2C-E
4-ethyl-2,5-dimethoxyphenethylamine
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2C-E (2,5-dimethoxy-4-ethylphenethylamine) is a synthetic psychedelic of the phenethylamine class. It is one of Shulgin's "magical half-dozen," distinguished from 2C-B by greater cognitive depth and a steeper dose-response curve. 2C-E is a partial agonist at serotonin 5-HT₂A receptors with a broad receptor interaction profile,[1][2] producing its effects by disrupting cortical filtering of sensory and cognitive input.
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Alexander Shulgin first synthesised the compound circa 1977 and documented it in PiHKAL (1991) as one of six phenethylamines he considered most pharmacologically significant.[3] A fatal mass poisoning in Minnesota in 2011 accelerated US scheduling.[4] 2C-E has been Schedule I in the United States since 2012 and is controlled in most jurisdictions that have specifically addressed it.[5]
Subjective effects include geometric visual patterns, time alteration, enhanced introspection, ego dissolution, and body load. The experience carries more cognitive weight than most 2C-series compounds — analytical and immersive rather than sensory, closer in reflective depth to mescaline than to 2C-B's lighter character.[3] Nausea, physical tension, and pronounced body load are characteristic unsought effects.
2C-E produces no physical dependence — tolerance develops rapidly via downregulation and cross-generalises to other classical psychedelics[6] — and the lethal dose is unknown. The steep dose-response curve is the defining risk: a few milligrams separate a manageable experience from an overwhelming one, and insufflation compresses onset in ways that remain pharmacokinetically uncharacterised. A single observational study of ten participants constitutes the only controlled human data; the current understanding rests largely on Shulgin's original reports and community experience.[1]
History[edit]
Discovery
Alexander Shulgin first synthesised 2C-E circa 1977 as part of his systematic exploration of substituted phenethylamines.[3] The compound was publicly documented in PiHKAL: A Chemical Love Story (1991), where Shulgin described it as "difficult and worth-while" and specifically warned of its steep dose-response curve — small dose increments producing disproportionately intense experiences. He designated 2C-E one of his "magical half-dozen," the six phenethylamine psychedelics he considered most significant, alongside mescaline, DOM, 2C-B, 2C-T-2, and 2C-T-7.
Key incidents and scheduling
2C-E entered online research chemical markets in the early 2000s and circulated legally in many jurisdictions for nearly a decade. In March 2011, a mass poisoning at a party in Blaine, Minnesota resulted in one death and ten hospitalisations after attendees insufflated 2C-E that had been mislabelled as 2C-I.[4][7] This incident was a significant driver of US scheduling: on 9 July 2012, the synthetic Drug Abuse Prevention Act placed 2C-E in Schedule I.[5]
Modern status
A second mass poisoning in Europe (2019) involved 2C-E combined with Bromo-DragonFly, an unusual case for both the polydrug combination and the older age profile of those involved.[8] No clinical trial of 2C-E has ever been conducted; the only controlled human data come from a single observational study of ten recreational users in Spain.[1] Schedule I classification in the United States and equivalent controls elsewhere have created substantial barriers to further research.
The "2C" designation refers to the two carbon atoms in the ethylamine side chain linking the aromatic ring to the terminal amine — a naming convention Shulgin applied across the entire series.[3] Among the magical half-dozen, 2C-E carries a distinctive reputation: users and commentators consistently describe it as the most cognitively demanding member of the 2C family, a compound that rewards preparation and punishes carelessness.
Chemistry[edit]
Structural class
2C-E belongs to the 2C series of substituted phenethylamines, a family defined by the 2,5-dimethoxy substitution pattern on the phenyl ring with a variable substituent at the 4-position.[3] The 4-ethyl group distinguishes 2C-E from other series members: 2C-B (4-bromo), 2C-I (4-iodo), 2C-D (4-methyl), and 2C-C (4-chloro).
Molecular properties
| Molecular formula | C₁₂H₁₉NO₂ |
| Molecular weight | 209.28 g/mol |
The molecule consists of a benzene ring bearing methoxy groups at the 2- and 5-positions and an ethyl group at the 4-position, with a two-carbon ethylamine chain extending from position 1. 2C-E is achiral — it lacks the alpha-methyl group present in the amphetamine-derived DO series, so no stereoisomers exist.
