This page describes pharmacological agents that may have legal restrictions, side effects, and drug interactions in your jurisdiction. Information is for educational research only — consult a clinician before considering any compound.
Surface here is educational only; do not use without medical supervision. Our editorial verdict is SKIP-FOR-NOW — current cost / risk / redundancy puts it below the line.
Masteron
DHT-derived AAS with mild anti-estrogenic activity — historical breast-cancer drug repurposed as the bodybuilding "hardening" compound.
Aliases (13)
Overview
What is Masteron?
Masteron (drostanolone) is a synthetic anabolic-androgenic steroid derived from dihydrotestosterone (DHT) with a 2α-methyl substitution. It was originally FDA-approved in 1961 as Drolban (drostanolone propionate) for inoperable / metastatic breast cancer in postmenopausal women, but was abandoned for tamoxifen by the late 1970s. Today the compound exists almost exclusively in bodybuilding gray-market form, where it is run for its signature "dry / hard / vascular" cosmetic effect in low-body-fat contest-prep states. Two esters dominate the modern market: propionate (Mast-P, ~2-3 day half-life, EOD injection) and enanthate (Mast-E, ~5-7 day half-life, weekly injection).
Key Benefits
Cosmetic 'hardening' in low-body-fat states (visible at <10% BF for men, invisible above): striated, dry, vascular muscle appearance for stage. Mild anti-estrogenic activity (peripheral AR/ER cross-talk + aromatase substrate competition) without the complete E2 crash of dedicated AIs. Modest androgen-receptor-mediated muscle protein synthesis (low absolute potency vs testosterone). Free-testosterone elevation via SHBG displacement. Preserved or modestly elevated libido in early-cycle (DHT-class CNS effect).
Mechanism of Action
Direct androgen receptor (AR) agonist with comparable peripheral AR affinity to testosterone but elevated activity at 'androgenic' tissues (scalp follicles, sebaceous glands, prostate) due to its DHT-class backbone. The 2α-methyl group blocks 3α-HSD inactivation in skeletal muscle (DHT alone is rapidly degraded there), maintains non-aromatizable structure (no E2 conversion), and provides a mild functional anti-estrogen effect via competitive aromatase substrate occupation — the pharmacological basis of the historical breast cancer indication. The enanthate ester (7-carbon chain) extends half-life to 5-7 days vs propionate's 2-3 days; pharmacodynamics are identical, only kinetics differ.
Pharmacokinetics
Research Indications
Structural identity
Drostanolone is 2α-methyl-5α-androstan-17β-ol-3-one (C20H32O2; MW 304.5 g/mol parent, 360.5 g/mol propionate, 416.6 g/mol enanthate) — a …
SHBG displacement — the under-discussed mechanism
DHT-class AAS bind sex hormone-binding globulin (SHBG) with high affinity. Saartok 1984 (PMID 6539197) documented that 1α-methyl-DHT (rel…
Ester pharmacokinetics
- Propionate (Mast-P, Drolban historical): 3-carbon ester; ~2-3 day half-life; requires EOD or 3×/week injection. More responsive titrati…
Receptor + signaling consequences
Drostanolone binds AR with affinity comparable to testosterone at peripheral AR (skeletal muscle, bone) and slightly elevated at "androge…
What it doesn't do
- No cognitive enhancement. Drostanolone is not a nootropic; AR signaling in CNS is real but does not produce meaningful cognitive benefi…
Peptide Interactions
Almost always run with test base; without it, mid-cycle hypogonadism symptoms (low libido, fatigue, mood drop) emerge. Test base is non-negotiable for any me…
Synergistic for cutting / contest prep — drostanolone "hardens," trenbolone "shreds"; together produce the harshest cosmetic effect at the highest cardiovasc…
Sometimes added late-cycle for additional "dryness" — compounds DHT-class side effects (HDL crash, hair loss) without proportional benefit.
Adds anabolic synergy; compounds cancer / cardiomyopathy / hypoglycemia risks.
Stacking multiple DHT-class compounds compounds androgenic side effects (hair, skin, prostate) and lipid impact without proportional muscle-building gain. Pa…
No direct contraindication but stacking creates pharmacological mess (different mechanism profiles, harder to attribute side effects); not commonly run toget…
Drostanolone already non-aromatizing + mild anti-E2; AI on top crashes E2 too low → joint pain, mood issues, lipid worsening, libido collapse. Only consider …
Ineffective for hair protection because drostanolone is already DHT-class (not a 5α-reductase substrate). The mechanism of finasteride / dutasteride does not…
No direct contraindication but mechanism-redundant for cutting goals; commonly stacked together in older bodybuilder protocols though less coherent than dros…
Quality Indicators
Clear oil, no precipitate or crystallization
Properly compounded drostanolone in carrier oil (typically grapeseed, MCT, or cottonseed) should be a clear, slightly viscous, pale-yellow solution. No cloudiness, no particulate matter, no crystalline deposits at the bottom of the vial.
Lab-tested COA (HPLC, mass spec)
Reputable suppliers provide certificates of analysis showing HPLC purity and mass-spec identity confirmation. Independent lab testing services (Anabolic Lab, Janoshik) verify UGL claims. Drostanolone is one of the more frequently counterfeited AAS — lab verification is not optional for users who proceed despite the SKIP-AT-20 verdict.
PIP (post-injection pain) — carrier oil sensitivity
Mast-P (propionate) is notorious for injection-site pain due to short ester / higher carrier-oil-to-active ratio. Mast-E (enanthate) is generally more comfortable but lower-quality UGL formulations may use inadequate carrier oils — cottonseed oil, high benzyl alcohol content, or unfiltered material can cause severe local reactions.
Unusually low price suggests counterfeit
Drostanolone is more expensive than testosterone esters at pharmaceutical-grade and at competent UGL level. "Mast" sold at testosterone-enanthate prices is statistically likely to be relabeled testosterone enanthate or boldenone (the cheapest oil-based AAS to manufacture). Independent lab testing flags meaningful counterfeit / underdosed rates across the gray market.
Cloudy oil or visible particles
Cloudiness, visible particles, color inconsistency, or sediment indicate degraded product, contaminated material, or improperly compounded oil. Do not inject.
What to Expect
- Week 1-2Subtle. Most users report "nothing happening yet" — consistent with the compound's modest absolute anabolic potency. Distinguishes Masteron from harsher cos…
- Week 2-4First subjective signals — slightly fuller / harder muscle appearance under low body fat conditions; "tighter" feel; slight increase in vascularity at low b…
- Week 4-8Peak cosmetic effect — visible "hardening" in low-body-fat states (8% or below for men): more striated muscle bellies, more pronounced vascularity, reduced …
- Week 8-12Full aesthetic effect on stage / in mirror; bloodwork typically shows lipid degradation (HDL drop 30-50%), mild HPG suppression, mild transaminase elevation…
Side Effects & Safety 12
Side Effects
- 1Atherogenic lipid changes — HDL drops 30-50%, LDL/ApoB rises. Worse on the lipid dimension than aromatizing AAS because the lack of estradiol means no E2-mediated HDL preservation. DHT-class compounds are particularly bad for HDL — drostanolone is at the worse end of the spectrum here.
- 2HPG axis suppression — less than testosterone monotherapy at equivalent doses, not zero. LH/FSH drop within weeks, endogenous T reduced. Recovery 4-8 weeks post-cycle with PCT.
- 3Accelerated androgenic alopecia in genetically predisposed users. Drostanolone is a potent peripheral androgen (DHT-class with 3α-HSD blocking) — for users with shorter AR CAG repeats and male-pattern baldness predisposition, this is one of the more aggressive AAS for hair loss. Finasteride / dutasteride cannot rescue because drostanolone is already DHT-class (not a 5α-reductase substrate).
- 4Acne / oily skin in susceptible users — DHT-class AR activation at sebaceous glands.
- 5Mild aggression / irritability / drive elevation (DHT-class CNS effects).
- 6Hematocrit elevation (red blood cell mass increase) — modest, less than testosterone esters.
- 7Mild blood pressure elevation — less than testosterone or trenbolone.
- 8Sleep disturbance in some users.
- 9Libido shifts (initially up via SHBG displacement / free-T elevation, later down as HPG suppression takes hold).
- 10Mild prostate hypertrophy effects in older users — less relevant for 20yo.
- 11Forearm / bicep "pumps" — transient, dehydration-related, typical of DHT-derived AAS.
- 12Injection site reactions — pain, mild inflammation, particularly with propionate ester (lower carrier oil-to-active ratio than enanthate, more painful injection).
When to Stop
- Severe atherogenic dyslipidemia leading to accelerated CVD with cumulative multi-cycle use over years — comparable to other DHT-class AAS profiles, possibly worse on HDL specifically. Baggish 2017 (PMID 28533317) cohort data shows accelerated coronary atherosclerosis tracking cumulative AAS exposure.
- Cardiomyopathy — extrapolated from broader AAS literature (Baggish cardiac MRI studies); cumulative exposure-dependent; drostanolone-specific cardiac data is sparse.
- Persistent post-cycle hypogonadism — documented in young AAS users with otherwise healthy HPG axes (Rasmussen 2016, PMID 27536957); risk likely higher when HPG axis is still maturing (late teens / early 20s). This is the core SKIP-AT-20 mechanism.
- Severe androgenic alopecia / accelerated male-pattern baldness in predisposed users — can be irreversible.
- Mood disorder triggering — supraphysiologic AR exposure during prefrontal maturation; case reports exist across AAS class (Pope 2014, PMID 24423981), drostanolone-specific data sparse.
- At age 20: HPG axis is still consolidating final adult set-point. Suppression at this age has higher theoretical risk of permanent change vs same suppression at 30. This is the core SKIP-AT-20 mechanism, applies to drostanolone same as other AAS.
- Week 4 of any cycle: ALT/AST + lipid panel — flag if HDL drops >50% or BP >140/90.
- End of cycle: Full HPG panel (T, LH, FSH, E2, DHT) to quantify suppression.
- Week 4-8 post-cycle: HPG recovery check; if still suppressed, formal PCT or endocrinology consult.
References
Saartok T, Dahlberg E, Gustafsson JA. (1984). "Relative binding affinity of anabolic-androgenic steroids: comparison of binding to androgen receptors in skeletal muscle and prostate, as well as to sex hormone-binding globulin." *Endocrinology* 114(6):2100-2106. PMID: 6539197.
Foundational AR + SHBG binding study including DHT-derivatives.
View StudyTalley RW et al. (1973). "A dose-response evaluation of androgens in the treatment of metastatic breast cancer." *Cancer* 32(2):315-320. PMID: 4515870.
32:2%3C315::AID-CNCR2820320206%3E3.0.CO;2-Q) — Historical breast cancer trial data including drostanolone propionate.
View StudyBaggish AL, Weiner RB, Kanayama G, et al. (2017). "Cardiovascular toxicity of illicit anabolic-androgenic steroid use." *Circulation* 135(21):1991-2002. PMID: 28533317.
Cardiac MRI cohort establishing AAS-class CV risk profile.
View StudyRasmussen JJ, Selmer C, Østergren PB, et al. (2016). "Former Abusers of Anabolic Androgenic Steroids Exhibit Decreased Testosterone Levels and Hypogonadal Symptoms Years after Cessation: A Case-Control Study." *PLoS One* 11(8):e0161208. PMID: 27536957.
Persistent post-AAS hypogonadism documentation; the empirical anchor for SKIP-AT-20.
View StudyPope HG Jr, Wood RI, Rogol A, et al. (2014). "Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement." *Endocrine Reviews* 35(3):341-375. PMID: 24423981.
Comprehensive AAS adverse-effect review.
View StudyHartgens F, Kuipers H. (2004). "Effects of androgenic-anabolic steroids in athletes." *Sports Medicine* 34(8):513-554. PMID: 15248788.
Class overview including drostanolone.
View StudyKicman AT. (2008). "Pharmacology of anabolic steroids." *British Journal of Pharmacology* 154(3):502-521. PMID: 18500378.
Mechanism review including DHT-derivatives.
View StudyDrolban (drostanolone propionate) — Wikipedia historical entry
historical FDA pathway, breast cancer indication, withdrawal context.
View StudyDrostanolone — Wikipedia
pharmacology overview, ester variants, historical use.
View StudyDrostanolone (DrugBank DB00858)
drug-database entry covering pharmacology, mechanism, ADME.
View StudyAnabolic Lab (anabolic.org)
Independent UGL/pharma testing data on AAS counterfeit rates including drostanolone.
View StudyJanoshik Analytical
Independent third-party AAS testing service; documents drostanolone counterfeit / underdosing rates.
View StudyHow was your experience with this compound?
Anonymous · one vote per session · results below at 5+ votes.
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