Question for chemists!

[rolemodel]

OK, let's say I was to run test/deca/winny...do they hit diff. receptor sites? If not, what would be the point in using diff. types of AAS, why not only use one compound?

I know winny is 17 alpha-methyl-5alpha- androstano
and Deca is 19-Nor-4-androstene-3-one,17b-ol
and test is 4-androstene-3-one,17beta-ol

But damed if I know if they hit different receptor sites?
Good question? I would like a good answer.
Thank you.

[alan1973]

OK, let's say I was to run test/deca/winny...do they hit diff. receptor sites? If not, what would be the point in using diff. types of AAS, why not only use one compound?

I know winny is 17 alpha-methyl-5alpha- androstano
and Deca is 19-Nor-4-androstene-3-one,17b-ol
and test is 4-androstene-3-one,17beta-ol

But damed if I know if they hit different receptor sites?
Good question? I would like a good answer.
Thank you.
yeah, that does sound like a good question.
Bumping for answers.

[rolemodel]

yeah, that does sound like a good question.
Bumping for answers.


Someone here should know, I hope.

[JustBecause]

OK, let's say I was to run test/deca/winny...do they hit diff. receptor sites? If not, what would be the point in using diff. types of AAS, why not only use one compound?

I know winny is 17 alpha-methyl-5alpha- androstano
and Deca is 19-Nor-4-androstene-3-one,17b-ol
and test is 4-androstene-3-one,17beta-ol

But damed if I know if they hit different receptor sites?
Good question? I would like a good answer.
Thank you.

Endocrine Index Glossary
Hormones, Receptors and Target Cells

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What exactly are hormones and how are they different from "non-hormones"? Hormones are chemical messengers secreted into blood or extracellular fluid by one cell that affect the functioning of other cells.

Most hormones circulate in blood, coming into contact with essentially all cells. However, a given hormone usually affects only a limited number of cells, which are called target cells. A target cell responds to a hormone because it bears receptors for the hormone.

In other words, a particular cell is a target cell for a hormone if it contains functional receptors for that hormone, and cells which do not have such a receptor cannot be influenced directly by that hormone. Reception of a radio broadcast provides a good analogy. Everyone within range of a transmitter for National Public Radio is exposed to that signal (even if they don't contribute!). However, in order to be a NPR target and thus influenced directly by their broadcasts, you have to have a receiver tuned to that frequency.


Hormone receptors are found either exposed on the surface of the cell or within the cell, depending on the type of hormone. In very basic terms, binding of hormone to receptor triggers a cascade of reactions within the cell that affects function. Additional details about receptor structure and function are provided in the section on hormone mechanism of action.

A traditional part of the definition of hormones described them as being secreted into blood and affecting cells at distant sites. However, many of the hormones known to act in that manner have been shown to also affect neighboring cells or even have effects on the same cells that secreted the hormone. Nonetheless, it is useful to be able to describe how the signal is distributed for a particular hormonal pathway, and three actions are defined:

Endocrine action: the hormone is distributed in blood and binds to distant target cells.
Paracrine action: the hormone acts locally by diffusing from its source to target cells in the neighborhood.
Autocrine action: the hormone acts on the same cell that produced it.

Two important terms are used to refer to molecules that bind to the hormone-binding sites of receptors:

Agonists are molecules that bind the receptor and induce all the post-receptor events that lead to a biologic effect. In other words, they act like the "normal" hormone, although perhaps more or less potently. Natural hormones are themselves agonists and, in many cases, more than one distinct hormone binds to the same receptor. For a given receptor, different agonists can have dramatically different potencies.
Antagonists are molecules that bind the receptor and block binding of the agonist, but fail to trigger intracellular signalling events. Antagonists are like certain types of bureaucrats - they don't themselves perform useful work, but block the activities of those that do have the capacity to contribute. Hormone antagonists are widely used as drugs.
Finally, a comment on the names given hormones and what some have called the tyranny of terminology. Hormones are inevitably named shortly after their discovery, when understanding is necessarily rudimentary. They are often named for the first physiologic effect observed or for their major site of synthesis. As knowledge and understanding of the hormone grow, the original name often appears inappropriate or too restrictive, but it has become entrenched in the literature and is rarely changed. In other situations, a single hormone will be referred to by more than one name. The problem is that the names given to hormones often end up being either confusing or misleading. The solution is to view names as identifiers rather than strict guidelines to source or function.

