Methenolone (Primobolan)

Methenolone (sold under the brand name Primobolan) is a lab-made anabolic-androgenic steroid built from dihydrotestosterone, or DHT (a strong natural male hormone). It is an androgen — a male-type hormone — not a peptide. Its genuine medical track record is small: a handful of old, modest studies in anemias caused by bone-marrow failure (when the body can’t make enough blood cells), plus a historical role in advanced breast cancer. Most of its fame today, though, comes from bodybuilding culture, where it’s sold as a “mild” steroid that helps hold onto lean muscle. That reputation is only partly earned, and partly a myth. Methenolone is gentle on the liver and doesn’t turn into estrogen, but it’s still a steroid that shuts down your natural hormones, can cause male-type changes in the body, and brings heart and hormone risks. And there’s no solid modern trial backing up its muscle or performance claims.

What it is

Methenolone (its official generic name is metenolone) is a DHT-derived anabolic-androgenic steroid. Its chemical name is 1-methyl-5α-androst-1-en-17β-ol-3-one (in shorthand, 1-methyl-δ¹-DHT). Two small tweaks to its structure — an added double bond between two carbon atoms (the C1–C2 spots) and an added methyl group at position 1 — slow down the enzyme (3α-hydroxysteroid dehydrogenase) that would normally break it down, and let some of it survive being swallowed. It works by directly switching on the androgen receptor (the docking point cells use to respond to male hormones), and it’s generally described as moderately muscle-building (anabolic) but only weakly masculinizing (androgenic). It does not convert into estrogen (it has little estrogen-like activity), and it barely binds to SHBG (a blood protein that mops up sex hormones).

One chemistry point matters a lot: methenolone is not 17α-alkylated. (17α-alkylation is a structural change drugmakers add so a steroid can survive being swallowed — but it’s the same change that tends to stress the liver.) Methenolone stays active in pill form thanks to its 1-methyl tweak instead, which is why it’s considered easier on the liver than true 17α-alkylated oral steroids (for example methyltestosterone, stanozolol, oxymetholone). It comes in two ester forms (an ester is a chemical “tail” that controls how fast the drug is released): metenolone acetate (the oral version; brands Primobolan, Nibal) and metenolone enanthate (an injected, slow-release “depot” version; brands Primobolan Depot, Nibal Injection).

The claims

• Medical (historical/approved): treatment of anemia caused by bone-marrow failure (aplastic and refractory anemias), plus an older, secondary use studied in advanced breast cancer and some exploration in wasting or muscle-loss conditions.
• Physique/performance (off-label): the idea that methenolone is a “mild and safe” muscle-builder that keeps or adds lean muscle without the harshness of other steroids — pitched as low-risk because it doesn’t convert to estrogen and isn’t tough on the liver.

This profile reports no doses, cycles, ester schedules, or post-cycle protocols. It is a reference, not a how-to.

What the evidence actually shows

Aplastic / refractory anemia (its real medical niche). Kaltwasser et al. (1988) ran a prospective randomized trial (a study where patients are randomly assigned to treatments, the strongest kind) in 30 people with aplastic anemia. Antithymocyte globulin, or ATG (a treatment that calms an overactive immune system), plus oral methenolone produced a 73% response (11 of 15 patients) versus 27% (4 of 15) with ATG alone (p = 0.01, meaning the difference was unlikely to be chance). There was also a survival edge (87% vs 43%), but that result wasn’t statistically firm (p = 0.15). The authors themselves noted that some American studies found no benefit, so the case for androgens in aplastic anemia isn’t settled. Lockner (1979) saw only modest, hit-or-miss improvement across different types of refractory anemia in 19 patients, with no clear gain in how long people lived even among those who responded (side effects were described as negligible). Palva & Wasastjerna (1972) and other older case reports describe partial improvements. Taken together, the anemia evidence is low-quality, old, and mixed, and it predates today’s standard treatments (modern immune-calming drugs and stem-cell transplants).

Breast cancer. Kennedy & Yarbro (1968) reported meaningful improvement in roughly 48% of 27 postmenopausal women with advanced breast cancer treated with methenolone enanthate (with no improvement among 13 patients given testosterone propionate). This is history, not part of how breast cancer is treated today. The 48% figure comes from later secondary summaries; the original PubMed listing has no abstract attached.

Lean mass / strength / bodybuilding use. There are no rigorous modern randomized controlled trials showing what methenolone does to lean muscle or strength in healthy athletes. Its reputation as a “mild” muscle-sparing steroid comes from its DHT-derived, non-estrogen-converting nature and from bodybuilding lore — not from controlled human performance studies. General findings about steroids as a class (very high androgen doses do add lean mass) don’t specifically prove methenolone’s marketed promises, and claims of big strength or size gains aren’t backed by good-quality evidence for this particular compound.

The bottom line here: a thin, dated set of human studies limited to anemia and historical breast cancer, with no strong modern evidence for the performance and physique uses that actually drive its popularity.

Legal and regulatory status

In the United States, anabolic steroids are Schedule III controlled substances (a legal category for drugs with real misuse potential and tight controls) under the Anabolic Steroid Control Act (1990, amended by the Anabolic Steroid Control Act of 2004, which took effect Jan 20, 2005), part of the Controlled Substances Act. Methenolone is named specifically in the federal definition of “anabolic steroid” — at 21 CFR 1300.01 (which mirrors 21 USC 802(41)) — as “1-methyl-17β-hydroxy-5α-androst-1-en-3-one” (methenolone). The Schedule III listing for anabolic steroids as a group is at 21 CFR 1308.13(f). There is no FDA-approved methenolone product in the US, and having, selling, or making it without a prescription is a federal crime.

