Ethylphenidate is a synthetic stimulant of the piperidine class and the ethyl analog of methylphenidate (Ritalin). What makes ethylphenidate pharmacologically unusual is its dual existence — it was first identified not as a designed drug but as ametabolite that forms naturally inside the human body when methylphenidate and ethanol are co-ingested, through a hepatic transesterification reaction . This metabolic curiosity was later exploited by research chemical vendors who began selling it as a standalone stimulant.
The Transesterification Discovery
In 1999, Markowitz and colleagues detected ethylphenidate in postmortem blood and liver samples from cases involving methylphenidate overdose with concurrent alcohol consumption . The reaction is catalyzed byhepatic carboxylesterase 1 (CES1), which transfers the ethyl group from ethanol to methylphenidate's ester linkage, producing ethylphenidate via transesterification — the same class of reaction that converts cocaine to cocaethylene in the presence of alcohol . This discovery raised important clinical implications: millions of people taking prescribed methylphenidate who also consume alcohol are unknowingly generating a pharmacologically active metabolite with distinct properties.
Research Chemical Market
By approximately 2010, ethylphenidate emerged on the novel psychoactive substances (NPS) market as a standalone stimulant, sold online as a "research chemical" under brand names including**"Gogaine," "Nopaine,"** and**"Burst"** . Users sought it as a legal alternative to cocaine, drawn by its short duration (2-4 hours), rapid onset when insufflated, and stimulant euphoria. However, the drug gained notoriety for causing significantnasal tissue damage when insufflated — substantially worse than cocaine or amphetamine — due to its caustic properties and the frequency of redosing driven by its short duration.
References
Markowitz JS et al. Detection of the novel metabolite ethylphenidate after methylphenidate overdose with alcohol coingestion. Journal of Clinical Psychopharmacology. 1999;19(4):362-366. Patrick KS et al. Synthesis and pharmacology of ethylphenidate enantiomers: the human transesterification metabolite of methylphenidate and ethanol. Journal of Medicinal Chemistry. 2005;48(8):2876-2881. ACMD. Methylphenidate-based NPS: A review of the evidence of use, harms, and availability. Advisory Council on the Misuse of Drugs. 2015.
Safety at a Glance
High Risk- Denmark: Ethylphenidate is illegal in Denmark as of 1 February 2013.
- Jersey: Ethylphenidate is illegal under the Misuse of Drugs (Jersey) Law 1978.
- Toxicity: The toxicity and long-term health effects of recreational ethylphenidate use do not seem to have been studied in any ...
- Dangerous with: 25x-NBOH, 25x-NBOMe, Atropa belladonna, Datura, MDMA (+3 more)
- Overdose risk: Stimulant overdose from Ethylphenidate is a medical emergency primarily involving cardiovascular ...
If someone is in crisis, call 911 or Poison Control: 1-800-222-1222
Dosage
oral
rectal
Duration
oral
Total: 4 hrs – 7 hrsrectal
Total: 2 hrs – 6 hrsHow It Feels
Ethylphenidate arrives with a clinical precision that mirrors its pharmaceutical cousin, methylphenidate. Within fifteen to thirty minutes of insufflation, a sharp, focused clarity descends upon the mind. The world does not become more beautiful or more interesting in any aesthetic sense. Instead, it becomes more manageable. Tasks that seemed tedious now appear straightforward. Distractions lose their pull. Attention narrows to a productive beam that can be directed and sustained with unusual ease. The onset when insufflated is accompanied by a significant nasal burn that lingers for several minutes, stinging and caustic in a way that distinguishes it from most other insufflated stimulants.
At the functional peak, which establishes itself within thirty to sixty minutes, ethylphenidate produces a state of concentrated, driven productivity. The euphoria is minimal, present only as a faint sense of satisfaction in accomplishment rather than as pleasure for its own sake. Conversation becomes efficient rather than expansive. Physical energy increases, but it is directed energy, purposeful and contained. The experience is fundamentally one of enhanced executive function: better planning, sharper prioritization, more sustained follow-through. This is a tool, not a toy, and its character reflects that distinction clearly.