Structure-activity relationships
The structural relationship between 2C-E and its amphetamine structural analog DOET (2,5-dimethoxy-4-ethylamphetamine) illustrates a key principle: the alpha-methyl group on the amphetamine side chain increases both potency and receptor activation at serotonergic targets.[9] 2C-E's two-carbon side chain confers lower intrinsic activity at 5-HT₂A compared to DOET, resulting in shorter duration and reduced potency.
Physical properties
2C-E is commonly encountered as the hydrochloride salt, a white to off-white crystalline powder. No published characterisation of melting point, solubility, or stability has appeared in peer-reviewed literature. Forensic detection methods using GC-MS and HPLC-MS[10] and UPLC-MS/MS in hair matrices[11] have been developed.
Pharmacology[edit]
Mechanism of action
2C-E acts primarily as a partial agonist at serotonin 5-HT₂A receptors, with additional activity at serotonin₂B and 5-HT₂C receptors and weak inhibition of serotonin and norepinephrine reuptake.[1] Activation of 5-HT₂A receptors on cortical pyramidal neurons enhances glutamate signalling, disrupting the brain's normal filtering of sensory and cognitive information.[12][13]
As a phenethylamine with a two-carbon side chain, 2C-E has lower receptor activation strength than its amphetamine-derived counterpart DOET.[9] The compound's psychoactive effects are receptor-mediated; its activity at monoamine transporters is weak compared to classical stimulants.[14]
Functional receptor activation has been confirmed in rat brain tissue, where 2C-E stimulated G-protein signalling at serotonin receptors in cortical membranes.[15] Receptor screening across 42 of 49 tested binding sites confirms a broad interaction profile typical of the phenethylamine class,[2] though the primary psychedelic effects are 5-HT₂A-mediated.
Pharmacokinetics
The only human pharmacokinetic data come from an observational study in Spain with ten recreational users who self-administered 2C-E orally at doses between 6.5 and 25 mg.[1] Peak drug levels in saliva were reached approximately two hours after ingestion. The study used saliva rather than blood plasma as its measurement matrix, which approximates free drug levels but is not equivalent to formal plasma pharmacokinetics.
No plasma pharmacokinetic study has been published — half-life, bioavailability, and volume of distribution remain unknown. Insufflated pharmacokinetics are entirely unstudied, despite insufflation being the route involved in the only confirmed fatality.
Metabolism
2C-E is metabolised primarily through removal of methoxy groups at the 2- and 5-positions, hydroxylation of the ethyl side chain, breakdown of the ethylamine portion, and conjugation of metabolites for excretion.[16] The specific liver enzymes responsible have not been individually characterised for 2C-E.[16]
The compound has also been confirmed as a metabolite of 25E-NBOH, formed by removal of the N-benzyl group.[17]
Neuroscience[edit]
Where it acts
No neuroimaging or electrophysiology studies of 2C-E have been published. Based on its established pharmacology — partial agonism at 5-HT₂A receptors — the compound is expected to disrupt default mode network integrity, reduce thalamic gating of sensory input, and increase global functional connectivity in the cortex.[12] These effects, characterised for LSD and psilocybin, produce the subjective experience of dissolved ego boundaries, visual distortion, and heightened pattern recognition.
2C-E's status as a partial agonist with lower intrinsic activity than DO-series compounds[9] suggests it may produce a submaximal version of these network disruptions — though whether this manifests as reduced intensity or qualitatively different neural patterns remains unknown.
Theoretical context
The REBUS model proposes that psychedelics loosen the brain's top-down predictions, allowing raw sensory data to propagate more freely through cortical hierarchies. 2C-E's perceptual effects — visual distortions, pattern recognition enhancement, synesthesia — fit this framework. The entropic brain hypothesis, which links psychedelic intensity to increased randomness in brain activity, may help explain the compound's steep dose-response curve: small increases in receptor occupancy could push neural entropy past a nonlinear tipping point.
Whether 2C-E promotes structural brain plasticity — as demonstrated for other 5-HT₂A agonists via growth factor signalling — has not been investigated.
- Does 2C-E promote neuroplasticity, and if so, at what doses relative to its psychoactive threshold?
- What neural mechanisms underlie the steep dose-response curve — receptor-level nonlinearity, network-level tipping points, or both?
- Why is the experience consistently described as more cognitively demanding than 2C-B, given similar primary receptor targets?