In sport, anabolic-androgenic steroids fall under WADA’s Class S1 (Anabolic Agents) and are banned at all times — both in competition and out of it. Within S1, lab-made steroids like metenolone sit in category S1.1a. The esters (the slow-release “tail” versions) of banned anabolic agents are also outlawed, so both metenolone acetate and enanthate are prohibited. For context: clenbuterol is also an S1 anabolic agent banned at all times (with no allowed threshold), while growth hormone and hCG are banned under a separate category, S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics).

Safety

• Hepatotoxicity (liver damage): Because methenolone isn’t 17α-alkylated, it’s thought to carry a low risk of the liver injuries (peliosis hepatis — blood-filled pockets in the liver — cholestasis, or backed-up bile, and liver tumors) seen with 17α-alkylated oral steroids. It looks comparatively kind to the liver — but not completely risk-free, and swallowed doses still pass through the liver.
• Cardiovascular / lipids (heart and blood fats): Like steroids in general, very high androgen doses push HDL (“good” cholesterol) down and LDL (“bad” cholesterol) up, which sets up an artery-clogging profile. The wider steroid research links abuse to high blood pressure, an enlarged or weakened heart, faster artery hardening, stiffer arteries, easier blood clotting, and a higher risk of heart attack and sudden cardiac death. Non-estrogen-converting DHT-based steroids like methenolone tend to be especially hard on HDL.
• HPTA suppression / infertility: Every steroid taken from outside the body quiets the hypothalamic-pituitary-testicular axis (the brain-to-testicle signaling loop that runs male hormone production). This lowers the signaling hormones LH and FSH and the body’s own testosterone, which can harm sperm production, shrink the testicles, and cause infertility (often reversible, but not always).
• Gynecomastia / estrogenic effects (breast tissue growth): Because methenolone doesn’t convert to estrogen, breast tissue growth caused directly by methenolone itself is unlikely.
• Virilization (masculinizing effects in women): Even though it’s called “mild,” it’s still a male hormone and can cause extra body or facial hair, a deeper voice, disrupted periods, and clitoral enlargement — and some of these changes are permanent.
• Hematologic (blood): Androgens spur the body to make more red blood cells and can raise hematocrit (the share of blood made up of red cells) and red-cell mass — that’s the very effect behind its anemia use — but at very high doses this can thicken the blood and raise clotting concerns.
• Other steroid-class risks: mood and behavior changes, acne, male-pattern hair loss, and the dangers of contaminated or wrongly-dosed black-market product — which is the main supply today.

Honest framing: the “mild and safe” reputation is relative. It mostly reflects the low liver risk and the lack of estrogen conversion — not an absence of heart, hormone, or masculinizing harm.

Bottom line

Methenolone is a DHT-derived anabolic steroid with a real but small and dated medical history — a few mixed studies in bone-marrow-failure anemias and a historical role in advanced breast cancer. Its modern popularity rests on a “mild and safe” physique reputation that controlled human trials have never confirmed. It really is gentler on the liver than 17α-alkylated oral steroids, and it doesn’t cause estrogen-driven breast growth, but it still shuts down natural hormone production, can masculinize the body, and drops HDL cholesterol — and it’s a Schedule III controlled substance in the US and banned at all times in sport. The honest read: for performance and physique claims, the evidence is preliminary at best, while the legal and health downsides are concrete.

Evidence grade: 8/10 · Good.

Sources

• Kaltwasser JP et al. Effect of androgens on the response to antithymocyte globulin in patients with aplastic anaemia. Eur J Haematol. 1988 (PMID 3278927)
• Lockner D. Treatment of refractory anemias with methenolone. Acta Med Scand. 1979 (PMID 367090)
• Palva IP, Wasastjerna C. Treatment of aplastic anaemia with methenolone. Acta Haematol. 1972 (PMID 4623546)
• Krug K. Pathophysiology of aplastic anemia and its treatment with methenolone enanthate. Z Gesamte Inn Med. 1980 (PMID 7467606)
• Kennedy BJ, Yarbro JW. Effect of methenolone enanthate (NSC-64967) in advanced cancer of the breast. Cancer. 1968 (PMID 4952912)
• Metenolone — Wikipedia (chemistry/pharmacology overview)
• Metenolone enanthate — Wikipedia (history, brands, indications)
• 21 CFR 1308.13 (Schedule III; anabolic steroids as a class at subsection (f))
• 21 USC 802(41) (federal definition of “anabolic steroid,” naming methenolone)
• WADA Prohibited List (S1 Anabolic Agents)
• WADA S1 Anabolic Agents (reference summary)
• WADA S2 Peptide Hormones, Growth Factors (reference summary)
• Liu JD, Wu YQ. Anabolic-androgenic steroids and cardiovascular risk. Chin Med J (Engl). 2019 (PMID 31478927)
• Hartgens F et al. Effects of androgenic-anabolic steroids on apolipoproteins and lipoprotein (a). Br J Sports Med. 2004 (PMID 15155420)
• Impact of Anabolic-Androgenic Steroid Abuse on the Cardiovascular System: Molecular Mechanisms and Clinical Implications. Int J Mol Sci. 2025 (PMC)