This page describes pharmacological agents that may have legal restrictions, side effects, and drug interactions in your jurisdiction. Information is for educational research only — consult a clinician before considering any compound.

Hepatotoxicity warning

Methyltestosterone is 17α-alkylated for oral bioavailability — a structural feature directly responsible for the most severe hepatotoxic class of AAS. Cholestatic injury, peliosis hepatis, and hepatic adenoma are all class-documented. Cycle length must be capped (typically < 6-8 weeks); LFTs (ALT, AST, GGT, bilirubin) baseline + every 2 weeks on cycle. Stop immediately on ALT/AST > 3× ULN or symptomatic jaundice.

High-risk compound

Surface here is educational only; do not use without medical supervision. Our editorial verdict is SKIP-PERMANENT — risk:benefit fails for the canonical archetype.

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Methyltestosterone

Emerging

The oldest oral anabolic steroid (synthesized 1935, marketed late 1930s), and now obsolete.

Aliases (9)

17α-Methyltestosterone · Metandren · Android · Testred · Methitest · Virilon · Oreton-M · MeT · 17a-MT

TYPICAL DOSE

5-25 mg/day

Daily

ROUTE

Oral (tablet)

Oral

CYCLE

Anabolic effect plateaus at 4-6 weeks at fixed …

Cycle length (4-6 wk)

STORAGE

Room temp; original container

Room temp

Overview

What is Methyltestosterone?

Methyltestosterone is a 17α-alkylated oral anabolic-androgenic steroid. It is one of the oldest oral testosterone analogs and is now rarely used clinically due to liver toxicity, with limited modern bodybuilding use.

Key Benefits

Provides oral testosterone replacement when injection is impractical, increases strength and aggression in performance contexts, and historically used for hypogonadism, delayed puberty, and breast cancer (largely supplanted).

Mechanism of Action

A 17α-methyl group prevents hepatic first-pass deactivation, allowing oral activity. Binds the androgen receptor and aromatizes partly to methyl-estradiol, with substantial hepatotoxicity from biliary stasis and oxidative stress.

Pharmacokinetics

PeakHalf-life

Approximate curve — visual aid only, not data-precise PK

▸ Cycle structure & PCT AAS oral

Ester

enanthate

PCT

Required

Phase 1 — On cycle

Ramp dose over week 1, hold steady through cycle weeks. Track baseline labs (TT/FT/E2/SHBG/HCT/lipids/LFTs) at week 0; recheck at week 4 and end-of-cycle.

Phase 2 — Bridge / cease

On the last dose, the ester clears over its half-life window (enanthate = est. 7 days). PCT begins after the active compound has cleared.

Phase 3 — PCT (post-cycle therapy)

Standard PCT is enclomiphene 12.5-25 mg/day or clomid 50/50/25/25 over 4 weeks (or nolvadex 20/20/10/10). HCG bridge optional during cycle to preserve testicular volume + faster restart. Bloodwork at PCT week 4 + 8 to confirm HPG axis recovery (LH, FSH, TT back to baseline).

Research Indications

Most Effective

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 ret…

Effective

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 rath…

Peptide Interactions

No legitimate synergy

Synergistic

in a 2026 protocol context. Historical bodybuilding stacks combined methyltestosterone with non-17αAA injectables (testosterone enanthate, nandrolone) to "sp…

Other 17α-alkylated AAS

Avoid

(oxandrolone, stanozolol, methandrostenolone, oxymetholone, fluoxymesterone, danazol) — additive hepatotoxicity. Stacking two oral 17αAA is one of the most h…

Alcohol

Avoid

dramatically additive hepatic load.

Acetaminophen/paracetamol

Avoid

at therapeutic dose — additive hepatotoxicity.

Statins

Avoid

additive lipid disruption + hepatic load.

NSAIDs (chronic)

Avoid

renal + hepatic compounding.

Modafinil / adrafinil / other prodrugs with hepatic processing

Avoid

additive load.

Hormonal contraceptives, HRT

Avoid

additive estrogenic effect + hepatic load.