Subjective Effects[edit]
Shulgin described the 2C-E experience as "difficult and worth-while"[3] — a characterisation that has held across decades of user reports. The steep dose-response curve means that precise dosing, mindset, and environment exert unusually strong influence on whether the experience resolves as deeply insightful or overwhelming. At lower doses the compound produces manageable visual and cognitive shifts; at higher doses it can become intensely immersive, with ego dissolution and heavy body load.
Compared to 2C-B, the most familiar reference in the series, 2C-E is consistently reported as more cognitively demanding and physically taxing. Where 2C-B leans sensory and recreational, 2C-E tends toward the analytical and reflective — closer in character to mescaline in its introspective depth, though shorter in duration and more stimulating in body profile.
Effect Grid
At common doses (10–15 mg oral), the full psychedelic experience develops: pronounced open- and closed-eye visuals including visual drifting, tracers, after-images, colour enhancement, and emerging internal hallucinations. Time distortion becomes significant. Thought connectivity increases substantially, often producing novel conceptual associations, creativity enhancement, and pattern recognition. Emotional responses intensify — music, art, and interpersonal exchanges take on heightened significance. Synesthesia may occur.
Physically, stimulation is prominent alongside nausea (particularly during onset), muscle tension, bruxism, pupil dilation, temperature dysregulation, and increased urination. The body load is a defining feature of 2C-E at this range, distinguishing it from the lighter somatic profile of 2C-B.
The experience demands 8–12 hours of committed time. Sleep is impossible during active effects. Functional impairment is substantial — driving, operating machinery, and complex decision-making are unsafe.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual breathing · Music enhancement · Symmetrical texture repetition · Tracers · Brightness alteration · Environmental patterning · After-images · Depth perception distortion · Light sensitivity · Peripheral vision distortion · Perspective distortion · Visual diffraction · Visual morphing · Holotropic state · Auditory enhancement · Sound sensitivity · Spatial disorientation · Visual haze / noise · Visual melting · Visual acuity enhancement · Touch enhancement · Auditory distortion · Auditory misinterpretation · Peripheral misidentification · Proprioceptive distortion · Vestibular distortion · Visual processing acceleration · Synesthesia · Dreaming enhancement · Visual magnification · Olfactory enhancement · Tinnitus · Flashbacks · Internal hallucinations · Object transformations · External hallucinations · Visual scenery slicing · Object activation · Visual recursion · Environmental orbism / cubism · Perspective hallucinations · Auditory hallucinations · Persisting hallucinations
Brightness alteration · Environmental patterning · After-images · Depth perception distortion · Light sensitivity · Peripheral vision distortion · Perspective distortion · Visual diffraction · Visual morphing · Holotropic state · Auditory enhancement · Sound sensitivity · Spatial disorientation · Visual haze / noise · Visual melting · Visual acuity enhancement · Touch enhancement · Auditory distortion · Auditory misinterpretation · Peripheral misidentification · Proprioceptive distortion · Vestibular distortion · Visual processing acceleration · Synesthesia · Dreaming enhancement · Visual magnification · Olfactory enhancement · Tinnitus · Flashbacks · Internal hallucinations · Object transformations · External hallucinations · Visual scenery slicing · Object activation · Visual recursion · Environmental orbism / cubism · Perspective hallucinations · Auditory hallucinations · Persisting hallucinations
Muscle tension · Stimulation · Body high · Nausea · Wakefulness · Insomnia · Physical fatigue · Restlessness · Tingling / electric sensations · Excessive sweating · Appetite suppression · Dry mouth · Heart rate perception changes · Nystagmus (eye wobbles) · Vasoconstriction · Dehydration sensation · Bodily heaviness · Bodily pressures · Body schema distortion · Breathing alteration · Dizziness · Headache · Tactile euphoria · Vibrations / buzzing · Increased urination · Bruxism · Diarrhea · Involuntary body movements · Laughter fits · Respiratory stimulation · Trembling · Sexual arousal enhancement · Abnormal heartbeat · Kundalini-like energy · Nasal congestion · Pain enhancement · Vomiting · Watery eyes · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Nausea · Wakefulness · Insomnia · Physical fatigue · Restlessness · Tingling / electric sensations · Excessive sweating · Appetite suppression · Dry mouth · Heart rate perception changes · Nystagmus (eye wobbles) · Dehydration sensation · Bodily heaviness · Bodily pressures · Body schema distortion · Breathing alteration · Dizziness · Headache · Tactile euphoria · Vibrations / buzzing · Increased urination · Bruxism · Diarrhea · Involuntary body movements · Laughter fits · Respiratory stimulation · Trembling · Sexual arousal enhancement · Abnormal heartbeat · Kundalini-like energy · Nasal congestion · Pain enhancement · Vomiting · Watery eyes · Seizure threshold reduction · Bodily dissociation · Tactile hallucination
