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 With the arrival of tamoxifen and modern endocrine therapies it was rendered obsolete, was withdrawn, and is no longer marketed anywhere as a pharmaceutical (NCATS lists it as "US Previously Marketed").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 known by the brand name Masteron, is a synthetic anabolic-androgenic steroid (AAS) of the dihydrotestosterone (DHT) family. It was once an FDA-approved palliative treatment for metastatic breast cancer but is now obsolete as a medicine, surviving only in the underground physique/performance market — where it is promoted for “hardening” and “dryness” despite a complete absence of controlled human evidence for those effects. It is not a peptide and not a SARM, and it carries the standard androgen-class harms.

What it is

Drostanolone (USAN: dromostanolone; INN/BAN: drostanolone) is a synthetic anabolic-androgenic steroid in the DHT family. Structurally it is 2α-methyl-5α-dihydrotestosterone (17β-hydroxy-2α-methyl-5α-androstan-3-one) — DHT with a methyl group added at the C2α position, which improves anabolic potency and metabolic stability. It is administered as injectable esters rather than as an oral; the classic ester is drostanolone propionate (“Masteron”), and a longer-acting enanthate ester circulates in the illicit market, though the pharmaceutical literature documents only the propionate. The ester is cleaved in the body to release free drostanolone and changes only release/duration, not the active molecule.

Importantly, drostanolone is not 17α-alkylated. 17α-alkylation is the modification responsible for liver toxicity in oral steroids such as methyltestosterone, stanozolol, and methasterone. Because drostanolone lacks it, the compound is not classically hepatotoxic — and is also not an effective oral.

Mechanistically, it acts primarily as an agonist of the androgen receptor (AR): it binds the receptor and drives nuclear translocation, dimerization, coactivator recruitment, and transcription of androgen-responsive genes, promoting protein synthesis and nitrogen retention in muscle and other androgen-sensitive tissues. As a 5α-reduced DHT derivative, it is not a substrate for aromatase and cannot be converted to estrogen (no estrogenic effect from the drug itself), and it is not a substrate for 5α-reductase. Its reported anabolic-to-androgenic ratio is roughly 1:3 to 1:4 in animal (Hershberger-type) assays — i.e., relatively androgenic and weakly anabolic versus reference standards, though these rodent-derived ratios do not map cleanly onto human muscle outcomes. It also has weak anti-estrogenic activity in breast tissue (the property that once made it a breast-cancer drug) and is essentially non-progestogenic.

The claims

Historically, the only legitimate medical claim was palliative hormonal treatment of inoperable or metastatic breast cancer in (typically postmenopausal) women, exploiting its androgenic plus weak anti-estrogenic action in breast tissue.

In bodybuilding and physique circles, drostanolone is promoted for cosmetic “hardening,” “dryness,” and a more defined look, plus strength gains, particularly during contest preparation or “cutting” phases. As detailed below, none of these physique/performance claims are supported by controlled human research.

What the evidence actually shows

Breast cancer is the only real clinical-trial setting. In the androgen-for-breast-cancer era, androgens including dromostanolone produced modest, minority tumor-regression rates — objective responses generally on the order of roughly 15-20% in metastatic disease across the broader androgen literature, with response correlating to a degree with hormone status. This was clinically meaningful palliation in the 1960s-70s before better agents existed, but response rates were low and effects were not curative. The Cooperative Breast Cancer Group dose-response trial (Talley et al., Cancer 1973) is the best-documented controlled human evaluation to include dromostanolone propionate; note that this paper has no online abstract, so the specific per-drug regression figures cannot be re-verified from the abstract, and the ~15-20% range reflects the general androgen-for-breast-cancer literature rather than a verifiable per-drug result.

Lean mass, strength, and athletic performance in healthy people have no credible, controlled human trials. Claims of “hardening,” “dryness,” or strength gains are anecdotal and non-evidence-based, not derived from clinical research. Whatever anabolic effect exists is a general AR-agonist effect shared by androgens, and drostanolone’s measured anabolic potency is comparatively weak.

Bottom line on evidence: real human data exist only for partial palliative activity in hormone-responsive breast cancer; 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 (anabolic steroids as a class). It is captured both by the statutory definition of “anabolic steroid” and is enumerated by name among the Schedule III anabolic steroids in the DEA schedules at 21 CFR 1308.13(f), listed verbatim as “drostanolone (17β-hydroxy-2α-methyl-5α-androstan-3-one).” Non-prescription possession or distribution 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 statute, 21 USC 333(e), rather than the CSA schedules.)

In sport, drostanolone is prohibited at all times (in- and out-of-competition) as an exogenous anabolic androgenic steroid under WADA Class S1.1 (anabolic androgenic steroids) on the Prohibited List in force for 2026. Esters of prohibited anabolic agents are explicitly prohibited, so drostanolone propionate and enanthate are covered. (For comparison, clenbuterol is also S1 — under S1.2, “other anabolic agents” — and human growth hormone falls under S2, peptide hormones.)

Safety

Even though it lacks the hepatotoxicity of 17α-alkylated oral steroids, drostanolone carries the standard androgen-class harms.

Cardiovascular and lipids: Like other AAS, it suppresses HDL-C and can raise LDL-C, worsening atherogenic lipid profiles. AAS use is associated with hypertension, adverse cardiac remodeling (left-ventricular hypertrophy, impaired function), and increased cardiovascular risk. Non-aromatizing DHT-derived androgens like drostanolone tend to be especially harsh on HDL and lipids.
Hepatotoxicity: Low for this compound specifically, because it is not 17α-alkylated and is injected — this is its main relative-safety distinction from oral AAS. It is not “liver-safe” in an absolute sense, but classic cholestatic injury and peliosis hepatis are not characteristic.
HPTA suppression and fertility: It suppresses the hypothalamic-pituitary-testicular axis, lowering endogenous testosterone, LH and FSH, and spermatogenesis, leading to testicular atrophy and impaired fertility or infertility, which can be prolonged after discontinuation.
Androgenic effects: As a potent DHT-type androgen, it is notable for androgenic alopecia (accelerated male-pattern hair loss), acne, and oily skin, and it can aggravate benign prostatic effects.
Virilization (women): High risk of irreversible virilization — voice deepening, hirsutism, clitoral enlargement, and menstrual disruption.
Gynecomastia: The drug itself does not aromatize and will not directly cause gynecomastia (it can even blunt estrogenic effects in breast tissue), but this offers no protection when it is used alongside aromatizing androgens.
Hematologic and other: AAS can raise hematocrit (erythrocytosis), increasing thrombotic risk, and are associated with mood and aggression changes, sleep disturbance, and dependence. Because the product is now exclusively underground, there are added risks of dosing inaccuracy and contamination.

Bottom line

Drostanolone is an obsolete medicine: a DHT-derived anabolic-androgenic steroid that once had a genuine but modest palliative role in metastatic breast cancer and was then made redundant by better drugs. Its modern physique and performance reputation for “hardening” and “dryness” 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 androgen-class risk profile — cardiovascular and lipid harm, HPTA suppression and infertility, strong androgenic and virilizing effects — even though it avoids the liver toxicity of oral 17α-alkylated steroids.

Evidence grade: Preliminary human.

Drostanolone (Masteron)