Bioavailability

Bioavailability is the fraction of administered compound reaching systemic circulation in active form. Intravenous defines 100%. Every other route loses mass to gut-wall CYP3A4, hepatic first-pass metabolism, or mucosal membrane impedance.

Parenteral routes:

– Intramuscular oil depot: 92–98%. Site-dependent — vastus lateralis > glute medius > deltoid at steady-state, reflecting local vascularity and adipose fraction.
– Subcutaneous oil depot: 85–95%. Adipose acts as a secondary depot; short-ester retention extends modestly.
– Intravenous: 100% by definition, clinically irrelevant for AAS — intolerable peaks, too-rapid clearance.

Oral routes, and why the answer spans three orders of magnitude:

– Unmodified testosterone: <5%. Portal circulation delivers almost the full dose to hepatocytes before systemic availability. The liver conjugates the 17β-hydroxyl and excretes biliarily; enterohepatic recycling completes the loss. No non-alkylated oral testosterone product exists in any pharmacopoeia for this reason.
– 17α-alkylated orals: 50–80%. The methyl or ethyl substituent sterically blocks glucuronidation at the 17β-position — the liver’s primary clearance pathway for sex steroids. Survival of the dose is bought at hepatocyte cost.
– Testosterone undecanoate (oral): 6–10%. The C11 ester permits absorption via intestinal lymphatics, bypassing portal circulation — but only with co-administered dietary fat to activate the pathway. Fasted dosing produces near-zero serum rise.

Transdermal routes:

– Gel (1–2% formulation): 10–14%. Stratum corneum is rate-limiting; twice-daily application compensates for short skin half-life.
– Patch (occlusive): 20–30%. Sustains steady-state at the price of predictable contact-site reactions.

The conversion-table fallacy:

Oral 25 mg and injected 25 mg do not produce equivalent serum curves. Different AUC, different peak-to-trough shape, different hepatic exposure, different metabolite fraction. Published equivalence tables circulating on forums are marketing lore, not pharmacokinetics. An honest comparison requires area-under-curve measured on validated assay in a matched population — and the matched population rarely exists in the AAS literature.

Bioavailability is not a conversion factor you punch into a spreadsheet. It is a separate pharmacokinetic variable travelling alongside potency, receptor affinity, and metabolic fate.