The body experiences the familiar constellation of stimulant effects. Heart rate elevates. Blood pressure rises. Appetite evaporates. Jaw tension is common but not severe. The most notable physical feature is the vasoconstriction, which can produce cold, pale fingers and toes, and at higher doses, an uncomfortable tightness in the chest. The nasal passages, if used as the route of administration, remain irritated and may produce nosebleeds with repeated use. There is a fine tremor in the hands that becomes noticeable when trying to perform precise tasks.
The duration is moderate, with the primary effects lasting two to four hours before gradually tapering. The comedown is functional in character, a gradual deflation of focus and energy rather than a crash. There may be mild irritability, slight headache, and a rebound of the very distractibility that the substance was taken to combat. Sleep is achievable within a reasonable timeframe, though the quality may be compromised by residual stimulation. The overall experience is utilitarian and efficient, valued by those seeking a study aid or productivity tool, and offering little to those seeking recreation or altered states.
Subjective Effects
The effects listed below are based on the Subjective Effect Index (SEI), an open research literature based on anecdotal reports and personal analyses. They should be viewed with a healthy degree of skepticism. These effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects.
Physical Effects
Physical(8)
- Headache— A painful sensation of pressure, throbbing, or aching in the head that can range from a dull backgro...
- Increased blood pressure— Increased blood pressure (hypertension) is an elevation of arterial pressure above the normal 120/80...
- Increased phlegm production— Increased phlegm production is the excessive generation of mucus in the throat and respiratory passa...
- Respiratory depression— A dangerous slowing and shallowing of breathing that can progress from barely noticeable reductions ...
- Seizure— Uncontrolled brain electrical activity causing convulsions and loss of consciousness -- a life-threa...
- Serotonin syndrome— Serotonin syndrome is a potentially fatal medical emergency caused by excessive serotonergic activit...
- Stimulation— A state of heightened physical and mental energy characterized by increased wakefulness, elevated mo...
- Vasoconstriction— A narrowing of blood vessels throughout the body that produces sensations of cold extremities, tingl...
Cognitive & Perceptual Effects
Cognitive(9)
- Amnesia— A complete or partial inability to form new memories or recall existing ones during and after substa...
- Delusion— A delusion is a fixed, false belief that is held with unshakeable certainty and is impervious to con...
- Depression— A persistent state of low mood, emotional numbness, hopelessness, and diminished interest or pleasur...
- Irritability— Irritability is a sustained state of emotional reactivity in which the threshold for annoyance, frus...
- Mania— Abnormally elevated mood, energy, and activity with impulsive behavior and grandiosity, associated w...
- Panic attack— A panic attack is a discrete episode of acute, overwhelming fear or terror that arises suddenly and ...
- Paranoia— Irrational suspicion and belief that others are watching, plotting against, or intending harm toward...
- Psychosis— Psychosis is a serious psychiatric state involving a fundamental break from consensus reality — char...
- Thought loops— Becoming trapped in a repeating cycle of thoughts, actions, and emotions that loops every few second...
Pharmacology
DAT and NET Reuptake Inhibition
Ethylphenidate, like its parent compound methylphenidate, acts as a dopamine-norepinephrine reuptake inhibitor (DNRI) — it blocks the dopamine transporter (DAT) and norepinephrine transporter (NET) without acting as a substrate or releasing monoamines . The pharmacologically actived-enantiomer (d-ethylphenidate) demonstrates potent DAT inhibition with an IC50 of approximately27 nM, remarkably close to d-methylphenidate's IC50 of 23 nM . However, ethylphenidate shows substantially greaterselectivity for DAT over NET, being approximately sevenfold less potent at NET (IC50 approximately 290 nM) compared to methylphenidate's more balanced inhibition of both transporters . This enhanced DAT selectivity may contribute to ethylphenidate's reportedly more euphoric and less anxiogenic subjective profile compared to methylphenidate.
