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Hepatotoxicity warning

Methyltrienolone 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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Methyltrienolone

Extensively Studied

17α-methylated trenbolone — the oral version of the most potent mainstream injectable AAS, sold via gray-market UGLs and used in lab…

Aliases (6)
Metribolone · R1881 · Mtren · Oral Tren · Methyltrenbolone · RU-1881
TYPICAL DOSE
500-1000 mcg/day
Daily (research)
ROUTE
Oral (tablet)
Oral
CYCLE
None
Cycle length (4-6 wk)
STORAGE
Room temp; original container
Room temp

Overview

What is Methyltrienolone?

Methyltrienolone (M3, "Metribolone") is an extremely potent oral 17α-methylated nor-19 anabolic-androgenic steroid. It is used in research as a high-affinity AR ligand and rarely in underground bodybuilding.

Key Benefits

Extremely high anabolic and androgenic potency relative to dose, useful as a research probe for the androgen receptor, and historically tested as a breast-cancer therapy; however, hepatotoxicity is severe.

Mechanism of Action

Binds the androgen receptor with very high affinity and very slow off-rate, producing potent and prolonged AR signaling. Cannot aromatize but interacts with progesterone and glucocorticoid receptors. The 17α-methyl group drives marked hepatotoxicity.

Pharmacokinetics

·
PeakHalf-life
Approximate curve — visual aid only, not data-precise PK
Cycle structure & PCT AAS oral
Ester
enanthate
Cycle
1-2 week
Frequency
weekly
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

Glucocorticoid receptor (GR) agonist

drives anxiety, sleep destruction, cardiovascular damage, connective-tissue catabolism (the "tren-class" subjective profile).

Effective

Progestogenic activity

prolactin elevation, gynecomastia risk that aromatase inhibitors don't address.

Investigational

Non-aromatizing

does not convert to estradiol, removing estrogen's cardioprotective effects (HDL crash, vascular endothelial damage).

Investigational

5α-reductase resistant

does not convert to DHT but is itself extraordinarily androgenic.

Investigational

HPG suppression: among the most severe of any AAS

LH/FSH crash within days; recovery post-cycle slow and uncertain.

Peptide Interactions

Other 17α-alkylated orals (methyltestosterone, oxandrolone, stanozolol, methandrostenolone, fluoxymesterone):
Avoid

hepatotoxicity additive and often catastrophic.

Other AAS:
Avoid

stacks tren-class CV/HPG damage non-linearly.

Stimulants (modafinil, amphetamines, high-dose caffeine):
Avoid

additive cardiovascular load.

Alcohol:
Avoid

additive hepatic stress (n/a for users in this archetype but noted for class context).

NSAIDs (chronic):
Avoid

additive hepatic + renal stress.

SSRIs / antidepressants:
Avoid

unpredictable interaction with AAS-mood axis.

Acetaminophen / paracetamol:
Avoid

additive hepatic stress on a 17α-methyl backbone is particularly poorly tolerated.

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

  • Common (>10% users): Insomnia, night sweats, severe mood lability, irritability, elevated BP, elevated resting HR, sexual dysfunction (mid-cycle ED), severe HPG suppression (universal at any meaningful dose), ALT/AST elevation within first 1-2 weeks, water retention modest.
  • Less common (1-10%): Cholestatic jaundice (yellowing, dark urine, pruritus), gynecomastia (progestogenic — AI does not address), aggression incidents, panic-attack-like episodes, severe acne, accelerated androgenic alopecia, kidney function decline, prostate symptoms.
  • Rare-serious (<1% but worth knowing):
    • Peliosis hepatis — blood-filled cystic lesions in the liver that can rupture catastrophically. 17α-methyl AAS are the primary pharmacologic cause; methyltrienolone is among the highest-risk in the class given its potency.
    • Hepatic adenoma / hepatocellular carcinoma — documented with prolonged 17α-methyl AAS use; methyltrienolone's potency means meaningful exposure happens at lower mg-doses than other 17α-AAS.
    • Acute liver failure — case reports exist for the 17α-methyl class with cholestatic liver failure progressing to ICU admission.
    • Cardiac event (MI, arrhythmia, cardiomyopathy) — HDL crash + hypertension + erythrocytosis + GR activation stack acutely on-cycle.
    • Acute kidney injury — case reports in the 19-nor / tren-class.
    • Psychotic episode, manic episode, suicidal ideation — vulnerable users.
    • Persistent post-cycle hypogonadism — failure to recover endogenous T after even short methyltrienolone exposures, given tren-class HPG suppression severity.
    • Tren cough analog — some users report acute respiratory reactions, though injection-route tren cough is not directly applicable to oral mtren.
  • Specific watch periods:
    • First 7 days: liver enzymes (ALT/AST/GGT/bilirubin) — methyltrienolone hits hepatic injury thresholds fastest of any commonly-discussed AAS.
    • Any RUQ pain, jaundice, dark urine, pruritus, or unexplained fatigue is an emergency stop.
    • First 4 weeks: psychiatric side effects peak (sleep, mood).
    • Mid-cycle through PCT: lipid panel, cardiac surveillance, kidney function.
    • 6-12 months post-cycle: ASIH may persist; some users never recover.
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