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11-keto-androstenetrione

Table of contents

Other Names

11-KA411-Keto-androstenedione11-Ketoandrostenedione11-OXO11-Oxo-androstenedione11-Oxoandrostenedione4-Androstene-3,11,17-trioneAdrenosteroneAndrost-4-ene-3,11,17-trioneAndrostenetrioneReichstein's substance G

Synopsis

11-Keto-Androstenetrione (Adrenosterone)

1. Identity: Chemical Names, Natural Sources, and Common Preparations

1.1 Chemical Identity and Nomenclature

11-Keto-Androstenetrione, more formally known as adrenosterone, is also designated by the synonyms Reichstein's substance G, 11-ketoandrostenedione (abbreviated 11-KA4), 11-oxoandrostenedione (11-OXO), and androst-4-ene-3,11,17-trione. It is a steroid hormone with an extremely weak androgenic effect, and functions as an intermediate and prohormone of 11-ketotestosterone. Its molecular formula is C19H24O3, with a CAS Registry Number of 382-45-6 and a molecular weight of 300.39. The IUPAC name, as listed in chemical reference databases, is androst-4-ene-3,11,17-trione. The molecule is characterized by three oxo (ketone) groups at positions 3, 11, and 17 on its androst-4-ene backbone.

The compound belongs to the broader family of 11-oxyandrogens — adrenal-derived androgens that all share an oxygen atom on carbon 11. Within modern endocrinology, 11-ketoandrostenedione (11-KA4) is recognized as one of the novel human androgens, produced primarily in the adrenal gland, exerting androgen receptor binding activity of various degrees.

1.2 Natural Sources and Endogenous Occurrence

Adrenosterone occurs in trace amounts in humans as well as most mammals and in larger amounts in fish, where it is a precursor to the primary androgen, 11-ketotestosterone. In the human body, adrenosterone represents an endogenous steroid in the metabolism of the adrenal glands and emerges in the metabolic pathways of corticosteroids and androst-4-ene-3,17-dione.

CYP11B1 catalyzes the 11β-hydroxylation of androstenedione in the adrenal cortex, yielding 11β-hydroxyandrostenedione (11OHA4), which is released into circulation. 11OHA4 can be converted to 11-ketoandrostenedione (11KA4) in mineralocorticoid tissues expressing HSD11B2. The resulting 11KA4 can subsequently be converted to 11-ketotestosterone in peripheral tissue, such as adipose tissue, which expresses AKR1C3.

The adrenal gland is considered a source of weak androgens, such as dehydroepiandrosterone, dehydroepiandrosterone sulfate, and androstenedione. Emerging evidence proposes a set of 11-oxygenated 19-carbon (11oxC19) adrenal-derived steroids as clinically important androgens. Such steroids include 11β-hydroxyandrostenedione, 11-ketoandrostenedione, 11β-hydroxytestosterone, and 11-ketotestosterone.

1.3 Common Preparations and Forms

Adrenosterone has been sold as a dietary supplement since 2007 as a fat loss and muscle gaining supplement. In the supplement market, it has been marketed under several trade names, with the pioneering product being "11-OXO" by Ergopharm. Popular commercial preparations have included 11-OXO by Ergopharm, 11-Sterone by CEL, 11-X by LGI Supplements, and 11-Test by Black China Labs.

Commercially, the compound has been formulated primarily as oral capsules. Supplement-facing sources have also described topical (transdermal) preparations and, more recently, sublingual cyclodextrin-complexed formulations intended to improve bioavailability by bypassing first-pass hepatic metabolism. Because adrenosterone is a non-methylated steroidal compound, it lacks the alpha-17 alkylation that characterizes many hepatotoxic designer steroids, and this feature has historically been used to distinguish it from methylated prohormones. It is worth noting that no published peer-reviewed pharmacokinetic study of these specific delivery vehicles exists at the time of writing.

2. Discovery and Historical Context

2.1 Scientific Discovery

Adrenosterone was first isolated in 1936 from the adrenal cortex by Tadeus Reichstein at the Pharmaceutical Institute in the University of Basel, and was originally called Reichstein's substance G.