In Vivo Formation: The Transesterification Mechanism
When methylphenidate and ethanol are co-ingested, hepatic carboxylesterase 1 (CES1) catalyzes a transesterification reaction that replaces the methyl ester group of methylphenidate with an ethyl group from ethanol, yielding ethylphenidate . This reaction isenantioselective — CES1 preferentially transesterifies the pharmacologically less active l-methylphenidate, producing predominantly l-ethylphenidate. The clinical consequence is paradoxical: the transesterification simultaneously removes l-methylphenidate (increasing the relative proportion of the more active d-enantiomer) while generating l-ethylphenidate (which has minimal pharmacological activity) . The net effect is increased early exposure to d-methylphenidate and rapid potentiation of subjective euphoria — a mechanism that may partially explain why some ADHD patients report enhanced medication effects when consuming alcohol.
Minimal Serotonergic Activity
Like methylphenidate, ethylphenidate has negligible affinity for the serotonin transporter (SERT), distinguishing it from amphetamine-type releasers and MDMA-like empathogens . This serotonergic absence accounts for the drug's purely stimulant subjective profile — increased energy, focus, confidence, and euphoria without the empathogenic warmth or emotional openness characteristic of serotonergic drugs.
References
Patrick KS et al. Ethylphenidate as a selective dopaminergic agonist and methylphenidate-ethanol transesterification biomarker. Journal of Pharmaceutical Sciences. 2014;103(12):3834-3842. Markowitz JS, Patrick KS. Differential pharmacokinetics and pharmacodynamics of methylphenidate enantiomers: does chirality matter? Journal of Clinical Psychopharmacology. 2008;28(3 Suppl 2):S54-61.
Detection Methods
Standard Drug Panel Inclusion
Ethylphenidate is a phenidate-class stimulant that is not detected on standard 5-panel, 10-panel, or 12-panel immunoassay drug screens. Phenidates are structurally distinct from amphetamines and do not cross-react with amphetamine or methamphetamine antibodies used in commercial immunoassays. There is no dedicated phenidate channel on any standard workplace or clinical drug panel.
Urine Detection
Ethylphenidate and its primary metabolite ritalinic acid (or the corresponding deesterified acid analogue) can be detected in urine for approximately 1 to 3 days after a single oral dose. The ester bond in phenidate compounds is rapidly hydrolyzed by plasma and hepatic esterases, producing the corresponding acid metabolite which is the dominant species found in urine. Higher doses or repeated administration may extend the detection window modestly.
Blood and Saliva Detection
Blood concentrations of Ethylphenidate decline rapidly due to ester hydrolysis, with a detection window of approximately 6 to 24 hours for the parent compound. The acid metabolite persists longer in plasma, detectable for up to 48 hours. Oral fluid testing can detect the parent compound for approximately 12 to 36 hours, though this route of detection is rarely employed for phenidates in practice.
Hair Follicle Detection
Hair follicle analysis may detect Ethylphenidate or its metabolites for up to 90 days. However, incorporation of phenidate-class compounds into hair has not been extensively studied, and commercial laboratories do not routinely test for these substances. Specialized forensic laboratories with LC-MS/MS capability and appropriate reference standards would be required.
Confirmatory Testing
Liquid chromatography-tandem mass spectrometry (LC-MS/MS) is the gold standard for confirming the presence of Ethylphenidate and its metabolites. The ester bond in phenidates makes them somewhat labile under GC-MS conditions, so LC-MS/MS is preferred. Both parent compound and the deesterified acid metabolite should be targeted for comprehensive analysis.
