes.

probably very expensive, rare and probably often counterfeited

Speculative.

dhb:
stronger than primo/mast

Says who?

liver toxicity in rats, anecdotal reports of problems with inflammatory markers in humans

Not toxicity in rats, just increased liver weight.

One might speculate that this is more likely due to hepatic strain given that it "must be," "intuitively," AR-mediated, and therefore of a category of hepatotoxic effects mediated by AR activation per se, increasing ROS, etc....

But this study has not been subjected to any replication of study methods. This is almost never done because researchers, kinda like bodybuilders, are always seeking out the "next great thing," and validating the reliability of a study's methods is booooooring.

This could be a mere artifact.

no tests

I don't know what this means. You mean no vendor has submitted it for public lab reports?

cheaper, my source has it for less than 60% of the price of primbolan

I believe you.

increasing DHT levels

Is this a benefit or a cost?