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Turinabol

4-Chlorodehydromethyltestosterone · Tbol

Turinabol (4-chlorodehydromethyltestosterone, "Tbol") is an orally active, 17-alpha-alkylated anabolic-androgenic steroid (AAS) originally made by Jenapharm as Oral-Turinabol and infamous as the primary drug of the East German (GDR) state doping program, where it was given to thousands of athletes — including women and minors — with documented damaging side effects, some requiring medical or surgical intervention. It is a chemical relative of methandienone (Dianabol) with an added 4-chloro group. There are essentially no modern controlled human safety-outcome studies of turinabol; almost everything known about its dangers comes from historical GDR-era observations of harm plus extrapolation from the broader AAS class. Because it is 17-alpha-alkylated and taken by mouth, it carries the class liver-toxicity profile of oral AAS (cholestasis, peliosis, tumors); like all AAS it suppresses the body's own testosterone production (HPTA suppression), worsens cholesterol/cardiovascular risk, and in women causes virilization that can be permanent. This monograph leads with risk and is educational only — not medical advice; anyone using or considering it should be under a physician's care with regular bloodwork. 21+ only.

Clinical readoutAAS · oral-17aa
Hepatic strainHigh
CardiovascularNone
HPTA suppressionHigh
Half-life
16 h
Route
Oral
Evidence
C
Active
Pharmacologic duration…
16 h32 h2 d2.7 d3.3 d
Illustrative single-compartment washout · each mark = one half-life · t½ ≈ The parent drug's elimination half-life is not well characterized in primary human literature (secondary sources often cite roughly 16 hours, which should be treated as uncertain). What is documented is that urinary metabolites persist far longer: after a single 5 mg oral dose in healthy men, long-term metabolites remained detectable for up to ~45 days.
Pharmacology

Mechanism of action

Turinabol is a synthetic derivative of testosterone that binds the androgen receptor and drives androgen-receptor-mediated anabolic (muscle protein synthesis, nitrogen retention) and androgenic signaling. Structurally it is methandienone with a 4-chloro substitution plus a 17-alpha-methyl group; the 17-alpha-alkylation lets it survive hepatic first-pass metabolism so it can be taken orally, and the 4-chloro group reduces its conversion to estrogen and its 5-alpha-reduction. Like all exogenous androgens it exerts negative feedback on the hypothalamic-pituitary-testicular (HPT) axis, suppressing LH/FSH and endogenous testosterone. Turinabol-specific receptor/mechanistic human data are sparse; the mechanism is inferred from its structure and the shared pharmacology of 17-alpha-alkylated AAS.
Kinetics

Pharmacokinetics

Half-life

The parent drug's elimination half-life is not well characterized in primary human literature (secondary sources often cite roughly 16 hours, which should be treated as uncertain). What is documented is that urinary metabolites persist far longer: after a single 5 mg oral dose in healthy men, long-term metabolites remained detectable for up to ~45 days.

Active duration

Pharmacologic duration of action is not rigorously defined in primary literature; the compound was historically dosed daily. Metabolite persistence over weeks reflects slow clearance of reduced metabolites, not sustained anabolic effect.

Route

Oral. It is 17-alpha-alkylated specifically to resist first-pass hepatic breakdown so it is orally bioavailable, the same feature that makes it hepatotoxic.

Metabolism & clearance

Extensively hepatically metabolized via phase I reduction of the A-ring and D-ring modifications and via 17-epimerization, followed by phase II glucuronidation; metabolites are excreted in urine (both glucuronidated and unconjugated fractions). PK/washout data are presented for monitoring and clinician discussion only, not for drug-test evasion.

For monitoring and washout planning, not drug-test evasion.

Reported effects

Physiological & performance effects

  • Increases lean muscle mass and strength via androgen-receptor-mediated anabolism (basis for its historical performance-enhancing misuse; documented in the GDR doping program)
  • Nitrogen retention and increased protein synthesis (class effect of AAS)
  • Comparatively low estrogenic activity due to the 4-chloro substitution (inferred from structure; limited direct human data)
  • In women and adolescents, produced measurable performance gains in the GDR program alongside virilizing side effects
  • No legitimate current medical indication; use is non-therapeutic/performance-driven
Safety

Adverse effects by system

Cardiovascular

No turinabol-specific cardiovascular outcome data exist. As an oral 17-alpha-alkylated AAS it is expected to adversely shift lipids (notably lowering HDL cholesterol) and raise blood pressure; the broader AAS class is associated with reduced left-ventricular systolic and diastolic function, accelerated coronary atherosclerosis, cardiomyopathy, and arrhythmia in long-term users.

Hepatic

17-alpha-alkylated oral AAS as a class cause dose- and duration-dependent liver injury: cholestasis (impaired bile flow), transaminase elevation, peliosis hepatis (blood-filled hepatic cavities), and benign/malignant liver tumors; fatal cholestatic necrosis has been reported with oral 17aa agents. Turinabol-specific hepatotoxicity reports are limited, but the structural class assignment makes this a primary concern.

Endocrine / HPTA

Suppresses the hypothalamic-pituitary-testicular axis, lowering LH/FSH and endogenous testosterone production (class effect of all AAS). This causes a functional hypogonadism during and after use.

Reproductive

In men: testicular atrophy and impaired spermatogenesis from HPTA suppression (recovery variable). In women and adolescent girls: virilization (deepening of the voice, clitoral enlargement, menstrual disruption, hirsutism) was documented in the GDR program, and some virilizing changes are irreversible; some GDR cases required surgical or medical intervention.

Neuropsychiatric

No adequate turinabol-specific psychiatric data. The GDR program documented damaging side effects broadly, and the wider AAS class is associated with neurological/behavioral effects including mood disturbance, irritability/aggression, and a dependence syndrome. Treat class-based; turinabol-specific magnitude is unquantified.

Renal

No turinabol-specific renal data. The broader AAS literature reports renal disorders among the multi-organ consequences of supraphysiologic long-term use; magnitude for turinabol specifically is unknown. Consider this an area of inadequate data.

Hematologic

No turinabol-specific hematologic data. AAS as a class can raise red-cell mass (erythrocytosis/polycythemia), which increases thrombotic risk; this should be monitored but is extrapolated, not turinabol-specific.

Dermatologic

Androgenic skin effects are expected: acne and oily skin; in women, hirsutism and other virilizing skin changes were documented in the GDR program.

Recovery

HPTA suppression & recovery

Suppression: Expected significant suppression. As an exogenous androgen, turinabol suppresses LH/FSH and endogenous testosterone (functional hypogonadism); turinabol-specific quantitative suppression data are lacking, so severity is assigned on class grounds.

Recovery from anabolic-steroid-induced hypogonadism is highly variable and depends on age and the degree/duration of use; a scoping review reports gonadotropin recovery typically over ~3-6 months and testosterone recovery over months, with testicular atrophy and spermatogenesis recovering over months to years and some effects (e.g., gynecomastia) often not resolving (PMID 37855241). Any recovery plan should be directed by an endocrinologist and based on serial bloodwork. Only single-SERM approaches are within scope here; multi-agent recovery protocols are out of scope and should not be self-directed.

Bloodwork & vitals

Monitoring

Recommended labs & checks
Liver function panel (ALT, AST, ALP, GGT, bilirubin) at baseline and periodicallyFull fasting lipid panel (especially HDL, LDL)Complete blood count including hematocrit/hemoglobin (erythrocytosis screen)Total and free testosterone, LH, FSH (to characterize HPTA suppression and recovery)Blood pressureEstradiol and PSA (in men) where clinically indicatedConsider echocardiography/lipid-and-imaging cardiac assessment for long-term users

Cadence: Baseline before any exposure, then approximately every 8-12 weeks during use, and again after cessation to track HPTA recovery; more frequently if abnormalities or symptoms appear. Monitoring should be arranged and interpreted by a clinician.

Warning signs — seek care
  • Jaundice (yellow skin/eyes), dark urine, pale stools, right-upper-quadrant abdominal pain, or unusual fatigue/nausea — possible liver injury; stop and seek urgent medical care
  • Chest pain, breathlessness, palpitations, fainting, or leg swelling — possible cardiac or thrombotic event; seek emergency care
  • New or worsening depression, aggression, or suicidal thoughts
  • In women: voice deepening, facial/body hair growth, clitoral enlargement, menstrual changes — some virilization may be permanent; stop and consult a clinician
  • In men: testicular shrinkage, loss of libido, infertility signs
  • Severe headache or visual changes (possible blood-pressure or hematocrit problem)
Do not use if

Contraindications

  • Pregnancy and breastfeeding (androgens cause fetal virilization; virilizing effects in females can be irreversible)
  • Women and adolescents generally, given documented and sometimes permanent virilization from AAS/turinabol exposure
  • Pre-existing liver disease or abnormal liver function (oral 17-alpha-alkylated hepatotoxicity)
  • Known or suspected androgen-sensitive cancer (e.g., prostate or breast carcinoma)
  • Pre-existing cardiovascular disease, uncontrolled hypertension, dyslipidemia, or erythrocytosis/polycythemia
  • History of AAS dependence or significant mood/psychiatric disorder
  • Any use without medical supervision and regular laboratory monitoring
Combinations

Interaction profile

  • MajorWith another anabolic steroid: Additive cardiovascular strain
  • MajorWith a thermogenic stimulant: Additive cardiovascular strain
  • ModerateWith thyroid hormone: Additive cardiovascular strain
  • ModerateWith growth hormone: Additive cardiovascular strain
  • MajorWith another 17α-alkylated oral: Additive liver strain
  • MajorWith a liver-signal SARM: Additive liver strain
  • MajorWith another anabolic steroid: Blood / clotting
  • MajorWith a clot-promoting SERM: Blood / clotting
  • ModerateWith an aromatase inhibitor: Hormonal
  • ModerateWith an anabolic steroid: Hormonal
  • ContraindicatedWith DNP: Additive cardiovascular strain

Check a specific combination in the interaction checker.