Reagent Testing
Marquis reagent typically shows no reaction or a very faint color change with Ethylphenidate, which helps distinguish it from amphetamines (orange-brown) and MDMA (purple-black). Mecke reagent generally shows no reaction. Mandelin reagent may produce a faint yellow or no change. The absence of strong reagent reactions is characteristic of the phenidate class and is itself a useful piece of information when combined with other reagent results.
Interactions
| Substance | Status | Note |
|---|---|---|
| 25x-NBOH | Dangerous | — |
| 25x-NBOMe | Dangerous | — |
| Atropa belladonna | Dangerous | Extreme cardiovascular strain from anticholinergic and stimulant effects combined |
| Datura | Dangerous | Extreme cardiovascular strain from anticholinergic and stimulant effects combined |
| Diphenhydramine | Dangerous | Extreme cardiovascular strain from anticholinergic and stimulant effects combined |
| Harmala alkaloid | Dangerous | Risk of hypertensive crisis and serotonin syndrome; potentially fatal combination |
| Peganum harmala | Dangerous | Risk of hypertensive crisis and serotonin syndrome; potentially fatal combination |
| MDMA | Unsafe | — |
| 1,3-Butanediol | Caution | Increases anxiety, cardiovascular stress, and psychological intensity |
| 25E-NBOH | Caution | Increases anxiety, cardiovascular stress, and psychological intensity |
| 2C-T | Caution | Increases anxiety, cardiovascular stress, and psychological intensity |
| 2C-T-2 | Caution | Increases anxiety, cardiovascular stress, and psychological intensity |
| 2C-T-21 | Caution | Increases anxiety, cardiovascular stress, and psychological intensity |
| Alcohol | Uncertain | — |
| Dissociatives | Uncertain | — |
History
Discovery as a Metabolite (1999)
Ethylphenidate was first identified in 1999 byJohn S. Markowitz and colleagues at the Medical University of South Carolina. While analyzing postmortem blood and liver samples from cases involving methylphenidate overdose with concurrent alcohol ingestion, the team detected an unexpected metabolite — ethylphenidate — formed by hepatic transesterification of methylphenidate in the presence of ethanol . This discovery paralleled the earlier identification of cocaethylene as a metabolite of cocaine and ethanol, establishing transesterification as a significant pharmacokinetic interaction for ester-containing stimulants.
From Metabolite to Research Chemical (2010-2014)
Following its characterization in the academic literature, ethylphenidate was synthesized and sold as a standalone research chemical by NPS vendors beginning around 2010 . It was marketed through online headshops and research chemical websites under various brand names including "Gogaine," "Nopaine," "Banshee Dust," and "Burst," primarily in theUnited Kingdom where it gained particular popularity as a cheap, legal alternative to cocaine. The drug was typically sold as a white powder for insufflation, with prices substantially below those of cocaine.
UK Temporary Class Drug Order (2015)
In response to growing evidence of harm — particularly an outbreak of soft tissue infections and abscesses among intravenous ethylphenidate users in Lothian, Scotland — the UK Home Secretary issued aTemporary Class Drug Order (TCDO) onApril 10, 2015, covering ethylphenidate and four related methylphenidate-based NPS . The TCDO made it illegal to produce, supply, or import these substances, with penalties of up to 14 years imprisonment. Ethylphenidate was subsequently permanently controlled under thePsychoactive Substances Act 2016, which broadly banned all psychoactive substances not specifically exempted .
References
Markowitz JS et al. Detection of the novel metabolite ethylphenidate after methylphenidate overdose with alcohol coingestion. Journal of Clinical Psychopharmacology. 1999;19(4):362-366. Patrick KS et al. Ethylphenidate as a selective dopaminergic agonist and methylphenidate-ethanol transesterification biomarker. Journal of Pharmaceutical Sciences. 2014;103(12):3834-3842. UK Home Office. Circular 015/2015: Temporary control of 5 methylphenidate-based NPS. Misuse of Drugs Act 1971 (Temporary Class Drug) Order 2015.
Harm Reduction
As with other stimulants,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.develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that,3 - 71 - 2 weeks to be back at baseline (in the absence of further consumption). ethylphenidate presents cross-tolerance with Cross-all dopaminergic stimulants, meaning that after the consumption of ethylphenidate all stimulants will have a reduced effect.
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). A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely. The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.
- Denmark: Ethylphenidate is illegal in Denmark as of 1 February 2013.
- Germany: Ethylphenidate is controlled under Anlage II BtMG (Narcotics Act, Schedule II) as of July 17, 2013. It is illegal to manufacture, possess, import, export, buy, sell, procure or dispense it without a license.
- Jersey: Ethylphenidate is illegal under the Misuse of Drugs (Jersey) Law 1978.
- The Neth
Toxicity & Safety
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.
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). A review on treatment for amphetamine, dextroamphetamine, and methamphetamine abuse-induced psychosis states that about 5–15% of users fail to recover completely. The same review asserts that, based upon at least one trial, antipsychotic medications effectively resolve the symptoms of acute amphetamine psychosis.
Dangerous interactions
Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.
25x-NBOMe & 25x-NBOH - 25x compounds are highly stimulating and physically straining. Combinations with Ethylphenidate should be strictly avoided due to the risk of excessive stimulation and heart strain. This can result in increased blood pressure, vasoconstriction, panic attacks, thought loops, seizures, and heart failure in extreme cases.
Alcohol - Combining alcohol with stimulants can be dangerous due to the risk of accidental over-intoxication. Stimulants mask alcohol's depressant effects, which is what most people use to assess their degree of intoxication. Once the stimulant wears off, the depressant effects will be left unopposed, which can result in blackouts and severe respiratory depression. If mixing, the user should strictly limit themselves to only drinking a certain amount of alcohol per hour.
DXM - Combinations with DXM should be avoided due to its inhibiting effects on serotonin and norepinephrine reuptake. There is an increased risk of panic attacks and hypertensive crisis, or serotonin syndrome with serotonin releasers (MDMA, methylone, mephedrone, etc.). Monitor blood pressure carefully and avoid strenuous physical activity.
MDMA - Any neurotoxic effects of MDMA are likely to be increased when other stimulants are present. There is also a risk of excessive blood pressure and heart strain (cardiotoxicity).
MXE - Some reports suggest combinations with MXE may dangerously increase blood pressure and increase the risk of mania and psychosis.
Dissociatives - Both classes carry a risk of delusions, mania and psychosis, and these risk may be multiplied when combined.
Stimulants - Ethylphenidate may be dangerous to combine with other stimulants like cocaine as they can increase one's heart rate and blood pressure to dangerous levels.
Tramadol - Tramadol is known to lower the seizure threshold and combinations with stimulants may further increase this risk.
MAOIs - This combination may increase the amount of neurotransmitters such as dopamine to dangerous or even fatal levels. Examples include syrian rue, banisteriopsis caapi, and some antidepressants.
MDMA - The neurotoxic effects of MDMA may be increased when combined with other stimulants.
Cocaine - This combination may increase strain on the heart.
Addiction Potential
moderately addictive with a high potential for abuse
Overdose Information
Stimulant overdose from Ethylphenidate is a medical emergency primarily involving cardiovascular and neurological toxicity.
Signs of overdose: Extremely rapid or irregular heartbeat, chest pain, severe headache, dangerously elevated body temperature, seizures, agitation progressing to psychosis, confusion, and loss of consciousness.
Emergency response:
- Call emergency services immediately
- Keep the person cool (remove excess clothing, apply cool water)
- If seizures occur, protect the head and clear the area of hard objects
- If the person loses consciousness, place in recovery position
- Do not give the person more stimulants, caffeine, or depressants unless directed by medical professionals
Prevention: Pre-measure doses. Avoid redosing. Stay hydrated (but don't overhydrate). Take breaks from physical activity. Monitor heart rate if possible. Have someone present who can recognize warning signs.