The Polish-Swiss biochemist Tadeus Reichstein shared the 1950 Nobel Prize for Physiology or Medicine with Philip S. Hench and Edward C. Kendall for discoveries concerning the structure and effects of hormones of the adrenal cortex. Reichstein's research on steroids, particularly on hormones of the adrenal cortex, paralleled that of Kendall in the United States. By 1936, Reichstein had isolated and identified adrenosterone; by 1942, Reichstein and colleagues had isolated 27 different adrenal corticosteroids in crystalline form.

Although the precursor 11β-hydroxyandrostenedione (11OHA4) was identified in the 1950s, it was considered a dead-end product of adrenal steroidogenesis and a way to prevent excessive androgen biosynthesis. Studies in the last decade, making use of mass spectrometry approaches, have shown that 11OHA4 is in fact a precursor to the potent androgen 11-ketotestosterone, that 11-oxygenated androgens contribute to the androgen pool in humans, and that they are important role players in several disease states.

2.2 Absence of Traditional Ethnobotanical Use

It is important to note that 11-Keto-Androstenetrione/adrenosterone does not have a documented pre-modern ethnobotanical or folk-medicine history. As an endogenous human hormone identified through twentieth-century laboratory techniques, there is no traditional herbal preparation, Ayurvedic formulation, traditional Chinese medicine preparation, or other historical use record attributable specifically to this compound. Its use is entirely a product of modern nutritional and sports supplementation science following laboratory identification of the molecule. Adrenosterone represents an endogenous steroid in the human metabolism of the adrenal glands that was characterized biochemically before any application in human supplementation was proposed.

Although the existence of 11-oxyandrogens has been acknowledged for several decades, exploration of their implications in human physiology and disease has been minimal until recently.

3. Key Constituents, Active Compounds, and Mechanisms of Action

3.1 Identity as a Prohormone

Adrenosterone is a steroid hormone with an extremely weak androgenic effect, and an intermediate/prohormone of 11-ketotestosterone. Its primary pharmacological relevance derives not from the parent molecule itself but from its downstream conversion and its inhibitory interaction with specific enzymes.

3.2 Conversion to 11-Ketotestosterone

11-Ketotestosterone, a downstream metabolite of 11β-hydroxyandrostenedione (which is mostly produced in peripheral tissues), and its 5α-reduced product, 11-ketodihydrotestosterone, are bioactive androgens, with potencies equivalent to those of testosterone and dihydrotestosterone. The clinical relevance of the 11oxC19 steroids resides in two key characteristics: the synthesis of all 11oxC19 originates predominantly in the adrenal cortex, and 11-ketotestosterone and its 5α-reduced metabolite, 11-ketodihydrotestosterone, are potent agonists of the human androgen receptor, similar to the classic androgens testosterone and dihydrotestosterone, respectively.

A landmark preclinical study confirmed this androgenic potency: this was the first study to show that 11-ketotestosterone and 11-ketodihydrotestosterone, like testosterone and DHT, are potent and efficacious agonists of the human androgen receptor and induced both the expression of representative AR-regulated genes as well as cellular proliferation in androgen-dependent prostate cancer cell lines.

3.3 Inhibition of 11β-Hydroxysteroid Dehydrogenase Type 1 (11β-HSD1)

It is proposed that adrenosterone may function as an inhibitor of the 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1), which is primarily responsible for reactivation of cortisol from cortisone. This proposed mechanism is the primary rationale for its use in sports and body-composition supplementation.

The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) contributes to intracellular glucocorticoid action by converting inactive cortisone to its receptor-active form, cortisol. 11β-HSD-1 is widely expressed, and particularly high expression levels are found in liver, brain, lung, adipose tissue, and vascular smooth muscle cells.

Adrenosterone is thought to be a competitive selective 11β-HSD1 inhibitor, which is responsible for activation of cortisol from cortisone. By competitively inhibiting 11β-HSD1, supplemental adrenosterone would theoretically reduce the local conversion of cortisone to the active glucocorticoid cortisol in tissues such as adipose and liver, thereby lowering tissue-level cortisol concentrations without necessarily disrupting circulating hormone levels.

