HackTwat
MuscleChemistry Registered Member
[h=2]Biochemistry and Pharmacology[/h]Because there are many agents in production and literally hundreds more that have been synthesized, this discussion focuses on the basics involving the steroid ring substitutions and how these substitutions affect the properties of the drug. Detailed analysis is limited to those agents that are available or have been approved for use in the United States.
Anabolic-androgenic steroid (AAS) development was centered on the need for agents that exhibited different characteristics than did testosterone. In general, the goal was to develop agents that were more anabolic and less androgenic than testosterone, that were capable of being administered orally, and that had less effect upon the hypothalamic-pituitary-gonadal axis. Most AASs are derived from 3 compounds: testosterone, dihydrotestosterone, and 19-nortestosterone. The third compound is structurally identical to testosterone except for the deletion of the 19th carbon (hence its name). These parent compounds offer different properties with regard to action and metabolism that are generally constant throughout the entire family of compounds.
One of the first changes made to the testosterone molecule was the addition of a methyl group or an ethyl group to the 17-carbon position. This addition was noted to inhibit the hepatic degradation of the molecule, greatly extending the molecule's half-life and making it active when administered orally. Prior to this, testosterone, dihydrotestosterone, and 19-nortestosterone all required parenteral administration due to hepatic metabolism of 17-ketosteroids; this metabolism occurred on the first pass, when the drugs were administered orally.
However, adding a methyl group or an ethyl group did not produce a drug with the exact properties of the parent compound. The alteration of hepatic metabolism was noted to cause strain on the liver, and indeed all oral compounds with this C-17 addition were found to cause dose-related hepatotoxicity. This small change was also found to lower these agents' interaction with aromatase.[SUP][9] [/SUP]Therefore, even small changes to these parent compounds cause multiple alterations in the inherent nature of AASs.
Anabolic-androgenic steroid (AAS) development was centered on the need for agents that exhibited different characteristics than did testosterone. In general, the goal was to develop agents that were more anabolic and less androgenic than testosterone, that were capable of being administered orally, and that had less effect upon the hypothalamic-pituitary-gonadal axis. Most AASs are derived from 3 compounds: testosterone, dihydrotestosterone, and 19-nortestosterone. The third compound is structurally identical to testosterone except for the deletion of the 19th carbon (hence its name). These parent compounds offer different properties with regard to action and metabolism that are generally constant throughout the entire family of compounds.
One of the first changes made to the testosterone molecule was the addition of a methyl group or an ethyl group to the 17-carbon position. This addition was noted to inhibit the hepatic degradation of the molecule, greatly extending the molecule's half-life and making it active when administered orally. Prior to this, testosterone, dihydrotestosterone, and 19-nortestosterone all required parenteral administration due to hepatic metabolism of 17-ketosteroids; this metabolism occurred on the first pass, when the drugs were administered orally.
However, adding a methyl group or an ethyl group did not produce a drug with the exact properties of the parent compound. The alteration of hepatic metabolism was noted to cause strain on the liver, and indeed all oral compounds with this C-17 addition were found to cause dose-related hepatotoxicity. This small change was also found to lower these agents' interaction with aromatase.[SUP][9] [/SUP]Therefore, even small changes to these parent compounds cause multiple alterations in the inherent nature of AASs.
