I should say that my earlier post is more oriented toward those who might lack the knowledge in these areas. The main message (to those who're interested) is that we shouldn't get carried away with predictions about a drug based on superficial, structural similarities to another, better known drug. Here are a couple of reasons off-hand, and in plain English: (those who know this stuff bear with me)
1. The 2a-methyl on masteron has different properties from the 2-methyl on msten or Mithras. This might or might not change how it affects the way the hormone is metabolized.
2. In my mind this is the more likely reason. I'll start by saying, DHT is readily converted to less active metabolites at certain places on the molecule (specifically C17 and C3). The 2a-methyl group (masteron) protects it at one of those vulnerable positions, meaning that the 2-CH3 essentially allows masteron to have a longer half-life in skeletal muscle than its parent molecule, DHT.
Now hormones like phera and M1T are also protected at this same vulnerable position on the molecule (like masteron). The double bond at C1 on M1T likely confers good protection to M1T from being converted to a less active metabolite. Adding a 2-CH3 (msten) will not add much more protection than it already has. If anything, it's conceivable that adding that 2-CH3 might be instead creating a less stable molecule.