Injectables

Masteron (Drostanolone Propionate)

Drostanolone propionate, widely known as Masteron, is an injectable anabolic-androgenic steroid (AAS) derived from dihydrotestosterone (DHT). It is DHT with one added methyl group, attached to a short propionate ester. In the 1960s and 1970s it was studied and used as a hormonal treatment for advanced breast cancer in women, sold under names such as Drolban, Masteril and Masterid.

The most important fact is that it is no longer a marketed medicine in the US. FDA’s drug database lists a single US product, Lilly’s Drolban injection, as discontinued (Drugs@FDA). No published study has measured its effects on muscle, strength or body composition in people, and no formal human pharmacokinetic study of the injected ester has been published. Today it is used mostly outside medicine, and it is one of the steroids most often found in doping and drug-abuse testing.

This page summarizes what the FDA record, the old breast cancer trials, anti-doping research and regulators report. It is for education only and is not medical advice.

Property Detail
Drug class Anabolic-androgenic steroid; 2α-methyl derivative of DHT
Other names Dromostanolone propionate (US name); Drolban, Masteril, Masterid
US product Drolban (Lilly), 50 mg/mL injection, NDA 012936; marketing status “Discontinued”
Route Injection (Drolban was an injectable; excretion studies used intramuscular injection)
Former medical use Hormonal treatment of advanced breast cancer in women
Half-life No published human pharmacokinetic data for the propionate ester
Drostanolone content ≈84% of the ester’s weight (304.5 of 360.5 g/mol)
Aromatizes to estrogen Not expected (5α-reduced, DHT-type structure); human metabolites identified are androgens, not estrogens
US status Schedule III anabolic steroid, listed by name with its esters
WADA status Prohibited at all times (S1.1 anabolic androgenic steroids)

What it is

Drostanolone’s chemical name is 17β-hydroxy-2α-methyl-5α-androstan-3-one (21 CFR 1308.13). In plain terms, it is DHT with a methyl group added at carbon 2 of the A-ring. FDA’s preferred substance name is dromostanolone (NCI Thesaurus).

Form Formula Molecular weight Notes
Drostanolone (free steroid) C₂₀H₃₂O₂ 304.5 g/mol The active hormone
Drostanolone propionate C₂₃H₃₆O₃ 360.5 g/mol Short ester; ≈84% drostanolone by weight
Drostanolone enanthate C₂₇H₄₄O₃ 416.6 g/mol Longer ester; ≈73% drostanolone by weight

Formulas and weights from PubChem (drostanolone; propionate; enanthate).

The propionate ester has no hormonal activity of its own. Enzymes cleave it after injection to release free drostanolone. The ester only changes how fast the drug is released from the injection site. The enanthate version is covered on its own page: Masteron Enanthate.

Two related compounds are easy to confuse with it:

How it acts

Drostanolone acts on the androgen receptor. Like DHT, it already has a saturated (5α-reduced) A-ring, so it does not need conversion by 5α-reductase to become a stronger androgen. Its documented human metabolites are reduced androstane steroids, mainly 2α-methyl-androsterone, rather than estrogens (de Boer et al., 1992).

The NCI Thesaurus describes it as a DHT-related steroid with antiestrogenic effects that inhibits the growth of estrogen receptor-positive breast cancers. It adds that masculinizing side effects limit its clinical usefulness (NCI Thesaurus).

About “anti-estrogen” and anabolic:androgenic claims. Online sources often call Masteron an anti-estrogen that prevents gynecomastia, or quote a fixed anabolic:androgenic ratio for it. The antiestrogenic description comes from its use against breast cancer, not from any trial of gynecomastia prevention in men, and we found no such trial. A widely cited pharmacology review notes that gynecomastia can occur even with steroids that resist aromatization (Kicman, Br J Pharmacol 2008). Its table of rat-assay anabolic:androgenic indices does not include drostanolone, and we could not trace the quoted ratios to an original assay, so we do not repeat them.

