Steroid Efficacy at Receptor

RzSco

Member
We know that steroids have different binding AFFINITY for the androgen receptor. For example testosterone is about five times less than Trenbolone.

Meaning that approximately equal number of receptor sites would be occupied either by a dose of 200mg tren or 1000mg tren. In rough terms.

What I can’t find is any information on whether the efficacy of steroids at the receptor is different - e.g. does a receptor with a Tren molecule have a stronger effect than the same receptor with a Test molecule (could also be influenced by stuff like 5a-reductase).

Anyone know?
 
We know that steroids have different binding AFFINITY for the androgen receptor. For example testosterone is about five times less than Trenbolone.

Meaning that approximately equal number of receptor sites would be occupied either by a dose of 200mg tren or 1000mg tren. In rough terms.

What I can’t find is any information on whether the efficacy of steroids at the receptor is different - e.g. does a receptor with a Tren molecule have a stronger effect than the same receptor with a Test molecule (could also be influenced by stuff like 5a-reductase).

Anyone know?

Sounds like a lot of minutiae. Muscle gain on 1000 mg tren is much greater than 200 mg test. Those binding affinity studies and androgen/anabolic ratios seem very loosely correlated with muscle building capacity at best.
 
Sounds like a lot of minutiae. Muscle gain on 1000 mg tren is much greater than 200 mg test. Those binding affinity studies and androgen/anabolic ratios seem very loosely correlated with muscle building capacity at best.

Sorry I typo’d it. Was meant to say 1000mg test and 200mg Tren.

Steroids bind to the androgen receptor primarily but can also bind to the glucocorticoid receptor as antagonists which prevent cortisol binding and thus catabolism.

Tren is particularly good at that, with almost the same affinity as cortisol itself - but unfortunately you’d have to take truly insane doses like 2 grams of tren to really begin fully exploiting that effect as there is a LOT of cortisol in the body.
 
Meaning that approximately equal number of receptor sites would be occupied either by a dose of 200mg tren or 1000mg tren. In rough terms.

No, you are oversimplifying. The binding affinity does not directly corelate to receptor occupancy. It does effect it, but it's not the sole determining factor. What it does effect though is the receptor lygand binding complex, specifically, the rate of dissociation, which does effect the "potency" of the steroid.

A more stable and longer lasting engagement with the receptor can enhance the efficiency of receptor dimerization, nuclear translocation, and interaction with DNA response elements which can lead to more effective transcriptional activation or repression of target genes.

Different aas can also recruit different coactivators or corepressors, which does effect transcriptional activity ...

The rate of dissociation also means longer lasting effects.

Long story short, to answer your question: yes. Binding affinity is important and does determine the potential of the strength of the drugs effect but it's also not the sole determining factor. Biology isn't that simple, there are always various cofactors which are important. And there is also the whole non genomic side of steroids which can't be disregarded. And there, again, the second messenger system activation varies vastly between lygands of the same receptor. And for instance, to complicate matters further, you also have to account for receptor hetero dimers activation ...
 
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