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Proviron

Mesterolone · Oral androgen (anabolic steroid)

Research reference only. Pepdex does not sell, supply or track this compound, and nothing here is guidance to use it — this page exists so the evidence and the risks are visible.

What it is

An oral DHT derivative with weak anabolic activity, historically prescribed in Europe for androgen deficiency and as an infertility adjunct. It also circulates in non-medical AAS contexts.

How it works

Mesterolone is a weak orally active androgen that is not 17-alpha-alkylated, which is what separates it from the rest of the oral group: substantially lower cholestatic risk, though its official product information still contraindicates prior or existing liver tumours and reports rare benign and rarer malignant ones, including life-threatening internal bleeding. Lower hepatic risk is not zero hepatic risk. The claim that its main job is displacing other steroids from their binding protein is stack lore rather than label pharmacology — no outcome benefit from that has been established, and no interaction studies were conducted. It is not meaningfully anabolic on its own.

What human evidence shows

Decades of European prescription use — modest, real androgenic effects, including mood and libido findings in older trials. Nothing about its physique-context reputation has controlled evidence behind it.

The studies, one by one

  • Prescribed in some countries for androgen deficiency and, in some national labelling, for male infertility associated with hypogonadism. At those regulated therapeutic exposures the product information states it does not significantly suppress gonadotropins or damage sperm production — which is a different situation from supratherapeutic or combination non-medical use.
  • Evidence for improving fertility outcomes is weak and it is not a current first-line treatment.
  • No trial supports its physique use, and it is generally described even in user communities as a supporting compound rather than an anabolic one.
  • Being non-alkylated, it lacks the case-report liver literature that defines the other orals here — its risk profile is androgenic and cardiovascular rather than hepatic.

Half-life and how long it lasts

Orally active without 17-alpha-alkylation, half-life around 12 hours. It is not converted to oestrogen and is not aromatisable. Its dominant pharmacological effect is displacing other hormones from sex hormone binding globulin, which is why its effects are largely about what else is present rather than about itself.

Risks

Milder than most entries in this class but not free: hair-loss pressure (it is essentially oral DHT), lipid effects, and HPG-axis suppression that users routinely underestimate because the drug "feels" mild. Counterfeits are common in the products that circulate.

Who should never touch it

  • Anyone with prostate cancer, or with a prior or existing liver tumour — both are label contraindications
  • Anyone with benign prostatic hyperplasia or male breast cancer, per national labelling
  • Women, for whom the label does not support use
  • Anyone experiencing prolonged or frequent erections, which is a labelled reason to seek care
  • Anyone with unfavourable lipids or cardiovascular disease
  • Anyone trying to conceive
  • Women, given virilisation risk

Interactions worth knowing

  • Other androgens. The belief that it makes them more active by freeing them from their binding protein is stack lore — no pharmacokinetic interaction studies were conducted and no outcome benefit is established.
  • Anticoagulants.
  • Finasteride, which does not block it in the usual way because of its structure.
  • Any lipid-lowering therapy, which it works against.

What a clinician would watch

  • Lipids — it still suppresses HDL despite the absence of liver toxicity.
  • Blood pressure.
  • Prostate symptoms and PSA in older men, since it is a pure androgen with no oestrogen conversion.
  • Total and free testosterone, LH and FSH. Suppression at regulated therapeutic exposure is described as not significant; at the amounts and combinations used non-medically, that reassurance does not carry over.
  • Hair loss in the predisposed, which it can accelerate.

What stopping looks like

No cholestatic recovery of the kind the 17-alpha-alkylated orals demand, which is the genuine difference — though lower hepatic risk is not none, and the label carries liver-tumour warnings. Suppression of natural testosterone recovers over weeks to months depending on what else was used alongside it, and lipids generally recover. Because it is almost always used with other compounds, what people experience on stopping is usually dominated by those rather than by mesterolone itself.

Myth vs evidence

It is a mild, side-effect-free addition.

It is not liver-toxic, which is a real difference, but it suppresses natural production, worsens lipids and can accelerate hair loss.

It restores fertility.

It is indicated for infertility associated with hypogonadism in some national labelling, at regulated therapeutic exposure. That does not transfer to the amounts and stacks used non-medically, and it is not a general fertility treatment.

It is an anabolic in its own right.

Its muscle-building effect is minimal. What it mostly does is change how much of the other compounds present are free to act.

Legal status

US: Schedule III anabolic steroid under the CSA; never FDA-approved. A prescription pharmaceutical in parts of Europe.

Research on this compound

Papers about this compound, not proof of the claims above. A title says what was studied, which is sometimes a negative result or a different question entirely.

  • Placebo-controlled trial of high-dose Mesterolone treatment of idiopathic male infertility
  • Mesterolone and idiopathic male infertility: a double-blind study. World Health Organization Task Force on the Diagnosis and Treatment of Infertility
  • The effects of mesterolone on sperm count in idiopathic oligospermia

Evidence base

A206 research papers
substantial literature

Strong human evidence: either a phase 3 or 4 trial report alongside review-level evidence, or ten or more randomised controlled trial reports.

phase 3/4
0
randomised
13
reviews
2
human trials
28

Counts are of published papers, not distinct trials, and they nest rather than add up: PubMed files every randomised trial as a clinical trial too. They measure how much research exists — not whether this works or is safe for you.

Research (12)

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