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DPreclinical / mechanistic only
CardiotoxicNeuropsychiatricHigh risk

Masteron Enanthate

Drostanolone Enanthate

Masteron Enanthate (drostanolone enanthate) is an injectable, DHT-derived anabolic-androgenic steroid (AAS) — the long-acting enanthate ester of drostanolone (2-alpha-methyl-dihydrotestosterone). Drostanolone was originally developed decades ago as an antineoplastic hormonal agent for advanced/metastatic breast cancer; it has no approved contemporary human indication and the enanthate ester in particular is used only non-medically in bodybuilding/physique settings. There are essentially no modern human safety, efficacy, or pharmacokinetic studies of drostanolone enanthate — most of what can be said is extrapolated from class-level AAS harm data and from forensic reports where the drug is detected in fatal steroid-abuse cases. Based on AAS-class data, the main risks include cardiovascular harm (reduced heart pumping/relaxation function and accelerated coronary plaque), atherogenic lipid changes, suppression of the body's own testosterone production (which can be slow or occasionally incomplete to recover), polycythemia (dangerously thick blood), and androgenic effects such as acne and accelerated male-pattern hair loss. Because it is a potent non-aromatizing androgen, it does not convert to estrogen, but this does not make it "safe." This monograph is risk-forward and educational only; anyone using or considering it should be under a physician's care with regular bloodwork.

Clinical readoutAAS · injectable-dht
Hepatic strainModerate
CardiovascularModerate
HPTA suppressionVery high
Half-life
5.5 d
Route
Intramuscular injection
Evidence
D
Active
Prolonged relative to s…
5.5 d11 d16.5 d3.1 wk3.9 wk
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ No published human pharmacokinetic study of drostanolone enanthate exists. The enanthate ester is a slow-release depot ester; by analogy to other enanthate-esterified injectable steroids its elimination half-life is on the order of several days (roughly ~4-7 days). Treat this as an uncertain estimate, not a measured value.
Pharmacology

Mechanism of action

Drostanolone is a synthetic derivative of dihydrotestosterone (DHT), structurally 2-alpha-methyl-DHT, that binds and activates the androgen receptor. As a 5-alpha-reduced (DHT-based) androgen it cannot be aromatized to estrogen, so it produces androgenic and anabolic signaling without direct estrogenic activity. Historically its antineoplastic use in breast cancer was attributed to androgen-receptor-mediated suppression of hormone-dependent tumor growth; in cell-culture work the parent compound inhibited growth of estrogen-responsive MCF-7 human breast cancer cells. As with all AAS, supraphysiologic androgen exposure feeds back on the hypothalamic-pituitary-gonadal (HPG) axis, suppressing LH and FSH and shutting down endogenous testosterone production. The enanthate ester is a pro-drug feature only: esterification at the 17-beta hydroxyl slows release from the intramuscular injection depot and is cleaved by esterases to liberate active drostanolone.
Kinetics

Pharmacokinetics

Half-life

No published human pharmacokinetic study of drostanolone enanthate exists. The enanthate ester is a slow-release depot ester; by analogy to other enanthate-esterified injectable steroids its elimination half-life is on the order of several days (roughly ~4-7 days). Treat this as an uncertain estimate, not a measured value.

Active duration

Prolonged relative to shorter esters (e.g., drostanolone propionate); clinically dosed at intervals of days to about weekly in non-medical use. No formal human duration-of-action data for the enanthate ester.

Route

Intramuscular injection (oil depot). Not orally active in this form.

Metabolism & clearance

Hepatic metabolism (reduction/oxidation of the steroid nucleus) with renal excretion of metabolites; being 5-alpha-reduced it is not aromatized to estrogen. Parent drostanolone and its esters are detectable in urine, hair, and nail matrices, with hair/nail windows of detection spanning months, relevant to washout reasoning and clinician discussion, not to evading testing. No compound-specific human clearance study is available.

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

Reported effects

Physiological & performance effects

  • Androgen-receptor activation producing anabolic (muscle/tissue) and androgenic effects
  • Non-aromatizing: does not raise estrogen directly (no direct estrogenic activity)
  • Historically produced measurable tumor responses when used as hormonal therapy for advanced breast cancer (drostanolone propionate)
  • Suppresses endogenous testosterone, LH and FSH via HPG-axis feedback
  • Commonly detected in real-world anabolic-steroid use, including fatal abuse cases
  • No credible evidence it is safer than other AAS; absence of human safety data is not evidence of safety
Safety

Adverse effects by system

Cardiovascular

Class-level human data on AAS show reduced left-ventricular systolic and diastolic function and accelerated, dose-related coronary atherosclerosis; anabolic-steroid-induced cardiomyopathy and fatal cardiovascular events are reported. No drostanolone-enanthate-specific cardiovascular study exists, but these class effects should be assumed to apply.

Hepatic

Lower direct hepatotoxic risk than oral 17-alpha-alkylated steroids because drostanolone enanthate is injectable and not 17-alpha-alkylated, bypassing the first-pass hepatic burden that drives cholestatic oral-AAS liver injury. A preclinical/in-vitro study found drostanolone can inhibit the human bile-acid enzyme AKR1D1, a mechanistic (not clinical) cholestasis signal. No human hepatotoxicity data specific to this drug.

