Testosterone or Masteron: What Is the Difference

Masteron is a trade name for drostanolone, a derivative of dihydrotestosterone. Unlike testosterone, it is not converted into estrogens, and it is with this property that both its reputation and its specific risks are associated. Our editorial team explains how these two substances differ at the level of the molecule, metabolism and effect on the body.

Two Different Families of Androgens

Synthetic anabolic-androgenic steroids are usually divided into several groups by their parent molecule: derivatives of testosterone, derivatives of 19-nortestosterone (nandrolone) and derivatives of dihydrotestosterone (DHT). Testosterone is the progenitor of the first group, while drostanolone belongs to the third.

This classification is not a formality. The parent molecule determines whether the substance can be converted into estrogens, whether it will be a substrate for 5α-reductase, and how it will be inactivated by enzymes in various tissues. It is these properties that determine the practical differences between the drugs.

In the human body, testosterone acts as a prohormone: part of it is converted into estradiol, part into DHT, and each of these metabolites has its own effects. Drostanolone, on the other hand, is already a "reduced" molecule, so these conversions are impossible for it.

Thus, when comparing testosterone and Masteron, we are comparing a universal hormone with a broad spectrum of action and a narrowly targeted DHT derivative in which part of the metabolic pathways is simply "switched off."

The Structure of the Molecule and What Follows from It

The chemical name of drostanolone is 2α-methyl-5α-androstan-17β-ol-3-one. It differs from DHT only by a methyl group at the second position of ring A. In pharmaceutical forms it was used as the propionate ester; on the illegal market the enanthate is also found.

DHT is a potent androgen, but in skeletal muscle it is quickly inactivated by the enzyme 3α-hydroxysteroid dehydrogenase. According to classical understanding, the methyl group at the 2α position makes drostanolone more resistant to such breakdown, which explains its anabolic activity being higher than that of DHT itself.

Testosterone has a double bond between the fourth and fifth carbon atoms. It is precisely this bond that allows enzymes to convert it into estradiol (aromatization) and into DHT (5α-reduction). Drostanolone lacks this bond, so both conversions are impossible.

As a result, testosterone acts "through three channels" — itself, through DHT and through estradiol — while drostanolone acts only through the androgen receptor. This explains why their profiles of action and side effects differ markedly.

Estrogens: Presence and Absence

The absence of aromatization is Masteron's key distinction. When testosterone is used in supraphysiological amounts, estradiol levels also rise, which can cause gynecomastia and fluid retention. Drostanolone by itself does not produce this effect.

However, estrogen is needed in men. It participates in maintaining bone mineral density, in the regulation of libido, in lipid metabolism and, probably, in the protection of blood vessels. An androgen that does not aromatize, when used on its own against the background of suppressed endogenous testosterone, can lead to estrogen deficiency.

Clinical studies with men in whom both testosterone and estradiol were artificially suppressed (in particular, the work of Finkelstein and colleagues, 2013) showed that it is estrogen that is responsible for part of the changes in adipose tissue and libido. This illustrates that the "absence of estrogens" is not an unambiguously positive property.

The second aspect is that drostanolone, as a DHT derivative, was studied in early works as an agent with antiestrogenic action in breast tissue. This property was used in oncology, but it should not be confused with safety for men.

History of Medical Use

Testosterone has been used in medicine since the 1930s and today is the basis of replacement therapy for hypogonadism. Its effectiveness and safety within physiological levels have been studied in large randomized trials, in particular in the TRAVERSE program on cardiovascular safety.

Drostanolone propionate appeared in the 1950s–1960s and was used mainly as an agent for palliative therapy of advanced breast cancer in postmenopausal women. Later it was displaced by more effective and better-tolerated drugs — antiestrogens and aromatase inhibitors.

As a result, in most countries pharmaceutical preparations of drostanolone have gone out of circulation. There are practically no modern clinical studies with it, and no new data on human safety are accumulating.

This is a typical situation for many "classic" anabolic steroids: their pharmacology is known from studies of the mid-20th century, while all modern information about their use in sport comes from unofficial sources, doping analysis and descriptions of complications.

Side Effects: Shared and Distinct

Common to both substances are the effects associated with activation of the androgen receptor at supraphysiological levels. Among them are suppression of the hypothalamic-pituitary-gonadal axis, a decrease in HDL, myocardial changes, psychoemotional effects and virilization in women.

The differences concern mainly estrogenic and androgenic effects in the skin and hair.

• Gynecomastia and fluid retention are more characteristic of testosterone due to the formation of estradiol.
• For drostanolone, as a DHT derivative, androgenic effects are considered typical: acne, oily skin, acceleration of androgenic alopecia in people with a genetic predisposition.
• 5α-reductase inhibitors (for example, finasteride) can reduce the DHT-dependent effects of testosterone, but do not affect drostanolone, since it is already a 5α-reduced molecule.
• Estrogen deficiency against the background of suppressed endogenous testosterone is a specific risk of non-aromatizing androgens.

As for the liver: the injectable esters of both substances do not have 17α-alkylation, so their hepatotoxicity is significantly lower than that of oral methylated steroids. However, the effect on lipids and the heart is not reduced by this.

Finally, Masteron, unlike testosterone, is almost always obtained from illegal sources. Thus, to the pharmacological risks are added the risks of an inconsistent composition, impurities and non-sterility.

Editorial Conclusions

Testosterone is a universal hormone whose action is realized both directly and through DHT and through estradiol. Masteron (drostanolone) is a DHT derivative that acts only through the androgen receptor and does not aromatize.

The absence of estrogenic effects does not make Masteron safer: it changes the risk profile — toward androgenic effects on the skin and hair and possible estrogen deficiency.

The key systemic risks — suppression of the hormonal axis, dyslipidemia, effect on the heart — are common to both substances.

We also recommend familiarizing yourself with our materials about the role of estradiol in the male body, about androgenic alopecia and DHT, and about monitoring the lipid profile.

References

1. Kicman AT. Pharmacology of anabolic steroids. Br J Pharmacol. 2008;154(3):502–521.
2. Schänzer W. Metabolism of anabolic androgenic steroids. Clin Chem. 1996;42(7):1001–1020.
3. Finkelstein JS, Lee H, Burnett-Bowie SA, et al. Gonadal steroids and body composition, strength, and sexual function in men. N Engl J Med. 2013;369(11):1011–1022.
4. Pope HG Jr, Wood RI, Rogol A, et al. Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Endocr Rev. 2014;35(3):341–375.
5. Lincoff AM, Bhasin S, Flevaris P, et al. Cardiovascular safety of testosterone-replacement therapy. N Engl J Med. 2023;389(2):107–117.
6. Bhasin S, Brito JP, Cunningham GR, et al. Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2018;103(5):1715–1744.
7. World Anti-Doping Agency. The Prohibited List. International Standard. Montreal: WADA; 2025.