Thought connectivity · Novelty enhancement · Aesthetic enhancement · Introspection enhancement · Openness enhancement · Thought acceleration · Cognitive flexibility · Multiple thought streams · Memory suppression · Cognitive euphoria · Cognitive fatigue · Cognitive impairment · Confusion · Increased nature relatedness · Memory fragmentation · Thought disorganization · Thought loops · Creativity enhancement · Analysis enhancement · Cognitive dysphoria · Focus suppression · Humor enhancement · Information processing suppression · Synchronicity · Information processing enhancement · Language enhancement · Language suppression · Memory replays · Motivation suppression · Focus enhancement · Motivation enhancement · Amnesia
Introspection enhancement · Openness enhancement · Thought acceleration · Cognitive flexibility · Multiple thought streams · Memory suppression · Cognitive euphoria · Cognitive fatigue · Cognitive impairment · Confusion · Increased nature relatedness · Memory fragmentation · Thought disorganization · Thought loops · Creativity enhancement · Analysis enhancement · Cognitive dysphoria · Focus suppression · Humor enhancement · Information processing suppression · Synchronicity · Information processing enhancement · Language enhancement · Language suppression · Memory replays · Motivation suppression · Focus enhancement · Motivation enhancement
Euphoria · Catharsis · Simultaneous emotions · Dysphoria · Irritability · Empathy enhancement · Anhedonia
Irritability · Empathy enhancement · Anhedonia
Disinhibition · Sociability suppression · Social connection · Social disconnection · Flow state · Communication enhancement · Sociability enhancement · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Flow state · Communication enhancement · Sociability enhancement · Boundary dissolution · Cognitive disconnection · Ego dissolution · Identity alteration · Telepathic feelings
Time cessation
Entity contact · Non-dual awareness · Cessation · Death-rebirth sequence · Transpersonal memory access · Voidness
Transpersonal memory access · Voidness
Mindfulness enhancement · Recursive awareness
Timeline
First alerts appear 20–45 minutes after ingestion: a subtle shift in visual texture, mild stomach awareness, and a growing sense that something has changed. The onset is slower than 2C-B.
Effects build steadily over 30–60 minutes. Nausea is most prominent during this phase. Colours brighten, visual drifting begins, and body stimulation increases.
Maximum intensity sustained for 2–3 hours, centred around the 2-hour saliva Tmax. Full visual phenomena, time distortion, thought connectivity, and emotional amplification. Body load peaks here — muscle tension, temperature dysregulation, and cardiovascular stimulation are most pronounced.
Effects sustain at a diminished but still significant level for 1. 5–3 hours. Visuals and cognitive effects remain active but less overwhelming.
A gradual return toward baseline over 1. 5–3 hours. Residual visual enhancement and thought patterns persist but functional capacity returns.
Residual mood elevation, enhanced colour perception, and reflective thinking persist for 6–12 hours. Mild physical fatigue is common. Sleep quality may be reduced even after subjective effects resolve.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Low
- Withdrawal
- None
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- LSD · psilo · mesc
Toxicity
Acute toxicity
No LD₅₀ data exist for 2C-E in any species, and the toxic dose in humans is unknown. One confirmed fatality is documented: a 19-year-old male died of cardiac arrest in March 2011 after insufflating 2C-E at a party in Blaine, Minnesota.[4] Ten others were hospitalised in the same incident, two in critical condition, with symptoms including delirium, paranoia, auditory distortions, and overheating.[7]
A second mass poisoning in Europe (2019) involved 2C-E combined with Bromo-DragonFly.[8] The polydrug nature of that case makes it impossible to attribute toxicity to 2C-E alone.
