Methyltestosterone

The oldest oral anabolic steroid (synthesized 1935, marketed late 1930s), and now obsolete. The 17α-methyl group that lets it survive oral first-pass is also the structural feature that produces the worst hepatotoxicity of any common AAS — cholestatic jaundice, peliosis hepatis, hepatic adenoma. Weaker anabolic potency than oxandrolone, methandrostenolone, or oxymetholone with substantially worse liver toxicity. SKIP-PERMANENT for every modern user archetype — anyone who wants oral androgen has cleaner orals, anyone who wants testosterone proper has injectable T at a fraction of the hepatic burden.

Methyltestosterone is testosterone with a methyl group added at the C17α position. That single structural change does two things, both important:

1. Enables oral bioavailability. Native testosterone, when swallowed, is almost entirely destroyed by hepatic 17β-hydroxysteroid dehydrogenase before reaching circulation (oral bioavailability of unmodified T is <1%). The 17α-methyl group sterically blocks this enzyme, allowing the molecule to survive first-pass and reach systemic circulation as an active androgen.

2. Forces metabolism through hepatotoxic pathways. The same C17α-alkyl group that protects against hepatic deactivation also (a) blocks normal glucuronidation/sulfation conjugation, (b) gets metabolized via reactive intermediates that interfere with bile salt export pump (BSEP) and MRP2 transporters, producing cholestasis, and (c) at chronic dose drives sinusoidal endothelial injury producing peliosis hepatis (blood-filled cystic spaces in the liver) and, rarely, hepatic adenoma → hepatocellular carcinoma. This is a structural class effect of all 17α-alkylated steroids (oxandrolone, stanozolol, methandrostenolone, oxymetholone, fluoxymesterone, danazol), but methyltestosterone is among the worst offenders per mg.

Once in circulation, methyltestosterone:

• Binds androgen receptor (AR) with affinity comparable to testosterone — direct anabolic + androgenic effects on muscle, bone, skin, prostate, hair, vocal cords.
• Aromatizes to 17α-methylestradiol — an estrogen analog that, like the parent compound, is harder for the liver to clear than native estradiol. Drives gynecomastia, water retention, and BP elevation more aggressively than native testosterone aromatization.
• Suppresses HPG axis via negative feedback at hypothalamus + pituitary → ↓GnRH → ↓LH/FSH → testicular atrophy and shutdown of endogenous testosterone production. This is universal to all exogenous androgens but compounded by methyltestosterone's poor anabolic-to-androgenic ratio.
• Does not 5α-reduce to a more potent DHT analog the way native testosterone does — the 17α-methyl group interferes with 5α-reductase activity, so DHT-driven effects (prostate, scalp hair) come from direct AR binding rather than DHT formation. Practically irrelevant from a side-effect standpoint.

Anabolic:androgenic ratio: ~1:1 (similar to testosterone), making it a relatively androgenic compound for the muscle-building it provides — worse than oxandrolone (10:1), nandrolone (10:1), or stanozolol (3:1) for body composition without virilizing side effects.