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Index of: Hormones, Receptors and Control Systems
Overview of Endocrinology Hormone Chemistry, Synthesis and Elimination

[JustBecause]

Steroid Hormone Receptors

The receptors to which steroid hormones bind are ligand-activated proteins that regulate transcription of selected genes. Unlike peptide hormone receptors, that span the plasma membrane and bind ligand outside the cell, steroid hormone receptors are found in the cytosol and the nucleus. The steroid hormone receptors belong to the steroid and thyroid hormone receptor super-family of proteins, that includes receptors for steroid hormones, thyroid hormones, vitamin D and vitamin A (retinoic acid).
When these receptors bind ligand they undergo a conformational change that renders them activated to recognize and bind to specific nucleotide sequences. These specific nucleotide sequences in the DNA are referred to as hormone-response elements (HREs). When ligand-receptor complexes interact with DNA they alter the transcriptional level (responses can be either activating or repressing) of the associated gene. Thus, the steroid-thyroid family of receptors all have three distinct domains: a ligand-binding domain, a DNA-binding domain and a transcriptional regulatory domain. Although there is the commonly observed effect of altered transcriptional activity in response to hormone-receptor interaction, there are family member-specific effects with ligand-receptor interaction. Binding of thyroid hormone to its receptor results in release of the receptor from DNA. Several receptors are induced to interact with other transcriptional mediators in response to ligand binding. Binding of glucocorticoid leads to translocation of the ligand-receptor complex from the cytosol to the nucleus.
The receptors for the retinoids (vitamin A and its derivatives) are identified as RARs (for retinoic acid, RA receptors) and exist in at least three subtypes, RARa, RARb and RARg. In addition, there is another family of nuclear receptors termed the retinoid X receptors (RXRs) that represents a second class of retinoid-responsive transcription factors. The RXRs have been shown to enhance the DNA-binding activity of RARs and the thyroid hormone receptors (TRs). There are also three distinct RXRs (a, b and g). The major difference between the RARs and RXRs is that the former exhibit highest affinity for all-trans-retinoic acid (all-trans-RA) and the latter for 9-cis-RA.
Additional super-family members are the peroxisome proliferator-activated receptors (PPARs). These receptors were originally discovered as proteins activated by agents that stimulate proliferation of peroxisomes in rat liver. An intracellular lipid-binding protein identified as aP2 is expressed exclusively in differentiated adipocytes. An adipocyte-specific enhancer of the aP2 gene is a target for peroxisome proliferators, fatty acids and 9-cis-RA. Subsequent to these observations it was found that there is an adipocyte-specific PPAR family identified as PPARg. The PPARg proteins form heterodimers with RXRs to activate adipocyte-specific enhancers such as the one in the aP2 gene.
Recent evidence has demonstrated a role for PPARg proteins in the etiology of type 2 diabetes. A relatively new class of drugs used to increase the sensitivity of the body to insulin are the thiazolidinedione drugs. These compounds bind to and alter the function of PPARg. Mutations in the gene for PPARg have been correlated with insulin resistance. It is still not completely clear how impaired PPARg signaling can affect the sensitivity of the body to insulin or indeed if the observed mutations are a direct or indirect cause of the symptoms of insulin resistance.

[rolemodel]

I found this also.

STACKING 101:

Okay, I'm going to attempt to address a piece of the puzzle towards effective combinations of compounds from a more scientific standpoint than just throwing two drugs together haphazardly so we can say we're"stacking". Keep in mind there are MANY variables here, and I'm only addressing one key (yet important) issue: Anabolic steroids work through more than one pathway-activating the androgen receptor (A/R) is only one of them. Some A/S is effective in certain pathways but not others. It's best to use a combination that covers both androgen receptors mediated activity and non-A/R mediated activity (outside of the A/R). Examples of drugs that do not bind well to the A/R and thus achieve their effectiveness through other pathways are Anadrol-50, Dianabol, and winstrol. Drugs that possess strong binding affinity to the A/R and thus achieve their effects through this mechanism are as follows: Oxandrolone, equipoise, primobolan depot, and nandrolone (deca). *Note-Testosterone exhibits powerful effects through both A/R and non-A/R pathways. This is one of the reasons that it is universally accepted as the most powerful "stand-alone" muscle builder (trenbolone also shares similar characteristics). Based on the above information, let's look at combining groups for complete growth through different pathways. Effective combinations could be (but are not limited to)--Testosterone/trenbolone + Dianabol or winstrol***Deca/equipoise + winstrol or dianabol***Primobolan/Equipoise + winstrol, d-bol or anadrol-50***Oxandrolone + winstrol or d-bol (*note-even though this would be a double AA-17 cycle, oxandrolone actually, for some odd reason exhibits very little liver toxicity, hence the 2 together should be okay). There are many different combinations that can be played with from the above selection, just be sure to include one from each group (A/R**non-A/R activity) for maximum effectiveness. Well, as stated above, this gives only a piece of the puzzle, but hopefully it will lay a little groundwork down for some of you guys, so you can start experimenting with different compounds with a direct purpose in mind.
A classic example of this type of synergy exists in the age-old deca/d-bol stack. Most users years ago probably had no idea why these two compounds worked so terrifically together, they just knew that when combined, they seemed to amplify the effects of each other. This is due to the fact that deca has a potent binding affinity to the A/R, whereas dianabol is very powerful outside of the A/R, thus each one takes up the space where the others weakness left off, making for a potent one-two punch of anabolic activity....
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[hooker]

There's only one androgen receptor, but there are different genes which are more readily activated by different steroids once they have bound to the androgen receptor.