It has also been proposed that 11-ketoandrostenedione (11KA4) functions as an inhibitor of 11β-HSD1, which catalyses the conversion of cortisone to cortisol. A reduction in cortisol, a catabolic hormone, is thought to be beneficial for increasing muscle mass.

3.4 Enzymatic Metabolism

The human metabolism of adrenosterone (11OXO) was already addressed in the 1950s and 1960s, and the main urinary metabolites were identified as 11β-hydroxy-androsterone (OHA), 11β-hydroxy-etiocholanolone (OHE), 11-oxo-androsterone (KA), and 11-oxo-etiocholanolone (KE).

From a doping-control investigation, substantially increased excretion of 11β-hydroxyandrosterone, 11β-hydroxyetiocholanolone, 11-oxoandrosterone, and 11-oxoetiocholanolone was observed after oral administration; minor metabolites such as 3α,17β-dihydroxy-5β-androstan-11-one, 3α-hydroxyandrost-4-ene-11,17-dione, and 3α,11β-dihydroxyandrost-4-en-17-one were also identified.

Both androstenedione and testosterone may undergo 11-hydroxylation catalyzed by P450c11β (CYP11B1 gene) to yield 11β-hydroxy-androstenedione and 11β-hydroxytestosterone, respectively. These 11-hydroxysteroids may be oxidized by 11β-hydroxysteroid dehydrogenase type 2 to 11-ketoandrostenedione and 11-ketotestosterone, respectively.

3.5 Non-Aromatizing Character

Unlike testosterone, adrenosterone and its principal metabolite 11-ketotestosterone are non-aromatizable; they cannot be converted by the aromatase enzyme into estrogens. This property is pharmacologically significant because supplemental use does not produce estrogenic side effects (such as gynecomastia) that are associated with many anabolic androgens and aromatizable prohormones. This structural feature has also been cited as a reason the compound does not require aromatase inhibitors when used in supplementation.

4. Scientific Evidence by Area of Use

4.1 Body Composition, Fat Loss, and Lean Mass

The primary proposed application of adrenosterone as a supplement is in body recomposition: reducing adipose tissue (particularly visceral/abdominal fat) while supporting lean muscle preservation or gain. The mechanistic basis links inhibition of 11β-HSD1 in adipose and liver tissue to reduced local cortisol exposure.

Excess cortisol is associated with numerous disorders, including diabetes, obesity, dyslipidemia, insulin resistance, and hypertension. The administration of 11β-HSD1 inhibitors decreases the level of cortisol and other 11β-hydroxysteroids in target tissues, thereby reducing the effects of excessive amounts of cortisol.

Targeted overexpression of 11β-HSD1 in adipocytes results in obesity owing to an increase in adipocyte differentiation and lipid accumulation. Conversely, in animal models, selective 11β-HSD1 inhibition has shown anti-obesity potential. Inhibition of 11β-HSD1 by a small molecule inhibitor decreased food intake and weight gain in diet-induced obese mice.

However, it is critical to distinguish these animal and in vitro findings from direct clinical evidence for adrenosterone itself. No peer-reviewed, placebo-controlled human clinical trial specifically examining adrenosterone/11-OXO supplementation on body composition has been published in the biomedical literature at the time of this writing. The body-composition claims circulating in the supplement market draw on mechanistic plausibility (the 11β-HSD1 inhibition pathway) and on animal data for related 11β-HSD1 inhibitors rather than direct human trials of the compound.

A relevant preclinical study in an animal model of metabolic syndrome showed that chronic 11β-HSD1 inhibition produced meaningful effects. A selective inhibitor of 11β-HSD1 significantly decreased 11β-HSD1 activity in adipose tissue and liver; in obese animals, it significantly decreased mean arterial pressure, glucose intolerance, insulin resistance, hypertriglyceridemia, and plasma renin activity. Whether adrenosterone achieves comparable enzyme inhibition at supplemental doses in humans has not been established in controlled trials.

