Ethylphenidate (EPH) is a psychostimulant and a close analog of methylphenidate.  Ethylphenidate acts as both a dopamine reuptake inhibitor and norepinephrine reuptake inhibitor, meaning it effectively boosts the levels of the norepinephrine and dopamine neurotransmitters in the brain, by binding to, and partially blocking the transporter proteins that normally remove those monoamines from the synaptic cleft. 

However, considering the close similarities between ethylphenidate and methylphenidate and the fact that methylphenidate, like cocaine, actually does not primarily act as a "classical" reuptake inhibitor, but rather as an "inverse agonist at the DAT" (also called a "negative allosteric modulator at the DAT"),[1] it is at least very likely that ethylphenidate also primarily acts as an inverse DAT agonist instead of (or at least only secondarily) as a classical reuptake inhibitor (which could be called a "competitive antagonist at the DAT" using a similar terminology as "negative allosteric modulator at the DAT", which per definition means that its mechanism is non-competitive)

Pharmacokinetics

Ethylphenidate metabolizes into methylphenidate and ritalinic acid.

Tiny amounts of ethylphenidate can be formed in vivo when a solvent (specifically ethanol) and methylphenidate are coingested, via hepatic transesterification. Ethylphenidate formation appears to be more common when large quantities of methylphenidate and alcohol are consumed at the same time, such as in non-medical use or overdose scenarios. However, the transesterfication process of methylphenidate to ethylphenidate, as tested in mice liver, was dominant in the inactive (−)-enantiomer but showed a prolonged and increased maximal plasma concentration of the active (+)-enantiomer of methylphenidate. Additionally, only a few percent of the consumed methylphenidate is converted to ethylphenidate.

This carboxylesterase-dependent transesterification process is also known to occur when cocaine and alcohol are consumed together, forming cocaethylene.

Pharmacodynamics

All available data on ethylphenidate's pharmacokinetics are drawn from studies conducted on rodents. Ethylphenidate is more selective to the dopamine transporter (DAT) than methylphenidate, having approximately the same efficacy as the parent compound,[5] but has significantly less activity on the norepinephrine transporter (NET).[7] Its dopaminergic pharmacodynamic profile is nearly identical to methylphenidate, and is primarily responsible for its euphoric and reinforcing effects.[8]

The eudysmic ratio for ethylphenidate is superior to that of methylphenidate.[5][failed verification] 

The following is ethylphenidate's binding profile in the mouse, alongside methylphenidate's. Figures for both the racemic and the dextrorotary enantiomers are given: