Orals

Boldione

Updated · 18 sources · Editorial policy

Boldione (androsta-1,4-diene-3,17-dione, also called 1,4-androstadienedione or “ADD”) is a steroid prohormone: a compound the body converts into a more active steroid. In its case that steroid is boldenone, the anabolic steroid sold for veterinary use as Equipoise. In the 2000s boldione was sold online and in health stores as a supplement “advertised as a highly anabolic/androgenic compound,” in the words of a Korean doping-control laboratory (Kim et al., Rapid Commun Mass Spectrom 2006).

The single most important fact: boldione has never been tested for muscle, strength or safety in a controlled human trial, and it has never been an approved medicine. Its human literature consists of a handful of urine studies run by anti-doping laboratories, usually after a single dose in one volunteer. It has been a Schedule III controlled substance in the US since January 2010, and it is banned in sport at all times.

This page summarizes what the doping-control studies, laboratory and animal research, and regulators report. It is for education only and is not medical advice.

Property Detail
Class Synthetic androgen precursor (“prohormone”); the 17-keto form of boldenone
Chemical name Androsta-1,4-diene-3,17-dione; C₁₉H₂₄O₂; 284.4 g/mol; CAS 897-06-3 (PubChem CID 13472)
Medical approval None; no approved indication or labeled dose
Route Oral (as former supplements)
Doses studied in humans A single 100 mg oral dose in one volunteer (urine excretion study); no efficacy trials
Half-life No human half-life has been published. Boldione and its metabolites were detectable in urine for 48 h after 100 mg; one metabolite for up to 5 days
Main active metabolite Boldenone (17β-hydroxyandrosta-1,4-dien-3-one)
Aromatase In human placental tissue in vitro, a substrate converted to estrogens and also a time-dependent inactivator of the enzyme
US status Schedule III anabolic steroid since January 4, 2010
WADA status Prohibited at all times (S1.1 anabolic androgenic steroids), non-Specified

What it is

Boldione is androstenedione with one extra double bond, between carbons 1 and 2 of the A-ring. The US Drug Enforcement Administration (DEA) described its structure as differing from testosterone in just two features: a ketone (C=O) group at carbon 17 instead of testosterone’s hydroxyl group, and the 1,2 double bond (DEA final rule, Federal Register 2009).

The 17-ketone is what makes it a precursor. Enzymes called 17β-hydroxysteroid dehydrogenases, found in many human tissues, convert a 17-ketone into a 17β-hydroxyl group. For boldione that reaction produces boldenone, and DEA cited human studies showing this conversion takes place (DEA final rule, 2009).

Compound Relationship to boldione
Boldione (this page) 17-keto prohormone; converted to boldenone
Boldenone The active anabolic steroid; sold as esters such as boldenone undecylenate, boldenone cypionate and boldenone acetate
Androstenedione (4-AD) Same 17-keto structure without the 1,2 double bond; precursor of testosterone
1-Androstenedione (1-AD) 1,2 double bond but no 4,5 double bond; precursor of 1-testosterone. Also found as a urinary metabolite of boldione
19-Norandrostenedione The equivalent prohormone of nandrolone

An industrial chemical and a trace natural compound

Outside supplements, boldione (“ADD”) is a bulk intermediate of the pharmaceutical industry. Bacteria such as Mycolicibacterium species convert plant sterols (phytosterols, often from soybean oil) into androstenedione and androstadienedione, which are then used to make other steroid drugs. A 2022 review put the world market for these two intermediates at over 1,000 tons per year (Nunes et al., Molecules 2022).

The approved breast cancer drug exemestane (Aromasin) is a close chemical relative: its label describes it as 6-methylenandrosta-1,4-diene-3,17-dione, an irreversible steroidal aromatase inactivator (Aromasin label, DailyMed). Boldione itself has never been developed as a drug.

Small amounts of boldione also turn up in human urine without any supplement use. In a 5-week study of 6 men and 6 women, endogenous boldione appeared sporadically at 0.751–1.73 ng/mL, and a daily phytosterol-enriched yogurt drink did not change this (Verheyden et al., J Steroid Biochem Mol Biol 2009). Endogenous boldenone could not be proven in the same study. In a separate pilot, 10 women eating 25 g/day of phytosterol-enriched margarine for one week had no detectable boldenone in their urine (Ros et al., Food Addit Contam 2007).

How it works in the body

There are no formal human pharmacokinetic studies (blood levels over time) of boldione. What is known comes from urine studies by anti-doping laboratories, each giving the drug to a single volunteer.

