Unanswered Molecular Biology. What do the different attachments of a steroid do?

Old Witch

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This will be an ongoing inquisition as to the effects of the variety of attachments which are a part of or can be made to a steroid molecule. Particularly the commonly known ones.

Any input is welcome. Cited sources are best.

Anyone with a degree in the subject, feel free to offer up a long winded dissertation.

I will post information I have found thus far and my suppositions as they come.
 
Kratom267

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Very good idea for a thread! I’ll delete this comment soon so I don’t junk up the thread...just wanted to give props since I don’t see the “like” on here anymore!
 
Old Witch

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“Favors anabolic activity” doesn’t go into much detail as to how the altered steroid shape changes its activity at the receptor.

Plus, we know 1T is more anabolic than primobolan, M1T more anabolic than stenbolone, etc. so on a dht itself, because the 1 or 2 position alkylation doesn’t spoil the flattened more flexible side the delta 1 steroid dhb has... it favors anabolic activity, npbut on dhb it spoils the flatter side, so it actually favors androgenic activity on a delta-1 steroid.

See? I think I can have a rational conversation about this. Maybe I’m wrong.
 

2kvette

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“Favors anabolic activity” doesn’t go into much detail as to how the altered steroid shape changes its activity at the receptor.

Plus, we know 1T is more anabolic than primobolan, M1T more anabolic than stenbolone, etc. so on a dht itself, because the 1 or 2 position alkylation doesn’t spoil the flattened more flexible side the delta 1 steroid dhb has... it favors anabolic activity, npbut on dhb it spoils the flatter side, so it actually favors androgenic activity on a delta-1 steroid.

See? I think I can have a rational conversation about this. Maybe I’m wrong.
Are you looking for specific values for each modification? Because thats not possible. Also, all those A:A ratios are done on the rat receptor, which is close to the human receptor but not exact. Additionally, certain AAS have tissue specific metabolism that are responsible for eliciting most of their effects. Delta one steroids have stronger anabolic effects because their activity in tissue is prolonged due to the double bond resisting metabolism in the liver and in the muscle by 3-HSD. So they get to do their thing longer.
 
Old Witch

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Are you looking for specific values for each modification? Because thats not possible. Also, all those A:A ratios are done on the rat receptor, which is close to the human receptor but not exact. Additionally, certain AAS have tissue specific metabolism that are responsible for eliciting most of their effects. Delta one steroids have stronger anabolic effects because their activity in tissue is prolonged due to the double bond resisting metabolism in the liver and in the muscle by 3-HSD. So they get to do their thing longer.
I wasn’t talking about the ratios. I was talking about in real life in humans.

Not specific values, no, but things such as what you just defined the 1,2 double bond as doing. Those types of definition. As in: “In what way?”

The double bonded side of a steroid is flatter and more flexible as well which does change its interaction with the androgen receptor itself, too. Any comments on that? That’s why I mention it seems to “spoil” it when the 1 or 2 position is alkylated on a delta one steroid, whereas on DHT it amplifies it as described in the diagram. DHB is really more anabolic than primobolan in real life usage. For sure. Heck, stenbolone (anatrofin) is too. And that’s probably because the alkylation is at the 2 position, it is not as wide as primobolan.
 
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Old Witch

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Lay some more knowledge on us.
 
Chados

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Well this might be out of my knowledge but as far as the ratio of androgenic and anabolic measurements they are measured either in rats or prostate. As far as the androgenic ratios they seem to be much more reliable as we can quite often if not always see which steroid will give androgenic sides. It's still not certain that the prostate is the best way of measuring but it seems to be quite reliable. As far as the anabolic ratio, well its completely flawed as anyone that ever used things like anavar or halotestin will notice far less muscle mass than the stronger bulkers.

To answer your question I don't think there is a way of measuring these ratios as steroids are either illegal or prescribed in medicin to people with aids or cancer which now most likely will be taken over by sarms due to the androgenic safety. It's highly unlikely given the time that they all of the sudden will do testing on trenbolone or even anadrol to see how much muscle one might add.
 
Kratom267

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Sorry to derail, but why are some ratios of anabolic:androgenic in the hundreds and some seem to be broken down to smaller numbers. Like Msten is 660/170 and Pmag is 55/50.
Is there any reason for that? Like it wouldn’t matter if you broke the Msten down to 330/85, etc?
 
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Old Witch

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Sorry to derail, but why are some ratios of anabolic:androgenic in the hundreds and some seem to be broken down to smaller numbers. Like Msten is 660/170 and Pmag is 55/50.
Is there any reason for that? Like it wouldn’t matter if you broke the Msten down to 330/85, etc?
These are numbers versus methyl testosterone.
 
Old Witch

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Well this might be out of my knowledge but as far as the ratio of androgenic and anabolic measurements they are measured either in rats or prostate. As far as the androgenic ratios they seem to be much more reliable as we can quite often if not always see which steroid will give androgenic sides. It's still not certain that the prostate is the best way of measuring but it seems to be quite reliable. As far as the anabolic ratio, well its completely flawed as anyone that ever used things like anavar or halotestin will notice far less muscle mass than the stronger bulkers.

