Masteron Propionate
Drostanolone Propionate
Masteron Propionate (drostanolone propionate) is the short-acting propionate ester of drostanolone, a synthetic injectable anabolic-androgenic steroid (AAS) derived from dihydrotestosterone (DHT; it is 2alpha-methyl-DHT propionate). It was originally marketed decades ago as an oncologic androgen (trade names Masteril, Masterid, Drolban) for advanced/metastatic breast cancer in women, and the only genuine human clinical trial data come from those old oncology studies, not from the cosmetic/performance context in which it is used today. As a DHT derivative it does not aromatize to estrogen and is not 17-alpha-alkylated, so it carries lower liver toxicity than oral steroids; it is used non-medically for a 'hard/dry' cosmetic look. The main risks are not compound-specific idiosyncrasies but the well-documented class harms of supraphysiologic androgen exposure: androgenic side effects and virilization (in the historical trials, virilization was the main dose-limiting toxicity), suppression of the body's own testosterone production (HPTA suppression) that can be slow or, rarely, incomplete to recover, adverse effects on cholesterol/lipids and cardiovascular remodeling, hair loss and acne, and potential prostate effects. There is no adequate modern human safety data for its use as a physique/performance drug; all systemic risk here is extrapolated from AAS-class literature. This is a reference summary, not medical advice or encouragement to use; anyone using or considering it should be under the care of a physician with baseline and ongoing bloodwork.
Mechanism of action
Pharmacokinetics
Short. The propionate ester confers a brief release/half-life on the order of ~1-3 days (propionate is the shortest common AAS ester); precise human pharmacokinetic parameters specific to drostanolone propionate are not well characterized in the modern literature. Parent drostanolone and its metabolites are detectable in urine/blood for longer (days) via conjugated metabolites.
Roughly 2-3 days of meaningful activity per injection, requiring frequent (e.g., every-other-day) dosing historically; this is stated for washout/monitoring purposes only, not to guide dosing.
Intramuscular injection (oil-based depot). Not orally active in this ester form.
Hepatic metabolism (reduction/hydroxylation) followed by phase II conjugation to glucuronides and sulfates that are renally excreted; drostanolone and its metabolites/conjugates are the targets of anti-doping urine and blood assays. Clearance is presented here for washout and clinical monitoring, not for evasion of testing.
For monitoring and washout planning, not drug-test evasion.
Physiological & performance effects
- Increased androgen-receptor signaling in muscle and skin (anabolic/androgenic effect)
- No estrogen conversion (does not aromatize), so no direct estrogenic effects such as gynecomastia from the drug itself
- Historically produced objective tumor regression in a subset of women with advanced/metastatic breast cancer when used as an oncologic androgen
- Cosmetic 'dry/hard' muscle appearance is the reason for non-medical use, but this is not supported by controlled human physique/performance trials
- Androgenic effects on hair follicles (scalp hair loss in predisposed individuals, increased body/facial hair) and sebaceous glands (acne)
Adverse effects by system
No drostanolone-propionate-specific human cardiovascular outcome data. As a class, supraphysiologic AAS use is associated with adverse lipid changes (notably lowered HDL), hypertension, left ventricular hypertrophy and dysfunction, accelerated atherosclerosis, cardiomyopathy, and increased risk of myocardial infarction and sudden cardiac death; some changes may persist after cessation. These risks are extrapolated to drostanolone from AAS-class evidence.
Lower hepatotoxic risk than oral 17-alpha-alkylated steroids because drostanolone propionate is injectable and not 17-alpha-alkylated. The historical breast-cancer literature did not flag it as notably hepatotoxic. There is no drostanolone-specific human evidence of serious liver injury; by contrast, 17-alpha-alkylated oral AAS (e.g., stanozolol) are associated with cholestatic injury and rare fatal hepatic necrosis. Liver risk is therefore rated low but not formally quantified for this compound.
Like all exogenous androgens, it suppresses the hypothalamic-pituitary-gonadal axis (reduced LH/FSH, endogenous testosterone and spermatogenesis). Recovery after stopping is variable and can be prolonged; rarely, hypogonadism may be incomplete/persistent. No drostanolone-specific recovery data exist; class data apply.
Suppressed spermatogenesis and fertility during use (class effect, variable recovery). In women, virilization was the principal dose-limiting adverse effect in the historical breast-cancer trials: deepening of the voice, hirsutism, clitoral enlargement and menstrual changes, some of which may be irreversible. Contraindicated in pregnancy (fetal virilization risk).
No drostanolone-specific psychiatric data. AAS class effects include idiosyncratic irritability, aggressiveness and hypomania during use and depressed mood during withdrawal, affecting a minority of users. Extrapolated to drostanolone.