Finding Study
After a single 100 mg oral dose, boldione and three metabolites appeared in urine and were detectable for 48 h Kim et al., Rapid Commun Mass Spectrom 2006
Maximum urinary excretion rates were reached 1.8 and 3.6 h after dosing Kim et al., 2006
Of the 100 mg dose, 34.45 mg was excreted in urine as unchanged boldione and 15.95 mg as boldenone Kim et al., 2006
15 metabolites were detected across free, glucuronide and sulfate fractions, including boldenone, 6β-hydroxy-boldenone, 1-androstenedione and 1-testosterone; the longest-detected metabolite was found up to 5 days after dosing Gómez et al., Drug Test Anal 2012
24 further metabolites were conjugated with cysteine or N-acetylcysteine, the first such report for an exogenous anabolic steroid Pozo et al., Drug Test Anal 2012
Boldione was rapidly converted to boldenone; reduction of the 1,2 double bond also produced metabolites identical to the body’s own androgens de la Torre et al., Drug Test Anal 2013

Two points stand out. First, about 34% of the dose came out in urine unchanged and about 16% as boldenone, all within two days, which fits a short-acting compound. Second, some metabolites are chemically identical to normal testosterone metabolites. The Rome anti-doping laboratory called these pseudoendogenous metabolites and showed that carbon isotope ratio testing (GC/C/IRMS, which can tell synthetic steroids from the body’s own) can still identify their synthetic origin (de la Torre et al., 2013).

Aromatase: substrate and inactivator, in vitro

Aromatase is the enzyme that turns androgens into estrogens. In human placental microsomes (a test-tube preparation of the enzyme), boldione was metabolized both to estrogens and to boldenone (Milewich et al., J Steroid Biochem 1981). In the same type of preparation it also caused a time-dependent loss of aromatase activity (Ki 0.32 µM), the pattern of a “suicide” inactivator (Covey & Hood, Cancer Res 1982).

These are enzyme experiments, not human studies. No study has measured estradiol or estrone in people taking boldione, so its net effect on estrogen levels in the body is unknown.

Regulatory status

  • United States. DEA classified boldione, along with desoxymethyltestosterone and 19-nor-4,9(10)-androstadienedione, as a Schedule III anabolic steroid in a final rule published December 4, 2009, effective January 4, 2010. As of August 2008, DEA had identified seven Internet-marketed dietary supplements claiming to contain boldione, and it received no comments describing any legitimate use (DEA final rule, Federal Register 2009). It is listed today in 21 CFR 1308.13, next to boldenone.
  • Sport. The WADA 2026 Prohibited List names “Boldione (androsta-1,4-diene-3,17-dione)” under S1.1 anabolic androgenic steroids, prohibited in and out of competition. All S1 substances are non-Specified Substances (WADA 2026 Prohibited List).
  • Medicine. There is no approved human or veterinary product containing boldione.

What the research shows

Humans: no efficacy data

No controlled trial has measured the effect of boldione on muscle mass, strength, body composition or performance in people. The only human studies are the single-volunteer urine studies above.

About “highly anabolic” claims. Supplement marketing presented boldione as a powerful muscle builder. That claim rests on its conversion to boldenone, not on any human outcome data. The evidence shows that people convert part of an oral dose to boldenone. It does not show how much muscle or strength, if any, results.

Animal and cell studies

DEA based its scheduling decision partly on two studies it sponsored. Both are described in the 2009 final rule, with the full reports placed in the rulemaking’s public docket (DEA final rule, 2009):

  • Castrated rats. Boldione delivered by capsules implanted under the skin prevented the shrinking of the prostate, seminal vesicles and levator ani muscle (a standard marker of anabolic effect) that follows castration. It also prevented the rise in LH and FSH (the pituitary hormones that drive the testes).
  • Intact rats. Boldione caused testicular atrophy (shrinking of the testes).
  • Cell culture. In C3H10T1/2 stem cells, boldione bound the androgen receptor and pushed the cells to form muscle cells. It was less potent than DHT in this assay.

In veal calves given boldenone or boldione at anabolic doses, as in illegal growth promotion, the prostate showed hypersecretion, and germ cells in the testes showed more cell death and less cell division, with the changes most marked in the boldione group (Cannizzo et al., J Vet Med Sci 2007). After a single oral dose of a boldione and boldenone combination in calves, boldione itself was never found in plasma or urine, while boldenone was (Draisci et al., Proteomics 2007).

These are rat, cell and cattle results. They show androgen-like activity, but they do not establish doses or effects in people.

Side effects and risks

No human safety data

Boldione has never been studied for safety in people, so there are no measured rates of side effects. Because part of each dose becomes boldenone, the androgen-related risks described for boldenone are the most relevant comparison; see the boldenone undecylenate page. Boldenone itself has never been tested in a controlled human trial either.

Suppression of the testes

The animal evidence points in one direction. In rats, boldione suppressed the rise in LH and FSH after castration and caused testicular atrophy in intact animals. In calves it increased germ-cell death in the testes (DEA final rule, 2009; Cannizzo et al., 2007). Whether and how strongly this happens in humans has not been measured.

Drug testing and contaminated supplements

Boldione is a doping risk even for people who do not knowingly take it:

  • A Dutch study of 66 high-risk sports supplements bought from web shops found undeclared doping substances in 25 of them (38%). Boldione was among the anabolic steroids detected (Duiven et al., J Sports Sci Med 2021).
  • The Cologne anti-doping laboratory reported that about 15% of 634 non-hormonal supplements bought in 13 countries in 2001–2002 contained undeclared anabolic steroids, mainly prohormones, and that products faked with boldenone and other steroids appeared from 2002 onward (Geyer et al., J Mass Spectrom 2008).

