Orals

Madol (DMT)

Madol, also called desoxymethyltestosterone (DMT), is a designer anabolic-androgenic steroid: a 17α-methylated steroid that was never developed as a medicine. On this page, DMT means desoxymethyltestosterone, the steroid. It has nothing to do with the psychedelic N,N-dimethyltryptamine, which shares the same abbreviation but is an unrelated tryptamine drug.

Madol was first reported in a doping context in 2005, when the UCLA Olympic Analytical Laboratory identified it in an oily product said to contain a steroid that routine doping tests did not screen for (Sekera et al., Rapid Commun Mass Spectrom 2005). It was later sold online in products marketed as “dietary supplements.” The single most important fact: there are no controlled human trials of madol. What is known comes from rat and cell studies, doping-control metabolism work and analyses of supplement products. In the US it has been a Schedule III controlled substance since January 2010, and WADA bans it by name.

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

Property Detail
Class Designer 17α-methylated anabolic-androgenic steroid without a 3-keto group
Other names Desoxymethyltestosterone, DMT, madol, 17α-methyl-5α-androst-2-en-17β-ol
Not to be confused with N,N-dimethyltryptamine (the psychedelic “DMT”)
Formula / weight C₂₀H₃₂O; 288.5 g/mol (PubChem)
Route Oral (capsules sold as “supplements”); never approved for any route
Medical approval None; never commercially marketed as a drug
Studied human doses None; no controlled human trials
Half-life Not established in humans; no published human pharmacokinetic data
US status Schedule III anabolic steroid, effective January 4, 2010
WADA status Prohibited at all times (S1.1 anabolic androgenic steroids), listed by name

What it is

Madol’s chemical name is 17α-methyl-5α-androst-2-en-17β-ol (PubChem CID 18651). In its 2009 scheduling rule, the DEA described four structural differences from testosterone (DEA final rule, Federal Register 2009):

Change vs testosterone Note
No ketone group at carbon 3 Doping chemists group it with “non-ketoic” steroids for this reason (Okano et al. 2009)
Double bond between carbons 2 and 3 Replaces the 4,5 double bond of testosterone
No double bond between carbons 4 and 5 The A-ring is otherwise 5α-reduced, as in DHT-derived steroids
17α-methyl group The same modification found in oral steroids such as methyltestosterone and Superdrol

The DEA noted that none of these four features is known to eliminate anabolic or androgenic activity. The compound itself is not new. The DEA rule cites rat studies from 1963–1966 in which it was given by injection and by mouth and prevented atrophy of the prostate, seminal vesicles and levator ani muscle in castrated rats.

Madol is closely related to other designer steroids:

History in doping

Sekera and colleagues at UCLA synthesized madol to confirm its identity and developed a urine screening test for it. They described it as only the third steroid that had never been commercially marketed to be found in the context of performance-enhancing drugs in sport (Sekera et al. 2005). A 2015 paper from the Hong Kong Jockey Club racing laboratory placed it after the athlete findings of norbolethone (2002) and tetrahydrogestrinone (THG, 2003). It stated that madol was seized by officials at the US-Canadian border in 2005 and that a mixed martial arts athlete tested positive two years later (Kwok et al., J Mass Spectrom 2015).

How it works in the body

Androgen receptor activity

The main pharmacology study comes from the German Sports University Cologne (Diel et al., Toxicol Lett 2007). In cell and rat experiments, madol:

  • activated androgen receptor (AR) reporter-gene expression with about half the potency of DHT;
  • bound the AR with high selectivity, with low binding to the progesterone receptor;
  • in castrated rats, increased the weight of the levator ani muscle without increasing prostate or seminal vesicle weight, and did not stimulate prostate cell proliferation, which testosterone propionate did;
  • like testosterone, raised IGF-1 and myostatin mRNA in the gastrocnemius (calf) muscle.

The authors described madol as a potent AR agonist with “SARM-like” (tissue-selective) properties in rats. A follow-up study from the same group gave castrated rats madol, 19-norandrostenedione or testosterone propionate at 1 mg/kg/day under the skin for 12 days (Frese et al., Arch Toxicol 2011). Madol again stimulated the levator ani but not the prostate or seminal vesicles, and shifted muscle myosin heavy chain expression toward the IId/x type, as testosterone did.

About “selective” or “dry” claims. The tissue-selective profile above comes from castrated rats in short experiments. No study has tested whether madol spares the prostate, the hormonal axis or other tissues in people, and the rat studies themselves reported possible harms (see below). The rat profile should not be assumed to carry over to humans.

Metabolism and detection

There is no published human pharmacokinetic study, so madol’s half-life in people is unknown. Doping-control research describes how it is broken down:

Finding Source
In human liver microsomes, madol formed the same metabolite seen in urine from a baboon given the drug Sekera et al. 2005
The main urinary metabolite, produced in cultures of fresh human liver cells, is 17α-methyl-2β,3α,17β-trihydroxy-5α-androstane Gauthier et al., Steroids 2012
In vitro, metabolism of madol and its analogues occurs mainly in the A-ring (enone formation, hydroxylation and reduction), with some hydroxylation of the 17α-methyl group Kwok et al. 2015
About 20 metabolites were found in human excretion urine. Newer long-term metabolites were detectable for at least 14 days, compared with 5–7 days for previously reported ones Sobolevsky and Rodchenkov, Drug Test Anal 2012

The detection windows above describe how long doping tests can find traces in urine. They are not a measure of how long the drug acts in the body.

Regulatory status

Madol has never been approved as a medicine anywhere we could verify.

  • United States. The DEA proposed control in April 2008 and issued a final rule classifying boldione, desoxymethyltestosterone and 19-nor-4,9(10)-androstadienedione as Schedule III anabolic steroids, effective January 4, 2010 (DEA final rule, Federal Register 2009). It is named in the current Schedule III list as “desoxymethyltestosterone (17α-methyl-5α-androst-2-en-17β-ol) (a.k.a. ‘madol’)” (21 CFR 1308.13). As of August 2008, the DEA had identified 23 dietary supplements claiming to contain madol, all sold online. It received no comments describing any legitimate use.
  • Sport. WADA lists desoxymethyltestosterone under S1.1 anabolic androgenic steroids, prohibited at all times, in and out of competition (WADA 2026 Prohibited List).

The related compounds boldione and 19-norandrostenedione have their own pages.

What the research shows

No controlled human trial of madol has been published, and no study has measured its effects on muscle mass, strength or performance in people. The evidence base consists of:

  • rat studies showing anabolic activity on the levator ani muscle and changes in muscle gene expression (Diel et al. 2007; Frese et al. 2011);
  • older castrated-rat studies from the 1960s cited by the DEA;
  • doping-control metabolism and detection studies;
  • product analyses and a small number of human case reports.

Claims about how much muscle or strength madol produces in people are therefore not supported by published data.

Side effects and risks

Findings from animal and cell studies

Finding Model Source
Significant increase in heart weight, which testosterone propionate did not cause Castrated rats Diel et al. 2007
Slight stimulation of the liver enzyme gene tyrosine aminotransferase, read by the authors as a possible sign of liver effects Castrated rats Diel et al. 2007
Concentration-dependent chromosome damage (micronuclei); the background rate doubled at 27 µM. The pattern pointed to a clastogenic (chromosome-breaking) mechanism Hamster V79 cells in culture Dorn et al., Toxicol Lett 2008

Dorn and colleagues concluded that genotoxic hazards could not be ruled out at the high doses used in doping. These are laboratory findings; whether they occur in people has not been studied.

Liver injury

A 2016 report described drug-induced liver injury in two deployed US service members who had taken “prohormone” supplements, and the authors called it the first report of clinical hepatotoxicity with desoxymethyltestosterone (Magee et al., Mil Med 2016). One patient developed cholestatic jaundice (yellowing from blocked bile flow) after 10 weeks; bilirubin normalized about 8 weeks after stopping. The other had liver enzyme rises and marked lipid changes after 21 days, which returned to baseline 4–8 weeks after stopping. When the products were tested, their contents did not match their labels, and 3 of 4 contained federally controlled anabolic steroids.

The authors noted that liver injury from anabolic steroids varies in pattern and that lipid changes may be an important clinical clue. Madol-specific human safety data are limited to case reports such as this one.

What has not been studied

No study has measured madol’s effects in people on the body’s own testosterone production, fertility, blood lipids, blood pressure, the heart or, in women, virilization. The size and frequency of these risks for madol are unknown.

Quality and contamination

Madol has mostly been sold in products labeled as supplements, and analyses repeatedly show that labels cannot be trusted:

  • Undeclared madol. An Epistane product labeled as containing only methylepitiostanol also contained madol, and a “P-PLEX” product contained madol plus its 3-ene isomer (Okano et al. 2009).
  • Missing madol. In 2025, the Beijing Anti-Doping Laboratory bought a “Pheraplex” product online whose label stated 10 mg of DMT per capsule. It contained no madol or any other routinely screened steroid. NMR analysis identified a different steroid, 17,17-dimethyl-18-nor-5α-androst-13-en-3β-ol, previously described as a metabolite of methyltestosterone (Zhu et al., Drug Test Anal 2025).
  • Mislabeled “prohormones.” In the 2016 liver-injury cases, product contents did not match their labels (Magee et al. 2016).