No drostanolone-specific human renal data exist. AAS abuse has been associated with nephrotoxicity in the broader literature and is considered a possible class effect, though direct data for this compound are lacking.
No drostanolone-specific human hematologic data. Androgens as a class can stimulate erythropoiesis and raise hematocrit/hemoglobin (secondary polycythemia risk); extrapolated to drostanolone. Direct data lacking.
Androgenic dermatologic effects are expected: acne/oily skin and, in predisposed individuals, accelerated male-pattern scalp hair loss and increased body/facial hair. In women these androgenic skin/hair effects were reported in the historical clinical use.
HPTA suppression & recovery
Suppression: Expected to be significant during use, as with all exogenous androgens (dose- and duration-dependent suppression of LH/FSH, endogenous testosterone and spermatogenesis). No drostanolone-specific quantification exists.
Recovery of the HPTA after stopping is variable and can take months; in some individuals it is prolonged or, rarely, incomplete (persistent post-AAS hypogonadism has been described). Any post-cycle recovery or fertility strategy should be directed by an endocrinologist / andrologist with laboratory monitoring; where pharmacologic stimulation is considered, the literature describes single-agent options (e.g., a selective estrogen receptor modulator such as clomiphene, or hCG) but these must be individualized by a clinician. This resource does not provide a recovery protocol and does not endorse self-managed multi-drug regimens.
Monitoring
Cadence: Establish a full baseline before any use, recheck within the first weeks to months of exposure, and monitor periodically thereafter and during any recovery period; frequency should be set by the supervising clinician. Women should be monitored closely for early virilization signs.
- Chest pain, breathlessness, palpitations, syncope, or reduced exercise tolerance (possible cardiomyopathy/ischemia) - seek emergency care
- Signs of virilization in women (voice deepening, hirsutism, clitoral enlargement, menstrual change) - stop and see a clinician, as some changes may be permanent
- Jaundice, dark urine, right-upper-quadrant pain, or persistent nausea (liver injury)
- Severe headache, visual changes, or very high blood pressure
- Ruddy complexion, headaches or thrombotic symptoms suggesting high hematocrit
- Persistent low libido, erectile dysfunction, fatigue, or low mood after stopping (possible persistent hypogonadism/depression)
- Marked mood change, aggression, or suicidal thoughts
Contraindications
- Pregnancy and breastfeeding (androgens cause fetal virilization)
- Known or suspected prostate carcinoma or male breast carcinoma (androgen-sensitive)
- Women who wish to avoid virilization, and generally women outside a supervised medical setting
- Pre-existing cardiovascular disease, hypertension, dyslipidemia, or cardiomyopathy
- Pre-existing significant liver disease
- Polycythemia / elevated hematocrit
- Men seeking to preserve current fertility (suppresses spermatogenesis)
- Adolescents (risk of premature epiphyseal closure and endocrine disruption)
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.
Reducing harm & when to stop
- This is educational harm-reduction information, not medical advice and not encouragement to use; the safest option is not to use, and any use should be supervised by a physician.
- Get comprehensive baseline bloodwork (lipids/HDL, CBC/hematocrit, testosterone/LH/FSH, liver and kidney function, PSA in older men, blood pressure) before any exposure and monitor on an ongoing basis with a clinician.
- There is no adequate modern human safety data for drostanolone as a physique/performance drug; do not assume 'mild' means safe - systemic AAS harms (cardiac, lipid, endocrine) still apply.
- Women should understand that virilizing effects (voice deepening, clitoral enlargement, hirsutism) were the main dose-limiting toxicity historically and can be permanent; stop at the earliest signs and consult a clinician.
- Stop use and seek prompt medical care for chest pain, breathlessness, palpitations, syncope, jaundice, severe headache/very high blood pressure, or thrombotic symptoms.
- HPTA recovery after stopping is variable and sometimes prolonged; do not self-manage recovery - see an endocrinologist/andrologist. This resource does not provide dosing or multi-drug post-cycle protocols.
- Never use in pregnancy or if trying to conceive; androgens suppress fertility and can virilize a fetus.
- Injection carries infection/abscess and vascular risks; unsterile technique adds serious harm - another reason for medical supervision.
Citations (13)
Every clinical claim above is tied to a primary source. Overall evidence grade C — graded to the best available evidence for its core claims.
- 01
Drostanolone propionate (Masteril) was studied as an androgen therapy for breast cancer, with objective response in a subset of patients, and its side effects were generally not serious but included androgenic/virilizing effects.
RCTHormonal therapy of breast cancer with special reference to Masteril therapy.PMID 1242823 ↗
- 02
Drostanolone propionate (Masterid) was used clinically for metastatic breast carcinoma; virilism was an associated adverse effect.
