Turinabol

updated

Turinabol (4-chlorodehydromethyltestosterone, sold as Oral Turinabol) is metandienone (Dianabol) with a chlorine at position 4, developed by Jenapharm in the 1960s. No controlled human efficacy trial has been found: the human work is a 1991 pharmacokinetic study, a five-volunteer excretion study run for doping control, three unabstracted 1965 and 1966 reports and one case report of an intratesticular leiomyosarcoma. A PubMed search on 9 October 2026 returned 108 records, none tagged as a clinical trial or randomized controlled trial.

17-alpha-methylated anabolic androgenic steroid (4-chloro derivative of metandienone)

  • Turinabol is 4-chloro-methandienone: metandienone (Dianabol) with a chlorine at position 4 (PubChem CID 98521, C20H27ClO2, molecular weight 334.9).
  • Jenapharm developed it in the 1960s and marketed it as Oral Turinabol. Three 1965 and 1966 clinical reports in East German journals have no abstract indexed, so no result is taken from them.
  • In the only human pharmacokinetic study, oral dosing showed marked enterohepatic circulation and a first-pass effect, and the terminal half-life after intravenous dosing was 16 hours.
  • In five healthy men given a single oral 5 mg dose for an excretion study, the long-term marker M3 was suitable in 4 of 5 and the last clearly positive urine sample came between 9.9 and 44.9 days.
  • One case report describes an intratesticular leiomyosarcoma in a 32-year-old man after 5 years of self-reported high-dose use. It is one case and a hypothesis, not a risk estimate.
  • A PubMed search on 9 October 2026 returned 108 records, and filtering to clinical trial and randomized controlled trial types returned 0. Turinabol is a Schedule III controlled substance in the United States.

What is Turinabol, and what is its legal status?

Turinabol is 4-chlorodehydromethyltestosterone, metandienone (Dianabol) with a chlorine at position 4. It is a Schedule III controlled substance in the United States, has no FDA label, and WADA prohibits it at all times.

The compound is PubChem CID 98521, C20H27ClO2, molecular weight 334.9, CAS 2446-23-3. PubChem synonyms include Oral Turinabol, Dehydrochlormethyltestosterone, 4-Chlorodehydromethyltestosterone, CDMT, 4-Chloro-methandienone and 4-Chlorodianabol. Chemically it is 4-chloro-17alpha-methyl-17beta-hydroxy-androsta-1,4-dien-3-one, which is metandienone (Dianabol) with a chlorine at position 4. The Dianabol relationship is literal.

Dehydrochloromethyltestosterone is a Schedule III controlled substance in the United States. 21 CFR 1308.13(f)(21) lists it as dehydrochloromethyltestosterone (4-chloro-17beta-hydroxy-17alpha-methyl-androst-1,4-dien-3-one), DEA code 4000, covering salts, esters and ethers. An openFDA Drugs@FDA substance-name query returned no matches and DailyMed returned no label on 9 October 2026. The WADA 2026 Prohibited List, in effect 1 January 2026, names Dehydrochlormethyltestosterone under S1.1, prohibited at all times as a non-specified substance. Legal status outside the United States is not covered here.

PubChem: Turinabol identity

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 98521, Oral Turinabol (dehydrochloromethyltestosterone).

The compound is PubChem CID 98521, C20H27ClO2, molecular weight 334.9, CAS 2446-23-3. PubChem synonyms include Oral turinabol, Oral-Turinabol, Dehydrochlormethyltestosterone, 4-Chlorodehydromethyltestosterone, CDMT, 4-Chloro-methandienone, 4-Chloromethandienone and 4-Chlorodianabol. Chemically it is 4-chloro-17alpha-methyl-17beta-hydroxy-androsta-1,4-dien-3-one, which is metandienone (Dianabol) with a chlorine at position 4.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule
Follow-up
Not applicable
Study design
Chemical database record
Funding
not stated in the source

The Dianabol relationship is literal: the same molecule with one added chlorine. Identity record only; it says nothing about activity or safety in people.

Read the original source
Schedule III (f)(21); WADA S1.1; 108 PubMed records, no trials

Regulatory record

Electronic Code of Federal Regulations, Title 21, section 1308.13, Schedule III. World Anti-Doping Agency, The 2026 Prohibited List, in effect 1 January 2026. openFDA Drugs@FDA, DailyMed, PubMed and ClinicalTrials.gov queries run 9 October 2026.

Dehydrochloromethyltestosterone is a Schedule III controlled substance in the United States: 21 CFR 1308.13(f)(21) lists it as dehydrochloromethyltestosterone (4-chloro-17beta-hydroxy-17alpha-methyl-androst-1,4-dien-3-one), DEA code 4000, covering salts, esters and ethers. The WADA 2026 Prohibited List names Dehydrochlormethyltestosterone under S1.1, prohibited at all times as a non-specified substance. An openFDA Drugs@FDA substance-name query returned no matches and DailyMed returned no label on 9 October 2026. On the same date, a PubMed search for dehydrochloromethyltestosterone or 4-chlorodehydromethyltestosterone or turinabol returned 108 records, and restricting to the clinical trial and randomized controlled trial publication types returned 0. A ClinicalTrials.gov query for turinabol and for dehydrochloromethyltestosterone each returned no studies. There is a real human literature for this compound, in pharmacokinetics and excretion, and there is no controlled human efficacy trial of any kind for lean mass, strength or athletic performance.

Participants / model
Regulatory records and reviewed literature, not a population
Treatment
Not applicable
Follow-up
Queries run 9 October 2026; WADA list in effect 1 January 2026
Study design
Codified federal regulation, official anti-doping record, dated literature and registry search
Funding
not stated in the source

Legal status outside the United States is not covered. The search counts are an absence finding as of 9 October 2026.

Read the original source

Where does Turinabol come from?

Jenapharm developed it in the 1960s and marketed it as Oral Turinabol. Three 1965 and 1966 clinical reports exist in East German journals but have no abstract indexed, so no result is taken from them. Documents of the East German doping program show androgens were given to thousands of athletes, without naming this compound.

Dehydrochloromethyltestosterone was developed by Jenapharm in the 1960s and marketed as Oral Turinabol. It is prohibited in sport at all times, and anti-doping laboratories report several findings every year.

The original clinical literature exists but is sparse, old, German-language and unabstracted. Three records from 1965 and 1966 describe clinical use: a 1965 report in Deutsche Gesundheitswesen titled [4-chloro-delta-1-methyltestosterone (Oral Turinabol), a new effective oral anabolic steroid], a 1965 report in Zeitschrift fuer die Gesamte Innere Medizin titled [Nitrogen metabolism in oral long-acting therapy with delta-1-4-chlormethyltestosterone (Oral Turinabol)], and a 1966 report titled [On the use of 'Oral-Turinabol' in pediatrics]. None has an abstract indexed in PubMed, so no result, dose, population size or outcome is taken from any of them. They establish only that the compound was clinically reported in East German journals in 1965 and 1966.