Harm reduction

Reducing harm & when to stop

  • This is educational information only, not medical advice, and does not endorse use; these substances carry serious risks. Anyone using or considering turinabol should be under a qualified physician's care with regular bloodwork. 21+ only.
  • Turinabol-specific human safety data are minimal; most known risks are extrapolated from the oral 17-alpha-alkylated AAS class, so absence of turinabol-specific reports is not evidence of safety.
  • Because it is an oral 17-alpha-alkylated steroid, avoid combining it with alcohol or other hepatotoxic drugs/supplements, and stop immediately and seek care for any sign of liver injury (jaundice, dark urine, right-upper-quadrant pain).
  • Get baseline and periodic liver panel, lipids, CBC/hematocrit, blood pressure, and testosterone/LH/FSH; interpret results with a clinician.
  • Women and adolescents face virilization that can be permanent; some GDR-era cases required surgical intervention. Any virilizing sign is a reason to stop and consult a clinician promptly.
  • Stop and seek emergency care for chest pain, breathlessness, palpitations, fainting, severe headache, or leg swelling.
  • HPTA suppression is expected; recovery is variable. Do not self-direct hormonal recovery. Consult an endocrinologist. Only single-SERM approaches are within scope; multi-agent recovery protocols are out of scope here.
  • Monitor for mood changes, aggression, or depression, and seek help for new or worsening psychiatric symptoms.
Evidence

Citations (11)

Every clinical claim above is tied to a primary source. Overall evidence grade C — graded to the best available evidence for its core claims.

  1. 01

    Turinabol (Oral-Turinabol, developed by Jenapharm) was the primary androgen of the GDR state doping program, administered to thousands of athletes including women and minors, with documented damaging side effects, some requiring surgical or medical intervention.

    Case seriesHormonal doping and androgenization of athletes: a secret program of the German Democratic Republic government.PMID 9216474 ↗

  2. 02

    Administration of androgens to women and adolescent girls in the GDR program produced virilization; damaging side effects were recorded.

    Case seriesHormonal doping and androgenization of athletes: a secret program of the German Democratic Republic government.PMID 9216474 ↗

  3. 03

    Turinabol (dehydrochloromethyltestosterone) was developed by Jenapharm and marketed as Oral-Turinabol; after a single 5 mg oral dose in healthy men, long-term urinary metabolites remained detectable for up to ~45 days.

    CohortControlled administration of dehydrochloromethyltestosterone in humans: Urinary excretion and long-term detection of metabolites for anti-doping purpose.PMID 34418529 ↗

  4. 04

    Turinabol is extensively hepatically metabolized to reduced long-term metabolites (A-ring/D-ring modified) excreted in urine in glucuronidated and unconjugated fractions.

    CohortDetection and mass spectrometric characterization of novel long-term dehydrochloromethyltestosterone metabolites in human urine.PMID 22142641 ↗

  5. 05

    4-Chlorodehydromethyltestosterone is a 17-alpha-methyl (17-alpha-alkylated) anabolic steroid that undergoes hepatic metabolism including 17-epimerization in humans.

    Cohort17-Epimerization of 17 alpha-methyl anabolic steroids in humans: metabolism and synthesis of 17 alpha-hydroxy-17 beta-methyl steroids.PMID 1448813 ↗

  6. 06

    4-Chlorodehydromethyltestosterone is classified among 17-alkyl-substituted (orally active) anabolic androgenic steroids.

    ReviewScreening of free 17-alkyl-substituted anabolic steroids in human urine by liquid chromatography-electrospray ionization tandem mass spectrometry.PMID 15013688 ↗

  7. 07

    Long-term AAS use is associated with reduced left-ventricular systolic and diastolic function and greater coronary atherosclerotic plaque volume scaling with cumulative exposure (class evidence).

    CohortCardiovascular Toxicity of Illicit Anabolic-Androgenic Steroid UsePMID 28533317 ↗

  8. 08

    Long-term AAS use is associated with cardiomyopathy, left-ventricular hypertrophy, and ventricular arrhythmia (class evidence, case report).

    Case reportNon-ischemic Cardiomyopathy Secondary to Left Ventricular Hypertrophy due to Long-term Anabolic-androgenic Steroid Use in a Former Olympic Athlete.PMID 30473946 ↗

  9. 09

    Oral 17-alpha-alkylated AAS as a class cause cholestasis, peliosis hepatis, and hepatic tumors, and supraphysiologic long-term AAS use affects cardiovascular, neurological, endocrine, renal, and hematologic systems.

    ReviewAnabolic androgenic steroid-induced liver injury: An update.PMID 36051334 ↗

  10. 10

    Oral 17-alpha-alkylated AAS can cause fatal cholestatic hepatic necrosis (analog stanozolol case).

    Case reportFatal anabolic androgenic steroid overdose in an amateur bodybuilder: a clinical and autopsy reportPMID 37948000 ↗

  11. 11

    Anabolic-steroid-induced hypogonadism recovery is variable: gonadotropins typically recover over ~3-6 months and testosterone over months, with testicular atrophy/spermatogenesis over months to years and some effects (e.g., gynecomastia) often not resolving.

    ReviewPhysical, psychological and biochemical recovery from anabolic steroid-induced hypogonadism: a scoping review.PMID 37855241 ↗

Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice