For MC-1, my comments aren't really based on the phase II results. It's just the fact that mc-1 is a major substrate in vit b6 metabolism. How can it not be rapidly metabolized and/or excreted if present at doses above what the body feels it needs? If you take vit b6, and you have insufficient p-5-p, wouldn't the metabolism simply make p-5-p from the ingested vit b6? If you ingest excess p-5-p, wouldn't it get dephosphorylated since an excess of products favours the reverse reaction of creating the substrates? What then, would be the advantage of ingesting p-5-p alone?
As for hospitals passing up a p-5-p supplement for a stringently formulated one from mcu... I can't deny that possibility. But the p-5-p supplement need not be 100% pure or anything like that. Chances are that any supplement on the market has more than enough p-5-p in it to be in excess; and the excess will be excreted. So I don't believe that formulation is strictly an advantage here.
In other words, I wouldn't expect p-5-p to be any different than vit b6. And we know what happened to b6:
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