A peer-reviewed analysis of classified documents preserved after the collapse of the German Democratic Republic in 1990 shows that from 1966 onward hundreds of physicians and scientists performed doping research and administered prescription drugs and unapproved experimental preparations. Several thousand athletes were treated with androgens every year, including minors of each sex. Androgens were emphasized for women and adolescent girls because that proved particularly effective for sports performance. Damaging side effects were recorded, some requiring surgical or medical intervention, and prominent GDR scientists and sports physicians helped develop administration methods designed to evade international doping controls. That analysis documents the androgen program as a whole and does not name Oral-Turinabol, so this page takes no turinabol-specific dose, athlete count or outcome from it.

Five men, single oral 5 mg dose, urine for 60 days

Human study

Loke S et al. J Steroid Biochem Mol Biol. 2021;214:105978. PMID 34418529.

Five healthy male volunteers received 5 mg of DHCMT orally and urine was collected for 60 days, with unconjugated and glucuronidated fractions analyzed separately by GC-MS/MS. The long-term metabolite M3 was identified against reference material and was a suitable long-term marker in 4 of the 5 volunteers, detectable for 45 days after a single oral dose in one of them. In two volunteers the older marker M5 gave longer detection, and in one M3 was undetectable while M2 lasted longest. Across the five, the last clearly positive sample was collected between 9.9 and 44.9 days. The study measured excretion only. Its introduction states that dehydrochloromethyltestosterone was developed by Jenapharm in the 1960s and marketed as Oral Turinabol, that it is prohibited in sport at all times, and that new long-term metabolites proposed in 2011 and 2012 produced adverse analytical findings in retests of samples from the 2008 and 2012 Olympic Games.

Participants / model
Five healthy male volunteers
Treatment
Single oral 5 mg dose
Follow-up
Urine collected for 60 days
Study design
Controlled administration study with urinary excretion profiling
Funding
not stated in the source

The best-documented human exposure on record. The dose was given to time a detection window and is not a use dose. It reports no efficacy, hormone or body composition outcome.

Read the original source
1965 and 1966 East German clinical reports, titles only

Human study

DOERNER G. Dtsch Gesundheitsw. 1965;20:670-4. PMID 14304129.

Three records from 1965 and 1966 describe clinical use: a 1965 report in Deutsche Gesundheitswesen titled [4-chloro-delta-1-methyltestosterone (Oral Turinabol), a new effective oral anabolic steroid], a 1965 report in Zeitschrift fuer die Gesamte Innere Medizin titled [Nitrogen metabolism in oral long-acting therapy with delta-1-4-chlormethyltestosterone (Oral Turinabol)], and a 1966 report titled [On the use of 'Oral-Turinabol' in pediatrics]. None has an abstract indexed in PubMed, so no result, dose, population size or outcome is carried from any of them.

Participants / model
Not stated; the records carry title and journal only
Treatment
Oral Turinabol
Follow-up
not stated in the source
Study design
Original clinical reports, title-level record only
Funding
not stated in the source

These establish only that the compound was clinically reported in East German journals in 1965 and 1966. No result is taken from them.

Read the original source
East German androgen program documents; compound not named

Human study

Franke WW et al. Clin Chem. 1997;43(7):1262-79. PMID 9216474.

Classified documents preserved after the collapse of the German Democratic Republic in 1990, including top-secret doctoral theses, scientific reports, grant progress reports, symposium proceedings, and reports by physicians and scientists serving as unofficial Stasi collaborators, show that from 1966 onward hundreds of physicians and scientists performed doping research and administered prescription drugs and unapproved experimental preparations. Several thousand athletes were treated with androgens every year, including minors of each sex. Androgens were emphasized for women and adolescent girls because that proved particularly effective for sports performance. Damaging side effects were recorded, some requiring surgical or medical intervention, and prominent GDR scientists and sports physicians helped develop administration methods designed to evade international doping controls.

Participants / model
Several thousand GDR athletes per year, including minors of both sexes
Treatment
Prescription and unapproved experimental androgen preparations
Follow-up
From 1966 onward
Study design
Peer-reviewed documentary analysis of preserved state records
Funding
not stated in the source

The abstract documents the androgen program as a whole and does not name Oral-Turinabol, so no turinabol-specific dose, athlete count or outcome is taken from it.

Read the original source

What have studies in people measured?

Pharmacokinetics and urinary excretion in volunteers, not benefit. There is no controlled human efficacy trial for lean mass, strength or performance. A PubMed search on 9 October 2026 returned 108 records, and none was a clinical trial or randomized controlled trial.

Human pharmacokinetics come from a single study, from 1991. Tritium-labeled Oral-Turinabol was given to male volunteers orally and intravenously; the number of volunteers is not stated in the abstract. After 10 mg orally per volunteer the compound was almost completely absorbed, with peak plasma concentrations of total radioactivity and of parent drug at about 3 hours. The plasma profile after both routes showed irregularities attributed to marked enterohepatic circulation. Oral administration was subject to a first-pass effect that reduced systemic availability, and the AUC ratio of unchanged drug to total radioactivity of 1 to 13 shows that metabolites predominate in plasma. After intravenous dosing, disposition of unchanged drug was biphasic with a terminal half-life of 16 hours. Urinary total radioactivity was about 60% of the dose by both routes. Through its affinity for SHBG, the drug competes for testosterone protein binding and raises plasma non-protein-bound testosterone.

The modern controlled administration study is the best-documented human exposure on record. Five healthy male volunteers received 5 mg of DHCMT orally, and urine was collected for 60 days. The dose was given to time a detection window. The study measured excretion only and reports no efficacy, hormone or body composition outcome.

A PubMed search on 9 October 2026 for dehydrochloromethyltestosterone, 4-chlorodehydromethyltestosterone or turinabol returned 108 records. Restricting to the clinical trial and randomized controlled trial publication types returned 0. A ClinicalTrials.gov query for turinabol and for dehydrochloromethyltestosterone each returned no studies. There is a real human literature for this compound, in pharmacokinetics and excretion, and there is no controlled human efficacy trial of any kind for lean mass, strength or athletic performance. The three 1965 and 1966 reports have no abstract indexed, so they cannot be assessed.

Only human pharmacokinetic study: oral and intravenous

Human study

Schumann W. Pharmazie. 1991;46(9):650-4. PMID 1798729.

Tritium-labeled Oral-Turinabol was given to male volunteers orally and intravenously. After 10 mg orally per volunteer the compound was almost completely absorbed, with peak plasma concentrations of total radioactivity and of parent drug at about 3 hours. The plasma profile after both routes showed irregularities attributed to marked enterohepatic circulation. Oral administration was subject to a first-pass effect that reduced systemic availability, and the AUC ratio of unchanged drug to total radioactivity of 1 to 13 shows metabolites predominate in plasma. After intravenous dosing, disposition of unchanged drug was biphasic with a terminal half-life of 16 hours. Urinary total radioactivity was about 60% of the dose by both routes. The paper also reports that, through its affinity for SHBG, the drug competes for testosterone protein binding and raises plasma non-protein-bound testosterone.

Participants / model
Male volunteers; number not stated in the abstract
Treatment
Oral 10 mg and intravenous tritium-labeled Oral-Turinabol
Follow-up
not stated in the source
Study design
Clinical pharmacokinetic study
Funding
not stated in the source

The 16-hour half-life is the terminal half-life of unchanged drug after intravenous dosing. The oral dose was given to measure absorption and clearance and is not a use dose.

Read the original source
Five men, single oral 5 mg dose, urine for 60 days

Human study

Loke S et al. J Steroid Biochem Mol Biol. 2021;214:105978. PMID 34418529.

Five healthy male volunteers received 5 mg of DHCMT orally and urine was collected for 60 days, with unconjugated and glucuronidated fractions analyzed separately by GC-MS/MS. The long-term metabolite M3 was identified against reference material and was a suitable long-term marker in 4 of the 5 volunteers, detectable for 45 days after a single oral dose in one of them. In two volunteers the older marker M5 gave longer detection, and in one M3 was undetectable while M2 lasted longest. Across the five, the last clearly positive sample was collected between 9.9 and 44.9 days. The study measured excretion only. Its introduction states that dehydrochloromethyltestosterone was developed by Jenapharm in the 1960s and marketed as Oral Turinabol, that it is prohibited in sport at all times, and that new long-term metabolites proposed in 2011 and 2012 produced adverse analytical findings in retests of samples from the 2008 and 2012 Olympic Games.

Participants / model
Five healthy male volunteers
Treatment
Single oral 5 mg dose
Follow-up
Urine collected for 60 days
Study design
Controlled administration study with urinary excretion profiling
Funding
not stated in the source

The best-documented human exposure on record. The dose was given to time a detection window and is not a use dose. It reports no efficacy, hormone or body composition outcome.

Read the original source
Schedule III (f)(21); WADA S1.1; 108 PubMed records, no trials

Regulatory record

Electronic Code of Federal Regulations, Title 21, section 1308.13, Schedule III. World Anti-Doping Agency, The 2026 Prohibited List, in effect 1 January 2026. openFDA Drugs@FDA, DailyMed, PubMed and ClinicalTrials.gov queries run 9 October 2026.

Dehydrochloromethyltestosterone is a Schedule III controlled substance in the United States: 21 CFR 1308.13(f)(21) lists it as dehydrochloromethyltestosterone (4-chloro-17beta-hydroxy-17alpha-methyl-androst-1,4-dien-3-one), DEA code 4000, covering salts, esters and ethers. The WADA 2026 Prohibited List names Dehydrochlormethyltestosterone under S1.1, prohibited at all times as a non-specified substance. An openFDA Drugs@FDA substance-name query returned no matches and DailyMed returned no label on 9 October 2026. On the same date, a PubMed search for dehydrochloromethyltestosterone or 4-chlorodehydromethyltestosterone or turinabol returned 108 records, and restricting to the clinical trial and randomized controlled trial publication types returned 0. A ClinicalTrials.gov query for turinabol and for dehydrochloromethyltestosterone each returned no studies. There is a real human literature for this compound, in pharmacokinetics and excretion, and there is no controlled human efficacy trial of any kind for lean mass, strength or athletic performance.

Participants / model
Regulatory records and reviewed literature, not a population
Treatment
Not applicable
Follow-up
Queries run 9 October 2026; WADA list in effect 1 January 2026
Study design
Codified federal regulation, official anti-doping record, dated literature and registry search
Funding
not stated in the source

Legal status outside the United States is not covered. The search counts are an absence finding as of 9 October 2026.

Read the original source

How long can tests detect Turinabol?

In five volunteers given a single oral 5 mg dose, the last clearly positive urine sample came between 9.9 and 44.9 days, and the long-term marker M3 was suitable in 4 of 5. These are study findings, not predictions for any individual.

In the five-volunteer study, urine was collected for 60 days and the unconjugated and glucuronidated fractions were analyzed separately by GC-MS/MS. The long-term metabolite M3 was identified against reference material and was a suitable long-term marker in 4 of the 5 volunteers, detectable for 45 days after a single oral dose in one of them. In two volunteers the older marker M5 gave longer detection, and in one M3 was undetectable while M2 lasted longest. Across the five, the last clearly positive sample was collected between 9.9 and 44.9 days.

Biotransformation of DHCMT in man was studied by fractionating pooled DHCMT-positive human urines, which showed about 50 metabolites. Six new long-term metabolites were identified, including M3, which the authors showed to be superior in most cases to the previously known markers. New long-term metabolites proposed in 2011 and 2012 produced adverse analytical findings in retests of samples from the 2008 and 2012 Olympic Games.

Five men, single oral 5 mg dose, urine for 60 days

Human study

Loke S et al. J Steroid Biochem Mol Biol. 2021;214:105978. PMID 34418529.

Five healthy male volunteers received 5 mg of DHCMT orally and urine was collected for 60 days, with unconjugated and glucuronidated fractions analyzed separately by GC-MS/MS. The long-term metabolite M3 was identified against reference material and was a suitable long-term marker in 4 of the 5 volunteers, detectable for 45 days after a single oral dose in one of them. In two volunteers the older marker M5 gave longer detection, and in one M3 was undetectable while M2 lasted longest. Across the five, the last clearly positive sample was collected between 9.9 and 44.9 days. The study measured excretion only. Its introduction states that dehydrochloromethyltestosterone was developed by Jenapharm in the 1960s and marketed as Oral Turinabol, that it is prohibited in sport at all times, and that new long-term metabolites proposed in 2011 and 2012 produced adverse analytical findings in retests of samples from the 2008 and 2012 Olympic Games.

Participants / model
Five healthy male volunteers
Treatment
Single oral 5 mg dose
Follow-up
Urine collected for 60 days
Study design
Controlled administration study with urinary excretion profiling
Funding
not stated in the source

The best-documented human exposure on record. The dose was given to time a detection window and is not a use dose. It reports no efficacy, hormone or body composition outcome.

Read the original source
Six new long-term metabolites, including M3

Human study

Sobolevsky T et al. J Steroid Biochem Mol Biol. 2012;128(3-5):121-7. PMID 22142641.

Biotransformation of DHCMT in man was studied by fractionating pooled DHCMT-positive human urines, finding about 50 metabolites. Six new long-term metabolites were identified, including M3, which the authors showed to be superior in most cases to the previously known DHCMT markers. This 2012 work is the methodological basis for the Olympic retest findings.

Participants / model
Pooled human urine from DHCMT-positive doping control samples
Treatment
Not applicable
Follow-up
Not applicable
Study design
Analytical metabolite identification study
Funding
not stated in the source

Detection-method literature. It reports no effect or safety outcome.

Read the original source

What did the mouse heart study find?

In female mice, only exercise alone significantly raised cardiac capillary density at 6 weeks. Adding Oral-Turinabol or Dianabol to exercise did not, and the authors conclude anabolic steroids with exercise impair cardiac microvascular adaptation.

Female SPF-NMRI mice were assigned to sedentary control, treadmill exercise, sedentary Dianabol, exercise plus Dianabol, or exercise plus Oral-Turinabol, and left ventricular papillary muscle was examined at 3 and 6 weeks. Only the steroid plus exercise groups showed mild myocyte hypertrophy. Only exercise alone significantly increased capillary density: at 6 weeks, capillaries per square millimetre were 4,272 +/- 287 for control, 5,411 +/- 755 for exercise, 4,004 +/- 333 for Dianabol, 4,076 +/- 403 for Dianabol plus exercise, and 4,053 +/- 306 for Oral-Turinabol plus exercise, p<0.05. Only exercise alone shortened intercapillary distance.

The authors conclude that anabolic steroids combined with exercise impair cardiac microvascular adaptation to physical conditioning, which may compromise myocardial oxygen supply during exercise. This is a mouse experiment and does not give a human risk estimate.

Female mice: Oral-Turinabol blocked exercise-induced capillary gain

Animal study

Tagarakis CV et al. Int J Sports Med. 2000;21(6):412-8. PMID 10961516.

Female SPF-NMRI mice were assigned to sedentary control, treadmill exercise, sedentary Dianabol, exercise plus Dianabol, or exercise plus Oral-Turinabol, and left ventricular papillary muscle was examined at 3 and 6 weeks. Only the steroid plus exercise groups showed mild myocyte hypertrophy. Only exercise alone significantly increased capillary density: at 6 weeks, capillaries per square millimetre were 4,272 +/- 287 for control, 5,411 +/- 755 for exercise, 4,004 +/- 333 for Dianabol, 4,076 +/- 403 for Dianabol plus exercise, and 4,053 +/- 306 for Oral-Turinabol plus exercise, p<0.05. Only exercise alone shortened intercapillary distance. The authors conclude that anabolic steroids combined with exercise impair cardiac microvascular adaptation to physical conditioning, which may compromise myocardial oxygen supply during exercise.

Participants / model
Female SPF-NMRI mice
Treatment
Oral-Turinabol or Dianabol with treadmill exercise; route not stated in the source record
Follow-up
3 and 6 weeks
Study design
Controlled preclinical study
Funding
not stated in the source

A direct experimental harm signal in mice. It does not give a human risk estimate.

Read the original source

Is Turinabol a lean-gain Dianabol relative with less water retention and moderate toxicity?

The chemistry is right, but no controlled human evidence supports the benefit claims. It is Dianabol with a chlorine, but no controlled trial measures lean gain, no published comparison supports less water retention, and the only human pharmacokinetic study does not support a moderate-toxicity description.

Sellers describe Turinabol as a lean gain and athleticism oral, a non-aromatizing Dianabol relative with less water retention and moderate oral-steroid toxicity. Non-aromatizing is correct on the chemical structure and on the shared 17-alpha-methyl group, but no aromatization assay was located, so that claim rests on structure and not on a measurement. Less water retention has no published comparison behind it in any species. Lean gain and athleticism have never been measured in a controlled human trial.

Moderate toxicity is the claim that the evidence argues against most. The only human pharmacokinetic study shows marked enterohepatic circulation and a first-pass effect, with an AUC ratio of unchanged drug to total radioactivity of 1 to 13, so metabolites predominate in plasma. Moderate is a comparative word, and no published comparison exists.

PubChem: Turinabol identity

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 98521, Oral Turinabol (dehydrochloromethyltestosterone).

The compound is PubChem CID 98521, C20H27ClO2, molecular weight 334.9, CAS 2446-23-3. PubChem synonyms include Oral turinabol, Oral-Turinabol, Dehydrochlormethyltestosterone, 4-Chlorodehydromethyltestosterone, CDMT, 4-Chloro-methandienone, 4-Chloromethandienone and 4-Chlorodianabol. Chemically it is 4-chloro-17alpha-methyl-17beta-hydroxy-androsta-1,4-dien-3-one, which is metandienone (Dianabol) with a chlorine at position 4.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule
Follow-up
Not applicable
Study design
Chemical database record
Funding
not stated in the source

The Dianabol relationship is literal: the same molecule with one added chlorine. Identity record only; it says nothing about activity or safety in people.

Read the original source
Only human pharmacokinetic study: oral and intravenous

Human study

Schumann W. Pharmazie. 1991;46(9):650-4. PMID 1798729.

Tritium-labeled Oral-Turinabol was given to male volunteers orally and intravenously. After 10 mg orally per volunteer the compound was almost completely absorbed, with peak plasma concentrations of total radioactivity and of parent drug at about 3 hours. The plasma profile after both routes showed irregularities attributed to marked enterohepatic circulation. Oral administration was subject to a first-pass effect that reduced systemic availability, and the AUC ratio of unchanged drug to total radioactivity of 1 to 13 shows metabolites predominate in plasma. After intravenous dosing, disposition of unchanged drug was biphasic with a terminal half-life of 16 hours. Urinary total radioactivity was about 60% of the dose by both routes. The paper also reports that, through its affinity for SHBG, the drug competes for testosterone protein binding and raises plasma non-protein-bound testosterone.

Participants / model
Male volunteers; number not stated in the abstract
Treatment
Oral 10 mg and intravenous tritium-labeled Oral-Turinabol
Follow-up
not stated in the source
Study design
Clinical pharmacokinetic study
Funding
not stated in the source

The 16-hour half-life is the terminal half-life of unchanged drug after intravenous dosing. The oral dose was given to measure absorption and clearance and is not a use dose.

Read the original source
Schedule III (f)(21); WADA S1.1; 108 PubMed records, no trials

Regulatory record

Electronic Code of Federal Regulations, Title 21, section 1308.13, Schedule III. World Anti-Doping Agency, The 2026 Prohibited List, in effect 1 January 2026. openFDA Drugs@FDA, DailyMed, PubMed and ClinicalTrials.gov queries run 9 October 2026.

Dehydrochloromethyltestosterone is a Schedule III controlled substance in the United States: 21 CFR 1308.13(f)(21) lists it as dehydrochloromethyltestosterone (4-chloro-17beta-hydroxy-17alpha-methyl-androst-1,4-dien-3-one), DEA code 4000, covering salts, esters and ethers. The WADA 2026 Prohibited List names Dehydrochlormethyltestosterone under S1.1, prohibited at all times as a non-specified substance. An openFDA Drugs@FDA substance-name query returned no matches and DailyMed returned no label on 9 October 2026. On the same date, a PubMed search for dehydrochloromethyltestosterone or 4-chlorodehydromethyltestosterone or turinabol returned 108 records, and restricting to the clinical trial and randomized controlled trial publication types returned 0. A ClinicalTrials.gov query for turinabol and for dehydrochloromethyltestosterone each returned no studies. There is a real human literature for this compound, in pharmacokinetics and excretion, and there is no controlled human efficacy trial of any kind for lean mass, strength or athletic performance.

Participants / model
Regulatory records and reviewed literature, not a population
Treatment
Not applicable
Follow-up
Queries run 9 October 2026; WADA list in effect 1 January 2026
Study design
Codified federal regulation, official anti-doping record, dated literature and registry search
Funding
not stated in the source

Legal status outside the United States is not covered. The search counts are an absence finding as of 9 October 2026.

Read the original source

How does the body absorb and clear Turinabol?

Oral Turinabol was almost completely absorbed, peaked at about 3 hours, and showed a first-pass effect and marked enterohepatic circulation. After intravenous dosing the terminal half-life was 16 hours, and the drug competes for testosterone binding at SHBG.

In the only human pharmacokinetic study, oral dosing gave almost complete absorption, with peak plasma concentrations of total radioactivity and of parent drug at about 3 hours. Oral administration was subject to a first-pass effect, the plasma profile after both routes showed irregularities attributed to marked enterohepatic circulation, and metabolites predominate in plasma. After intravenous dosing, unchanged drug showed biphasic disposition with a terminal half-life of 16 hours. About 60% of the dose appeared in urine as total radioactivity by both routes.

Through its affinity for SHBG, the drug competes for testosterone protein binding and raises plasma non-protein-bound testosterone. The study did not state the number of volunteers in its abstract.

Only human pharmacokinetic study: oral and intravenous

Human study

Schumann W. Pharmazie. 1991;46(9):650-4. PMID 1798729.

Tritium-labeled Oral-Turinabol was given to male volunteers orally and intravenously. After 10 mg orally per volunteer the compound was almost completely absorbed, with peak plasma concentrations of total radioactivity and of parent drug at about 3 hours. The plasma profile after both routes showed irregularities attributed to marked enterohepatic circulation. Oral administration was subject to a first-pass effect that reduced systemic availability, and the AUC ratio of unchanged drug to total radioactivity of 1 to 13 shows metabolites predominate in plasma. After intravenous dosing, disposition of unchanged drug was biphasic with a terminal half-life of 16 hours. Urinary total radioactivity was about 60% of the dose by both routes. The paper also reports that, through its affinity for SHBG, the drug competes for testosterone protein binding and raises plasma non-protein-bound testosterone.

Participants / model
Male volunteers; number not stated in the abstract
Treatment
Oral 10 mg and intravenous tritium-labeled Oral-Turinabol
Follow-up
not stated in the source
Study design
Clinical pharmacokinetic study
Funding
not stated in the source

The 16-hour half-life is the terminal half-life of unchanged drug after intravenous dosing. The oral dose was given to measure absorption and clearance and is not a use dose.

Read the original source

What harms are documented for Turinabol?

No controlled human safety study exists. The record has one case report of an intratesticular leiomyosarcoma after 5 years of reported high-dose use, a mouse study showing impaired cardiac capillary adaptation, and a human pharmacokinetic study with marked enterohepatic circulation and a first-pass effect.

A 32-year-old man underwent right radical orchiectomy for a tumor of the upper pole of the right testicle, identified by growth pattern and immunohistochemistry as an intratesticular leiomyosarcoma. He reported a 5-year history of systematic high-dose Oral-Turinabol use beginning at age 18 and stopping about 9 years before presentation. The authors argue that the rarity of the tumor, the experimental induction of similar tumors in animals by androgens and estrogens, and the unusually young presentation support a cocarcinogenic role. That is a hypothesis in a single case, not an established causal link and not a risk estimate.

In female mice, Oral-Turinabol combined with exercise did not raise cardiac capillary density at 6 weeks (4,053 +/- 306 per square millimetre, against 5,411 +/- 755 for exercise alone), and the authors conclude that anabolic steroids with exercise impair cardiac microvascular adaptation.

The human pharmacokinetic study shows marked enterohepatic circulation and a first-pass effect. Documents of the East German androgen program record damaging side effects, some requiring surgical or medical intervention, but they do not name Oral-Turinabol. Turinabol is a Schedule III controlled substance in the United States.

One 32-year-old man: leiomyosarcoma after 5 years of use

Case report

Froehner M et al. Cancer. 1999;86(8):1571-5. PMID 10526287.

A 32-year-old man underwent right radical orchiectomy for a tumor of the upper pole of the right testicle, identified by growth pattern and immunohistochemistry as an intratesticular leiomyosarcoma. He reported a 5-year history of systematic high-dose Oral-Turinabol (4-chloro-1-dehydro-17alpha-methyltestosterone) use beginning at age 18 and stopping about 9 years before presentation. The authors argue that the rarity of the tumor, the experimental induction of similar tumors in animals by androgens and estrogens, and the unusually young presentation support a cocarcinogenic role.

Participants / model
One 32-year-old man
Treatment
Oral-Turinabol, high dose, self-reported over 5 years
Follow-up
5 years of reported use, stopping about 9 years before presentation
Study design
Case report
Funding
not stated in the source

A cocarcinogenic role is a hypothesis in a single case, not an established causal link and not a risk estimate.

Read the original source
Female mice: Oral-Turinabol blocked exercise-induced capillary gain

Animal study

Tagarakis CV et al. Int J Sports Med. 2000;21(6):412-8. PMID 10961516.

Female SPF-NMRI mice were assigned to sedentary control, treadmill exercise, sedentary Dianabol, exercise plus Dianabol, or exercise plus Oral-Turinabol, and left ventricular papillary muscle was examined at 3 and 6 weeks. Only the steroid plus exercise groups showed mild myocyte hypertrophy. Only exercise alone significantly increased capillary density: at 6 weeks, capillaries per square millimetre were 4,272 +/- 287 for control, 5,411 +/- 755 for exercise, 4,004 +/- 333 for Dianabol, 4,076 +/- 403 for Dianabol plus exercise, and 4,053 +/- 306 for Oral-Turinabol plus exercise, p<0.05. Only exercise alone shortened intercapillary distance. The authors conclude that anabolic steroids combined with exercise impair cardiac microvascular adaptation to physical conditioning, which may compromise myocardial oxygen supply during exercise.

Participants / model
Female SPF-NMRI mice
Treatment
Oral-Turinabol or Dianabol with treadmill exercise; route not stated in the source record
Follow-up
3 and 6 weeks
Study design
Controlled preclinical study
Funding
not stated in the source

A direct experimental harm signal in mice. It does not give a human risk estimate.

Read the original source
Only human pharmacokinetic study: oral and intravenous

Human study

Schumann W. Pharmazie. 1991;46(9):650-4. PMID 1798729.

Tritium-labeled Oral-Turinabol was given to male volunteers orally and intravenously. After 10 mg orally per volunteer the compound was almost completely absorbed, with peak plasma concentrations of total radioactivity and of parent drug at about 3 hours. The plasma profile after both routes showed irregularities attributed to marked enterohepatic circulation. Oral administration was subject to a first-pass effect that reduced systemic availability, and the AUC ratio of unchanged drug to total radioactivity of 1 to 13 shows metabolites predominate in plasma. After intravenous dosing, disposition of unchanged drug was biphasic with a terminal half-life of 16 hours. Urinary total radioactivity was about 60% of the dose by both routes. The paper also reports that, through its affinity for SHBG, the drug competes for testosterone protein binding and raises plasma non-protein-bound testosterone.