Pharmacokinetics

No formal human pharmacokinetic study of injected drostanolone propionate has been published, so its absorption rate and half-life in people are unknown. What is known comes from metabolism and anti-doping excretion studies:

Study Finding
Human urine after use (de Boer et al., 1992) Main metabolite 2α-methyl-androsterone; parent drug and 3α,17β-diol metabolites also found; all conjugated to glucuronic acid
Human liver cells in culture (Gauthier et al., 2009) 3α-reduced (major) and 3β-reduced metabolites, plus hydroxylated forms; the same metabolites appeared in a volunteer’s urine
One male volunteer, IM injection (Liu et al., Steroids 2016) 11 urinary metabolites; two new markers detectable for up to 24 days
Two excretion studies (Albertsdóttir et al., Drug Test Anal 2020) Main glucuronide metabolite detectable for up to 29 days; a sulfate metabolite for up to 24 days

These are detection windows for sensitive anti-doping tests, not elimination half-lives. Being able to find a trace metabolite weeks later does not mean the drug is still active.

Former medical use

Drostanolone propionate was studied as a hormonal treatment for advanced (metastatic or inoperable) breast cancer from the early 1960s. A US cooperative group report on “2α-methyldihydrotestosterone propionate” in advanced breast cancer appeared in 1962 (Blackburn, Cancer Chemother Rep 1962).

In the US it was marketed by Lilly as Drolban, a 50 mg/mL injection. Drugs@FDA lists the product as discontinued (Drugs@FDA, NDA 012936). We could not find the original US label online, so the exact labeled indication wording and dose are not given here.

We did not find a primary source documenting when or why Drolban was discontinued.

What the research shows

Breast cancer trials

The comparative data in people come from breast cancer studies in women published between 1968 and 1982. Most are available only as short abstracts, and several were not in English:

Study Design Main finding
Gaertner et al., Johns Hopkins Med J 1968 Triple-blind study, 68 patients, dromostanolone and fluorometholone Results not available in the indexed abstract
Bennett et al., S Afr Med J 1975 Trial 1968–1972, three menopausal groups, each vs a standard treatment See table below
Rieche & Wolff, Arch Geschwulstforsch 1975 Randomized: testosterone decanoate vs drostanolone vs testolactone, then each plus cyclophosphamide Similar response rates for the hormones alone; adding cyclophosphamide raised responses from 22–25% to 46–55%, with drostanolone plus cyclophosphamide doing less well than the other two combinations
Wolff & Rieche, Onkologie 1978 Controlled trial, 91 patients: testolactone vs drostanolone vs nandrolone No difference between the three drugs; average remission 24% at 4 weeks and 46% at 16 weeks (after cyclophosphamide was added)
Clavel et al., Sem Hop 1982 Randomized, 98 postmenopausal women: tamoxifen plus drostanolone (n = 34) vs CMF chemotherapy (n = 30) vs both (n = 34) Hormonal therapy alone gave the best immediate responses and the fewest side effects

The South African trial reported these response rates (Bennett et al., 1975):

Patient group Drostanolone (Masteril) Comparator
Premenopausal 44% 22% (surgical removal of the ovaries)
Perimenopausal 34.5% 39% (nandrolone phenylpropionate)
Postmenopausal 38.5% 57% (ethinyl estradiol)

The authors judged its side effects to be generally mild in this setting, rarely a reason to stop treatment. Overall, drostanolone performed about as well as other androgens of its era, such as nandrolone and testolactone, against breast cancer. These trials measured tumor response, not muscle or body composition, and the abstracts do not report side-effect rates.

Other medical uses

The evidence outside breast cancer is very thin:

  • Anemia: two patients with acquired aplastic anemia who responded to oxymetholone had no blood-count response to dromostanolone (Azen & Shahidi, Am J Med 1977). A 1974 report described high blood triglycerides in hemodialysis patients given oral dromostanolone for anemia (Choi et al., Am J Clin Nutr 1974).
  • Animal tumor models: in rats with chemically induced mammary tumors, the propionate at 1.25–5 mg/kg/day for 4 weeks produced complete tumor remission in 15–48% of tumors, and more when combined with 5-fluorouracil (Teller et al., Cancer Res 1982). These are results in rats.

Muscle, strength and performance

No study has measured muscle mass, strength or athletic performance in people given drostanolone. Claims that it “hardens” the physique or suits pre-contest use come from user culture, not from published research.

Side effects and risks

Because there are no modern controlled trials, the true rates of side effects are unknown. The evidence comes from the old cancer literature, general knowledge of the AAS class, and case reports.

Virilization in women

Masculinizing (virilizing) effects were the main limit on its medical use in women (NCI Thesaurus). Across anabolic steroids, these effects include deepening of the voice, facial and body hair growth (hirsutism), clitoral enlargement and menstrual disruption. Voice changes and clitoral growth can be permanent (Kicman, 2008).