Clinical presentation
2C-drug poisoning typically presents with hallucinations, agitation, aggression, elevated blood pressure, rapid heart rate, seizures, and dangerously high body temperature.[18] Excited delirium — a state of extreme agitation, confusion, and physiological crisis — was the most consistent pattern among reported 2C-class deaths.[18]
The presentation can resemble either a stimulant overdose or serotonin syndrome, reflecting 2C-E's combined receptor activation and mild reuptake inhibitor.[1][18] Severe cases may progress to muscle breakdown, cardiovascular collapse, and metabolic crisis.[19]
Heart and circulation
In the only controlled human observation (n=10, oral 6.5–25 mg), elevated blood pressure and heart rate were documented, with no serious adverse events at these doses.[1]
Treatment of 2C-E poisoning is primarily supportive. Benzodiazepines are first-line for agitation and seizure control. Active cooling is critical for dangerously high body temperature. No specific antidote exists.[18]
Psychological Risks
Acute psychological distress is a recognised risk with all serotonergic psychedelics. 2C-E's steep dose-response curve amplifies this risk — Shulgin explicitly warned that a few milligrams can separate a manageable experience from a very frightening one.[3] Survivors of the 2011 Minnesota incident reported paranoia, auditory distortions, and delirium.[7]
No substance-specific data on persistent perceptual changes (HPPD) or psychosis following 2C-E use have been published. Individuals with personal or family history of psychotic disorders or bipolar disorder face elevated risk of psychiatric destabilisation after any serotonergic psychedelic. The prolonged duration (8–12 hours) increases the cumulative psychological burden of difficult experiences.
Tolerance & Dependence
2C-E produces rapid tolerance through downregulation of 5-HT₂A receptors in the frontal cortex.[6] Tolerance typically develops within days of repeated use and subsides within several days of abstinence. Cross-tolerance with other classical psychedelics — LSD, psilocybin, mescaline, DMT, and other 2C compounds — is established for the class.[6] This cross-tolerance is specific to psychedelic 5-HT₂A agonists and does not extend to non-psychedelic 5-HT₂A agonists such as lisuride.[6]
2C-E is not considered habit-forming. No cases of physical dependence, withdrawal, or compulsive use have been reported. Rapid tolerance development itself limits reinforcing properties.
Drug Interactions
The principal interaction risk stems from 2C-E's serotonergic activity — receptor activation combined with weak serotonin and norepinephrine reuptake inhibition.[1]
Tramadol is classified as dangerous. Tramadol blocks serotonin reuptake[20] and is associated with serotonin syndrome when combined with other serotonergic agents.[21] The combination with 2C-E substantially increases the risk of serotonin syndrome through dual elevation of synaptic serotonin.[20]
MAOIs represent a likely dangerous combination: blocking serotonin breakdown while 2C-E activates serotonin receptors and mildly inhibits reuptake creates significant serotonin syndrome risk. inferred
SSRIs and SNRIs present dual risk: chronic use may blunt psychedelic effects, while acute co-administration could increase serotonin toxicity risk. inferred
Lithium has been associated with seizures when combined with psychedelics; the mechanism is unclear. inferred
Stimulants (amphetamines, cocaine) carry additive cardiovascular strain risk. inferred
Bromo-DragonFly was documented in a mass poisoning event combined with 2C-E;[8] the specific mechanism of combined toxicity is uncharacterised.
Cannabis may potentiate psychedelic effects or increase psychological distress in some individuals; no 2C-E-specific data exist.
Contraindications
No contraindications specific to 2C-E have been established. The following are inferred from the compound's pharmacological class:
Psychotic disorders and bipolar disorder — personal or family history represents an absolute contraindication for serotonergic psychedelic use, owing to risk of psychosis or psychiatric destabilisation. inferred
Heart conditions — 2C-E produces elevated blood pressure and heart rate.[1] Individuals with high blood pressure, irregular heart rhythm, or structural heart disease face increased risk. inferred
Seizure disorders — seizures are a documented feature of 2C-class poisoning,[18] indicating that 2C-E may lower the seizure threshold. inferred
Concurrent serotonergic medications — MAOIs, tramadol, SSRIs, and SNRIs are contraindicated due to serotonin syndrome risk.
Pregnancy and breastfeeding — no reproductive or developmental toxicity data exist. Psychoactive substance use during pregnancy is generally contraindicated absent established safety data. inferred
Harm Reduction[edit]
Forms & Identification
The steep dose-response curve that defines 2C-E makes accurate dosing more consequential than with most psychedelics — a difference of 2–3 mg can shift the experience from manageable to overwhelming. Volumetric dosing (dissolving a known quantity in a measured volume of liquid) is strongly preferred over weighing individual doses, as few consumer-grade scales reliably measure single-milligram differences in the 10–25 mg range.