Participants / model
Male volunteers; number not stated in the abstract
Treatment
Oral 10 mg and intravenous tritium-labeled Oral-Turinabol
Follow-up
not stated in the source
Study design
Clinical pharmacokinetic study
Funding
not stated in the source

The 16-hour half-life is the terminal half-life of unchanged drug after intravenous dosing. The oral dose was given to measure absorption and clearance and is not a use dose.

Read the original source
East German androgen program documents; compound not named

Human study

Franke WW et al. Clin Chem. 1997;43(7):1262-79. PMID 9216474.

Classified documents preserved after the collapse of the German Democratic Republic in 1990, including top-secret doctoral theses, scientific reports, grant progress reports, symposium proceedings, and reports by physicians and scientists serving as unofficial Stasi collaborators, show that from 1966 onward hundreds of physicians and scientists performed doping research and administered prescription drugs and unapproved experimental preparations. Several thousand athletes were treated with androgens every year, including minors of each sex. Androgens were emphasized for women and adolescent girls because that proved particularly effective for sports performance. Damaging side effects were recorded, some requiring surgical or medical intervention, and prominent GDR scientists and sports physicians helped develop administration methods designed to evade international doping controls.

Participants / model
Several thousand GDR athletes per year, including minors of both sexes
Treatment
Prescription and unapproved experimental androgen preparations
Follow-up
From 1966 onward
Study design
Peer-reviewed documentary analysis of preserved state records
Funding
not stated in the source

The abstract documents the androgen program as a whole and does not name Oral-Turinabol, so no turinabol-specific dose, athlete count or outcome is taken from it.

Read the original source

Why does Turinabol sit in F tier?

The human record is pharmacokinetics and excretion with no efficacy trial, while the harm record is specific: marked enterohepatic circulation and first-pass loss, one case report of intratesticular leiomyosarcoma, and a mouse study showing impaired cardiac capillary adaptation.

Turinabol is methandienone with a chlorine, but its record differs in kind from that of a conventionally studied oral steroid. Its best-documented human exposures are five volunteers given 5 mg so a laboratory could time a detection window and a 1991 tritium pharmacokinetic study, and no controlled human efficacy trial of any kind has been found.

Against that sit a 17-alpha-methylated oral with marked enterohepatic circulation and a first-pass burden, a single case report of intratesticular leiomyosarcoma after 5 years of high-dose use starting at age 18, and a mouse experiment in which Oral-Turinabol did not allow the capillary growth that exercise alone produced. F reflects documented harm signals against a published upside of close to zero.

Only human pharmacokinetic study: oral and intravenous

Human study

Schumann W. Pharmazie. 1991;46(9):650-4. PMID 1798729.

Tritium-labeled Oral-Turinabol was given to male volunteers orally and intravenously. After 10 mg orally per volunteer the compound was almost completely absorbed, with peak plasma concentrations of total radioactivity and of parent drug at about 3 hours. The plasma profile after both routes showed irregularities attributed to marked enterohepatic circulation. Oral administration was subject to a first-pass effect that reduced systemic availability, and the AUC ratio of unchanged drug to total radioactivity of 1 to 13 shows metabolites predominate in plasma. After intravenous dosing, disposition of unchanged drug was biphasic with a terminal half-life of 16 hours. Urinary total radioactivity was about 60% of the dose by both routes. The paper also reports that, through its affinity for SHBG, the drug competes for testosterone protein binding and raises plasma non-protein-bound testosterone.

Participants / model
Male volunteers; number not stated in the abstract
Treatment
Oral 10 mg and intravenous tritium-labeled Oral-Turinabol
Follow-up
not stated in the source
Study design
Clinical pharmacokinetic study
Funding
not stated in the source

The 16-hour half-life is the terminal half-life of unchanged drug after intravenous dosing. The oral dose was given to measure absorption and clearance and is not a use dose.

Read the original source
Five men, single oral 5 mg dose, urine for 60 days

Human study

Loke S et al. J Steroid Biochem Mol Biol. 2021;214:105978. PMID 34418529.

Five healthy male volunteers received 5 mg of DHCMT orally and urine was collected for 60 days, with unconjugated and glucuronidated fractions analyzed separately by GC-MS/MS. The long-term metabolite M3 was identified against reference material and was a suitable long-term marker in 4 of the 5 volunteers, detectable for 45 days after a single oral dose in one of them. In two volunteers the older marker M5 gave longer detection, and in one M3 was undetectable while M2 lasted longest. Across the five, the last clearly positive sample was collected between 9.9 and 44.9 days. The study measured excretion only. Its introduction states that dehydrochloromethyltestosterone was developed by Jenapharm in the 1960s and marketed as Oral Turinabol, that it is prohibited in sport at all times, and that new long-term metabolites proposed in 2011 and 2012 produced adverse analytical findings in retests of samples from the 2008 and 2012 Olympic Games.

Participants / model
Five healthy male volunteers
Treatment
Single oral 5 mg dose
Follow-up
Urine collected for 60 days
Study design
Controlled administration study with urinary excretion profiling
Funding
not stated in the source

The best-documented human exposure on record. The dose was given to time a detection window and is not a use dose. It reports no efficacy, hormone or body composition outcome.

Read the original source
One 32-year-old man: leiomyosarcoma after 5 years of use

Case report

Froehner M et al. Cancer. 1999;86(8):1571-5. PMID 10526287.

A 32-year-old man underwent right radical orchiectomy for a tumor of the upper pole of the right testicle, identified by growth pattern and immunohistochemistry as an intratesticular leiomyosarcoma. He reported a 5-year history of systematic high-dose Oral-Turinabol (4-chloro-1-dehydro-17alpha-methyltestosterone) use beginning at age 18 and stopping about 9 years before presentation. The authors argue that the rarity of the tumor, the experimental induction of similar tumors in animals by androgens and estrogens, and the unusually young presentation support a cocarcinogenic role.

Participants / model
One 32-year-old man
Treatment
Oral-Turinabol, high dose, self-reported over 5 years
Follow-up
5 years of reported use, stopping about 9 years before presentation
Study design
Case report
Funding
not stated in the source

A cocarcinogenic role is a hypothesis in a single case, not an established causal link and not a risk estimate.

Read the original source
Female mice: Oral-Turinabol blocked exercise-induced capillary gain

Animal study

Tagarakis CV et al. Int J Sports Med. 2000;21(6):412-8. PMID 10961516.

Female SPF-NMRI mice were assigned to sedentary control, treadmill exercise, sedentary Dianabol, exercise plus Dianabol, or exercise plus Oral-Turinabol, and left ventricular papillary muscle was examined at 3 and 6 weeks. Only the steroid plus exercise groups showed mild myocyte hypertrophy. Only exercise alone significantly increased capillary density: at 6 weeks, capillaries per square millimetre were 4,272 +/- 287 for control, 5,411 +/- 755 for exercise, 4,004 +/- 333 for Dianabol, 4,076 +/- 403 for Dianabol plus exercise, and 4,053 +/- 306 for Oral-Turinabol plus exercise, p<0.05. Only exercise alone shortened intercapillary distance. The authors conclude that anabolic steroids combined with exercise impair cardiac microvascular adaptation to physical conditioning, which may compromise myocardial oxygen supply during exercise.

Participants / model
Female SPF-NMRI mice
Treatment
Oral-Turinabol or Dianabol with treadmill exercise; route not stated in the source record
Follow-up
3 and 6 weeks
Study design
Controlled preclinical study
Funding
not stated in the source

A direct experimental harm signal in mice. It does not give a human risk estimate.

Read the original source
Schedule III (f)(21); WADA S1.1; 108 PubMed records, no trials

Regulatory record

Electronic Code of Federal Regulations, Title 21, section 1308.13, Schedule III. World Anti-Doping Agency, The 2026 Prohibited List, in effect 1 January 2026. openFDA Drugs@FDA, DailyMed, PubMed and ClinicalTrials.gov queries run 9 October 2026.

Dehydrochloromethyltestosterone is a Schedule III controlled substance in the United States: 21 CFR 1308.13(f)(21) lists it as dehydrochloromethyltestosterone (4-chloro-17beta-hydroxy-17alpha-methyl-androst-1,4-dien-3-one), DEA code 4000, covering salts, esters and ethers. The WADA 2026 Prohibited List names Dehydrochlormethyltestosterone under S1.1, prohibited at all times as a non-specified substance. An openFDA Drugs@FDA substance-name query returned no matches and DailyMed returned no label on 9 October 2026. On the same date, a PubMed search for dehydrochloromethyltestosterone or 4-chlorodehydromethyltestosterone or turinabol returned 108 records, and restricting to the clinical trial and randomized controlled trial publication types returned 0. A ClinicalTrials.gov query for turinabol and for dehydrochloromethyltestosterone each returned no studies. There is a real human literature for this compound, in pharmacokinetics and excretion, and there is no controlled human efficacy trial of any kind for lean mass, strength or athletic performance.

Participants / model
Regulatory records and reviewed literature, not a population
Treatment
Not applicable
Follow-up
Queries run 9 October 2026; WADA list in effect 1 January 2026
Study design
Codified federal regulation, official anti-doping record, dated literature and registry search
Funding
not stated in the source

Legal status outside the United States is not covered. The search counts are an absence finding as of 9 October 2026.

Read the original source

Studies and sources

PubChem: Turinabol identity

Chemical identity record

PubChem, National Library of Medicine. Compound summary for CID 98521, Oral Turinabol (dehydrochloromethyltestosterone).

The compound is PubChem CID 98521, C20H27ClO2, molecular weight 334.9, CAS 2446-23-3. PubChem synonyms include Oral turinabol, Oral-Turinabol, Dehydrochlormethyltestosterone, 4-Chlorodehydromethyltestosterone, CDMT, 4-Chloro-methandienone, 4-Chloromethandienone and 4-Chlorodianabol. Chemically it is 4-chloro-17alpha-methyl-17beta-hydroxy-androsta-1,4-dien-3-one, which is metandienone (Dianabol) with a chlorine at position 4.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined molecule
Follow-up
Not applicable
Study design
Chemical database record
Funding
not stated in the source

The Dianabol relationship is literal: the same molecule with one added chlorine. Identity record only; it says nothing about activity or safety in people.

Read the original source
1965 and 1966 East German clinical reports, titles only

Human study

DOERNER G. Dtsch Gesundheitsw. 1965;20:670-4. PMID 14304129.

Three records from 1965 and 1966 describe clinical use: a 1965 report in Deutsche Gesundheitswesen titled [4-chloro-delta-1-methyltestosterone (Oral Turinabol), a new effective oral anabolic steroid], a 1965 report in Zeitschrift fuer die Gesamte Innere Medizin titled [Nitrogen metabolism in oral long-acting therapy with delta-1-4-chlormethyltestosterone (Oral Turinabol)], and a 1966 report titled [On the use of 'Oral-Turinabol' in pediatrics]. None has an abstract indexed in PubMed, so no result, dose, population size or outcome is carried from any of them.

Participants / model
Not stated; the records carry title and journal only
Treatment
Oral Turinabol
Follow-up
not stated in the source
Study design
Original clinical reports, title-level record only
Funding
not stated in the source

These establish only that the compound was clinically reported in East German journals in 1965 and 1966. No result is taken from them.

Read the original source
Only human pharmacokinetic study: oral and intravenous

Human study

Schumann W. Pharmazie. 1991;46(9):650-4. PMID 1798729.

Tritium-labeled Oral-Turinabol was given to male volunteers orally and intravenously. After 10 mg orally per volunteer the compound was almost completely absorbed, with peak plasma concentrations of total radioactivity and of parent drug at about 3 hours. The plasma profile after both routes showed irregularities attributed to marked enterohepatic circulation. Oral administration was subject to a first-pass effect that reduced systemic availability, and the AUC ratio of unchanged drug to total radioactivity of 1 to 13 shows metabolites predominate in plasma. After intravenous dosing, disposition of unchanged drug was biphasic with a terminal half-life of 16 hours. Urinary total radioactivity was about 60% of the dose by both routes. The paper also reports that, through its affinity for SHBG, the drug competes for testosterone protein binding and raises plasma non-protein-bound testosterone.

Participants / model
Male volunteers; number not stated in the abstract
Treatment
Oral 10 mg and intravenous tritium-labeled Oral-Turinabol
Follow-up
not stated in the source
Study design
Clinical pharmacokinetic study
Funding
not stated in the source

The 16-hour half-life is the terminal half-life of unchanged drug after intravenous dosing. The oral dose was given to measure absorption and clearance and is not a use dose.

Read the original source
Five men, single oral 5 mg dose, urine for 60 days

Human study

Loke S et al. J Steroid Biochem Mol Biol. 2021;214:105978. PMID 34418529.

Five healthy male volunteers received 5 mg of DHCMT orally and urine was collected for 60 days, with unconjugated and glucuronidated fractions analyzed separately by GC-MS/MS. The long-term metabolite M3 was identified against reference material and was a suitable long-term marker in 4 of the 5 volunteers, detectable for 45 days after a single oral dose in one of them. In two volunteers the older marker M5 gave longer detection, and in one M3 was undetectable while M2 lasted longest. Across the five, the last clearly positive sample was collected between 9.9 and 44.9 days. The study measured excretion only. Its introduction states that dehydrochloromethyltestosterone was developed by Jenapharm in the 1960s and marketed as Oral Turinabol, that it is prohibited in sport at all times, and that new long-term metabolites proposed in 2011 and 2012 produced adverse analytical findings in retests of samples from the 2008 and 2012 Olympic Games.