Effects shared with other anabolic steroids

No drostanolone-specific human data exist for most of these. The class risks listed in a major pharmacology review include (Kicman, 2008):

  • Hormone suppression and fertility: suppression of the body’s own testosterone production and testicular shrinkage; recovery of fertility can take months up to about a year after stopping.
  • Blood lipids and heart: higher LDL (“bad”) cholesterol, lower HDL (“good”) cholesterol, a higher hematocrit (the share of blood made up of red cells), and links to heart muscle damage and thrombotic events such as heart attack and stroke.
  • Skin and hair: acne, which can be severe, and acceleration of male-pattern hair loss.
  • Mood: irritability, aggression and, on withdrawal, depression.

Liver toxicity in this class is linked mainly to 17α-alkylated oral steroids. Drostanolone propionate is not 17α-alkylated (21 CFR 1308.13), but that does not mean its liver safety has been studied; it has not.

Dependence

In male hamsters, animals self-administered drostanolone directly into the brain about as readily as nandrolone, and more than the oral steroids oxymetholone and stanozolol (Ballard & Wood, Behav Neurosci 2005). These are results in hamsters, but they fit the broader concern that injectable AAS can be reinforcing.

Deaths and case reports

Drostanolone appears in forensic reports, almost always alongside other drugs. In one case, a young bodybuilder was found dead the day before a competition. His urine contained the main drostanolone metabolite (202 ng/mL) along with clenbuterol and a raised testosterone/epitestosterone ratio (11), and autopsy showed an enlarged heart (Favretto et al., Drug Test Anal 2022). Cases like this cannot show which drug, if any, caused death.

Product quality

With no marketed pharmaceutical product in the US, drostanolone used outside medicine comes from unregulated sources. Dose, sterility and identity are not controlled by any regulator.

In the US, drostanolone is listed by name as a Schedule III anabolic steroid, and the listing covers its salts, esters and ethers (21 CFR 1308.13).

Drostanolone is named in section S1.1 (anabolic androgenic steroids) of the World Anti-Doping Agency 2026 Prohibited List, in force from January 1, 2026, and is prohibited at all times (WADA; Tractatenblad 2026, 25).

Testing data show how widely it is used:

  • Anti-doping researchers describe it as one of the most frequently detected AAS in doping control (Liu et al., 2016).
  • In 21,172 samples tested at a Swedish drug-abuse laboratory from 2014 to 2023, the most common AAS detected were consistently testosterone, nandrolone and drostanolone (Bohlin et al., Drug Test Anal 2025).
  • In doping controls of competing bodybuilders in Flanders, drostanolone was among the injectable steroids in use from 1990 on (Delbeke et al., Int J Sports Med 1995).

Key takeaways

  • A methylated DHT with a short ester. Drostanolone is DHT with a 2α-methyl group; the propionate ester is about 84% drostanolone by weight and only sets the release rate.
  • A former breast cancer drug. It was used in the 1960s–1980s against advanced breast cancer, where it performed about as well as other androgens. The only US product, Lilly’s Drolban, is discontinued.
  • No human data on muscle or performance. No study has tested its effects on muscle, strength or body composition, and no human half-life has been published.
  • “Anti-estrogen” is not a proven benefit for men. That description comes from its anti-tumor use in breast cancer; no trial has tested it for preventing gynecomastia.
  • Class risks apply. Expect suppression of natural testosterone, unfavorable lipid changes and, in women, virilization that may be permanent.
  • Controlled and banned in sport. It is Schedule III in the US, prohibited at all times by WADA, and detectable in urine for weeks.

Sources

  1. Food and Drug Administration. Drugs@FDA: NDA 012936, Drolban (dromostanolone propionate) injection, 50 mg/mL, Lilly. Drugs@FDA.
  2. National Center for Biotechnology Information. Drostanolone, PubChem CID 6011; drostanolone propionate, CID 224004; drostanolone enanthate, CID 13014314; methasterone, CID 237186. PubChem (drostanolone); PubChem (propionate); PubChem (enanthate); PubChem (methasterone).
  3. National Cancer Institute. NCI Thesaurus: Dromostanolone Propionate (C1077) and Dromostanolone (C1076). NCI Thesaurus.
  4. Drug Enforcement Administration. 21 CFR 1308.13(f) Schedule III anabolic steroids. Electronic Code of Federal Regulations. eCFR.
  5. World Anti-Doping Agency. The 2026 Prohibited List, in force January 1, 2026. WADA; published text in Tractatenblad 2026, 25.
  6. Blackburn CM. Use of 2alpha-methyldihydrotestosterone propionate in treatment of advanced cancer of the breast: a group report. Cancer Chemother Rep. 1962;16:279–282. PubMed.
  7. Gaertner RA, Lewison EF, Finney GG Jr, Montague AC. Combined hormone therapy in advanced breast cancer. Triple-blind study of 68 patients treated with dromostanolone and fluorometholone. Johns Hopkins Med J. 1968;123(3):138–141. PubMed.
  8. Bennett MB, Helman P, Palmer P. Hormonal therapy of breast cancer with special reference to Masteril therapy. S Afr Med J. 1975;49(49):2036–2040. PubMed.
  9. Rieche K, Wolff G. Comparison of testosterone decanoate, drostanolone and testololactone in disseminated breast cancer–a randomized clinical study. Arch Geschwulstforsch. 1975;45(5):485–488. PubMed.
  10. Wolff G, Rieche K. Androgen therapy of incurable breast neoplasms. Controlled clinical study: nandrolone-testololactone-drostanolone [in German]. Onkologie. 1978;1(4):172–174. PubMed.
  11. Clavel B, Cappelaere JP, Guerin J, et al. Management of advanced breast cancer in post-menopausal women. A comparative trial of hormonal therapy, chemotherapy, and a combination of both [in French]. Sem Hop. 1982;58(34):1919–1923. PubMed.
  12. Azen EA, Shahidi NT. Androgen dependency in acquired aplastic anemia. Am J Med. 1977;63(2):320–324. PubMed.
  13. Choi ES, Chung T, Morrison RS, et al. Hypertriglyceridemia in hemodialysis patients during oral dromostanolone therapy for anemia. Am J Clin Nutr. 1974;27(9):901–904. PubMed.
  14. Teller MN, Stock CC, Bowie M, et al. Therapy of 7,12-dimethylbenz(a)anthracene-induced rat mammary carcinomas with combinations of 5-fluorouracil and 2 alpha-methyldihydrotestosterone propionate. Cancer Res. 1982;42(11):4408–4412. PubMed.
  15. de Boer D, de Jong EG, Maes RA, van Rossum JM. The methyl-5 alpha-dihydrotestosterones mesterolone and drostanolone; gas chromatographic/mass spectrometric characterization of the urinary metabolites. J Steroid Biochem Mol Biol. 1992;42(3-4):411–419. PubMed.
  16. Gauthier J, Goudreault D, Poirier D, Ayotte C. Identification of drostanolone and 17-methyldrostanolone metabolites produced by cryopreserved human hepatocytes. Steroids. 2009;74(3):306–314. PubMed.
  17. Liu Y, Lu J, Yang S, et al. New drostanolone metabolites in human urine by liquid chromatography time-of-flight tandem mass spectrometry and their application for doping control. Steroids. 2016;108:61–67. PubMed.
  18. Albertsdóttir AD, Van Gansbeke W, Coppieters G, et al. Searching for new long-term urinary metabolites of metenolone and drostanolone using gas chromatography-mass spectrometry with a focus on non-hydrolysed sulfates. Drug Test Anal. 2020;12(8):1041–1053. PubMed.
  19. Kicman AT. Pharmacology of anabolic steroids. Br J Pharmacol. 2008;154(3):502–521. PubMed; PMC.
  20. Ballard CL, Wood RI. Intracerebroventricular self-administration of commonly abused anabolic-androgenic steroids in male hamsters (Mesocricetus auratus): nandrolone, drostanolone, oxymetholone, and stanozolol. Behav Neurosci. 2005;119(3):752–758. PubMed.
  21. Favretto D, Stocchero G, Pertile R, et al. Post-mortem investigation into a death involving doping agents: the case of a body builder. Drug Test Anal. 2022;14(10):1795–1799. PubMed.
  22. Bohlin KP, Villén T, Hopcraft O, et al. Prevalence of AAS-positive samples at Drug Abuse Laboratory Sweden between 2014 and 2023 and sub-study of dual use of AAS and narcotics. Drug Test Anal. 2025;17(12):2421–2428. PubMed.
  23. Delbeke FT, Desmet N, Debackere M. The abuse of doping agents in competing body builders in Flanders (1988-1993). Int J Sports Med. 1995;16(1):66–70. PubMed.