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BHuman cohort / observational

Proviron

Mesterolone

Proviron (mesterolone) is an orally active synthetic androgen, chemically 1-alpha-methyl-5-alpha-dihydrotestosterone (a DHT derivative). It is a weak anabolic but relatively potent androgen that does not aromatize to estrogen and binds sex hormone-binding globulin (SHBG) very strongly. It was developed for androgen deficiency and empirically tried for male infertility. The main risks are an atherogenic shift in blood lipids in humans (large drop in HDL, large rise in LDL and triglycerides) even at replacement doses, which is the dominant documented harm. As a DHT-type androgen it can worsen acne and male-pattern hair loss, promote prostate growth, and cause virilization in women. Contrary to common belief it does not provide a demonstrated fertility benefit in controlled trials, and unlike aromatizing steroids it still suppresses the reproductive axis in a dose-dependent way at higher doses. Human data are old, small, and drawn from hypogonadal/infertility populations rather than performance users, so certainty is limited. Anyone using it should be under clinician supervision with periodic bloodwork.

Clinical readoutAAS · oral-dht
Hepatic strainLow
CardiovascularModerate
HPTA suppressionLow
Half-life
12 h
Route
Oral
Evidence
B
Active
Short
12 h24 h36 h2 d2.5 d
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ Formal human PK data are sparse; the parent compound is short-acting (commonly cited elimination half-life on the order of ~12 hours), consistent with clinical multiple-daily dosing. Treat this as approximate given the limited primary PK literature.
Pharmacology

Mechanism of action

Mesterolone is 1-alpha-methyl-5-alpha-dihydrotestosterone, a synthetic androgen receptor (AR) agonist. The 1-methyl substitution confers oral activity (it is not 17-alpha-alkylated). Because it is already 5-alpha-reduced (a DHT analogue), it cannot be aromatized to estrogen, so it produces no estrogenic effects. In receptor-binding studies it binds the AR in skeletal muscle and prostate relatively weakly compared with reference anabolic steroids, but binds SHBG with high affinity (roughly 4x that of DHT), which is the basis for its clinical use as an androgen and its purported ability to displace testosterone/estradiol from SHBG and raise free androgen fraction. Its anabolic (myotrophic) potency is weak relative to its androgenic activity.
Kinetics

Pharmacokinetics

Half-life

Formal human PK data are sparse; the parent compound is short-acting (commonly cited elimination half-life on the order of ~12 hours), consistent with clinical multiple-daily dosing. Treat this as approximate given the limited primary PK literature.

Active duration

Short; clinically administered 1-3 times daily (e.g., 25-100 mg/day divided), reflecting a short active window.

Route

Oral (tablet).

Metabolism & clearance

Hepatic metabolism to 1-methyl-androstane metabolites; excreted in urine as sulfate and glucuronide conjugates. Urinary metabolites (e.g., 1-alpha-methyl-5-alpha-androstan-3-one-17-sulfate) are detectable up to ~9 days after a single oral dose, which is relevant for washout/monitoring timelines, not for evading testing.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • Acts as an androgen: improved some sexual (libido, erections) and mental-state parameters in hypogonadal men, but significantly less effectively than oral testosterone undecanoate in a double-blind RCT.
  • Weak anabolic effect: minimal effect on bone mineral density in hypogonadal men (+0.8% vs larger gains with testosterone esters) in a randomized trial.
  • Does not aromatize; produces no estrogenic activity.
  • Binds SHBG with high affinity (~4x DHT), the pharmacologic basis for its use to affect free androgen fraction.
  • No demonstrated fertility benefit: a Cochrane systematic review found androgens including mesterolone did not improve sperm parameters or pregnancy rates in idiopathic oligo/asthenospermia.
  • Preclinical (avian/rodent) studies show androgen-driven skeletal muscle hypertrophy and satellite-cell proliferation, but these do not establish meaningful anabolic efficacy in humans.
Safety

Adverse effects by system

Cardiovascular

Documented adverse lipid changes in humans: in a randomized trial of hypogonadal men, mesterolone 100 mg/day raised total cholesterol ~19%, LDL-C ~46%, and triglycerides ~46%, and lowered HDL-C ~35% - an atherogenic profile. This is the best-documented harm.

Hepatic

No adequate human hepatotoxicity data specific to mesterolone. Unlike classic oral 17-alpha-alkylated steroids, mesterolone is 1-methylated (not 17-alkylated), so the structural feature most associated with cholestatic/oral steroid liver injury is absent; clinically significant hepatotoxicity has not been characterized. State explicitly: evidence is essentially absent, not reassuring proof of safety.

