Orals

Ethylestrenol

Updated · 26 sources · Editorial policy

Ethylestrenol is an oral anabolic steroid from the 19-nortestosterone (nandrolone) family. Organon sold it in the US as Maxibolin, approved by the FDA in 1964, and in other countries under names such as Orabolin and Orgabolin (Ward et al., J Steroid Biochem 1977; Nilsson et al., Acta Med Scand 1981). Both US Maxibolin products are now listed as discontinued.

Ethylestrenol has an unusual history. Besides its use as a general “anabolic,” it was studied in the 1960s and 1970s mainly as a drug to boost fibrinolysis (the body’s system for dissolving blood clots), often combined with the diabetes drug phenformin. Its most unusual chemical feature is that it lacks the 3-keto group that most steroids need to bind the androgen receptor. Laboratory and animal work suggests it acts largely after the liver converts it to norethandrolone.

This page summarizes what the FDA record, the older clinical studies and regulators report. It is for education only and is not medical advice.

Property Detail
Drug class 17α-alkylated anabolic-androgenic steroid (19-nortestosterone derivative)
Brands Maxibolin (Organon, US); Orabolin and Orgabolin in other markets
Route Oral (tablet, elixir)
Former US strengths 2 mg tablet; 2 mg/5 mL elixir
Doses in cited studies 4–8 mg/day (thrombosis studies); 30 mg/day for 4 days (one menstrual-cycle study)
Half-life No published human half-life found
Key mechanism fact Lacks a 3-keto group; androgen receptor binding too low to measure in one assay; converted to norethandrolone by liver preparations
US status FDA-approved 1964; both NDAs listed as discontinued; Schedule III anabolic steroid
WADA status Prohibited at all times (S1.1, named)

What it is

Ethylestrenol has the formula C₂₀H₃₂O and a molecular weight of 288.5 g/mol (PubChem). The DEA lists its chemical name as 17α-ethyl-17β-hydroxyestr-4-ene (21 CFR 1308.13). The structure is easiest to understand next to its close relatives:

Compound DEA chemical name Difference
Ethylestrenol 17α-ethyl-17β-hydroxyestr-4-ene No oxygen at carbon 3
Norethandrolone 17α-ethyl-17β-hydroxyestr-4-en-3-one Same skeleton, with the 3-keto group

Both are “estr-” steroids, meaning they lack the carbon-19 methyl group, like nandrolone. Both also carry a 17α-ethyl group. Like the 17α-methyl group on methyltestosterone or oxandrolone, this slows breakdown in the liver and allows oral use.

The missing 3-keto group matters. In a receptor-binding study using rat and rabbit tissue, ethylestrenol’s binding to the androgen receptor in skeletal muscle and prostate was too low to measure (Saartok et al., Endocrinology 1984). Liver studies point to how it still works:

These are animal and in-vitro findings. They suggest ethylestrenol acts largely as a prodrug of norethandrolone, but this has not been mapped in comparable detail in people.

About anabolic:androgenic ratios. Ethylestrenol is often described online as a highly “anabolic” steroid with weak androgenic effects. A 1963 rat study compared its oral anabolic and androgenic activity (Arnold et al., Acta Endocrinol 1963), but we could not access its figures, so we do not quote a ratio. Rat assays of this kind do not predict effects in people.

Pharmacokinetics

Human pharmacokinetic data are very limited. We found no published human half-life, peak level or bioavailability figure. A 1977 study examined its metabolism in people and marmoset monkeys, but we could not access the full report (Ward et al., J Steroid Biochem 1977).

The best-described kinetics come from rats given radiolabeled ethylestrenol by stomach tube (Steele et al., Xenobiotica 1981):

Measure (in rats) Result
Share of oral dose absorbed About one third
Excretion within 10 days 17% in urine, 83% in feces
Tissue concentration Liver 5–7 times and kidney 2.5–3 times the average of other tissues
Urinary component Unchanged ethylestrenol only

In cattle, both ethylestrenol and norethandrolone are excreted largely as the same metabolite, 17α-ethyl-5β-estrane-3α,17β-diol, which residue laboratories use to detect illegal use of either drug as a growth promoter (Van Puymbroeck et al., J Chromatogr B 1999).

