History
Drostanolone was first described around 1959 and introduced for medical use circa 1961. As dromostanolone propionate it was an FDA-approved drug (US brand Drolban, by Eli Lilly; international brands including Masteril, Masteron, Masterid, Metormon, and Permastril), used as a palliative hormonal treatment for inoperable or metastatic breast cancer in (typically postmenopausal) women, working as an androgen with weak anti-estrogenic effect in breast tissue. With the arrival of tamoxifen and modern endocrine therapies it was rendered obsolete, was withdrawn, and is no longer marketed anywhere as a pharmaceutical (NCATS lists it as "US Previously Marketed"). There is no current FDA-approved human indication.
Drostanolone, almost always called by its brand name Masteron, is a lab-made anabolic-androgenic steroid (a synthetic version of a male sex hormone, built to grow muscle). It belongs to the dihydrotestosterone (DHT) family — DHT is a potent natural form of testosterone. It was once an FDA-approved treatment to ease symptoms in advanced breast cancer, but it is obsolete as a medicine today. It now survives only in the underground physique and performance market, where it’s sold on promises of “hardening” and “dryness” — even though no controlled human studies back up those effects. It is not a peptide and not a SARM, and it comes with the same risks as other androgens (male-hormone drugs).
What it is
Drostanolone (its other approved names are dromostanolone in the US and drostanolone internationally) is a man-made anabolic-androgenic steroid in the DHT family. Chemically, it is DHT with a small methyl group attached at one spot on the molecule (called the C2α position). That tweak makes it a bit stronger at building tissue and helps it survive longer in the body. It is given as an injection, not a pill. The classic version is drostanolone propionate (“Masteron”), and a longer-lasting form called the enanthate ester floats around the illegal market — though the published pharmaceutical literature only documents the propionate. An “ester” is just a chemical tail attached to the drug; the body snips it off to release the active steroid. The ester only changes how fast and how long the drug is released, not what the drug actually does.
One important point: drostanolone is not 17α-alkylated. 17α-alkylation is the chemical change that makes many oral steroids (like methyltestosterone, stanozolol, and methasterone) hard on the liver. Because drostanolone doesn’t have it, it isn’t the kind of steroid that’s classically toxic to the liver — but that same fact is also why it doesn’t work well as a pill.
How does it work? It mainly switches on the androgen receptor (AR), the cellular “docking station” for male hormones. Once it binds there, it sets off a chain of steps inside the cell that turn on androgen-responsive genes, which boosts protein building and helps muscle and other hormone-sensitive tissues hold onto nitrogen (a sign of muscle growth). Because it is already a 5α-reduced DHT-type molecule, it cannot be turned into estrogen by the enzyme aromatase — so the drug itself causes no estrogen effects — and it is also not acted on by the enzyme 5α-reductase. In animal tests (the Hershberger-type assay, a standard rodent screen), its anabolic-to-androgenic ratio is roughly 1:3 to 1:4 — meaning it’s relatively androgenic but only weakly muscle-building compared with reference standards. That said, these rodent numbers don’t translate neatly to what happens in human muscle. It also has weak anti-estrogen activity in breast tissue (the very property that once made it a breast-cancer drug), and it has essentially no progesterone-like activity.
The claims
Historically, the one legitimate medical use was to ease symptoms in advanced or inoperable metastatic breast cancer, usually in postmenopausal women. It worked through a mix of androgenic and weak anti-estrogen action in breast tissue.
In bodybuilding and physique circles, drostanolone is sold as a way to get a “harder,” “drier,” more defined look, plus a bit more strength — especially during contest prep or “cutting” phases (leaning out). As the next section explains, none of these physique or performance claims hold up in controlled human research.
What the evidence actually shows
Breast cancer is the only area with real clinical-trial data. Back when androgens were used against breast cancer, drugs like dromostanolone shrank tumors in a modest minority of patients — across the broader androgen literature, measurable responses generally ran about 15-20% in metastatic disease, with results tied somewhat to a patient’s hormone status. In the 1960s and 70s, before better drugs existed, this was genuinely useful for easing symptoms — but the response rates were low and it never cured anyone. The best-documented controlled human study to include dromostanolone propionate is the Cooperative Breast Cancer Group dose-response trial (Talley et al., Cancer 1973). One caveat: that paper has no abstract available online, so we cannot re-verify the exact per-drug shrinkage figures from it, and the ~15-20% range reflects the general androgen-for-breast-cancer literature rather than a confirmed number for this specific drug.
Lean mass, strength, and athletic performance in healthy people have no credible, controlled human trials at all. The claims of “hardening,” “dryness,” or extra strength are based on personal anecdotes, not clinical research. Whatever muscle-building effect the drug has is just the general androgen-receptor effect shared by all androgens, and on the measured scale drostanolone’s muscle-building potency is comparatively weak.
Bottom line on the evidence: the only real human data show partial, symptom-easing activity in hormone-responsive breast cancer. The physique and performance effects are unproven in the scientific literature.
Legal and regulatory status
In the United States, drostanolone is a Schedule III controlled substance under the Anabolic Steroid Control Act (which covers anabolic steroids as a group). It’s covered both by the law’s general definition of “anabolic steroid” and by being named specifically in the DEA’s Schedule III list at 21 CFR 1308.13(f), written out as “drostanolone (17β-hydroxy-2α-methyl-5α-androstan-3-one).” Possessing or selling it without a prescription is a federal crime. (For comparison, since they often come up alongside it: clenbuterol is not FDA-approved for human use and is not a scheduled controlled substance; human growth hormone is governed by its own law, 21 USC 333(e), rather than the controlled-substance schedules.)
