Drostanolone (Masteron)
A breast-cancer drug from 1960s oncology wards, resurrected as a cutting-season favorite. It has three real randomized trials — in metastatic breast cancer — and essentially no modern human pharmacology. The compound nobody measured.
The short version
- The only clinical human dose: 100 mg IM three times weekly = 300 mg/week propionate, run double-blind against testosterone propionate at identical mg. DATA
- Head-to-head vs testosterone: 26% vs 22% tumor response, with less virilization — the entire documented efficacy case. DATA
- No measured Kd / Ki / IC50 exists for drostanolone at any steroid receptor. The famous “62:25 anabolic:androgenic ratio” is unverifiable. DATA (an absence, verified by search)
- Its anti-estrogenic reputation comes from breast-tumor experiments — redundant in anyone already controlling estradiol. MODEL
What it was, before it was a cutting drug
Drostanolone propionate (Drolban/Masteril) was an oncology agent for inoperable metastatic breast cancer in women — the same therapeutic niche as testosterone propionate, which is exactly how it was tested:
| Trial | Design | Drostanolone arm | Comparator |
|---|---|---|---|
| Gordan 1963, double-blind | alternating-patient crossover vs TP at identical mg | 300 mg/wk — 26% objective response | testosterone propionate 300 mg/wk — 22%, more virilization |
| Blackburn 1964 extension | same protocol, more patients | ~26% | ~25% — response parity confirmed |
| Wolff 1978, RCT n=91 | added to cyclophosphamide + fluorouracil | remission 46% | 24% without drostanolone |
| Rieche 1975, RCT | added to cyclophosphamide | 46–55% | 22–25% without |
| Clavel 1982, RCT n=98 | endocrine combination arm | tamoxifen + drostanolone: best responses, fewest side effects | vs cyclophosphamide-based chemo |
PMID 13949172 · Gordan 1963
PMID 5536155 · Heney 1970
PMID 362297 · Wolff 1978
PMID 1243528 · Rieche 1975
PMID 6293073 · Clavel 1982
Longest documented exposure: one case of 100 mg/week for 17 months in a woman with zero masculinization (Heney 1970) — a virilization data point, not a safety trial.
Receptor pharmacology: the void
No binding constant has ever been published DATA
The classic steroid-RB panels (Saartok 1984, which assayed 42 steroids) simply do not include drostanolone. Kicman 2008 lists only rodent myotrophic:androgenic quotients of roughly 1:3–1:4 (from Potts 1976). No Ki, no Kd, no IC50, at AR or anywhere else, in any species.
“62:25 anabolic:androgenic ratio” CLAIM
Repeated in every forum profile. Source: not found — no archived primary paper contains it. The only quotable number is the 1:3–1:4 rodent quotient above, which says drostanolone was less myotrophic per unit androgenic effect than testosterone in rats.
Detection: 24–29 days after a single 100 mg dose DATA
The best modern human data drostanolone has — doping-control excretion studies. Detection window 24–29 d; long-term metabolites characterized for LC-MS screening. It remains a top-3 most-detected steroid in Scandinavian doping samples.
The anti-estrogen story
Real anti-estrogenic activity — measured in breast cancer models DATA
Drostanolone inhibited estradiol-stimulated MCF-7 breast-cancer cell growth by 16–94% depending on line, and induced remissions in DMBA-induced rat mammary tumors. That is where “Masteron is anti-estrogenic” comes from — tumor and rodent data, in women with breast cancer.
Which makes it redundant under an AI or low estradiol MODEL
Premise (data): the anti-estrogen effect is competition at estrogen-responsive tissue. Premise: it is not an aromatase inhibitor (DHT-family structure — no substrate). Logic: its “hardening” benefit can only matter when estradiol signaling is present to oppose. Prediction: in someone whose E2 is already suppressed, drostanolone contributes androgens, not anti-estrogenism. Reject the premise, reject the conclusion.
Hair — the one thing its structure does tell you
Pre-reduced: finasteride cannot touch it DATA
Drostanolone is already 5α-reduced (DHT-family). Finasteride blocks the 5α-reductase conversion of testosterone to DHT — there is nothing to convert. The drug arrives at the androgen receptor of the hair follicle in its final, most androgenic form.
Minoxidil still works downstream MODEL
Minoxidil acts via follicular blood flow / potassium channels, below receptor level — mechanistically unaffected by any steroid. Assumption: that pathway remains rate-limiting. If follicle miniaturization is receptor-driven and advanced, no vasodilator rescues it.
Market reality
More than half of black-market “Masteron” was mislabeled DATA
2025 forensic analysis of 28 seized drostanolone products: 15 mislabeled — wrong compound, wrong ester, or no drug. The compound with the least pharmacology also has among the worst label integrity.
What does not exist
No healthy-subject trial · no PK · no half-life · no stacking study DATA
Verified by search (2026-08-31): no trial of drostanolone in healthy subjects of either sex, no human pharmacokinetic study, no measured half-life of any ester (propionate or enanthate), no combination trial with any 19-nor or any other AAS. The “test:masteron ratio” doctrine traces to no archived primary source at all. Every dosing conversation about this drug is extrapolation from 1960s oncology.