Former medical use

The FDA approved Maxibolin tablets (NDA 014005) on May 28, 1964, as a new molecular entity, and Maxibolin elixir (NDA 014006) on January 7, 1965. Both are now listed as discontinued (Drugs@FDA, NDA 014005; Drugs@FDA, NDA 014006). We could not find the original US label online, so its approved indications and doses are not given here.

Outside the US, ethylestrenol was tried in several settings, including weight gain in children (Borniche, Med Infant 1965) and asthmatic children on corticosteroids (Kerrebijn and Delver, Scand J Respir Dis Suppl 1969). Most of these reports from the 1960s and 1970s are small, uncontrolled or without published abstracts, so they are not summarized further here.

What the research shows

Fibrinolysis and recurrent venous thrombosis

Most of the clinical literature studied ethylestrenol as a way to raise fibrinolytic activity in people with low baseline activity. One Swedish group reported a series of open studies:

Study Design and n Dose Main finding
Nilsson et al., Acta Med Scand 1975 Open, 75 patients (60 with recurrent deep venous thrombosis) Phenformin 100 mg + ethylestrenol 8 mg daily for 3–48 months Fibrinolytic activity rose significantly by 3 months (p under 0.001); 9 thrombotic episodes during treatment; one patient developed lactic acidosis
Hedner et al., BMJ 1976 Open, 49 patients with low fibrinolytic activity, plus 15 with normal activity Ethylestrenol alone, 8 or 4 mg/day for 3–17 months 8 mg/day raised fibrinolytic activity; 4 mg/day had no effect; no change in patients with normal baseline activity
Nilsson et al., Acta Med Scand 1981 Open, 21 patients with recurrent thrombosis 6 mg/day, up to 56 months Fibrinolytic activity improved; significantly lower incidence of thrombosis reported (p under 0.001)

These were not placebo-controlled trials, so the drop in clot recurrence cannot be separated from chance, patient selection or other treatment.

Ethylestrenol was not unique here. In men with ischemic heart disease, five 17α-alkylated steroids, ethylestrenol among them, all raised plasma plasminogen activator, while the one non-17α-alkylated steroid tested (methenolone acetate) did not (Walker et al., Thromb Diath Haemorrh 1975). A small study of phenformin plus ethylestrenol found that the fall in plasma fibrinogen probably reflected lower production of fibrinogen by the liver, rather than faster breakdown (Hickman, J Clin Pathol 1970).

Prevention of clots after surgery

The largest controlled trial was negative. In a double-blind randomized trial of 314 surgical patients, phenformin plus ethylestrenol increased laboratory markers of fibrinolysis but did not lower the rate of postoperative deep venous thrombosis (Atkins et al., Thromb Haemost 1978).

Cutaneous vasculitis

A small double-blind study compared phenformin plus ethylestrenol, phenformin plus stanozolol, and placebo in 13 patients with cutaneous vasculitis (inflammation of small skin blood vessels). Eight patients improved considerably on phenformin plus an anabolic steroid, and low fibrinolytic activity before treatment predicted a better response (Dodman et al., BMJ 1973). The study was too small to show a reliable effect of ethylestrenol itself.

Muscle, strength and body composition

We found no controlled trial measuring lean mass, muscle size or strength with ethylestrenol in adults. Its reputation as a muscle-building drug is not backed by modern human data.

