Ethylphenidate

Structure of Ethylphenidate

Ethylphenidate (EPH) is a psychostimulant and a close analog of methylphenidate. The two drugs have very similar pharmacological effects.

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.

Ethylphenidate in its free base form is a highly caustic substance, and as a result, some anecdotal reports on internet forums such as Bluelight indicate that even just a few uses via the insufflation (snorted) route of administration can result in a perforated septum.

Pharmacokinetics


Ethylphenidate can be formed in vivo when 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. This carboxylesterase-dependent transesterification process is also known to occur when cocaine and alcohol are consumed together, forming cocaethylene. 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 (+)-enanatiomer of methylphenidate. Additionally, only a few percent of the consumed methylphenidate is converted to ethylphenidate so a pharmacologically significant dose would never be produced.

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, but has significantly less activity on the norepinephrine transporter (NET). Its dopaminergic pharmacodynamic profile is nearly identical to methylphenidate, and is primarily responsible for its euphoric and reinforcing effects.

The eudysmic ratio for ethylphenidate is superior to that of methylphenidate.

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

Compound Binding DAT Binding NET Uptake DA Uptake NE
d-methylphenidate 139 408 28 46
d-ethylphenidate 276 2479 24 247
dl-methylphenidate 105 1560 24 31
dl-ethylphenidate 382 4824 82 408

Legality


  • Ethylphenidate is not controlled internationally, see Convention on Psychotropic Substances
  • Ethylphenidate is not controlled in the Netherlands, as the Opium Law does not cover it, nor is there any law covering analogs of controlled drugs (methylphenidate is covered).
  • Ethylphenidate is not explicitly controlled in US but it could possibly be considered an analog of a Schedule II substance (methylphenidate) under the Federal Analog Act.
  • Ethylphenidate is illegal in Sweden as of 15 December 2012.
  • Ethylphenidate is controlled in the UK
  • Ethylphenidate is illegal in Jersey under the Misuse of Drugs (Jersey) Law 1978.
  • Australian state and federal legislation contains provisions that mean that analogues of controlled drugs are also covered by the legislation. Ethylphenidate would be an analogue of methylphenidate under this legislation.[citation needed]
  • Ethylphenidate is not controlled in Canada under the Controlled Drugs and Substances Act as the inclusion of methylphenidate in Schedule III only bans salts, not analogues (unlike drugs covered by Schedule I).
  • Ethylphenidate is illegal in Germany as of 05.07.2013
  • Ethylphenidate is illegal in Austria by the “Neue Psychoaktive Substanzen Gesetz” (=new psychoactive substances act) NPSG since 1 January 2012
  • Ethylphenidate is illegal in Denmark as of 1 February 2013.

The above article was sourced from http://en.wikipedia.org/wiki/Ethylphenidate