Trenbolone (enanthate / acetate / hex)
The most-used injectable after testosterone has zero modern human trials. The only human efficacy data ever collected: 1967, at 17.5–35 mg/week, measured as nitrogen balance. Everything you have read about dosing schedules was written without a single measured human half-life.
The short version
- Zero modern human trials of trenbolone at any dose, for any indication. DATA
- The only labeled human dose ever: Parabolan (France, 1987–1997), 76 mg hexahydrobenzylcarbonate per 10 days ≈ 35 mg base/week. DATA
- Receptor pharmacology is real and strong — AR potency DHT-grade, ~3× testosterone affinity — but the famous “500:500 anabolic:androgenic ratio” appears nowhere in indexed literature. DATA
- No human half-life has been measured for any trenbolone ester — every injection-schedule calculation rests on unsourced estimates. DATA (systematic negative)
What humans were ever given
| Year | What | Dose | Outcome |
|---|---|---|---|
| 1967 | Trenbolone acetate, male & female volunteers, 14 days | 5 or 10 mg IM every other day = 17.5–35 mg/wk | Nitrogen retention at 5 mg (the anabolic effect, measured); menstrual disturbances at 10 mg; liver, cholesterol, coagulation unchanged |
| 1965–70 | Oral tren (metribolone/R1881), clinical era | not recoverable | Real human clinical series — nitrogen balance, calcium, liver workups, a breast-cancer trial — then abandoned for hepatotoxicity |
| 1987–97 | Parabolan (hex), only human-approved product | 76 mg / 10 days ≈ 35 mg base/wk | Discontinued; overdose case needed 5 liver-support (MARS) cycles for cholestatic jaundice |
PMID 5632439 · Krüskemper 1967
PMID 5955468 · metribolone liver study 1966
PMID 4946014 · metribolone cancer trial 1970
PMID 16436902 · Parabolan jaundice case
Receptor pharmacology — measured, unlike the doses
DHT-grade androgen, no aromatization, weak SHBG grip DATA
Binding: IC50 ≈ 4 nM at rat prostate AR, ≈ 33 nM at transfected human AR (vs 1 nM R1881); AR gene-expression potency ≥ DHT; nuclear translocation from 1 pM; ~3× testosterone affinity; main metabolites carry ~5% (17α-trenbolone) and ~0.4% (trendione) of parent affinity. At any supraphysiological dose the AR is saturated orders of magnitude above Ki — full DHT-like agonism in every AR tissue, not just muscle.
Not AR-selective: progesterone-receptor and mineralocorticoid-receptor activity are real DATA
17β-trenbolone displaced labeled progesterone from bovine uterine PR with slightly higher affinity than progesterone itself. The oral relative R1881 binds the human mineralocorticoid receptor with the same affinity as aldosterone and is a potent MR antagonist (order R1881 > DHT > testosterone). Relative binding of metribolone (reference = 100): PR 208, AR 204, GR 26, MR 18, ER <0.1. Human-PR Ki: not found anywhere.
“500:500 anabolic:androgenic ratio” CLAIM
Appears nowhere in indexed literature. Kicman 2008’s myotrophic:androgenic table peaks at 20 (norbolethone) and omits trenbolone entirely. Classic Hershberger rat data actually show trenbolone as potent as testosterone propionate in 5α-reductase-poor muscle but less effective in reductase-rich tissue (prostate, seminal vesicles) — tissue selectivity is metabolic, not a super-potent receptor.
The myth column
“Tren raises prolactin” — the direct measurement says no DATA
The inference chain (PR binding → prolactin → cabergoline) is unverified. The only direct endocrine measurement: castrated male sheep with a 140 mg trenbolone implant — prolactin unaltered. What the same study did find: total thyroxine depressed to 45% of basal — trenbolone can distort thyroid labs.
Black-market vials: every deviation was underdosing DATA
The only published lab quantification of trenbolone injectables (Australia, 58 AAS samples, LC-MS): five trenbolone-enanthate products all labeled 200 mg/mL tested 199, 204, 200, 167 and 34 mg/mL; one acetate labeled 100 tested 45. No trenbolone product was overdosed. Any mg/week calculation inherits this label uncertainty.
Harm data — human, non-randomized
| Self-report | Tren users (n=237) | Other AAS (n=909) |
|---|---|---|
| Heart problems | 54.4% | 31.2% |
| Restlessness | 29.1% | 12.9% |
| Hair loss | 42.6% | 27.6% |
| Liver | 42.2% | 22.4% |
| Depression / mood swings | 23.6% each | 12.0 / 9.5% |
| Anger | 21.1% | 9.2% |
Cardiovascular damage tracks cumulative YEARS, not weekly mg DATA
164 athletes, median 2.2 years of AAS: each AAS-year independently worsened LV strain (β 0.08, CI 0.03–0.12) and raised coronary-calcium odds OR 1.23/y and non-calcified plaque OR 1.17/y; 35/36 men with >5 y use had ventricular mass above and ejection fraction below the normal median. In n=140 weightlifters, ejection fraction was 52±11% (users) vs 63±8%; on-drug 49±10 vs off-drug 58±10 — a ~9-point active-use penalty, partial recovery off-drug. Verified ≥3-year users: HDL 0.69 vs 1.25 mmol/L in non-users.
Growing skeleton (all animal)
No premature-closure signal — if anything the opposite DATA
Best 19-nor dataset (nandrolone laurate, 3 controlled experiments, 25 treated colts vs 15 controls): plates did not close early — “closure appeared to be DELAYED,” with a warning of cartilage-injury susceptibility during exercise; testosterone stayed suppressed 4.5 months after stopping. Trenbolone itself: 1,480 veal calves at 10–25× implant dose — serum and bone calcium/phosphorus unaltered. In adult orchiectomized rats it was bone-anabolic. None of this is human, and none covers open plates in humans.
What does not exist
No human half-life · no human PK at labeled+ doses · no tren-specific dosing survey DATA
Systematic negatives, each across many query phrasings: terminal half-life of trenbolone enanthate or ANY injectable ester has never been measured in humans (the “acetate ~1–3 d, enanthate ~5 d, hex ~8–14 d” figures are unsourced); no study relates trenbolone serum levels to dose; the Global Drug Survey 2024 dataset contains no dosing variables. Per-compound mg/week exists only at case-report level (e.g. one powerlifter at 100 mg/wk inside a 1,100 mg/wk stack). All schedule math is gray literature.