I'm sure that if you have taken an interest in anabolic steroids you have noticed the similarities on the labeling of many drugs. Let's look at testosterone for example. One can find compounds like testosterone cypionate, enanthate, propionate, heptylate; caproate, phenylpropionate, isocaproate, decanoate, acetate, the list goes on and on. In all such cases the parent hormone is testosterone, which had been modified by adding an ester (enanthate, propionate etc.) to its structure. The following question arises: What is the difference between the various esterified versions of testosterone in regards to their use in bodybuilding?
An ester is a chain composed primarily of carbon and hydrogen atoms. This chain is typically attached to the parent steroid hormone at the 17th carbon position (beta orientation), although some compounds do carry esters at position 3 (for the purposes of this article it is not crucial to understand the exact position of the ester). Esterification of an injectable anabolic/androgenic steroid basically accomplishes one thing, it slows the release of the parent steroid from the site of injection. This happens because the ester will notably lower the water solubility of the steroid, and increase its lipid (fat) solubility. This will cause the drug to form a deposit in the muscle tissue, from which it will slowly enter into circulation as it is picked up in small quantities by the blood. Generally, the longer the ester chain, the lower the water solubility of the compound, and the longer it will take to for the full dosage to reach general circulation.
Slowing the release of the parent steroid is a great benefit in steroid medicine, as free testosterone (or other steroid hormones) previously would remain active in the body for a very short period of time (typically hours). This would necessitate an unpleasant daily injection schedule if one wished to maintain a continuous elevation of testosterone (the goal of testosterone replacement therapy). By adding an ester, the patient can visit the doctor as infrequently as once per month for his injection, instead of having to constantly re-administer the drug to achieve a therapeutic effect. Clearly without the use of an ester, therapy with an injectable anabolic/androgen would be much more difficult.
Esterification temporarily deactivates the steroid molecule. With a chain blocking the 17th beta position, binding to the androgen receptor is not possible (it can exert no activity in the body). In order for the compound to become active the ester must therefore first be removed. This automatically occurs once the compound has filtered into blood circulation, where esterase enzymes quickly cleave off (hydrolyze) the ester chain. This will restore the necessary hydroxyl (OH) group at the 17th beta position, enabling the drug to attach to the appropriate receptor. Now and only now will the steroid be able to have an effect on skeletal muscle tissue. You can start to see why considering testosterone cypionate much more potent than enanthate makes little sense, as your muscles are seeing only free testosterone no matter what ester was used to deploy it.
An ester is a chain composed primarily of carbon and hydrogen atoms. This chain is typically attached to the parent steroid hormone at the 17th carbon position (beta orientation), although some compounds do carry esters at position 3 (for the purposes of this article it is not crucial to understand the exact position of the ester). Esterification of an injectable anabolic/androgenic steroid basically accomplishes one thing, it slows the release of the parent steroid from the site of injection. This happens because the ester will notably lower the water solubility of the steroid, and increase its lipid (fat) solubility. This will cause the drug to form a deposit in the muscle tissue, from which it will slowly enter into circulation as it is picked up in small quantities by the blood. Generally, the longer the ester chain, the lower the water solubility of the compound, and the longer it will take to for the full dosage to reach general circulation.
Slowing the release of the parent steroid is a great benefit in steroid medicine, as free testosterone (or other steroid hormones) previously would remain active in the body for a very short period of time (typically hours). This would necessitate an unpleasant daily injection schedule if one wished to maintain a continuous elevation of testosterone (the goal of testosterone replacement therapy). By adding an ester, the patient can visit the doctor as infrequently as once per month for his injection, instead of having to constantly re-administer the drug to achieve a therapeutic effect. Clearly without the use of an ester, therapy with an injectable anabolic/androgen would be much more difficult.
Esterification temporarily deactivates the steroid molecule. With a chain blocking the 17th beta position, binding to the androgen receptor is not possible (it can exert no activity in the body). In order for the compound to become active the ester must therefore first be removed. This automatically occurs once the compound has filtered into blood circulation, where esterase enzymes quickly cleave off (hydrolyze) the ester chain. This will restore the necessary hydroxyl (OH) group at the 17th beta position, enabling the drug to attach to the appropriate receptor. Now and only now will the steroid be able to have an effect on skeletal muscle tissue. You can start to see why considering testosterone cypionate much more potent than enanthate makes little sense, as your muscles are seeing only free testosterone no matter what ester was used to deploy it.
Added your blog, my friend!