Participants / model
Five healthy male volunteers
Treatment
Single oral 5 mg dose
Follow-up
Urine collected for 60 days
Study design
Controlled administration study with urinary excretion profiling
Funding
not stated in the source

The best-documented human exposure on record. The dose was given to time a detection window and is not a use dose. It reports no efficacy, hormone or body composition outcome.

Read the original source
Six new long-term metabolites, including M3

Human study

Sobolevsky T et al. J Steroid Biochem Mol Biol. 2012;128(3-5):121-7. PMID 22142641.

Biotransformation of DHCMT in man was studied by fractionating pooled DHCMT-positive human urines, finding about 50 metabolites. Six new long-term metabolites were identified, including M3, which the authors showed to be superior in most cases to the previously known DHCMT markers. This 2012 work is the methodological basis for the Olympic retest findings.

Participants / model
Pooled human urine from DHCMT-positive doping control samples
Treatment
Not applicable
Follow-up
Not applicable
Study design
Analytical metabolite identification study
Funding
not stated in the source

Detection-method literature. It reports no effect or safety outcome.

Read the original source
East German androgen program documents; compound not named

Human study

Franke WW et al. Clin Chem. 1997;43(7):1262-79. PMID 9216474.

Classified documents preserved after the collapse of the German Democratic Republic in 1990, including top-secret doctoral theses, scientific reports, grant progress reports, symposium proceedings, and reports by physicians and scientists serving as unofficial Stasi collaborators, show that from 1966 onward hundreds of physicians and scientists performed doping research and administered prescription drugs and unapproved experimental preparations. Several thousand athletes were treated with androgens every year, including minors of each sex. Androgens were emphasized for women and adolescent girls because that proved particularly effective for sports performance. Damaging side effects were recorded, some requiring surgical or medical intervention, and prominent GDR scientists and sports physicians helped develop administration methods designed to evade international doping controls.

Participants / model
Several thousand GDR athletes per year, including minors of both sexes
Treatment
Prescription and unapproved experimental androgen preparations
Follow-up
From 1966 onward
Study design
Peer-reviewed documentary analysis of preserved state records
Funding
not stated in the source

The abstract documents the androgen program as a whole and does not name Oral-Turinabol, so no turinabol-specific dose, athlete count or outcome is taken from it.

Read the original source
One 32-year-old man: leiomyosarcoma after 5 years of use

Case report

Froehner M et al. Cancer. 1999;86(8):1571-5. PMID 10526287.

A 32-year-old man underwent right radical orchiectomy for a tumor of the upper pole of the right testicle, identified by growth pattern and immunohistochemistry as an intratesticular leiomyosarcoma. He reported a 5-year history of systematic high-dose Oral-Turinabol (4-chloro-1-dehydro-17alpha-methyltestosterone) use beginning at age 18 and stopping about 9 years before presentation. The authors argue that the rarity of the tumor, the experimental induction of similar tumors in animals by androgens and estrogens, and the unusually young presentation support a cocarcinogenic role.

Participants / model
One 32-year-old man
Treatment
Oral-Turinabol, high dose, self-reported over 5 years
Follow-up
5 years of reported use, stopping about 9 years before presentation
Study design
Case report
Funding
not stated in the source

A cocarcinogenic role is a hypothesis in a single case, not an established causal link and not a risk estimate.

Read the original source
Female mice: Oral-Turinabol blocked exercise-induced capillary gain

Animal study

Tagarakis CV et al. Int J Sports Med. 2000;21(6):412-8. PMID 10961516.

Female SPF-NMRI mice were assigned to sedentary control, treadmill exercise, sedentary Dianabol, exercise plus Dianabol, or exercise plus Oral-Turinabol, and left ventricular papillary muscle was examined at 3 and 6 weeks. Only the steroid plus exercise groups showed mild myocyte hypertrophy. Only exercise alone significantly increased capillary density: at 6 weeks, capillaries per square millimetre were 4,272 +/- 287 for control, 5,411 +/- 755 for exercise, 4,004 +/- 333 for Dianabol, 4,076 +/- 403 for Dianabol plus exercise, and 4,053 +/- 306 for Oral-Turinabol plus exercise, p<0.05. Only exercise alone shortened intercapillary distance. The authors conclude that anabolic steroids combined with exercise impair cardiac microvascular adaptation to physical conditioning, which may compromise myocardial oxygen supply during exercise.

Participants / model
Female SPF-NMRI mice
Treatment
Oral-Turinabol or Dianabol with treadmill exercise; route not stated in the source record
Follow-up
3 and 6 weeks
Study design
Controlled preclinical study
Funding
not stated in the source

A direct experimental harm signal in mice. It does not give a human risk estimate.

Read the original source
Schedule III (f)(21); WADA S1.1; 108 PubMed records, no trials

Regulatory record

Electronic Code of Federal Regulations, Title 21, section 1308.13, Schedule III. World Anti-Doping Agency, The 2026 Prohibited List, in effect 1 January 2026. openFDA Drugs@FDA, DailyMed, PubMed and ClinicalTrials.gov queries run 9 October 2026.

Dehydrochloromethyltestosterone is a Schedule III controlled substance in the United States: 21 CFR 1308.13(f)(21) lists it as dehydrochloromethyltestosterone (4-chloro-17beta-hydroxy-17alpha-methyl-androst-1,4-dien-3-one), DEA code 4000, covering salts, esters and ethers. The WADA 2026 Prohibited List names Dehydrochlormethyltestosterone under S1.1, prohibited at all times as a non-specified substance. An openFDA Drugs@FDA substance-name query returned no matches and DailyMed returned no label on 9 October 2026. On the same date, a PubMed search for dehydrochloromethyltestosterone or 4-chlorodehydromethyltestosterone or turinabol returned 108 records, and restricting to the clinical trial and randomized controlled trial publication types returned 0. A ClinicalTrials.gov query for turinabol and for dehydrochloromethyltestosterone each returned no studies. There is a real human literature for this compound, in pharmacokinetics and excretion, and there is no controlled human efficacy trial of any kind for lean mass, strength or athletic performance.

Participants / model
Regulatory records and reviewed literature, not a population
Treatment
Not applicable
Follow-up
Queries run 9 October 2026; WADA list in effect 1 January 2026
Study design
Codified federal regulation, official anti-doping record, dated literature and registry search
Funding
not stated in the source

Legal status outside the United States is not covered. The search counts are an absence finding as of 9 October 2026.

Read the original source

Why is Turinabol in F tier?

F fits a compound whose human record, apart from three unabstracted 1965 and 1966 reports, is pharmacokinetics and excretion rather than benefit, with no controlled efficacy trial found. The harm record is specific: marked enterohepatic circulation and a first-pass effect in the only human pharmacokinetic study, one case report of intratesticular leiomyosarcoma, and a mouse experiment in which Oral-Turinabol did not allow the capillary growth that exercise alone produced.