Adrenosterone, also called 11-ketoandrostenedione (11KA4) and sold as “11-OXO,” is a steroid the human adrenal glands make naturally. It belongs to the family of 11-oxygenated androgens, adrenal steroids that endocrinologists now see as an important part of the body’s androgen supply. It has been marketed as a dietary supplement for reducing body fat and increasing muscle mass (Brooker et al., Drug Test Anal 2009).
The most important fact: no controlled trial has tested adrenosterone for fat loss, muscle gain or performance. The human studies that exist are small metabolism and doping-control studies. In the body, adrenosterone is a precursor of 11-ketotestosterone, an androgen about as potent as testosterone, and it is banned in sport under the WADA Prohibited List.
This page summarizes what the endocrine research, the doping-control literature and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Class | Endogenous 11-oxygenated C19 steroid; androgen precursor |
| Chemical name | Androst-4-ene-3,11,17-trione; C₁₉H₂₄O₃, 300.4 g/mol |
| Medical approval | None; no FDA-approved drug product contains it |
| Route studied in humans | Oral |
| Doses used in human studies | Single doses of 75 mg and 100 mg; 150 mg/day for 7 days |
| Half-life | Not established in humans; after one 100 mg dose, urinary metabolites peaked at 3–5.5 h |
| Key conversion | Converted to 11-ketotestosterone, which activates the androgen receptor about as well as testosterone |
| US status | Not named as a Schedule III anabolic steroid in 21 CFR 1308.13 |
| WADA status | Prohibited at all times (S1.1, named explicitly) |
What it is
Adrenosterone is androstenedione with an extra ketone (oxygen) group at carbon 11. Its formula is C₁₉H₂₄O₃ and its molecular weight is 300.4 g/mol (PubChem). Despite the similar “OXO” name, it is a different compound from 6-OXO (androst-4-ene-3,6,17-trione), which is marketed as an aromatase inhibitor.
For decades the adrenal steroid 11β-hydroxyandrostenedione (11OHA4) was treated as a dead-end product. More recent work showed it is the starting point of a separate androgen pathway (Pretorius et al., Mol Cell Endocrinol 2017; Turcu & Auchus, Curr Opin Endocrinol Diabetes Obes 2017):
| Step | Enzyme | Product |
|---|---|---|
| 11OHA4 to adrenosterone | 11β-HSD2 (11β-hydroxysteroid dehydrogenase type 2) | 11-ketoandrostenedione (adrenosterone) |
| Adrenosterone to 11-ketotestosterone | AKR1C3 (aldo-keto reductase 1C3) | 11-ketotestosterone (11KT) |
| 11KT to 11-ketodihydrotestosterone | 5α-reductase | 11-ketodihydrotestosterone (11KDHT) |
| Adrenosterone back to 11β-hydroxy forms | 11β-HSD1, mainly in the liver | 11OHA4 and its metabolites |
Adrenosterone itself is a precursor. Its activity comes from what it turns into. 11KT binds and activates the androgen receptor with potency similar to testosterone (McDonnell et al., Eur J Endocrinol 2025). Supporting lab data:
- In cell studies, 11KT and 11KDHT were potent, efficacious agonists of the human androgen receptor, much like testosterone and DHT, and were broken down more slowly than them (Pretorius et al., PLoS One 2016). An earlier study found 11KDHT acted as a full agonist with activity similar to DHT at 1 nM (Storbeck et al., Mol Cell Endocrinol 2013).
- The enzyme AKR1C3 converted adrenosterone 8 times more efficiently than it converted androstenedione, in laboratory enzyme assays (Barnard et al., J Steroid Biochem Mol Biol 2018).
- 11β-HSD2 favors making adrenosterone from 11OHA4, while 11β-HSD1 favors reducing the 11-keto steroids back to their 11β-hydroxy forms (Gent et al., J Steroid Biochem Mol Biol 2019).
In the body
Adrenosterone is a normal part of human steroid biology. Some measured findings:
- Across adulthood: in 590 adults, serum adrenosterone was stable with age in women but fell by about 0.06 ng/dL per year in men (Davio et al., JCEM 2020).
- In polycystic ovary syndrome (PCOS): serum adrenosterone and the other 11-oxygenated androgens were higher in 114 women with PCOS than in 49 controls. These steroids made up 53.0% of total serum androgens in PCOS vs 44.0% in controls, and adrenosterone correlated with markers of insulin resistance (O’Reilly et al., JCEM 2017).
- In other conditions: 11-oxygenated androgens are raised in 21-hydroxylase deficiency (a form of congenital adrenal hyperplasia) and are thought to contribute to castration-resistant prostate cancer (Turcu & Auchus 2017).
Pharmacokinetics
No formal pharmacokinetic study (blood levels, half-life, bioavailability) of oral adrenosterone in humans has been published. What is known comes from urine studies.
In a single male volunteer given one 100 mg oral dose from a dietary supplement product, all measured urinary metabolites rose sharply (Piper et al., Metabolites 2024):
| Measure | Result after 100 mg |
|---|---|
| Time to peak urinary metabolite levels | 3 or 5.5 h |
| Return to normal endogenous ranges | After 10–14 h (slightly elevated until 33 h) |
| Urinary 11-ketotestosterone | Rose from under 10 ng/mL to over 70 µg/mL |
| Urinary 11-oxoetiocholanolone | Rose from about 100 ng/mL to over 330 µg/mL |
The authors called this a proof-of-concept with one volunteer. It does show that oral adrenosterone is converted to 11-ketotestosterone in people.
The main urinary metabolites are 11β-hydroxyandrosterone, 11β-hydroxyetiocholanolone, 11-oxoandrosterone and 11-oxoetiocholanolone (Brooker et al. 2009). Most of these overlap with the breakdown products of cortisol and cortisone, which makes them hard to attribute; 11-ketoandrosterone is the only one specific to 11-oxygenated androgens (McDonnell et al. 2025).
In a 2025 study, 20 women with PCOS were randomized (open label) to 150 mg/day of oral DHEA or oral adrenosterone for 7 days (McDonnell et al. 2025). After adrenosterone, the median rises in urinary metabolites were:
| Urinary metabolite | Median fold increase (IQR) |
|---|---|
| 11-ketoandrosterone | 89.9 (57.8–142.5) |
| 11-ketoetiocholanolone | 32.1 (22.0–35.0) |
| 11β-hydroxyandrosterone | 17.7 (16.1–18.0) |
| 11β-hydroxyetiocholanolone | 6.5 (4.0–8.6) |
Classic androgen metabolites did not rise significantly. Liver tissue studies in the same paper showed that 11β-HSD1 in the liver converts much of the 11-keto steroid to 11β-hydroxy forms. The paper did not report blood levels or side effects.
A registered trial from the same Irish group with the same two 150 mg/day arms, NCT05263557, aims to measure muscle insulin sensitivity. Its last registry update (2023) listed it as recruiting with status now unknown, and no results have been posted.
Regulatory status
- FDA: adrenosterone is not an approved drug, and no product containing it appears in the FDA’s drug approval database (openFDA Drugs@FDA).
- DEA: adrenosterone is not among the anabolic steroids named in the US Schedule III list (21 CFR 1308.13), which does name its close relative 4-androstenedione.
- WADA: “Androst-4-ene-3,11,17-trione (11-ketoandrostenedione, adrenosterone)” is listed by name under S1.1 anabolic androgenic steroids, prohibited at all times and as a non-Specified Substance (WADA 2026 Prohibited List).
What the research shows
Fat loss and muscle
No randomized, controlled or even uncontrolled trial has measured body fat, lean mass, strength or performance after adrenosterone. The fat-loss claim rests on the proposal that adrenosterone inhibits 11β-HSD1, the enzyme that turns inactive cortisone back into cortisol inside tissues (Brooker et al. 2009). No human study has shown that adrenosterone lowers cortisol or body fat.
About the “cortisol blocker” claim. In human liver tissue, adrenosterone is a substrate of 11β-HSD1: the enzyme converts it to 11β-hydroxy steroids (McDonnell et al. 2025). Whether it competes enough with cortisone to change cortisol levels in people has not been measured.
Other research
In a zebrafish model of liver cancer spread, a drug screen identified adrenosterone, described as an 11β-HSD1 inhibitor, as suppressing cancer cell dissemination. Blocking 11β-HSD1 also reduced the spread of human cancer cell lines transplanted into zebrafish, and adrenosterone-treated cells regained markers of non-invasive cells (Nakayama et al., Mol Cancer Res 2020). These are animal and cell findings and have not been tested in people.
Side effects and risks
No human safety data
None of the human studies reported safety outcomes. The largest exposure studied is 150 mg/day for 7 days in 10 women (McDonnell et al. 2025). Long-term effects on lipids, liver, blood pressure, hormones or fertility are unknown.
Androgen exposure
Because oral adrenosterone is converted to 11-ketotestosterone (Piper et al. 2024), it is a source of an active androgen. Higher 11-oxygenated androgens are linked in observational studies to PCOS and to markers of insulin resistance (O’Reilly et al. 2017), and they are being studied as drivers of castration-resistant prostate cancer (Barnard et al. 2018). Whether supplement doses cause effects such as acne, hair changes, virilization in women or suppression of natural testosterone has not been studied.
Drug testing
Athletes who take adrenosterone risk an anti-doping rule violation. Laboratories can confirm its use with carbon isotope ratio testing, which tells synthetic from naturally made steroids (Brooker et al. 2009). In the one-dose study, urinary 11-ketotestosterone exceeded the proposed screening threshold of 130 ng/mL from 1 to 14 h after the dose (Piper et al. 2024). Because its metabolites overlap with those of cortisone, laboratories need isotope analysis of the main cortisol metabolites to tell adrenosterone use from cortisone use; that study gave 75 mg orally to volunteers (Brooker et al., Drug Test Anal 2012).