4.2 Cortisol Modulation and Stress Response

11β-HSD1 inhibitors partially inhibit the enzymatic conversion of cortisone to cortisol, thereby adjusting cortisol levels. Inhibitors of 11β-HSD1 are believed to lower cortisol selectively within the tissues without impacting the normal variations of plasma cortisol during stress response. This selective tissue-level modulation, if achievable with adrenosterone in humans, would be mechanistically distinct from systemic cortisol suppression.

Reducing glucocorticoid exposure through 11β-HSD1 inhibition showed therapeutic promise across several cardiometabolic outcomes, including lowering weight, blood glucose, blood pressure, and cholesterol; however, variable efficacy and inconsistent effect sizes have delayed clinical progress for the pharmaceutical 11β-HSD1 inhibitor drug class broadly. This caveat applies equally to adrenosterone-based supplementation.

Evidence for cortisol modulation by adrenosterone in healthy human subjects remains largely theoretical or based on self-reported user experiences. No published, peer-reviewed pharmacodynamic study in humans measuring urinary free cortisol or tissue cortisol/cortisone ratios in response to adrenosterone supplementation could be identified.

4.3 Androgenic / Anabolic Activity

The conversion of adrenosterone to 11-ketotestosterone in peripheral tissues provides a pathway to androgenic activity. 11-Ketotestosterone is a bioactive 11-oxyandrogen, with a potency similar to that of testosterone, and its concentrations exceed those of testosterone in prepubertal children and in postmenopausal women.

11-ketotestosterone and 11-ketodihydrotestosterone, like testosterone and DHT, are potent and efficacious agonists of the human androgen receptor and induced both the expression of representative AR-regulated genes as well as cellular proliferation; proteomic analysis revealed that 11-ketodihydrotestosterone regulated the expression of more AR-regulated proteins than DHT in certain prostate cancer cell lines, while in vitro conversion assays showed that 11-ketotestosterone and 11-ketodihydrotestosterone are metabolized at a significantly lower rate compared to testosterone and DHT. The latter finding — slower metabolism — could theoretically prolong androgenic activity relative to classic androgens, though this has not been studied in the context of supplementation.

The overall evidence for anabolic effects of supplemental adrenosterone in humans is limited to anecdotal user reports and pharmacological inference. No randomized controlled trial has assessed muscle hypertrophy or strength gains attributable to adrenosterone supplementation.

4.4 Adrenal Androgen Physiology: Congenital Adrenal Hyperplasia and PCOS

The broader scientific relevance of 11-ketoandrostenedione (the endogenous equivalent of adrenosterone) has become increasingly apparent in clinical endocrinology. Accumulating evidence suggests that 11-oxyandrogens contribute to androgen excess in patients with 21-hydroxylase deficiency or polycystic ovary syndrome (PCOS). Unlike classic androgens, 11-oxyandrogens produced in maternal tumors can pass through the placenta without being converted into estrogens, and cause severe virilization of female fetuses.

Concentrations of 11-oxyandrogens are elevated in several disorders of androgen excess, making 11-ketoandrostenedione a potentially valuable biomarker rather than a therapeutic target in these conditions. These research findings pertain to endogenous 11-oxyandrogen biology, not to supplementation; they are cited here because they establish the physiological significance of the compound.

4.5 Adrenarche and Pediatric Endocrinology

Advanced bone age greater than one year compared to chronological age was positively associated with 11-ketotestosterone and 11β-hydroxytestosterone in girls with clinical signs of premature adrenarche. Investigators proposed that 11-oxo-androgens are a more sensitive steroid to be measured when premature adrenarche is suspected. This is a diagnostic rather than a therapeutic finding.

4.6 Metabolic Disease (Animal and Translational Data)

Scientific reports confirm that inhibition of 11β-HSD1 activity brings beneficial results for the alleviation of the course of metabolic syndrome in animal models. Cortisol in excess can trigger triglyceride formation and VLDL secretion in the liver, contributing to hyperlipidemia and associated dyslipidemia; 11β-HSD1 knockout mice have markedly lower plasma triglyceride levels and increased HDL cholesterol levels, indicating a potential atheroprotective phenotype.