Endocrine / HPTA

Suppresses the hypothalamic-pituitary-gonadal axis, lowering LH, FSH and endogenous testosterone. AAS-induced hypogonadism can persist after discontinuation and is occasionally slow or incomplete to recover.

Reproductive

Testicular atrophy, reduced sperm production and potential infertility, and suppressed endogenous testosterone via HPG-axis shutdown, documented for AAS as a class. In women, androgenic/virilizing and menstrual effects would be expected. No compound-specific human fertility data.

Neuropsychiatric

Class-level AAS data describe mood disturbance, irritability/aggression, hypomanic or depressive symptoms, dependence syndromes, and withdrawal-related depression (linked to hypogonadism). No drostanolone-specific psychiatric data.

Renal

No direct nephrotoxicity data for drostanolone. AAS abuse has been broadly associated with renal disease in forensic/fatal-abuse reports; any renal harm is plausibly secondary (e.g., to hypertension, polycythemia, rhabdomyolysis) rather than a documented direct effect.

Hematologic

Androgens stimulate erythropoiesis; AAS use is associated with polycythemia/erythrocytosis (e.g., a reported hematocrit of 56.9%), raising thrombosis, stroke and cardiovascular risk. No drostanolone-specific hematologic study, but this is a well-recognized androgen class effect.

Dermatologic

As a potent non-aromatizing DHT-derived androgen, expected to drive androgenic skin effects (acne and acceleration of male-pattern scalp hair loss) and, in women, virilization (voice deepening, hirsutism, clitoral enlargement). These are class/androgen-mechanism expectations; no drostanolone-enanthate-specific dermatologic human data.

Recovery

HPTA suppression & recovery

Suppression: Marked: expected strong suppression of endogenous testosterone, LH and FSH, as with other AAS

Recovery of the hypothalamic-pituitary-gonadal axis after stopping is variable: many recover over months, but AAS-induced hypogonadism can be prolonged or, in some reported cases, incomplete. Any recovery strategy must be individualized and directed by an endocrinologist, who may consider single-agent approaches (e.g., a SERM such as tamoxifen, or hCG) and appropriate monitoring. Dual-SERM protocols are out of scope and not endorsed here. This content is conservative and not a substitute for specialist care.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Complete blood count with hematocrit/hemoglobin (monitor for polycythemia)Fasting lipid panel (total, LDL, HDL, triglycerides)Total and free testosterone, LH, FSH (HPG-axis suppression/recovery)Liver function tests (AST, ALT, bilirubin, GGT)Renal function (creatinine, eGFR)Blood pressure at every assessmentEstradiol and PSA where clinically indicatedConsider echocardiography/cardiology evaluation with prolonged use or symptoms

Cadence: Baseline before any use, then periodically during use (e.g., every 8-12 weeks is commonly advised for high-risk parameters such as hematocrit, lipids and blood pressure), and after discontinuation to track HPG-axis recovery, all under a clinician's direction.

Warning signs — seek care
  • Chest pain, shortness of breath, palpitations, or exertional intolerance (seek emergency care)
  • Signs of stroke/clot: sudden weakness, facial droop, speech difficulty, leg swelling
  • Very high hematocrit or symptoms of hyperviscosity (headache, flushing, dizziness)
  • Marked blood-pressure elevation
  • Jaundice, dark urine, right-upper-quadrant pain, or unexplained fatigue (possible liver injury)
  • Persistent low mood, aggression, or suicidal thoughts
  • Testicular shrinkage, low libido, or infertility
  • In women: voice deepening, facial hair, clitoral enlargement (virilization, often irreversible)
Do not use if

Contraindications

  • Pre-existing cardiovascular disease, cardiomyopathy, heart failure, or significant coronary artery disease
  • Hypertension (uncontrolled or poorly controlled)
  • Polycythemia / elevated hematocrit or other thrombophilic/erythrocytosis states
  • Known or suspected prostate or breast cancer in men (hormone-sensitive malignancy risk)
  • Pregnancy and breastfeeding (androgenic/virilizing harm to the fetus); women generally, given virilization risk
  • Adolescents/those with open growth plates (premature epiphyseal closure)
  • Significant hepatic or renal impairment
  • History of AAS-induced mood disorder, aggression, or dependence
  • Any use without medical supervision and baseline/interval bloodwork
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

  • This is educational information only, not medical advice, and does not endorse use; these substances carry serious risks. Use, if it occurs, should be under a physician with regular bloodwork. 21+ only.
  • There is no adequate human safety or pharmacokinetic data specific to drostanolone enanthate. The lack of documented harm is not evidence of safety.
  • Obtain baseline labs (CBC/hematocrit, lipids, liver and kidney function, testosterone/LH/FSH, blood pressure) before any use and monitor periodically thereafter.
  • Polycythemia is a concrete, measurable danger: rising hematocrit sharply increases clot, stroke and heart-attack risk; have it checked and stop and seek care if it is high.
  • Stop and seek medical care immediately for chest pain, breathlessness, palpitations, stroke symptoms, jaundice, or severe mood changes/suicidal thoughts.
  • Do not combine with other AAS or stimulants to 'push results'; polypharmacy compounds cardiovascular and psychiatric risk.
  • HPG-axis recovery is variable and can be prolonged; any recovery plan should be directed by an endocrinologist. Only single-agent approaches are discussed here; dual-SERM protocols are out of scope.
  • Women face a high risk of irreversible virilization (voice deepening, facial hair, clitoral enlargement); pregnant or breastfeeding individuals must not use it.
  • This monograph does not provide sourcing, dosing-to-maximize, or acquisition guidance of any kind.
Evidence

Citations (12)

Every clinical claim above is tied to a primary source. Overall evidence grade D — this compound lacks adequate human data; claims rest on preclinical or mechanistic evidence.

  1. 01

    Drostanolone (as the propionate ester) was used clinically as hormonal therapy for advanced/postmenopausal breast cancer in a randomized trial, establishing historical human antineoplastic use.

    RCT[Management of advanced breast cancer in post-menopausal women. A comparative trial of hormonal therapy, chemotherapy, and a combination of both].PMID 6293073 ↗

  2. 02

    Drostanolone propionate was administered to women with disseminated breast cancer as an antineoplastic hormonal agent (historical clinical use).

    Case series[Drostanolone propionate (masteril) in disseminated breast cancer in women. Immediate results].PMID 2830431 ↗

  3. 03

    Drostanolone (2-alpha-methyl-DHT propionate) inhibits growth of estrogen-responsive MCF-7 human breast cancer cells in vitro, supporting an androgen-receptor/antitumor mechanism.

    PreclinicalEffects of 5-fluorouracil and 2 alpha-methyldihydrotestosterone propionate on the growth of human breast carcinoma MCF-7 in vitro.PMID 6688585 ↗

  4. 04

    Drostanolone can competitively inhibit the human bile-acid-synthesizing enzyme AKR1D1 in vitro, a mechanistic cholestasis signal (not clinical hepatotoxicity).

    PreclinicalAssessment of the inhibitory potential of anabolic steroids towards human AKR1D1 by computational methods and in vitro evaluation.PMID 37451653 ↗

  5. 05

    Drostanolone and drostanolone enanthate are detected in real-world anabolic-steroid use, including a fatal abuse case, where long-term AAS abuse is described as causing cardiac, hepatic and renal disease; drug is detectable in hair over long windows (washout relevance).

    Case reportThe Power of Keratinous Matrices (Head Hair, Body Hair and Nail Clippings) Analysis in a Case of Death Involving Anabolic Agents.PMID 36516229 ↗

  6. 06

    Drostanolone is detectable in nail clippings with detection windows of several months, relevant to washout/monitoring reasoning.

    Case seriesTesting for anabolic steroids in human nail clippings.PMID 33885144 ↗

  7. 07

    Drostanolone is among the most commonly detected anabolic-androgenic steroids in routine drug-abuse laboratory testing.

    CohortPrevalence of AAS-Positive Samples at Drug Abuse Laboratory Sweden Between 2014 and 2023 and Sub-Study of Dual Use of AAS and Narcotics.PMID 40992881 ↗

  8. 08

    Long-term AAS use in men is associated with reduced left-ventricular systolic and diastolic function and greater, dose-dependent coronary atherosclerotic plaque compared with non-users.

    CohortCardiovascular Toxicity of Illicit Anabolic-Androgenic Steroid UsePMID 28533317 ↗

  9. 09

    Long-term AAS abuse is linked to cardiovascular toxicity (cardiomyopathy, atherosclerosis), hypogonadism, liver injury, and neuropsychiatric/dependence effects; hepatotoxicity is chiefly associated with oral 17-alpha-alkylated steroids.

    ReviewLong-term psychiatric and medical consequences of anabolic-androgenic steroid abuse: a looming public health concern?PMID 18599224 ↗

  10. 10

    AAS suppress the hypothalamic-pituitary-gonadal axis causing hypogonadism during withdrawal; endocrine reactivation may involve single agents such as hCG or clomiphene, and dependence involves muscle dysmorphia and hedonic mechanisms.

    ReviewTreatment of anabolic-androgenic steroid dependence: Emerging evidence and its implications.PMID 20188494 ↗

  11. 11

    AAS abuse can cause hypogonadotropic hypogonadism with testicular atrophy and suppressed LH/FSH that is sometimes slow or not fully reversible after cessation.

    Case report[Case of androgenic anabolic steroid abuse caused hypogonadotropic hypogonadism].PMID 19068689 ↗

  12. 12

    Non-medical androgen use is associated with anabolic-steroid-induced cardiomyopathy, progressive polycythemia (hematocrit 56.9%), testicular atrophy, suppressed LH/FSH and hypogonadism; managed with endocrinologist-directed care and, despite abstinence, a fatal cardiovascular event occurred.

    Case reportHarm reduction measures in a recreational gym user with anabolic androgenic steroid dependence: a case report in the context of current best clinical practice.PMID 40841640 ↗

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