To answer your question I don't think there is a way of measuring these ratios as steroids are either illegal or prescribed in medicin to people with aids or cancer which now most likely will be taken over by sarms due to the androgenic safety. It's highly unlikely given the time that they all of the sudden will do testing on trenbolone or even anadrol to see how much muscle one might add.
Actually I was more looking for a diagram like what 2k posted, but with a bit more depth and detail of explanation. A lot more, actually.

This is a rabbit hole I’ve only just barely begun to enter.
 

2kvette

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I wasn’t talking about the ratios. I was talking about in real life in humans.

Not specific values, no, but things such as what you just defined the 1,2 double bond as doing. Those types of definition. As in: “In what way?”

The double bonded side of a steroid is flatter and more flexible as well which does change its interaction with the androgen receptor itself, too. Any comments on that? That’s why I mention it seems to “spoil” it when the 1 or 2 position is alkylated on a delta one steroid, whereas on DHT it amplifies it as described in the diagram. DHB is really more anabolic than primobolan in real life usage. For sure. Heck, stenbolone (anatrofin) is too. And that’s probably because the alkylation is at the 2 position, it is not as wide as primobolan.
Yes, the double bond does seem to ruin it in some ways. That's because the molecule itself waves around like a flag in the wind. The lack of rigidity from loss of the double bond allows tighter binding with the receptor because the molecule is more flexible and can conform to the shape of the receptor more uniformly. But the lack of the double bond makes it more susceptible to 3-HSD degradation near the receptor, which mostly makes the increased flexibility useless in human tissues. Thats why you have things like msten where you have 2 methylation to block the effects of 3-HSD in the tissue but still have the 1-2 double bond to increase half life. These two changes are synergistic and compliment one another in terms of the sum of the tissue effects, which is why Msten has a higher myotrophic rating than superdrol.
 
Old Witch

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Yes, the double bond does seem to ruin it in some ways. That's because the molecule itself waves around like a flag in the wind. The lack of rigidity from loss of the double bond allows tighter binding with the receptor because the molecule is more flexible and can conform to the shape of the receptor more uniformly. But the lack of the double bond makes it more susceptible to 3-HSD degradation near the receptor, which mostly makes the increased flexibility useless in human tissues. Thats why you have things like msten where you have 2 methylation to block the effects of 3-HSD in the tissue but still have the 1-2 double bond to increase half life. These two changes are synergistic and compliment one another in terms of the sum of the tissue effects, which is why Msten has a higher myotrophic rating than superdrol.
I thought it was the double bond that made it more flexible, and the lack of a double bond made it wider and less flexible. Hence tren. Triple-double bonded in such a way as to make it impervious to all metabolism and fits every receptor like a glove. So much so, in fact, it can damage them.


Also, MSten has the higher anabolic rating, but superdrol has the higher Q rating overall, it’s androgenic rating and anabolic rating are much more widely disparate. This is why MSten doesn’t do what superdrol does. Why nothing does what superdrol does except maybe M1T, phera, and a select few others.

But then, Hexadrone should have an even higher Q... but it doesn’t.

So this would mean androgenic potency does matter for anabolism/myotropic activity as well.
 
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2kvette

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I thought it was the double bond that made it more flexible, and the lack of a double bond made it wider and less flexible. Hence tren. Triple-double bonded in such a way as to make it impervious to all metabolism and fits every receptor like a glove. So much so, in fact, it can damage them.


Also, MSten has the higher anabolic rating, but superdrol has the higher Q rating overall, it’s androgenic rating and anabolic rating are much more widely disparate. This is why MSten doesn’t do what superdrol does. Why nothing does what superdrol does except maybe M1T, phera, and a select few others.

But then, Hexadrone should have an even higher Q... but it doesn’t.

So this would mean androgenic potency does matter for anabolism/myotropic activity as well.
double bond makes it less flexible. nothing changes its width. Tren is impervious to metabolism because of the double bond, leading to its awesome effects. Q rating doesn't matter, its meaningless in practicality, it's just a trivial mathematical representation of androgens from a data set. For example, Tren has a Q ratio of 1, which is the same as testosterone.
 
Old Witch

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double bond makes it less flexible. nothing changes its width. Tren is impervious to metabolism because of the double bond, leading to its awesome effects. Q rating doesn't matter, its meaningless in practicality, it's just a trivial mathematical representation of androgens from a data set. For example, Tren has a Q ratio of 1, which is the same as testosterone.
Fair enough.
 
THOR 70

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Very much Subbed. And have an awkward biology/chem boner now. Thanks guys
 
Chados

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Actually I was more looking for a diagram like what 2k posted, but with a bit more depth and detail of explanation. A lot more, actually.

This is a rabbit hole I’ve only just barely begun to enter.

Yeah I got you it's just that I don't think there is any good explanation. Some steroids just binds differently to the receptors and with different potency regardless if it's on paper weaker or stronger you won't know for sure before you try.

Many if not most prefer anadrol above dbol but I am quite confident when I day that dbol is stronger per mg. There's so many variables but to get in to detail why each steroid do what it does I don't think is fully established. You have testosterone and you change the structure of the compound to get other steroids and when the steroid gets more androgenic and anabolic you'll notice it when running it not by reading the ratios in rats. I just don't think there's any studies especially on illegal steroids.
 

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