Key takeaways

  • Not the psychedelic. Here DMT means desoxymethyltestosterone, a 17α-methylated designer steroid, not N,N-dimethyltryptamine.
  • Never a medicine. Madol was studied in rats in the 1960s but never marketed; it surfaced in doping in 2005 and then in online “supplements.”
  • No human trials. Its anabolic activity is documented in castrated rats and cell assays; there is no human efficacy, dosing or pharmacokinetic data.
  • Warning signs in the lab. Rat studies found increased heart weight and a possible liver signal, and cell studies found chromosome damage at high concentrations. A 2016 case report linked it to liver injury.
  • Labels are unreliable. Products have contained madol without declaring it, or claimed madol and contained a different steroid.
  • Controlled and banned. Schedule III in the US since January 4, 2010, and prohibited at all times by WADA.

Sources

  1. Sekera MH, Ahrens BD, Chang YC, et al. Another designer steroid: discovery, synthesis, and detection of ‘madol’ in urine. Rapid Commun Mass Spectrom. 2005;19(6):781–784. PubMed.
  2. Kwok WH, Kwok KY, Leung DK, et al. In vitro metabolism studies of desoxy-methyltestosterone (DMT) and its five analogues, and in vivo metabolism of desoxy-vinyltestosterone (DVT) in horses. J Mass Spectrom. 2015;50(8):994–1005. PubMed.
  3. 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.
  4. 21 CFR 1308.13 — Schedule III. Electronic Code of Federal Regulations. eCFR.
  5. World Anti-Doping Agency. The 2026 Prohibited List, International Standard. In effect January 1, 2026. WADA.
  6. National Center for Biotechnology Information. PubChem Compound Summary for CID 18651, Madol. PubChem.
  7. Diel P, Friedel A, Geyer H, et al. Characterisation of the pharmacological profile of desoxymethyltestosterone (Madol), a steroid misused for doping. Toxicol Lett. 2007;169(1):64–71. PubMed.
  8. Frese S, Velders M, Schleipen B, et al. Myosin heavy chain expression pattern as a marker for anabolic potency: desoxymethyltestosterone (madol), norandrostenedione and testosterone repress MHC-IIb expression and stimulate MHC-IId/x expression in orchiectomized rat gastrocnemius muscle. Arch Toxicol. 2011;85(6):635–643. PubMed.
  9. Dorn SB, Bolt HM, Thevis M, et al. Micronucleus induction in V79 cells by the anabolic doping steroids desoxymethyltestosterone (madol) and 19-norandrostenedione. Toxicol Lett. 2008;183(1–3):58–64. PubMed.
  10. Gauthier J, Poirier D, Ayotte C. Characterization of desoxymethyltestosterone main urinary metabolite produced from cultures of human fresh hepatocytes. Steroids. 2012;77(6):635–643. PubMed.
  11. Sobolevsky T, Rodchenkov G. Mass spectrometric description of novel oxymetholone and desoxymethyltestosterone metabolites identified in human urine and their importance for doping control. Drug Test Anal. 2012;4(9):682–691. PubMed.
  12. Okano M, Sato M, Ikekita A, et al. Analysis of non-ketoic steroids 17alpha-methylepithiostanol and desoxymethyl-testosterone in dietary supplements. Drug Test Anal. 2009;1(11–12):518–525. PubMed.
  13. Waller CC, Weththasinghe SA, McClure L, et al. In vivo metabolism of the designer anabolic steroid hemapolin in the thoroughbred horse. Drug Test Anal. 2020;12(6):752–762. PubMed.
  14. Magee CD, Witte S, Kwok RM, et al. Mission compromised? Drug-induced liver injury from prohormone supplements containing anabolic-androgenic steroids in two deployed U.S. service members. Mil Med. 2016;181(9):e1169–e1171. PubMed.
  15. Zhu S, Wang S, Liu X, et al. A “Pheraplex” capsule labeled as desoxymethyltestosterone from the market turned out to be 17,17-dimethyl-18-nor-5α-androst-13-en-3β-ol. Drug Test Anal. 2025;17(10):2032–2035. PubMed.