Case series[The treatment of metastasising mammary carcinoma with drostanolone propionate (masterid)]PMID 4216810 ↗
- 03
Clinical experience with dromostanolone propionate in breast carcinoma documents its historical human medical use.
Case seriesClinical experience with dromostanolone propionate (NSC-12198) in breast carcinoma.PMID 5067664 ↗
- 04
Drostanolone (2alpha-methyldihydrotestosterone propionate) directly inhibits growth of human MCF-7 breast cancer cells, supporting an androgen-receptor-mediated antitumor mechanism (preclinical).
PreclinicalEffects of 5-fluorouracil and 2 alpha-methyldihydrotestosterone propionate on the growth of human breast carcinoma MCF-7 in vitro. (PMID 6688585)DOI 10.1016/0277-5379(83)90200-6 ↗
- 05
Drostanolone and its metabolites are metabolized to glucuronide and sulfate conjugates that are renally excreted and detectable in urine, informing metabolism/clearance and washout.
PreclinicalAnalysis of anabolic androgenic steroids as sulfate conjugates using high performance liquid chromatography coupled to tandem mass spectrometry. (PMID 26472592)DOI 10.1002/dta.1895 ↗
- 06
Drostanolone is among the commonly misused synthetic anabolic-androgenic steroids detectable in blood/urine by mass spectrometry, relevant to monitoring and clearance.
PreclinicalDetermination of anabolic steroids in dried blood using microsampling and gas chromatography-tandem mass spectrometry: Application to a testosterone gel administration study. (PMID 32822984)DOI 10.1016/j.chroma.2020.461445 ↗
- 07
Long-term supraphysiologic androgen (AAS) use produces cardiovascular toxicity (cardiomyopathy, atherosclerosis), and withdrawal after long-term use may produce prolonged and sometimes irreversible hypogonadism; psychiatric effects (irritability/aggression during use, depression on withdrawal) are idiosyncratic; hepatotoxicity and nephrotoxicity have been described.
ReviewPublic health impact of androgens. (PMID 29369918)DOI 10.1097/MED.0000000000000404 ↗
- 08
AAS use is associated with elevated blood pressure, adverse lipid profiles, accelerated atherosclerosis, cardiomyopathy, left ventricular hypertrophy/dysfunction, and increased risk of myocardial infarction and sudden cardiac death, with some changes persisting after cessation.
ReviewAnabolic-androgenic steroids among recreational athletes and cardiovascular risk. (PMID 40401476)DOI 10.1097/HCO.0000000000001235 ↗
- 09
Long-term AAS abuse can cause nonischemic cardiomyopathy/heart failure, illustrated by a bodybuilder with left ventricular thrombus and emboli who partially recovered after cessation.
Case reportFor the love of muscles: a bodybuilder with complicated left ventricular heart failure. (PMID 35972452)DOI 10.1080/00015385.2022.2080919 ↗
- 10
After stopping androgen abuse the HPG axis needs time to recover; endogenous testosterone often recovers within about 3 months but prolonged or persistent post-androgen-abuse hypogonadism occurs, and management should be clinician-directed.
ReviewClinical question: How to manage symptoms of hypogonadism in patients after androgen abuse? (PMID 35133022)DOI 10.1111/cen.14686 ↗
- 11
TRT and AAS suppress spermatogenesis; recovery after cessation is variable and depends on baseline function, duration of use and age, and may require clinician-directed hormonal stimulation.
ReviewUnderstanding and managing the suppression of spermatogenesis caused by testosterone replacement therapy (TRT) and anabolic-androgenic steroids (AAS). (PMID 35783920)DOI 10.1177/17562872221105017 ↗
- 12
Exogenous androgen administration suppresses gonadotropins causing hypogonadotropic hypogonadism and impaired spermatogenesis; recovery is variable and single-agent stimulation (clomiphene or hCG) may be used under specialist care.
Case series[Risk of Male Infertility Due to Testosterone Replacement Therapy for Late-Onset Hypogonadism (LOH)] (PMID 33271659)DOI 10.14989/ActaUrolJap_66_11_407 ↗
- 13
17-alpha-alkylated oral anabolic steroids (e.g., stanozolol) are associated with cholestatic liver injury and can cause fatal hepatic necrosis, contrasting with the lower hepatotoxic risk of injectable non-17-alpha-alkylated steroids like drostanolone.
Case reportFatal anabolic androgenic steroid overdose in an amateur bodybuilder: a clinical and autopsy report. (PMID 37948000)DOI 10.1007/s12024-023-00747-7 ↗
Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice