Methyltestosterone
Also known as: Methyltestosterone, 17α-Methyltestosterone, Android, Metandren, Testred, Oreton, Virilon
Lower numbers = closer to natural. Higher numbers = more enhanced.
Why this rating?
Methyltestosterone is an orally active 17α-methylated derivative of testosterone with an anabolic:androgenic ratio close to 1:1, making it roughly testosterone-equivalent in potency but among the most androgenic AAS. It aromatizes efficiently to a metabolism-resistant estrogen (17α-methylestradiol) and is meaningfully hepatotoxic. It clearly places a user beyond natural limits like any exogenous androgen, but it is a modest oral rather than a mass monster, rated 7, similar to testosterone with the added liver and estrogen burden of an oral 17-alkylated drug.
Overview
One of the first orally active anabolic steroids, a 17α-methylated form of testosterone that survives first-pass liver metabolism. FDA-approved for male hypogonadism, delayed puberty and advanced breast cancer, it is now largely superseded but still illustrates the classic trade-off of oral 17-alkylated androgens: convenience at the cost of liver strain and strong estrogenicity.
Purpose & Use Cases
Androgen Replacement (medical)
Its approved role: treating male hypogonadism and delayed puberty when an oral androgen is wanted.
Oral Anabolic / Strength
Historically used by athletes as a convenient oral androgen for strength and mass before more selective orals existed.
Breast Cancer (palliative, historical)
Approved at higher doses for advanced inoperable breast cancer in women as an androgen therapy.
Benefits
- Orally active: no injections needed
- Roughly testosterone-equivalent anabolic potency (A:A ~1:1)
- Strongly androgenic: drive, libido and aggression
- Increases protein synthesis and nitrogen retention
- Well-characterised, FDA-approved pharmacology
Good to Know
The archetypal oral 17-alkylated androgen
The 17α-methyl group is what makes methyltestosterone survive the liver and work orally (~70% bioavailable), but the very same modification is what makes it hepatotoxic. This is the fundamental trade-off of every oral 17-alkylated steroid (Dianabol, Anadrol, Winstrol, Superdrol): oral convenience bought with liver strain.
It aromatizes to a "stubborn" estrogen
Unlike testosterone's estradiol, methyltestosterone converts to 17α-methylestradiol, which resists the enzymes that normally clear estrogen. That is why it is relatively estrogenic for its dose and why gyno/water can appear even though it is "just oral test."
One of the few orals where finasteride helps hair
Because it is a 5α-reductase substrate (converting to methyl-DHT/mestanolone), finasteride or dutasteride can blunt its scalp and prostate effects. The same logic that applies to testosterone. This is NOT true of DHT-derivative orals like Superdrol, Anavar or Winstrol, which are already past that step.
Muscle memory raises your natural ceiling afterward
Any effective androgen adds myonuclei to muscle fibres, and those are retained long after the drug clears ("muscle memory"). A past methyltestosterone run keeps nudging your "natural" ceiling upward. Relevant to how the natty scale treats prior use even during fully natural phases.
Dosage Guidelines
| Experience Level | Dosage Range |
|---|---|
| Beginner | 10 – 25 mg/day |
| Intermediate | 25 – 50 mg/day |
| Advanced | 50 – 100 mg/day |
FDA label range is 10-50 mg/day in men for hypogonadism/delayed puberty (2.5 mg/day in women for menopausal symptoms; 50-200 mg/day historically for breast cancer, a dose that risked severe, largely irreversible virilization in women). Harm-reduction sources report a bodybuilding "standard" of roughly 40-50 mg/day for about 6-8 weeks, noting few athletes gain enough advantage over other orals to justify the added liver/estrogen burden. Doses meaningfully above 50 mg/day are poorly documented and sharply raise hepatotoxicity and estrogenicity risk.
Elimination half-life is roughly 2.5-3.5 hours; the duration of androgenic action is longer at about 1-3 days.
Side Effects
Hepatotoxicity
very commonAs a 17α-alkylated oral it can cause elevated liver enzymes, cholestatic jaundice, peliosis hepatis, and with prolonged use hepatic adenomas and hepatocellular carcinoma.
Keep cycles short, avoid alcohol and other hepatotoxic orals, use TUDCA, and monitor liver enzymes with bloodwork.
Gynecomastia / Estrogenic Effects
commonAromatizes efficiently to 17α-methylestradiol, a potent metabolism-resistant estrogen, giving relatively high estrogenicity, gyno and water retention.
An aromatase inhibitor (e.g. anastrozole) or a SERM for gyno, dosed to bloodwork.