Nephrotoxic compounds

Avoid

(high-dose creatine combined with dehydration in MMA cut, e.g.) — synergistic kidney stress in already androgen-strained kidneys.

AI (anastrozole, letrozole)

Compatible

historically used to mitigate aromatization; mechanically logical but doesn't address hepatotoxicity (the dominant problem).

the user's V stack supplements

Compatible

mechanistically neutral, but the hepatic load of methyltestosterone would compound with NAC's hepatoprotective load (which would be a band-aid, not a fix).

Quality Indicators

✓

Pharmacy-dispensed, intact packaging

Prescription tablets in original sealed packaging from a licensed pharmacy.

Generic vs branded

Generics are usually fine but bioavailability can vary slightly; track if you switch.

✗

Unbranded blister or counterfeit risk

Counterfeit pharmaceuticals are a known issue; verify pharmacy and lot if buying internationally.

What to Expect

Week 1-2
Frontload phase. Strength gains start; appetite up.
Week 3-4
Visible muscle fullness and recovery acceleration.
Week 5-8
Peak performance window. Monitor blood pressure + libido.
Post-cycle
PCT week 1-4. Bloodwork at week 6 post-cycle.

Side Effects & Safety 16

Side Effects

1Elevated ALT/AST — most consistent finding. Often 2-5× ULN within 4-6 weeks at 30+ mg/day.
2Elevated GGT and alkaline phosphatase — cholestatic pattern.
3HDL-C suppression — often >50% reduction within 6-8 weeks; cardiovascular risk implication.
4LDL-C / ApoB elevation — additive CV risk.
5Water retention, hypertension — aromatization-driven.
6Gynecomastia (irreversible if untreated past nodule formation) — aromatization to 17α-methylestradiol.
7HPG axis suppression — testicular atrophy, ↓endogenous T, ↓libido on cessation.
8Acne, oily skin, accelerated androgenic alopecia — direct AR effects.
9Mood changes, irritability, aggression, sleep disruption.
10Increased hematocrit / polycythemia — direct erythropoietin pathway stimulation.
11Cholestatic jaundice — yellowing of skin/sclera, dark urine, pruritus. Typical onset 2-5 months chronic dosing. Reversible if caught early; can require hospitalization.
12Erectile dysfunction during use — paradoxical at supraphysiologic dose due to HPG suppression overriding direct androgen effects.
13Voice changes in females (irreversible vocal cord thickening). MeT is one of the most virilizing androgens for women historically — not used in modern female endocrinology.
14Menstrual irregularity, clitoral enlargement in females.
15Prostate hypertrophy / accelerated BPH in older males.
16Increased aggression / "roid rage" — especially at higher doses or in users with mood instability.

When to Stop

Peliosis hepatis — blood-filled cystic spaces in liver parenchyma. Can rupture → fatal hemorrhage. Detected on imaging; often asymptomatic until advanced.
Hepatic adenoma → hepatocellular carcinoma — long-term chronic use. Documented in chronic AAS users; methyltestosterone among the most associated agents.
Stroke, MI, sudden cardiac death — via combined hypertension + adverse lipid + polycythemia + LV hypertrophy effects.
Thromboembolic events — DVT, PE driven by polycythemia + altered coagulation.
Psychiatric — mania, psychosis, suicidality (rare but documented in AAS literature).
Sleep apnea exacerbation — soft tissue effects + polycythemia.
Weeks 2-4: liver enzyme baseline establishment — full LFT panel before starting (mandatory) and at 2 weeks; >3× ULN ALT/AST = stop drug.
Weeks 4-12: cholestasis watch — monitor bilirubin, GGT, alkaline phosphatase; clinical symptoms (jaundice, dark urine, RUQ pain, pruritus).
Weeks 6-8: HDL-C nadir — cardiovascular lipid impact.
Months 3-12: peliosis hepatis / adenoma watch — abdominal imaging (US, MRI) for chronic users.
Indefinite: hematocrit watch — HCT >54% = stop drug.