Related pages
- Androstenedione (4-AD), the classic adrenal precursor without the 11-oxygen.
- DHEA and 7-Keto DHEA, other adrenal steroids sold as supplements.
Key takeaways
- A natural adrenal androgen precursor. Adrenosterone (11-ketoandrostenedione) is part of the 11-oxygenated androgen pathway and is converted to 11-ketotestosterone, which is about as potent as testosterone in cell studies.
- No efficacy trials. No study has tested it for fat loss, muscle or performance; the human data are small metabolism and doping-control studies.
- The cortisol claim is unproven. In human liver tissue it is processed by 11β-HSD1, and no human study shows it lowers cortisol or fat.
- Safety is unstudied. Human exposure in research has been limited to single doses and one 7-day course of 150 mg/day.
- Banned in sport, not a US scheduled drug. WADA names it under S1.1 (prohibited at all times); it is not named in the US Schedule III list and is not FDA-approved.
Sources
- Brooker L, Parr MK, Cawley A, et al. Development of criteria for the detection of adrenosterone administration by gas chromatography-mass spectrometry and gas chromatography-combustion-isotope ratio mass spectrometry for doping control. Drug Test Anal. 2009;1(11-12):587–595. PubMed.
- Brooker L, Cawley A, Kazlauskas R, et al. Carbon isotope ratio analysis of endogenous glucocorticoid urinary metabolites after cortisone acetate and adrenosterone administration for doping control. Drug Test Anal. 2012;4(12):951–961. PubMed.
- Piper T, Fußhöller G, Thevis M. Employing 11-ketotestosterone as a target analyte for adrenosterone (11OXO) administration in doping controls. Metabolites. 2024;14(3):141. PubMed.
- McDonnell T, Anthony AV, Clarke G, et al. Hepatic metabolism of 11-oxygenated androgens in humans: an integrated in vivo and ex vivo approach. Eur J Endocrinol. 2025;193(3):340–347. PubMed.
- Royal College of Surgeons in Ireland. Dissecting the IMpact of 11-OXygenated and Classic Androgens on Skeletal Muscle Insulin Sensitivity (DIMOXIS). NCT05263557. ClinicalTrials.gov.
- Turcu AF, Auchus RJ. Clinical significance of 11-oxygenated androgens. Curr Opin Endocrinol Diabetes Obes. 2017;24(3):252–259. PubMed.
- Pretorius E, Arlt W, Storbeck KH. A new dawn for androgens: novel lessons from 11-oxygenated C19 steroids. Mol Cell Endocrinol. 2017;441:76–85. PubMed.
- Pretorius E, Africander DJ, Vlok M, et al. 11-Ketotestosterone and 11-ketodihydrotestosterone in castration resistant prostate cancer: potent androgens which can no longer be ignored. PLoS One. 2016;11(7):e0159867. PubMed.
- Storbeck KH, Bloem LM, Africander D, et al. 11β-Hydroxydihydrotestosterone and 11-ketodihydrotestosterone, novel C19 steroids with androgenic activity: a putative role in castration resistant prostate cancer? Mol Cell Endocrinol. 2013;377(1-2):135–146. PubMed.
- Barnard M, Quanson JL, Mostaghel E, et al. 11-Oxygenated androgen precursors are the preferred substrates for aldo-keto reductase 1C3 (AKR1C3): implications for castration resistant prostate cancer. J Steroid Biochem Mol Biol. 2018;183:192–201. PubMed.
- Gent R, du Toit T, Bloem LM, et al. The 11β-hydroxysteroid dehydrogenase isoforms: pivotal catalytic activities yield potent C11-oxy C19 steroids with 11βHSD2 favouring 11-ketotestosterone, 11-ketoandrostenedione and 11-ketoprogesterone biosynthesis. J Steroid Biochem Mol Biol. 2019;189:116–126. PubMed.
- Davio A, Woolcock H, Nanba AT, et al. Sex differences in 11-oxygenated androgen patterns across adulthood. J Clin Endocrinol Metab. 2020;105(8):e2921–e2929. PubMed.
- O’Reilly MW, Kempegowda P, Jenkinson C, et al. 11-Oxygenated C19 steroids are the predominant androgens in polycystic ovary syndrome. J Clin Endocrinol Metab. 2017;102(3):840–848. PubMed.
- Nakayama J, Lu JW, Makinoshima H, et al. A novel zebrafish model of metastasis identifies the HSD11β1 inhibitor adrenosterone as a suppressor of epithelial-mesenchymal transition and metastatic dissemination. Mol Cancer Res. 2020;18(3):477–487. PubMed.
- National Center for Biotechnology Information. PubChem Compound Summary for CID 223997, Adrenosterone. PubChem.
- US Food and Drug Administration. openFDA Drugs@FDA API (search for adrenosterone returned no products). openFDA.
- Code of Federal Regulations. 21 CFR 1308.13, Schedule III. eCFR.
- World Anti-Doping Agency. The 2026 Prohibited List, International Standard. In effect January 1, 2026. WADA 2026 Prohibited List.