refer to methyltrienolone as oral trenbolone. It was first explored quite some time ago by Negma in France, the same company that marketed Parabolan (trenbolone). But the drug was never approved by the French government and was hence never produced. The reason was extreme hepatoxicity. Bill Roberts, the biochemist, once commented that taking methyltrienolone made taking insane doses of anadrol and Halotestin together look mild on the liver. While I was unable to find anything in the literature that describes the extent of the liver toxicity, it's a generally accepted fact. That's also why, to the dissapointment of many, you will never find a commercially marketed methyltrienolone product. Its only sold in bulk to labs and universities for research studies involving androgens.
Mainly because (and those who wish it was available will wish so even more now) its such a potent androgen. There is some conflicting information in that regard however. Organic chemist Patrick Arnold, head of LPJ research, once stated that methyltrienolone was the most powerful steroid ever, and that statement has been blown out of proportion and taken on a life of its own. While androgenically a very potent steroid, methyltrienolone is still basically trenbolone with a 17-alpha-methyl group. A group that has the tendency to actually reduce the androgenic potency. So it may actually be somewhat milder than trenbolone, on the contrary to what many pseudo steroid guru's are now claiming after reading Pat Arnold's statement. I can't find any other documented effects of the 17-alpha-alkylation influencing androgen binding in a positive way. It's a potent androgen, with more binding than even DHT2, but the study that claims that is mild at the very best about quantifications, whereas people have used the term 1000 times more powerful than testosterone, which is surely exaggerated.
What is interesting is that it seems to show nearly no binding for sex-hormone binding proteins, which makes it a popular choice in androgen receptor studies3, since it will demonstrate equal binding in all tissues regardless of the presence and amount of these proteins. No doubt this plays a role in its supposed binding capacity. In this instance the 17-alpha-alkylation may have played a key role, since it has been demonstrated a multitude of times that 17-alpha-methyl groups decrease the binding for sex-hormone binding proteins as well as most other structures, and due to its triple double bond, trenbolone really didn't bind well to these to begin with.
One of the findings made in clinical tests with methyltrienolone was the discovery of high amounts of the DHT-deactivating enzyme 3alpha-hydroxysteroid dehydrogenase in muscle tissue4. Once again proof that God meant to keep us humans weak. Hurray for science. Follow-up studies then went on to show that DHT nonetheless showed similar binding in the prostate, and showing little or no presence of the deactivating enzyme. So God would rather have us all die of prostate cancer than gain a few ounces of muscle. It's a comforting thought, no?
What methyltrienolone, despite its amazing capacity, still doesn't overcome are the basic problems with any 19Nor compound. First of all its effects on libido. Methyltrienolone still seems to affect our sex drive in such a potent manner that the dreaded Deca Dick (temporary impotence) is a very real threat5. Another is that it still binds almost equipotently to the progesterone receptor3. The latter would be of little concern as long as no circulating estrogen is present since methyltrienolone does not aromatize, but could cause problems such as aggravating water retention and gyno (growth of breast tissue in men) if combined with an aromatizing androgen or an estrogen.
While many may wish that an incredibly strong androgenic, non-aromatizing compound as this was available for daily use, its not. And if the indications are true, its probably best. I've warned many people for the toxicity of fluoxymesterone, and everything points to it that methyltrienolone makes fluoxymesterone look like Tums tablets in terms of liver toxicity.