Pro-hormone version of Anabolic Steroid Trenbolone


The breakthrough came in 2012, for the pro-hormone analogue of the anabolic steroid trenbolone. Chemical bodybuilders who had tried the new designer supplement and were convinced of its effectiveness wrote about their experiences on all international forums. Trendione, the name we’ll use for the active ingredient in these products, is apparently active when taken orally. And sure enough, we found an animal study that confirms this.

Trenbolone is an expensive hormone. On the raw materials market a kilogram of trenbolone costs over six times as much as a kilogram of testosterone. This is because trenbolone, with three double bonds in its skeleton, is an anabolic steroid that requires considerable chemical gymnastics to produce.

The three double bonds make trenbolone a slim and flexible molecule, which fits better in the androgen receptor than testosterone does, better in the progesterone receptor than progesterone does, and above all is resists metabolization. That’s why trenbolone is such an effective steroid – and why it’s not without side effects. Take a look in Llewellyn’s Anabolics. []

On the side effects: it may well be the case that in ten to twenty years we’ll realise that these are more serious than we originally thought. Animal [Toxicol Sci. 2002 Dec;70(2):202-11.] and in-vitro studies suggest that trenbolone can change DNA.


Above left is the trenbolone molecule in the form that is used for injectable preparations. Usually there’s still one ester group attached.

In the middle is trendione, the analogue that’s turned up in the form of designer supplements. It is probably slightly active itself, but is also capable of partially converting itself in the body into fully active trenbolone.

And above right is 17-alpha-hydroxytrenbolone or epitrenbolone. This substance is virtually inactive: it’s by far the most important trenbolone metabolite that researchers detect in human urine.

A steroid that is so difficult to metabolise should be orally active, you’d think. Well – that’s what the makers of designer supplements like Methoxy-TST and Methoxy-TRN thought too. They put trenbolone in their products – and the things worked too.

The figure below is from the animal study we mentioned above. It shows the anabolic effect of injected [sc] and orally administered trenbolone [oral]. And orally administered trenbolone is active – but is a hundred times less active than the trenbolone given through a needle.


We compiled the figure below using data from the same study. It shows the effect of oral doses of 0 [olie], 0.1, 10.0 and 50.0 mg trenbolone per kg bodyweight per day on male rats incapable of synthesising testosterone.

The back row shows the effect on the muscles [levator ani], the second row from the back shows the effect on the prostate, the third row the effect on the seminal vesicles and the front row shows the effect on the penis.

The values on the y-axis are in milligrams.

So oral trenbolone is active, and oral trendione is probably active too.


If you convert the dose of 10 mg/kg/day to the dose for an adult human weighing 80 kg, then you’d need about 130 mg per day. Steroids expert HenryV – clever, knowledgeable, active on the better bulletin boards and writer of superior posts – suspects however that people react better to oral trenbolone, and therefore also to trendione, than rats do. Click here for a copy of HenryV’s trendione profile.

He compiled it from an animal study in which researchers analysed trenbolone metabolites in the gall bladder of rats [Xenobiotica. 1981 Jul;11(7):489-500.] and PhD research done by a Dutchman, Douwe de Boer. [Biol Mass Spectrom. 1991 Aug;20(8):459-66.] These studies suggest that rats neutralise trenbolone faster than humans do, and that humans therefore probably need less trendione than you’d expect based on the animal studies.

The first reports from users seem to confirm HenryV’s view. Users have reported anabolic effects at doses of 40 – 90 mg trendione per day. At the higher dose androgenic side effects come into play.


In vitro and in vivo effects of 17beta-trenbolone: a feedlot effluent contaminant.

Wilson VS, Lambright C, Ostby J, Gray LE Jr.


US Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research

Laboratory, Reproductive Toxicology Division, MD-72, Research Triangle Park, North Carolina 27711, USA.


Concern has arisen regarding the presence and persistence of trenbolone in the environment. Trenbolone acetate is an anabolic steroid used to promote growth in beef cattle. It is hydrolyzed to the active compound, 17beta-trenbolone (TB), which is also one of the metabolites excreted by cattle. Reproductive alterations have been reported in fish living in waters receiving cattle feedlot effluent, and in vitro androgenic activity displayed by feedlot effluent samples has been related to these effects. In the current study, the androgenic potency of TB was examined both in vitro and in short-term in vivo assays. TB was a high affinity ligand for the androgen receptor (AR), with an IC(50) of about 4 nM in rat ventral prostate cytosol and about 33 nM in cells transfected with the human AR when competed with 1 nM [3H]R1881. TB induced AR-dependent gene expression in MDA-kb2 cells with a potency equal to or greater than dihydrotestosterone. In immunocytochemistry experiments with the human AR, concentrations as low as 1 pM significantly induced androgen-dependent translocation of the AR into the cell nucleus. TB also displayed antiglucocorticoid activity in vitro, inhibiting dexamethasone-induced transcriptional activity, and reduced adrenal gland size in vivo. In the Hershberger assay (in vivo), TB was as potent as testosterone propionate in tissues that lack 5alpha-reductase but less effective at increasing weight of tissues with this enzyme. Such tissue specificity was anticipated because other C-19 norsteroidal androgens display a similar profile in this assay. Subcutaneous TB treatment was about 50- to 100-fold more effective in stimulating growth of androgen-dependent tissues than was oral treatment. In our in utero screening assay, maternal TB administration increased AGD and attenuated the display of nipples in female offspring in a dose-related manner, similar to the published effects of testosterone propionate. Previous studies have documented that these types of malformations in newborn and infant rats are not only permanent effects but are also highly correlated with serious reproductive malformations as adults. In summary, TB is a potent environmental androgen both in vitro and in vivo and, in contrast to other reports, can induce developmental abnormalities in the fetus.

PMID: 12441365 [PubMed – indexed for MEDLINE]