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4F-MPH & Ethanol — Patrician Pharmacology
The study that’s often cited as evidence against any conversion of methylphenidate to ethylphenidate is skimmed over too often. Especially when there’s an abundance of better studies available. This study showing the conversion rate to be rather insignificant was dose related. They only administered a therapeutic dose of the parent compound, MPH, after one standard drink. The researchers subsequently admitted that EPH concentrations could become relevant in the event that supratherapeutic doses of MPH binge-drinking settings.
The more fascinating studies indicate that even at relatively low doses, ethanol before dl-MPH greatly amplified psychoactive plasma concentrations of MPH. Interestingly this is because the ethanol—dl-MPH interaction caused a change in enantioselectively for d-MPH.
There was a significant increase in maximum plasma concentration of d-MPH. This was biphasic, first during absorption and secondly at peak blood serum levels. During absorption phase of dl-MPH, concomitant ethanol significantly elevated d-MPH plasma concentrations by 44-99%. When the MPH was maximally absorbed, d-MPH plasma concentrations were increased by 21%.
d-MPH exhibits more pronounced effects on the central nervous system, typically associated with rewarding effects. Subjective effects of "high," "good," "like," "stimulated," and overall "effect" were significantly potentiated.
These studies found that the transesterification into EPH was more of a secondary effect, and yielded more of the biologically inactive l-EPH opposed to the euphoric d-EPH component of ethylphenidate.
Can’t think of any reasons why these pharmacokinetics wouldn’t extend to racemic 4F-MPH.