These animal and genetic knockout findings provide a mechanistic rationale for 11β-HSD1 inhibition as a metabolic strategy, but they do not constitute clinical evidence for adrenosterone supplementation in metabolic disease. Translation of this research from preclinical studies has proved challenging so far; however, this is a growing area of research and more studies should focus on understanding the complex relationships between 11β-HSD1 and disease pathology.

4.7 Cognitive Function and Brain (Preclinical)

Inhibition of 11β-HSD1 activity in the brain, so as to lower cortisol levels, may also be useful to treat or reduce anxiety, depression, cognitive impairment, or age-related cognitive dysfunction. These are proposals based on the neurological role of cortisol and on studies of pharmaceutical 11β-HSD1 inhibitors, not on any clinical study of adrenosterone supplementation itself.

4.8 Prostate Cancer (Preclinical/In Vitro Only)

Research into the 11-oxyandrogen pathway has demonstrated relevance to castration-resistant prostate cancer. The adrenal steroid 11β-hydroxyandrostenedione serves as the precursor to the androgens 11-ketotestosterone and 11-ketodihydrotestosterone, and these compounds have been detected in prostate cancer tissue. 11-Ketotestosterone and 11-ketodihydrotestosterone are potent and efficacious agonists of the human androgen receptor and induced cellular proliferation in androgen-dependent prostate cancer cell lines. This finding is relevant to understanding disease mechanisms but does not support supplementation use; it raises the concern that supplemental adrenosterone, through conversion to 11-ketotestosterone, could potentially stimulate androgen-receptor-positive tissue.

5. Body Systems Associated with 11-Keto-Androstenetrione

  • Endocrine system / HPA axis: Directly involves the adrenal cortex as site of origin; modulates the cortisol–cortisone equilibrium via 11β-HSD1; relevant to the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis is the body's major neuroendocrine system secreting cortisol; when functioning normally, cortisol follows a diurnal rhythm with exposure to stress activating the HPA axis to temporarily increase cortisol.
  • Adipose tissue and metabolic regulation: High expression of 11β-HSD1 is found in adipose tissue; inhibition of this enzyme in adipose tissue is a primary proposed mechanism for fat-loss effects. 11β-HSD1 activity is elevated in subcutaneous adipose tissue in obese patients.
  • Liver: 11β-HSD1 is abundant in the liver; the liver is a key site for glucocorticoid reactivation and a target for the anti-lipogenic effects of 11β-HSD1 inhibition.
  • Skeletal muscle: Cortisol is catabolic to muscle protein; reducing tissue-level cortisol activation is proposed to preserve lean mass. A reduction in cortisol, a catabolic hormone, is thought to be beneficial for increasing muscle mass.
  • Reproductive / androgenic system: Via conversion to 11-ketotestosterone, adrenosterone engages the androgen receptor; 11-ketotestosterone and 11-ketodihydrotestosterone are bioactive androgens with potencies equivalent to testosterone and dihydrotestosterone.
  • Cardiovascular system: The role of cortisol in nitric oxide signaling and hence vasoconstriction has been investigated; these findings render 11β-HSD1 a potential target for controlling hypertension.
  • Central nervous system: Inhibition of 11β-HSD1 activity in the brain may be useful in reducing anxiety, depression, cognitive impairment, or age-related cognitive dysfunction — a preclinical hypothesis.
  • Skeletal system: Glucocorticoid-induced osteoporosis is the most common and serious side effect for patients receiving glucocorticoids; loss of bone mineral density is greatest in the first few months of use. 11β-HSD1 inhibition has been proposed as a strategy to protect bone, though no adrenosterone-specific bone data exist.

6. Dosage Forms and Doses Reported in Sources

No peer-reviewed pharmacokinetic or dose-ranging clinical trial specifically for adrenosterone (11-OXO) has been published. The following dosage information derives from supplement-industry sources, a doping-control research study, and non-peer-reviewed practitioner references, and is presented only as information found in identified sources — not as recommendations.

  • Doping-control research (single oral dose, 2009 study): The developed doping-control protocols for 11-ketotestosterone were tested to detect the administration of adrenosterone (11OXO) after a single oral dose of 100 mg. This was the dose used in a human pharmacokinetic/metabolite characterization study.
  • Supplement-industry beginner dosing: One supplement product label states "beginners 300 mg daily: three times a day with food, up to 8 weeks; advanced 300–500 mg daily, up to 12 weeks." (Source: supplement retail label as cited in available commercial documentation.) These are not clinically validated dosing regimens.
  • Forum-level practitioner dosing: User-community sources describe 300 mg/day for cutting purposes, 600 mg/day for moderate anabolic effects, and up to 900 mg/day for more pronounced effects over 7-week cycles, with the explicit caveat that these represent user reports rather than clinical data.
  • Delivery form considerations: As adrenosterone is not 17α-methylated, oral first-pass hepatic metabolism may significantly reduce bioavailability. Topical and sublingual cyclodextrin-complexed preparations have been marketed to improve systemic exposure, though no published bioavailability comparison study was identified.

A closely related compound, androst-4-ene-3,6,17-trione (6-OXO), has been studied in a peer-reviewed placebo-controlled trial at doses of 300 mg and 600 mg for eight weeks. Sixteen males were supplemented with either 300 mg or 600 mg of 6-OXO in a double-blind manner for eight weeks; blood and urine samples were analyzed for total testosterone, free testosterone, dihydrotestosterone, estradiol, estriol, estrone, SHBG, LH, FSH, growth hormone, and cortisol. For all of the serum hormones, there were no significant differences between groups; compared to baseline, free testosterone underwent overall increases of 90% for 300 mg and 84% for 600 mg; DHT underwent significant overall increases of 192% and 265% with 300 mg and 600 mg, respectively; and the T/E ratio increased 53% and 67% for the respective doses. This study is cited here for contextual comparison only; 6-OXO differs structurally from 11-OXO/adrenosterone in its ketone position (C-6 vs. C-11) and in its primary mechanism (aromatase inhibition rather than 11β-HSD1 inhibition), and the results of the 6-OXO trial cannot be extrapolated to adrenosterone.

7. Safety Considerations, Regulatory Status, and Drug Interactions

7.1 Anti-Doping and Regulatory Status

Adrenosterone (Androst-4-ene-3,11,17-trione, 11OXO) is forbidden in sports according to the Prohibited List of the World Anti-Doping Agency (WADA). In the context of doping controls, 11OXO belongs to the compounds forbidden for athletes at all times by WADA, and it is explicitly mentioned on WADA's Prohibited List.

The administration of 11OXO may be detected by monitoring the urinary concentrations of its main human metabolites 11β-hydroxy-androsterone and 11β-hydroxy-etiocholanolone. Preliminary urinary concentration and concentration ratio thresholds have been established for sports drug testing purposes, but adaptations are desirable as the suggested limits would result in numerous suspicious findings due to naturally elevated concentrations and ratios — reflecting the challenge that adrenosterone is also an endogenous human hormone.

Gas chromatography–mass spectrometry (GC-MS) and gas chromatography–combustion–isotope ratio mass spectrometry (GC-C-IRMS) methods have been developed specifically for discriminating exogenous administration from endogenous production, using carbon isotope ratio analysis as a confirmatory technique.

7.2 Non-Methylation and Hepatotoxicity

Adrenosterone is a non-17α-methylated steroid. The 17α-methyl group present in many designer steroids (e.g., methyltestosterone) is the primary structural feature associated with oral hepatotoxicity ("liver stress") in that class of compounds, because it inhibits first-pass hepatic oxidation. Because adrenosterone lacks this modification, it is not expected to produce the same degree of direct hepatotoxicity as methylated oral steroids. However, as a steroidal compound administered at supplemental doses exceeding endogenous levels by orders of magnitude, the absence of controlled long-term human safety data means definitive claims of hepatic safety cannot be made.