Endocrine / HPTA

Dose-dependent suppression of the hypothalamic-pituitary-gonadal axis. At low doses (25 mg/day) it did not change FSH, LH, or testosterone in one study; at higher/androgenic exposures endogenous testosterone can fall, though production recovered after discontinuation in a Klinefelter cohort. Because it does not aromatize, estrogen-mediated feedback is absent, but androgenic negative feedback still occurs.

Reproductive

No fertility benefit demonstrated (Cochrane review). As a DHT-type androgen it promotes prostate growth and, at suppressive doses, can impair spermatogenesis via HPTA suppression. In women it causes virilization; contraindicated in pregnancy due to fetal virilization risk.

Neuropsychiatric

Limited data: mesterolone improved mental-state scores in hypogonadal men (less than testosterone undecanoate). No mesterolone-specific data on mood destabilization, aggression, or dependence; neuropsychiatric risks described for the broader anabolic-androgenic steroid class cannot be excluded and are not adequately studied for this compound.

Renal

No adequate human data specific to mesterolone. No characterized direct renal toxicity; state explicitly that renal safety data are lacking.

Hematologic

No mesterolone-specific human data. Androgens as a class can stimulate erythropoiesis and raise hematocrit; this cannot be excluded for mesterolone but has not been specifically quantified - state that direct data are lacking.

Dermatologic

Androgenic dermatologic effects expected as a DHT derivative: acne and acceleration of male-pattern (androgenetic) hair loss. Skin reactions/exanthema were reported among adverse effects in androgen infertility trials.

Recovery

HPTA suppression & recovery

Suppression: Dose-dependent: minimal at low doses, meaningful at higher androgenic doses

Low-dose mesterolone (25 mg/day) did not measurably change LH/FSH/testosterone in one study, and endogenous testosterone production recovered after discontinuation in a Klinefelter cohort, suggesting suppression is often reversible. However, data are old and small, and higher or stacked exposures can suppress the axis. This is not a substitute for endocrine evaluation. Any recovery concern should be managed by an endocrinologist with formal testing (LH, FSH, total/free testosterone). If restart of endogenous function is a goal, that must be individualized by a clinician; a single-SERM approach, if any pharmacologic support is considered, should only be undertaken under medical supervision - do not self-direct axis-recovery protocols.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Fasting lipid panel (total cholesterol, LDL-C, HDL-C, triglycerides)Complete blood count / hematocrit and hemoglobinTotal and free testosterone, LH, FSH (to assess axis)Liver function tests (AST, ALT, bilirubin) as general androgen due-diligence despite non-17aa structurePSA and prostate assessment in men over ~40 or with prostate riskBlood pressure

Cadence: Baseline before use, an early recheck (about 6-12 weeks), then every 6-12 months while continuing; sooner if abnormal or symptomatic.

Warning signs — seek care
  • Chest pain, shortness of breath, or exertional symptoms (cardiovascular)
  • New or worsening urinary hesitancy/retention or a rising PSA
  • Jaundice, dark urine, right-upper-quadrant pain (seek care promptly even though hepatotoxicity is not established)
  • Marked mood change, aggression, or depressive symptoms
  • Signs of high hematocrit (headache, flushing, visual changes)
  • In women: voice deepening, hirsutism, clitoral enlargement (largely irreversible - stop and seek care)
Do not use if

Contraindications

  • Known or suspected prostate carcinoma (androgen-dependent).
  • Male breast carcinoma.
  • Pregnancy and women who may become pregnant (fetal virilization).
  • Pre-existing dyslipidemia or established atherosclerotic cardiovascular disease (given documented adverse lipid effects) - use only with specialist oversight.
  • Untreated significant benign prostatic hyperplasia / urinary obstruction.
  • Polycythemia / elevated hematocrit (relative, given androgen class erythropoietic effect).
  • Hypersensitivity to the drug.
Combinations

Interaction profile

  • MajorWith another anabolic steroid: Additive cardiovascular strain
  • MajorWith a thermogenic stimulant: Additive cardiovascular strain
  • ModerateWith thyroid hormone: Additive cardiovascular strain
  • ModerateWith growth hormone: Additive cardiovascular strain
  • MajorWith another anabolic steroid: Blood / clotting
  • MajorWith a clot-promoting SERM: Blood / clotting
  • ModerateWith an aromatase inhibitor: Hormonal
  • ModerateWith an anabolic steroid: Hormonal
  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • Do not use without clinician oversight and baseline plus periodic bloodwork (lipids, CBC/hematocrit, testosterone/LH/FSH, LFTs, PSA where age-appropriate).
  • The best-documented harm is an atherogenic lipid shift (large HDL fall, LDL/triglyceride rise); if you use it, monitor lipids and stop if they deteriorate, especially with any cardiovascular risk factors.
  • Do not use it as a fertility aid - controlled evidence shows no benefit for sperm parameters or pregnancy.
  • Recognize it still suppresses the reproductive axis at higher doses; do not assume it is 'axis-safe' just because it does not aromatize.
  • Stop and seek medical care for chest pain, jaundice/dark urine, marked mood change, urinary obstruction or rising PSA, or (in women) any signs of virilization.
  • Any concerns about hormonal recovery after stopping should be evaluated by an endocrinologist with formal testing - do not self-manage recovery protocols.
  • Women: virilizing effects (voice deepening, clitoral enlargement, hirsutism) can be permanent; discontinue at the earliest signs.
  • Human evidence is old, small, and from patient populations, not performance users - the true risk profile at higher self-administered doses is not well characterized.
Evidence

Citations (11)

Every clinical claim above is tied to a primary source. Overall evidence grade B — graded to the best available evidence for its core claims.

  1. 01

    Mesterolone is 1-alpha-methyl-5-alpha-dihydrotestosterone; binds SHBG with ~4x the affinity of DHT and binds skeletal muscle/prostate androgen receptor relatively weakly versus reference anabolic steroids (mechanism, weak anabolic vs androgenic).

    PreclinicalRelative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin.PMID 6539197 ↗

  2. 02

    In hypogonadal men, mesterolone 100 mg/day produced an atherogenic lipid shift: total cholesterol +~18.8%, LDL-C +~46.4%, triglycerides +~46.4%, HDL-C -~34.9%, without normalization on follow-up.

    RCTInfluence of various modes of androgen substitution on serum lipids and lipoproteins in hypogonadal men.DOI 10.1016/s0026-0495(99)90056-2 ↗

  3. 03

    Mesterolone raised LDL/VLDL and blunted exercise-induced HDL increases in a CETP transgenic mouse model (mechanistic support for adverse lipid effect).

    PreclinicalChronic Exercise Reduces CETP and Mesterolone Treatment Counteracts Exercise Benefits on Plasma Lipoproteins Profile: Studies in Transgenic Mice.DOI 10.1007/s11745-017-4299-1 ↗

  4. 04

    In a double-blind RCT, mesterolone improved sexual activity and mental state in hypogonadal men but significantly less than testosterone undecanoate.

    RCTDouble-blind group comparative study of testosterone undecanoate and mesterolone in hypogonadal male patients.DOI 10.1007/BF03348281 ↗

  5. 05

    Mesterolone produced only minimal bone mineral density change (+0.8%) in hypogonadal men versus larger gains with testosterone esters (weak anabolic effect).

    RCTOsteoporosis in male hypogonadism: responses to androgen substitution differ among men with primary and secondary hypogonadism.DOI 10.1159/000070823 ↗

  6. 06

    Androgens including mesterolone did not improve sperm parameters or pregnancy rates in idiopathic oligo/asthenospermia; adverse effects such as headaches and exanthema were reported.

    Meta-analysisAndrogens versus placebo or no treatment for idiopathic oligo/asthenospermia.DOI 10.1002/14651858.CD000150 ↗

  7. 07

    Low-dose mesterolone (25 mg/day) did not significantly change plasma FSH, LH, or testosterone, indicating predominantly peripheral action at low dose.

    CohortMesterolone treatment of patients with pathospermia.DOI 10.1007/BF02082034 ↗

  8. 08

    In Klinefelter patients, mesterolone did not severely impair endogenous testosterone production after discontinuation, supporting dose-dependent and often reversible axis effects.

    CohortTestosterone levels and gonadotrophins in Klinefelter's patients treated with injections of mesterolone cipionate.DOI 10.1007/BF00561132 ↗

  9. 09

    Urinary mesterolone metabolites (sulfate/glucuronide conjugates) are detectable up to ~9 days after a single oral dose (metabolism/washout).

    Case seriesNew potential biomarkers for mesterolone misuse in human urine by liquid chromatography quadrupole time-of-flight mass spectrometry.DOI 10.1002/jms.3508 ↗

  10. 10

    Mesterolone (marketed as Proviron) has been used clinically among testosterone-replacement options in men, with long-term observational follow-up.

    CohortEvolution of testosterone treatment over 25 years: symptom responses, endocrine profiles and cardiovascular changes.DOI 10.3109/13685538.2015.1048218 ↗

  11. 11

    Mesterolone induces androgen-mediated skeletal muscle hypertrophy and satellite-cell proliferation in avian models (preclinical anabolic mechanism; not proof of human efficacy).

    PreclinicalInfluence of mesterolone on satellite cell distribution and fiber morphology within maturing chicken pectoralis muscle.DOI 10.1002/ar.22439 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice