turinabol

Turinabol was made in East Germany and is best known for being given to around ten thousand athletes, often without them knowing, as part of a secret state doping programme. It stopped being produced in 1994, has no approved medical use anywhere, and there is essentially no proper clinical research showing what it does or how safe it is.

regulatory status

US Schedule III controlled substance; UK Class C (Misuse of Drugs Act). NO approved medical indication in any major market; production discontinued 1994.

Turinabol is Schedule III under the US Controlled Substances Act and Class C under the UK Misuse of Drugs Act; Australia classifies it in its highest-risk category. It was patented in 1961 and introduced for clinical use in 1965 by Jenapharm in East Germany, and was NEVER approved for medical use in the United States. Production ceased in 1994 and it retains no approved medical indication in any major market. It is prohibited at all times in sport under the WADA List and has been central to retrospective doping reanalyses of stored samples.

The composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.

documented safety signals

• HEPATOTOXICITY BY STRUCTURAL CLASS: turinabol is 17α-alkylated, the specific structural feature NIH LiverTox identifies as causing cholestatic injury — noting that cholestasis has NOT been described with unmodified testosterone. Class incidence of acute cholestasis is approximately 1% of treated patients, onset typically 1-4 months, delayed presentation to 6-24 months.
• PELIOSIS HEPATIS: documented across the 17α-alkylated class at 2-27 months of therapy, with potential for asymptomatic progression to fatal hepatic rupture and haemorrhage.
• HEPATIC ADENOMA AND HEPATOCELLULAR CARCINOMA: associated with long-term androgen exposure, typically after 5-15 years, with cases documented within 2 years.
• NO COMPOUND-SPECIFIC HEPATIC SURVEILLANCE DATA: turinabol is absent from the NIH LiverTox roster entirely, so unlike oxymetholone and stanozolol there is no agent-specific likelihood score or case-series characterisation — the absence of data is itself a safety concern, not evidence of safety.
• ADVERSE LIPID EFFECTS: oral 17α-alkylated androgens markedly suppress HDL cholesterol and raise LDL through hepatic triglyceride lipase induction; the closest characterised comparator, stanozolol, showed a 33% HDL fall and 29% LDL rise in six weeks.
• CARDIOMYOPATHY AND ATHEROSCLEROSIS: Baggish et al. (Circulation 2017) documented reduced LVEF (52±11% vs 63±8%, p<0.001), impaired diastolic relaxation velocity (9.3±2.4 vs 11.1±2.0 cm/s, p<0.001), and lifetime-dose-dependent coronary atherosclerosis in long-term AAS users.
• HPG AXIS SUPPRESSION: suppression of GnRH and pituitary LH/FSH with testicular atrophy, impaired spermatogenesis and suppressed endogenous testosterone production.
• VIRILISATION IN WOMEN: the East German programme produced extensive testimony of irreversible virilisation in female athletes, including voice deepening, hirsutism and clitoral enlargement, alongside reported gynaecological and psychiatric sequelae.
• GROWTH-PLATE EFFECTS IN ADOLESCENTS: many State Plan 14.25 subjects were adolescents, a population in which androgens accelerate epiphyseal maturation and risk premature growth-plate closure with permanent loss of adult height.
• UNREGULATED SUPPLY: no legitimate pharmaceutical production has existed since 1994, so all circulating material is of unverified identity, purity and dose.
• ETHICAL AND CONSENT CONTEXT: the compound's principal human exposure occurred without informed consent in minors and adults, a fact relevant to how its historical 'experience' should be weighted as evidence.