Side effects and risks

Liver

Ethylestrenol carries a 17α-alkyl group. A 2022 review notes that 17α-alkyl-substituted steroids cause a characteristic form of acute cholestasis (slowed bile flow), with itching, jaundice and dark urine, and that anabolic steroids as a class are linked to peliosis hepatis (blood-filled cysts in the liver) and liver tumors (Petrovic et al., World J Gastroenterol 2022). We found no published case series specific to ethylestrenol. Its main metabolite, norethandrolone, caused total cholestasis within 3 hours when infused into rat liver (Phillips et al., Am J Pathol 1978).

Menstrual changes and virilization in women

  • In the 1976 thrombosis series, 2 of the 3 women of reproductive age developed irregular cycles and bleeding between periods, which stopped when treatment was withdrawn (Hedner et al., BMJ 1976).
  • In a study of women given anabolic steroids after ovulation, ethylestrenol 30 mg/day for 4 days significantly shortened the luteal phase (the second half of the cycle; p under 0.001), though the authors noted the sample was small (Bolch and Warren, Am J Obstet Gynecol 1973).

Hormonal suppression

In pubertal rats, ethylestrenol suppressed ovulation at doses of 100 micrograms/day or more, consistent with antigonadotropic activity (suppression of the pituitary hormones that drive the gonads) (Boris et al., Contraception 1972). In adult male rats, ethylestrenol caused extensive testicular damage and inhibited growth of accessory sex organs (Sarkar and Jogi, Indian J Med Res 1971). These are animal results; comparable human data on testosterone or sperm suppression were not found.

Interactions

  • Anticoagulants: a 1968 Lancet letter reported a suspected interaction between ethylestrenol and the oral anticoagulant phenindione (Vere and Fearnley, Lancet 1968).
  • Phenformin combination: in the largest combination series of phenformin plus ethylestrenol, one patient developed lactic acidosis (Nilsson et al., Acta Med Scand 1975).
  • United States: ethylestrenol is named as an anabolic steroid in Schedule III of the Controlled Substances Act, entry (f)(32) (21 CFR 1308.13). With both NDAs discontinued, there is no FDA-approved product on the US market.
  • Sport: it is named under S1.1 anabolic androgenic steroids on the WADA list and is prohibited in and out of competition (WADA 2026 Prohibited List).
  • Food animals: residue laboratories treat ethylestrenol and norethandrolone as illegal growth promoters in cattle and monitor a shared urinary and fecal metabolite (Van Puymbroeck et al., J Chromatogr B 1999).

Key takeaways

  • A 19-nor oral steroid without a 3-keto group. Its own androgen receptor binding was too low to measure in one assay; in rat and bovine liver preparations it is converted mainly to norethandrolone.
  • Formerly approved, now discontinued in the US. Maxibolin tablets (2 mg) and elixir (2 mg/5 mL) were approved in 1964–1965 and are listed as discontinued.
  • Studied mostly for blood clotting, not muscle. Open studies at 6–8 mg/day raised fibrinolytic activity, but a 314-patient randomized trial found no reduction in postoperative venous thrombosis.
  • No modern human data on muscle or strength. Claims that it is a strongly “anabolic” steroid are not supported by human trials; the only potency comparison found is a 1963 rat assay.
  • Class risks apply. As a 17α-alkylated steroid, it carries the class risk of cholestatic liver injury; menstrual disturbance was reported in women at therapeutic doses.
  • Controlled and banned in sport. It is a US Schedule III substance and is named on the WADA Prohibited List.

Sources

  1. National Center for Biotechnology Information. Ethylestrenol, CID 13765. PubChem. PubChem.
  2. US Food and Drug Administration. Drugs@FDA: Maxibolin (ethylestrenol) tablet, NDA 014005, Organon USA Inc. FDA.
  3. US Food and Drug Administration. Drugs@FDA: Maxibolin (ethylestrenol) elixir, NDA 014006, Organon USA Inc. FDA.
  4. Drug Enforcement Administration. Schedule III, 21 CFR 1308.13. eCFR.
  5. World Anti-Doping Agency. The 2026 Prohibited List. WADA.
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