Androgenic Effects (acne, hair loss, prostate)
commonAmong the most androgenic AAS; acne, accelerated male-pattern hair loss in the predisposed and prostate effects are likely.
Because it is a 5α-reductase substrate, finasteride/dutasteride can blunt scalp/prostate DHT effects (as with testosterone).
HPTA Suppression
very commonLike any exogenous androgen it suppresses natural testosterone production, requiring PCT after use.
Full SERM PCT after the cycle; hCG can preserve testicular size on longer runs.
General Mitigation Strategies
Treat it as a hepatotoxic oral 17-alkylated androgen: keep cycles short (4-6 weeks), avoid alcohol and stacking with other orals, run liver support (TUDCA/NAC) and monitor liver enzymes. Because it aromatizes efficiently, keep an AI or SERM on hand for estrogen control. Standard SERM PCT restores natural testosterone afterwards. Unlike DHT-derivatives, finasteride does help its androgenic hair/prostate effects because it is a 5α-reductase substrate.
Support Supplements
Ancillary supplements commonly run alongside Methyltestosterone to manage side effects, support the target tissue, or fill nutrient demands it creates.
Liver support (TUDCA + NAC)
KeyMethyltestosterone is a 17α-alkylated oral implicated in cholestasis, peliosis hepatis and liver tumours. TUDCA supports bile flow; NAC replenishes hepatic glutathione. Support only: dose/duration limits and bloodwork are the real protection.
- Dose
- TUDCA 500-1,000 mg/day; NAC 600-1,200 mg/day
- Timing
- Throughout the oral cycle
Lipid support (omega-3 + citrus bergamot)
Oral 17-alkylated androgens are hard on cholesterol (HDL suppression). Omega-3 lowers triglycerides; citrus bergamot lowers LDL via statin-like flavonoids.
- Dose
- Omega-3 2-4 g/day; citrus bergamot 500-1,000 mg/day
- Timing
- With meals
Aromatase inhibitor on hand (anastrozole)
It aromatizes efficiently to a potent metabolism-resistant estrogen, so an AI may be needed for gyno/water at higher doses.
- Dose
- Anastrozole 0.25-0.5 mg, dosed to E2 bloodwork
- Timing
- As needed
- When
- Only if estrogenic symptoms appear: do not crash estrogen.
Post Cycle Therapy (PCT)
Methyltestosterone suppresses the HPTA like any exogenous androgen, so PCT is needed after a cycle. Standard SERM protocol (e.g. Nolvadex 40/40/20/20 mg/day or Clomid 50/50/25/25 mg/day over 4 weeks). Because it is short-acting and cleared quickly, PCT can begin soon after the last dose. Confirm recovery with bloodwork (LH, FSH, total/free testosterone, E2).
How It Works
Methyltestosterone is a synthetic 17α-alkylated androstane steroid, differing from testosterone only by a methyl group at C17α. That group creates steric hindrance that blocks hepatic breakdown, giving roughly 70% oral bioavailability, but the same modification drives its liver toxicity. It is an agonist of the androgen receptor like testosterone and DHT. It is a 5α-reductase substrate, being potentiated in androgenic tissues into mestanolone (17α-methyl-DHT), and it aromatizes efficiently to 17α-methylestradiol, a potent, metabolism-resistant estrogen.
Hormonal & Androgenic Profile
~1:1 (close to testosterone): which makes it among the most androgenic AAS relative to its anabolic strength
Aromatizes efficiently into 17α-methylestradiol, a potent estrogen that resists metabolism, giving relatively high estrogenicity. An AI or a gyno SERM may be needed at higher doses, dosed to bloodwork.
A testosterone derivative, not a DHT-derivative, and it is a 5α-reductase substrate, potentiated in skin/scalp/prostate into mestanolone (17α-methyl-DHT). This is one of the cases where finasteride/dutasteride actually help, cutting the DHT-mediated hair/prostate effect much as they do on testosterone.
Oral 17-alkylated androgens suppress HDL and worsen lipids; efficient aromatization also brings estrogenic water retention and blood-pressure rise. Monitor a full lipid panel and BP.
Fundamentals
Reference on the practices relevant to Methyltestosterone: how they are done and where they go wrong. Not a recommendation to use it.
Legal Status
Schedule III controlled substance (USA); Schedule IV (Canada). An FDA-approved prescription drug (hypogonadism, delayed puberty, inoperable breast cancer in women).
Legal status varies by country and changes over time. This is a general summary, not legal advice.
WADA Status
Methyltestosterone is explicitly prohibited at all times as an exogenous anabolic androgenic steroid.