Ethylphenidate

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Summary sheet: Ethylphenidate
Ethylphenidate
Ethylphenidate.svg
Chemical Nomenclature
Common names Ethylphenidate, EPH
Substitutive name Ethylphenidate
Systematic name Ethyl 2-phenyl-2-(piperidin-2-yl)acetate
Class Membership
Psychoactive class Stimulant
Chemical class Phenidate / Piperidine
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.



Oral
Dosage
Threshold Common Heavy
10 - 20 - 40 - 80 - 120 mg
Light Strong
Threshold 10 mg
Light 20 - 40 mg
Common 40 - 80 mg
Strong 80 - 120 mg
Heavy 120 mg+
Duration
Total 4 - 7 hours
Onset 40 - 120 minutes




Rectal
Dosage
Threshold Common Heavy
- 5 - 15 - 30 - 50 mg
Light Strong
Threshold < 5 mg
Light 5 - 15 mg
Common 15 - 30 mg
Strong 30 - 50 mg
Heavy 50 mg+
Duration
Total 2 - 6 hours
Onset 5 - 20 minutes





DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

Ethylphenidate (also known as EPH) is a novel stimulant substance of the piperidine class that produces traditional stimulant effects when administered.

It is a closely related analog of methylphenidate (brand names Ritalin, Concerta). The two substances have very similar pharmacological mechanisms but discernible differences in their subjective effects with ethylphenidate often considered to be recreational.

Ethylphenidate is most commonly distributed as a research chemical by online vendors, due to its grey-area legal status in certain countries.

Chemistry

Ethylphenidate is a synthetic molecule of the substituted phenethylamine class. It contains a phenethylamine core featuring a phenyl ring bound to an amino -NH2 group through an ethyl chain. It is structurally similar to amphetamine, featuring a substitution at Rα which is incorporated into a piperdine ring ending at the terminal amine of the phenethylamine chain. Additionally, it contains an ethyl acetate bound to R2 or its structure. Ethylphenidate is structurally differed to methylphenidate by elongation of the carbon chain. Ethyl- regards the side chain of two carbon atoms, phen- indicates the phenyl ring, id- is contracted from a piperidine ring, and -ate indicates the acetate group containing the oxygens. Ethylphenidate is a chiral compound, presumably produced as a racemic mixture.

Pharmacology

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. This allows dopamine and norepinephrine to accumulate within the brain, resulting in stimulating and euphoric effects.

All available data on ethylphenidate's pharmacokinetics are drawn from studies conducted on rodents. It has been found that ethylphenidate is more selective to the dopamine transporter (DAT) than methylphenidate, having approximately the same efficacy as the parent compound,[1] but with significantly less activity on the norepinephrine transporter (NET).[2] Its dopaminergic pharmacodynamic profile is nearly identical to methylphenidate and is primarily responsible for its euphoric and reinforcing effects.[3]

The following is ethylphenidate's binding profile in the mouse, alongside methylphenidate's. Figures for both the racemic and the dextrorotary enantiomers are given:[4]

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

Ethylphenidate can be formed within the body (in the liver), when alcohol and methylphenidate are co-ingested.[5] This is most common when large quantities of methylphenidate and alcohol are consumed at the same time, such as in non-medical use or overdose scenarios.[6] A similar process is also known to occur when cocaine and alcohol are consumed together, forming cocaethylene.[7] However, only a few percent of the consumed methylphenidate is converted to ethylphenidate, so a pharmacologically significant dose with measurable physiological effects would never be produced.[8][9]

Subjective effects

he general headspace of ethylphenidate is described by many as one of extreme mental stimulation, increased focus, and powerful euphoria. It contains a large number of typical stimulant cognitive effects. Although negative side effects are usually mild at low to moderate dosages, they become increasingly likely to manifest themselves with higher amounts or extended usage. This particularly holds true during the offset of the experience.

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances and are more likely to induce a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include serious injury or death.

Physical effects
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Cognitive effects
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After effects
Aftereffects (3).svg

Experience reports

There are currently anecdotal reports which describe the effects of this compound within our experience index.

Additional experience reports can be found here:

Toxicity and harm potential

The toxicity and long-term health effects of recreational ethylphenidate use do not seem to have been studied in any scientific context and the exact toxic dosage is unknown. This is because ethylphenidate has a very limited history of human usage.

Anecdotal evidence from people who have tried ethylphenidate within the community suggests that there do not seem to be any negative health effects attributed to simply trying this substance at low to moderate doses by itself and using it sparingly (but nothing can be completely guaranteed).

It is worth noting that ethylphenidate crystals are particularly abrasive and somewhat caustic to mucous membranes. Careless use will deteriorate the chosen routes of administration so it is important to practice routine maintenance such as soaking the sinus cavity with water prior to and following insufflation.

It will also irritate lung tissue if inhaled, resulting in the production of phlegm and an irritated cough.

It is strongly recommended that one use harm reduction practices when using this substance.

Tolerance and addiction potential

As with other stimulants, the chronic use of ethylphenidate can be considered moderately addictive with a high potential for abuse and is capable of causing psychological dependence among certain users. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage.

Tolerance to many of the effects of ethylphenidate develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). ethylphenidate presents cross-tolerance with all dopaminergic stimulants, meaning that after the consumption of ethylphenidate all stimulants will have a reduced effect.

Psychosis

Main article: Stimulant psychosis

Abuse of compounds within the stimulant class at high dosages for prolonged periods of time can potentially result in a stimulant psychosis that may present with a variety of symptoms (e.g., paranoia, hallucinations, or delusions).[10] A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely.[11][12] The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.[13]

Dangerous interactions

Although many psychoactive substances are safe to use on their own, they can become dangerous or even life-threatening when taken with other substances. The list below contains some potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses but still increase the possibility of injury of death. Independent research should always be conducted to ensure that a combination of two or more substances is safe before consumption.

  • 25x-NBOMe - Members of the 25x-NBOMe family are very stimulating and should not be combined with stimulants due to the risk of excessive stimulation. This can result in panic attacks, thought loops, seizures, increased blood pressure, vasoconstriction, and heart failure in extreme cases.
  • Alcohol - Alcohol can be dangerous to combine with stimulants due to the risk of accidental over-intoxication. Stimulants mask the sedative effects of alcohol, which is the main factor people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects of alcohol are left unopposed, which can result in blackouts and respiratory depression. If combined, one should strictly limit themselves to only drinking a certain amount of alcohol per hour.
  • DXM - DXM should not be combined with stimulants due to its effects on serotonin and dopamine reuptake. This can lead to panic attacks, hypertensive crisis, or serotonin syndrome.
  • MXE - Combining stimulants with MXE may dangerously elevate blood pressure and increase the risk of psychosis.
  • Tramadol - Combining stimulants with tramadol increases the risk of seizures.
  • MAOIs - This combination may increase the amount of neurotransmitters such as dopamine to dangerous or even fatal levels. Examples include syrian rue, banisteriopsis caapi, 2C-T-2, 2C-T-7, αMT, and some antidepressants.[14]
  • MDMA - The neurotoxic effects of MDMA may be increased when combined with other stimulants.
  • Cocaine - This combination may increase strain on the heart.

Legal status

Ethylphenidate is not controlled internationally and remains easily accessible through online research chemical vendors. It is, however, illegal or at least potentially illegal within certain jurisdictions, each of which are listed below:

  • USA: Ethylphenidate is not explicitly controlled in the US, but it could possibly be considered an analog of a Schedule II substance (methylphenidate) under the Federal Analog Act.
  • Sweden: Ethylphenidate is illegal as of 15 December 2012.[15]
  • Jersey: Ethylphenidate is illegal under the Misuse of Drugs (Jersey) Law 1978.[16]
  • Australia: 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.
  • Germany: Ethylphenidate is illegal in Germany as of 05.07.2013.[17]
  • Austria: Since January 1, 2012, Ethylphenidate is illegal to possess, produce and sell under the NPSG. (Neue-Psychoaktive-Substanzen-Gesetz Österreich)
  • Denmark: Ethylphenidate is illegal in Denmark as of 1 February 2013.[18]
  • United Kingdom - Ethylphenidate is a class B drug in the UK as of 31st May 2017 and is illegal to possess, produce or supply. [19]

See also

External links

References

  1. Synthesis and pharmacology of ethylphenidate enantiomers: the human transesterification metabolite of methylphenidate and ethanol (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/15828826
  2. Methylphenidate and its ethanol transesterification metabolite ethylphenidate: brain disposition, monoamine transporters and motor activity (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/17218796
  3. Methylphenidate and its ethanol transesterification metabolite ethylphenidate: brain disposition, monoamine transporters and motor activity (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/17218796
  4. Methylphenidate and its ethanol transesterification metabolite ethylphenidate: brain disposition, monoamine transporters and motor activity | http://journals.lww.com/behaviouralpharm/pages/articleviewer.aspx?year=2007&issue=02000&article=00005&type=abstract
  5. Ethylphenidate formation in human subjects after the administration of a single dose of methylphenidate and ethanol (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/10820132
  6. Detection of the novel metabolite ethylphenidate after methylphenidate overdose with alcohol coingestion (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/10440465
  7. Carboxylesterase-mediated transesterification of meperidine (Demerol) and methylphenidate (Ritalin) in the presence of [2H6]ethanol: preliminary in vitro findings using a rat liver preparation (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/9423167
  8. Ethylphenidate formation in human subjects after the administration of a single dose of methylphenidate and ethanol (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/10820132
  9. Methylphenidate and its ethanol transesterification metabolite ethylphenidate: brain disposition, monoamine transporters and motor activity (PubMed.gov / NCBI) | http://www.ncbi.nlm.nih.gov/pubmed/17218796
  10. Treatment for amphetamine psychosis | [1]
  11. Treatment for amphetamine psychosis | [2]
  12. Hofmann FG (1983). A Handbook on Drug and Alcohol Abuse: The Biomedical Aspects (2nd ed.). New York: Oxford University Press. p. 329. ISBN 9780195030570.
  13. Treatment for amphetamine psychosis | [3]
  14. Gillman, P. K. (2005). Monoamine oxidase inhibitors, opioid analgesics and serotonin toxicity. British Journal of Anaesthesia, 95(4), 434-441. https://doi.org/10.1093/bja/aei210
  15. http://www.riksdagen.se/sv/Dokument-Lagar/Lagar/Svenskforfattningssamling/Forordning-19921554-om-kont_sfs-1992-1554/?bet=1992:1554
  16. http://www.jerseylaw.je/law/Display.aspx?url=/law/lawsinforce/consolidated/08/08.680.60_MisuseofDrugs(GeneralProvisions)Order2009_RevisedEdition_1January2014.pdf
  17. http://www.gesetze-im-internet.de/btmg_1981/anlage_ii_60.html
  18. https://www.retsinformation.dk/Forms/R0710.aspx?id=145195
  19. The Misuse of Drugs Act 1971 (Amendment) Order 2017 (Legislation.gov.uk) | http://www.legislation.gov.uk/uksi/2017/634/made