EmergingResearch compound

Turinabol (4‑Chlorodehydromethyltestosterone)

Oral-Turinabol (Chlorodehydromethyltestosterone, CDMT), 17α-alkylated chlorinated Dianabol-analog oral AAS. Jenapharm 1962, infamous as the main agent of the GDR state doping program 1968-1989 ("Komplex 08"). Notorious for long-term detection metabolites.

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WHAT IS TURINABOL (4-CHLORODEHYDROMETHYLTESTOSTERONE)?

Detailed overview

Turinabol (4-chlorodehydromethyltestosterone, CDMT) is a 17α-alkylated chlorinated Dianabol structural analog oral AAS, synthesized by Jenapharm (East Germany, Jena) in 1962, marketed in 1965 as Oral-Turinabol Rx. It became the MAIN agent of the GDR state doping program ("Staatsplanthema 14.25", Stasi code-named "Komplex 08", 1968-1989); ~10,000+ GDR athletes received Turinabol unknowingly or undocumented, mainly in swimming, athletics, rowing programs. The 1990s Stasi archive openings document the harms (liver damage, cardiomyopathy, virilization in female athletes, neonatal anomalies in doped mothers' children). Anabolic:androgenic ratio 53:6 – high anabolic, virtually zero androgenic ("drier Anavar"). Does NOT aromatize (4-chloro substitution blocks CYP19 substrate binding). 17α-methyl → moderate hepatotoxicity (the 4-chloro reduces it, similar to Anavar). Schänzer 2006 (PMID 17042466) describes extra-long detection metabolites (6β-OH-CDMT and others) – urinary 12-18 month detection is possible, basis of the 2016 Olympic (Rio) IOC re-test: 100+ athletes retrospectively disqualified after 2008-2012 sample re-evaluation. WADA-banned year-round.

Mechanism

AR agonist, 17α-methyl-4-chloro-Δ1-T, NOT aromatized

Anabolic:Androgenic

53:6

Half-life

16 hours (oral)

Onset

2-3 h (oral)

Legal status

Jenapharm Rx (DE) discontinued 1994; UGL today. Schedule III.

Data console

Lab data

/lab/molecular-data.jsonLIVE
> Androgenic:Anabolic53:6
> AR bindingModerate-high AR affinity; virtually zero 5α-reductase subs…
> Active half-life16 h (parent), plus 6β-OH and 3α-OH metabolites ~24-48 h
> Detection windowEXTRA LONG – urinary 12-18 months (Schänzer 2006 6β-OH-CDMT and 3α-hydroxy-3-one metabolites). 2016 Rio Olympics retrospective re-test disqualified 100+ athletes based on 2008-2012 reevaluation. WADA-accredited LC-MS/MS.
> AromatizationNo – 4-chloro substitution blocks CYP19 binding; clinically E2 elevation essentially zero (Pope-Kanayama 2014 PMID 24423981, Schänzer 2006 PMID 17042466)
> HepatotoxicityModerate – 17α-methyl group hepatic first-pass stress, BUT 4-chloro reduces hepatic toxicity vs other 17α-alkylated AAS (Dianabol, Anadrol). ALT/AST 2-3x rise common at 6+ week cycle, clinically milder than Dianabol or Anadrol (Hartgens-Kuipers 2004 PMID 15233599)

Safety

Side effects, stop signs, contraindications

Side effects · 7

  • HPTA suppression: endogenous testosterone production shuts down (LH/FSH suppression), testicular atrophy, reduced libido and fertility; prolonged hypogonadism without PCT.
  • Adverse lipid changes: moderate-to-marked HDL drop (15-25%) and LDL rise, pronounced with oral 17alpha-alkylated AAS; long-term atherosclerosis risk.
  • Hepatotoxicity (oral 17alpha-methyl): ALT/AST elevation 2-3x over 6+ week cycles; clinically milder than Dianabol/Anadrol (4-chloro protection), but liver stress is real, with rare cholestasis and peliosis hepatis.
  • Virilization in women: despite the low androgenic ratio, >10 mg/day and longer exposure can cause IRREVERSIBLE voice deepening, clitoral enlargement, hirsutism (documented GDR case: Heidi/Andreas Krieger).
  • Elevated blood pressure: hypertension is common during AAS cycles; combined with HDL decline and hematocrit changes it increases cardiovascular load.
  • Psychiatric effects: irritability, aggression, mood swings on cycle, plus depression and low libido during cessation/PCT; AAS dependence can develop.
  • Androgenic skin effects: acne and oily skin can occur; scalp hair-loss risk is low, however, since Turinabol is not a 5alpha-reductase substrate (no DHT conversion).

Contraindications · 7

  • Pregnancy and breastfeeding: absolutely contraindicated due to virilization and risk of fetal developmental abnormalities (the GDR program documented neonatal abnormalities in children of doped mothers).
  • Any liver disease or elevated liver enzymes: the 17alpha-methyl group adds hepatic stress, so it must not be used with pre-existing liver impairment.
  • Cardiovascular disease, hypertension or adverse lipid profile: HDL decline and raised blood pressure worsen existing cardiovascular risk.
  • Hormone-sensitive tumors (prostate or breast carcinoma): contraindicated as an androgen-receptor agonist.
  • WADA-tested athletes: extra-long detection window (12-18 months in urine due to Sobolevsky-Rodchenkov 2012 long-term metabolites); to be avoided at any career stage.
  • Psychiatric predisposition (depression, bipolar disorder, aggression-control problems): mood side effects and post-cycle depression can exacerbate it.
  • Adolescents and growing youths: AAS can cause premature epiphyseal closure and irreversible developmental effects.

Related Performance Compounds

Same therapeutic category

Studies

Related research and clinical findings

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MolekulaX Editorial Team·Source-verified · PubMed · FDA · EMA
Updated: June 19, 2026

The information here is for educational and scientific purposes only. Performance-enhancing compounds (AAS, prohormones, stimulants, doping agents) are illegal without prescription in Hungary and most of the EU, and carry serious health and legal risks. WADA bans them in competitive sport. This is NOT a usage guide, and we do not encourage any illegal use. If you do use them, medical supervision and regular bloodwork are ESSENTIAL. Severe endocrine, cardiovascular, hepatic and psychiatric side effects are possible.