Dangerous Interactions
The combinations listed below may be life-threatening. Independent research should always be conducted to ensure safety when combining substances.
Extreme cardiovascular strain from anticholinergic and stimulant effects combined
Extreme cardiovascular strain from anticholinergic and stimulant effects combined
Extreme cardiovascular strain from anticholinergic and stimulant effects combined
Risk of hypertensive crisis and serotonin syndrome; potentially fatal combination
Risk of hypertensive crisis and serotonin syndrome; potentially fatal combination
Tolerance
| Full | develops with prolonged and repeated use |
| Half | 3 - 7 days |
| Zero | 1 - 2 weeks |
Cross-tolerances
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:
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.
Austria: Since January 1, 2012, Ethylphenidate is illegal to possess, produce and sell under the NPSG. (Neue-Psychoaktive-Substanzen-Gesetz Österreich)
Canada: Ethylphenidate is listed on the CDSA in Schedule III as of May 5, 2017.
Denmark: Ethylphenidate is illegal in Denmark as of 1 February 2013.
Germany: Ethylphenidate is controlled under Anlage II BtMG (Narcotics Act, Schedule II) as of July 17, 2013. It is illegal to manufacture, possess, import, export, buy, sell, procure or dispense it without a license.
Jersey: Ethylphenidate is illegal under the Misuse of Drugs (Jersey) Law 1978.
The Netherlands: Ethylphenidate is listed in the Opiumwet (Opium Act)) on Lijst I as of April 27, 2018.
Sweden: Ethylphenidate is illegal as of 15 December 2012.
Switzerland: Ethylphenidate is a controlled substance specifically named under Verzeichnis D.
United Kingdom: Ethylphenidate is a class B drug in the UK as of 31st May 2017 and is illegal to possess, produce or supply.
United States: 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.
Responsible use
Research chemical
Stimulant
Methylphenidate
Ethylphenidate (Wikipedia)
Ethylphenidate (Erowid Vault)
Ethylphenidate (Isomer Design)
Ethylphenidate (Drugs-Forum)
Experience Reports (1)
Tips (6)
Monitor your heart rate and blood pressure when using Ethylphenidate. Sustained elevated cardiovascular stress causes cumulative damage. If you experience chest pain, irregular heartbeat, or numbness in extremities, seek medical attention.
Weigh your dose of Ethylphenidate with a milligram scale. Street stimulants vary wildly in purity and potency. What looks like a normal amount could be significantly stronger than expected, especially with a new batch.
Ethylphenidate is actually formed in your body when you combine methylphenidate (Ritalin) with alcohol via transesterification. This is not a safe way to produce it. The combination puts enormous strain on your liver and cardiovascular system and the dose is completely unpredictable.
If you snort Ethylphenidate, use a clean straw (never shared), crush the powder as finely as possible, alternate nostrils, and rinse with saline spray after your session. Chronic insufflation damages nasal tissue and septum.
Ethylphenidate is extremely caustic to nasal tissue when insufflated. It causes significantly more damage than most other stimulants. If you must use this route, dissolve it in saline solution first and use a nasal spray bottle. Oral dosing is much safer for your mucous membranes.
Ethylphenidate is roughly equipotent to methylphenidate but with a shorter duration. Start with 10-15mg orally. Insufflated doses should be lower, around 5-10mg, due to higher bioavailability. The compulsive redosing urge is strong with this one, so set a firm limit beforehand.
See Also
References (4)
- Amphetamine: new content for an old topic — Heal et al. Neuropsychopharmacology Reviews (2013)paper
- PubChem: Ethylphenidate
PubChem compound page for Ethylphenidate (CID: 3080846)
pubchem - Ethylphenidate - TripSit Factsheet
TripSit factsheet for Ethylphenidate
tripsit - Ethylphenidate - Wikipedia
Wikipedia article on Ethylphenidate
wikipedia