7.3 Androgenic Side Effects and Suppression of Endogenous Production

Because adrenosterone is a prohormone for 11-ketotestosterone — itself an active androgen receptor agonist — administration at higher doses raises the possibility of androgen-mediated effects including suppression of the hypothalamic-pituitary-gonadal (HPG) axis. 11-Oxyandrogens are present in cord blood and placenta as well as in the blood of men and women of various ages and are produced primarily in the adrenal gland; supraphysiological exogenous levels could theoretically suppress endogenous adrenal and gonadal androgen production through negative feedback, though no clinical study has formally quantified HPG suppression from adrenosterone supplementation.

Unlike classic androgens, 11-oxyandrogens can pass through the placenta without being converted into estrogens, and can cause severe virilization of female fetuses. This finding — derived from studies of virilizing tumors — highlights that 11-oxyandrogens are not without androgenic risk, and that use by pregnant or potentially pregnant women carries potential fetal risk.

7.4 Prostate Cancer Relevance

The adrenal steroid 11β-hydroxyandrostenedione serves as the precursor to 11-ketotestosterone and 11-ketodihydrotestosterone; comprehensively assessed androgenic activity showed that 11-ketotestosterone and 11-ketodihydrotestosterone are potent and efficacious agonists of the human androgen receptor and induced cellular proliferation in androgen-dependent prostate cancer cell lines. Individuals with androgen-sensitive conditions — including prostate cancer or benign prostatic hyperplasia — should be aware of this evidence when evaluating supplemental adrenosterone.

7.5 Polycystic Ovarian Syndrome and Female Hyperandrogenism

Accumulating evidence suggests that 11-oxyandrogens contribute to androgen excess in patients with polycystic ovary syndrome. Women with PCOS or other states of hyperandrogenism may exhibit an elevated baseline of endogenous 11-oxyandrogens; supplemental adrenosterone would be expected to further elevate this pool and potentially worsen androgenic symptoms.

7.6 Overall Evidence Characterization for Safety

There are no published long-term randomized controlled safety trials of adrenosterone supplementation in humans. The compound's safety profile is characterized predominantly by mechanistic inference, single-dose pharmacokinetic/metabolite identification studies (for anti-doping purposes), and anecdotal user experience. The lack of clinical safety data should be considered when evaluating this ingredient. The World Anti-Doping Agency's prohibition reflects regulatory concern about its androgenic properties at supraphysiological dosing levels.

Summary of Evidence Quality

The table below summarizes the strength of available evidence for the main proposed uses of 11-Keto-Androstenetrione (adrenosterone):

  • Mechanism of action (11β-HSD1 inhibition): Biochemically proposed and supported by the compound's structure and in vitro enzyme kinetics. No published in vivo human pharmacodynamic study directly measuring 11β-HSD1 inhibition by supplemental adrenosterone was identified.
  • Body composition (fat loss / lean mass): Mechanistically plausible; supported by animal studies of related 11β-HSD1 inhibitors. No peer-reviewed human clinical trial of adrenosterone for body composition exists. Evidence level: preclinical / theoretical only.
  • Androgenic activity (via 11-ketotestosterone): In vitro evidence confirms potent androgen receptor agonism of the metabolite 11-ketotestosterone. In vivo conversion efficiency in humans from supplemental doses is not characterized in peer-reviewed literature. Evidence level: in vitro / mechanistic.
  • Cortisol modulation: Supported by the 11β-HSD1 inhibitor mechanism and animal studies. No controlled human study with adrenosterone measuring cortisol outcomes was identified. Evidence level: preclinical / mechanistic.
  • Metabolic disease (obesity, insulin resistance, dyslipidemia): Supported by animal models of 11β-HSD1 inhibition. No human clinical trial data for adrenosterone specifically. Evidence level: animal / preclinical only.
  • Safety (human): Only single-dose metabolite characterization studies for anti-doping purposes. No long-term safety studies. WADA-prohibited substance. Evidence level: very limited.

References

Health Conditions

Health conditions that 11-keto-androstenetrione may help support.

  • No conditions available.

Body Systems

Body systems that 11-keto-androstenetrione may help support.

  • No body systems available.
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