Many will have heard the rumour at, one time or another, that the prohormone/designer steroid “epistane” (also known as havoc, and 17α-methyl-epithiostanol) can convert to “pheraplex” (also known as phera, madol, and desoxymethyltestosterone). Often it’s suggested that epi that is past its use-by date can degrade in the bottle into phera; occasionally it’s suggested that epi may even convert in the body to phera, acting as a sort of “prohormone” to phera.
There’s a profound difference in reported effects between the drugs, which has raised doubts over their suspected relationship. Epi is reported to be very effective as a cutting agent, inducing fat-loss and a “dry” appearance, with lean muscle acquisition often accompanied by sore joints and a low libido. Phera, in contrast, is promoted as a “bulker,” with which the gains are “wet,” and it’s described as being a “feel-good” compound with a positive effect on libido.
While the question of whether conversion is possible is an interesting riddle for some, for others it may have more serious repercussions – though epistane is not currently scheduled at the time of writing, phera (desoxymethyltestosterone) is a Class C controlled substance in the UK,  and a Schedule III controlled substance in the US. 
But is it true, or is it broscience?
Let’s look at the evidence.
- The chemical nomenclature for phera is 17α-methyl 5α-androst-2-ene-17β-ol
- The nomenclature for epistane is 2α,3α-epithio-17α-methyl-5α-androstan-17β-ol
At first glance, when they’re written down, they look sufficiently different to make the conversion of one into the other appear an unlikely prospect.
Now let’s look at them represented as structural diagrams:
They start to look a lot more similar.
Evidence for Epi degrading to Phera
The conversion of epistane to desoxymethyltestosterone would require oxygenation of the episulphide and dethionylation (loss of the sulphur moiety). It is known that 2α,3α-episulphides (like 2α,3α-epithio-17α-methyl-5α-androstan-17β-ol) can be reduced under certain circumstances to the 2-olefins (2-dehydro steroids like desoxymethyltestosterone). Chemical reduction of 2α,3α-episulphides into 2-olefins was demonstrated in 1965.  Recent analytical testing of supplements containing 17α-methylepithiostanol has been confounded by the pyrolization of epithio steroids to 2-dehydro steroids in the heat of the GC/MS port. 
The unmethylated analogue has poor oral bioavailability, so a metabolism study was done in 1991 in Japan to ascertain how and where it was metabolised (probably in order to demonstrate the superiority of the highly lipophilic methoxycyclopentane-etherified analogue mepitiostane, which is lymphatically absorbed ).  The drug was administered directly into the portal vein (of rats) and into the intestine, and then blood was drawn which, when analysed, showed that epithiostanol was converted to the 2-olefin both in the liver and intestine.
Circled in blue is the administered epitiostanol (which is unmethylated epistane/havoc), and in red is indicated 2-androstenol (unmethylated phera), which was found to be a metabolite.
Obviously phera and epi are both 17α-methylated compounds – unlike those in the diagram above – which can change their metabolism quite significantly. The main effect of the 17α-methyl functional group is to protect the 17β-hydroxyl, which will prevent the formation of all of the 17-keto metabolites presented above (greyed out), significantly limiting the routes of metabolism available to epistane.
A study published in the journal Drug Testing Analysis in 2009 studied the metabolites of an off-the-shelf methylepithiostanol-containing supplement in the urine of a volunteer. Neither 17α-methylepithiostanol nor desoxymethyltestosterone were detected in the urine, but the main metabolite of desoxymethyltestosterone (17α-methyl-2β,3α,17β-trihydroxy-5α-androstane ) was detected. 
“It is known that epithiostanol is metabolized to olefin steroid (5α-androst-2-en-17β-ol) by oxygenation and dethionylation; it is therefore suggested that 17α-methylepithiostanol, which is a 17-methylated analogue of epithiostanol, might be metabolized to olefin steroid desoxymethyltestosterone” 
Unfortunately the researchers could not determine if the trihydroxy steroid detected resulted from metabolism of 17α-methylepithiostanol or from contamination, as some desoxymethyltestosterone had been found to be present in the caps in addition to the 17α-methylepithiostanol.
The drug 17α-methylepithiostanol itself was first synthesized in 1966 by researchers at Searle & Co.  They also examined the activity of the 2β,3β-episulphide, as well as the olefin, and their unmethylated analogues. All of the 2β,3β compounds were relatively inactive, and the unmethylated olefin was inactive by oral administration (probably due to poor solubility).
The researchers noted that the anabolic activities of 2α,3α-epithio-17α-methyl-5α-androstan-17β-ol and desoxymethyltestosterone were similarly high, and were also of the opinion that one could reasonable expect some in vivo metabolism of the epithio compounds into the olefins, though they speculated that this appeared not to be the case with the 2β,3β-episulphide compounds (because of their inactivity relative to the 2-dehydro compounds). Interestingly, the 2β,3β-episulphides were in fact synthesized from 2-dehydro compounds (by way of 2α,3α-epoxides).
Though there appears to be no conclusive proof of the metabolism of methylepithiostane to desoxymethyltestosterone, this article should at least give a better understanding of the likelihood, as it would seem highly probable from the weight of evidence presented above.