In sport, drostanolone is banned at all times — both in and out of competition — as an outside-source anabolic androgenic steroid. It falls under WADA Class S1.1 (anabolic androgenic steroids) on the Prohibited List in force for 2026. The esters (those chemical tails) of banned anabolic agents are explicitly banned too, so both drostanolone propionate and enanthate are covered. (For comparison, clenbuterol is also in S1 — under S1.2, “other anabolic agents” — and human growth hormone falls under S2, peptide hormones.)
Safety
Even though it avoids the liver toxicity of 17α-alkylated oral steroids, drostanolone still carries the usual risks that come with androgens.
- Cardiovascular and lipids: Like other anabolic steroids, it lowers HDL (“good” cholesterol) and can raise LDL (“bad” cholesterol), pushing your blood-fat profile in a heart-unhealthy direction. Anabolic steroid use is linked to high blood pressure, harmful changes to the heart’s structure (a thickened, weaker-pumping left ventricle), and higher cardiovascular risk overall. Non-aromatizing DHT-type androgens like drostanolone tend to be especially rough on HDL and blood fats.
- Hepatotoxicity (liver harm): Low for this particular drug, because it isn’t 17α-alkylated and is injected rather than swallowed — this is its main relative-safety edge over oral steroids. That does not make it “liver-safe” in an absolute sense, but the classic bile-flow injury and blood-filled liver cysts (peliosis hepatis) seen with oral steroids aren’t typical of it.
- HPTA suppression and fertility: It shuts down the body’s own hormone control loop (the hypothalamic-pituitary-testicular axis, which manages testosterone production), lowering natural testosterone along with the signaling hormones LH and FSH and reducing sperm production. This leads to shrinking testicles and reduced fertility or infertility, which can linger for a while after stopping.
- Androgenic effects: As a strong DHT-type androgen, it’s known for speeding up male-pattern hair loss (androgenic alopecia), causing acne and oily skin, and it can worsen prostate enlargement.
- Virilization (in women): High risk of permanent masculinizing changes — a deeper voice, extra body and facial hair, an enlarged clitoris, and disrupted periods.
- Gynecomastia (breast tissue growth in men): The drug itself doesn’t convert to estrogen and won’t directly cause breast growth (it can even dampen estrogen effects in breast tissue) — but that gives no protection when it’s stacked with other steroids that do convert to estrogen.
- Blood and other effects: Anabolic steroids can thicken the blood by raising hematocrit (the share of the blood made up of red cells), which raises the risk of clots, and they’re linked to mood and aggression changes, disrupted sleep, and dependence. Because the product is now sold only on the black market, there are added dangers of wrong dosing and contamination.
Bottom line
Drostanolone is an obsolete medicine: a DHT-derived anabolic-androgenic steroid that once had a real but modest role in easing symptoms of advanced breast cancer, before better drugs made it unnecessary. Its modern reputation for “hardening” and “dryness” in physique and performance circles rests entirely on anecdote, with no controlled human evidence behind it. It is a Schedule III controlled substance with no current FDA-approved use, banned at all times in sport, and it carries the full set of androgen risks — heart and cholesterol harm, shutdown of natural hormone production and infertility, and strong androgenic and masculinizing effects — even though it sidesteps the liver toxicity of oral 17α-alkylated steroids.
Evidence grade: 8/10 · Good.
Sources
- Drostanolone — Wikipedia
- Drostanolone propionate — Wikipedia
- Dromostanolone propionate — NCATS Inxight Drugs (UNII X20UZ57G4O)
- Talley RW et al. 1973 — dose-response evaluation of androgens in metastatic breast cancer, Cancer (PMID 4579091)
- Marinov L et al. 1987 — drostanolone propionate (masteril) in disseminated breast cancer, Khirurgiia (Bulgarian; no abstract) (PMID 2830431)
- 21 CFR § 1308.13 (Schedule III, anabolic steroids) — Cornell Legal Information Institute
- DEA Drug Fact Sheet: Steroids
- WADA — The Prohibited List
- WADA — 2026 Prohibited List now in force (news)
- WADA — 2026 Prohibited List (resource)
Checking ClinicalTrials.gov…
- What is Drostanolone (Masteron)?
- A synthetic anabolic-androgenic steroid (AAS) of the dihydrotestosterone (DHT) family — 2α-methyl-DHT, given as injectable esters. Not a peptide, not a SARM.
- What is Drostanolone (Masteron) used for?
- Drostanolone (Masteron) is mainly studied for historically: palliative hormonal treatment of metastatic breast cancer. In fitness use: 'hardening,' 'dryness,' and strength — none of which have controlled human evidence.
- Is Drostanolone (Masteron) FDA-approved or legal?
- No current FDA-approved indication; DEA Schedule III controlled substance; prohibited at all times in sport (WADA S1.1).
- How strong is the evidence for Drostanolone (Masteron)?
- On the Codex Scale, Drostanolone (Masteron) grades 8/10 — Good. RCTs with consistent results — some scale, duration, or population limits.
- What else is Drostanolone (Masteron) called?
- Masteron; dromostanolone (USAN); drostanolone propionate; historic brands Drolban, Masteril, Masterid, Metormon, Permastril.
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