Because traces of boldione can also occur naturally, laboratories use carbon isotope ratio testing to confirm a synthetic origin (de la Torre et al., 2013; Verheyden et al., 2009).

Key takeaways

  • A prohormone of boldenone. Boldione is androstenedione with an extra 1,2 double bond. The body converts part of an oral dose to boldenone, which carries the 17β-hydroxyl group of active androgens.
  • Short-acting in urine studies. After a single 100 mg dose in one volunteer, 34.45 mg was excreted unchanged and 15.95 mg as boldenone, and boldione and its metabolites were detectable in urine for 48 h. No human half-life has been published.
  • No human efficacy or safety trials. Claims of strong anabolic effects come from marketing and from rat and cell studies, not from controlled human research.
  • Aromatase effects are known only in vitro. In placental enzyme preparations it is both converted to estrogens and inactivates aromatase over time.
  • Controlled and banned. It has been a US Schedule III anabolic steroid since January 4, 2010, and is prohibited at all times under WADA S1.1.
  • A supplement-contamination finding. It has been found as an undeclared ingredient in sports supplements, and laboratories use isotope testing to separate it from the small amounts the body makes naturally.

Sources

  1. Kim Y, Jun M, Lee W. Characterization of boldione and its metabolites in human urine by liquid chromatography/electrospray ionization mass spectrometry and gas chromatography/mass spectrometry. Rapid Commun Mass Spectrom. 2006;20(1):9–20. PubMed.
  2. Gómez C, Pozo OJ, Fabregat A, et al. Detection and characterization of urinary metabolites of boldione by LC-MS/MS. Part I: Phase I metabolites excreted free, as glucuronide and sulfate conjugates, and released after alkaline treatment of the urine. Drug Test Anal. 2012;4(10):775–785. PubMed.
  3. Pozo OJ, Gómez C, Marcos J, et al. Detection and characterization of urinary metabolites of boldione by LC-MS/MS. Part II: Conjugates with cysteine and N-acetylcysteine. Drug Test Anal. 2012;4(10):786–797. PubMed.
  4. de la Torre X, Curcio D, Colamonici C, et al. Metabolism of boldione in humans by mass spectrometric techniques: detection of pseudoendogenous metabolites. Drug Test Anal. 2013;5(11-12):834–842. PubMed.
  5. Verheyden K, Noppe H, Vanhaecke L, et al. Excretion of endogenous boldione in human urine: influence of phytosterol consumption. J Steroid Biochem Mol Biol. 2009;117(1-3):8–14. PubMed.
  6. Ros MM, Sterk SS, Verhagen H, et al. Phytosterol consumption and the anabolic steroid boldenone in humans: a hypothesis piloted. Food Addit Contam. 2007;24(7):679–684. PubMed.
  7. Milewich L, Bradfield DJ, Coe LD, et al. Metabolism of 1,4-androstadiene-3,17-dione by human placental microsomes. Enzyme properties and kinetic parameters in the formation of estrogens and 17 beta-hydroxy-1,4-androstadien-3-one. J Steroid Biochem. 1981;14(11):1115–1125. PubMed.
  8. Covey DF, Hood WF. A new hypothesis based on suicide substrate inhibitor studies for the mechanism of action of aromatase. Cancer Res. 1982;42(8 Suppl):3327s–3333s. PubMed.
  9. Drug Enforcement Administration. Classification of three steroids as schedule III anabolic steroids under the Controlled Substances Act. Final rule. Federal Register. December 4, 2009;74(232):63603–63610 (FR Doc E9-28572). govinfo.
  10. 21 CFR 1308.13, Schedule III. Electronic Code of Federal Regulations. eCFR.
  11. World Anti-Doping Agency. The 2026 Prohibited List, International Standard. In effect January 1, 2026. WADA 2026 Prohibited List.
  12. National Center for Biotechnology Information. Boldione (androsta-1,4-diene-3,17-dione), PubChem CID 13472. PubChem.
  13. Pharmacia & Upjohn. Aromasin (exemestane) tablets prescribing information. DailyMed.
  14. Nunes VO, Vanzellotti NC, Fraga JL, et al. Biotransformation of phytosterols into androstenedione—a technological prospecting study. Molecules. 2022;27(10):3164. PubMed.
  15. Cannizzo FT, Zancanaro G, Spada F, et al. Pathology of the testicle and sex accessory glands following the administration of boldenone and boldione as growth promoters in veal calves. J Vet Med Sci. 2007;69(11):1109–1116. PubMed.
  16. Draisci R, Montesissa C, Santamaria B, et al. Integrated analytical approach in veal calves administered the anabolic androgenic steroids boldenone and boldione: urine and plasma kinetic profile and changes in plasma protein expression. Proteomics. 2007;7(17):3184–3193. PubMed.
  17. Duiven E, van Loon LJC, Spruijt L, et al. Undeclared doping substances are highly prevalent in commercial sports nutrition supplements. J Sports Sci Med. 2021;20(2):328–338. PubMed.
  18. Geyer H, Parr MK, Koehler K, et al. Nutritional supplements cross-contaminated and faked with doping substances. J Mass Spectrom. 2008;43(7):892–902. PubMed.