Oral AAS Guide17α-Alkylated Anabolic Steroids — Complete Research Reference by QSC Peptides

17α-Alkylated (17α-AA) oral AAS achieve oral bioavailability through a C17α methyl group that sterically blocks hepatic 17β-hydroxysteroid dehydrogenase (17β-HSD) from oxidizing the C17β-hydroxyl to an inactive 17-ketone during first-pass metabolism. Without this protection, orally ingested steroids are rapidly inactivated by the liver before reaching systemic circulation.

The tradeoff is direct hepatic exposure during portal circulation — the methyl group-protected compound passes through the liver intact, where it exerts direct effects on hepatocytes. This is the pharmacological basis of 17α-AA hepatotoxicity, including cholestasis, peliosis hepatis, and hepatocellular adenoma in long-term models.

17α-Methyl: How It Works Chemically

The 17α-methyl group creates steric hindrance at C17 that prevents 17β-HSD from approaching the substrate. The enzyme requires access to the β-face of C17 to oxidize the hydroxyl — the α-axial methyl group physically blocks this approach. The result: the compound passes through the liver essentially unchanged, achieving ~70–85% oral bioavailability depending on the compound.

Oral AAS Comparison — All QSC Peptides Oral Compounds

Research Design Considerations for Oral AAS

• Short half-lives (3–9 hrs): Frequent dosing required in research but enables rapid on/off kinetics; useful for short washout between treatment phases
• Hepatotoxicity models: All oral 17α-AA compounds produce hepatic enzyme elevation in a dose and duration-dependent manner — making them model compounds for 17α-AA hepatotoxicity research
• Dianabol injectable: QSC Peptides uniquely offers injectable Dianabol (50mg/mL oil) alongside oral tablets — enabling oral vs parenteral bioavailability comparison studies
• Anadrol injectable: Similarly available as injectable (50mg/mL) for direct vs oral PK comparison research