Reagent testing confirms compound class but cannot distinguish between individual 2C-series members. The 2011 Minnesota fatality occurred because 2C-E was mislabelled as 2C-I[7] — reagent kits would not have caught this substitution. When positive identification matters, quantitative analysis (FTIR or laboratory testing services) is the only reliable method.
Guidelines
- Test every batch. Reagent testing confirms phenethylamine presence but cannot distinguish 2C-E from other 2C compounds. Quantitative analysis is preferred when available.
- Use a milligram-precision scale and consider volumetric dosing for greater accuracy.
- Start low. First-time users should begin at the lower end of the common dose range and wait the full onset period (30–90 minutes oral) before considering any redose.
- Do not insufflate. Insufflation dramatically compresses onset, amplifies peak intensity, and increases body load. The only confirmed fatality involved this route. Insufflated pharmacokinetics are entirely uncharacterised.
- Clear your schedule. The experience lasts 8–12 hours, and residual effects may persist beyond that. Do not plan to drive, work, or meet obligations.
- Eat lightly 2–3 hours before ingestion. An empty stomach intensifies nausea; a full stomach may delay onset and lead to impatient redosing.
- Stay hydrated but avoid excessive water intake.
- Prepare for body load. Have blankets, comfortable seating, and temperature control available. Heat packs or a warm bath can ease physical tension.
Set & Setting
2C-E's cognitive depth and prolonged duration demand more preparation than lighter psychedelics. A familiar, comfortable environment with minimal external demands is essential. The compound is poorly suited to social or public settings, particularly at moderate-to-high doses, where cognitive load can become isolating.
An experienced, sober sitter is strongly recommended for anyone unfamiliar with the compound or working above their established dose range. The sitter should be briefed on the expected duration, the possibility of intense body load and psychological difficulty, and the importance of calm reassurance over active intervention.
Aftercare & integration. The cognitive intensity of a 2C-E experience often benefits from deliberate processing afterward. Journaling within the first 24–48 hours — while impressions are still accessible — can help consolidate insights and identify themes worth revisiting.
Allow at least one full day of rest. Sleep may be disrupted the first night; this typically normalises within 24 hours. Eat nutritious food, hydrate, and avoid stimulants or other psychoactive substances for several days.
If the experience was difficult, talking with a trusted person or an integration-trained therapist can help contextualise distressing material. Persistent anxiety, depersonalisation, or intrusive imagery lasting more than two weeks warrants professional support.
Recovery & Support
2C-E does not produce physical dependence, and compulsive use patterns are rare due to rapid tolerance. If psychedelic use has become a way of avoiding difficult emotions or responsibilities, or if experiences are causing lasting distress, support is available.
- Fireside Project (62-FIRESIDE / 623-473-7433) — psychedelic peer support line
- MAPS Integration List — directory of therapists experienced with psychedelic integration
- SAMHSA National Helpline (1-800-662-4357) — free, confidential referral service
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognising an emergency
Most 2C-E experiences involve discomfort that resolves without intervention. Seek immediate help if any of the following occur:
- Seizure or convulsions
- Chest pain or irregular heartbeat
- Body temperature that feels dangerously hot through clothing
- Loss of consciousness or unresponsiveness
- Severe confusion with inability to recognise surroundings or people
- Self-harm behaviour or complete disconnection from reality
Immediate steps
- 1. Call emergency services if any of the above signs are present.
- 2. Move the person to a quiet, cool space.
- 3. If unconscious but breathing, place in the recovery position (on their side, airway clear).
- 4. If overheating, apply cool water to skin, fan the person, and remove excess clothing.
- 5. Do not restrain a person in delirium unless they pose immediate physical danger to themselves or others.
- 6. Do not induce vomiting.
What to tell the dispatcher
State that the person took a synthetic psychedelic (2C-E), the approximate amount and time of ingestion, the route of administration, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Medical management
No specific antidote exists for 2C-E. Hospital treatment is supportive: benzodiazepines for agitation and seizures, active cooling for dangerously high body temperature.[18]
Legal Status[edit]
2C-E is controlled as a prohibited substance in most jurisdictions that have specifically addressed it. In the United States, it was placed in Schedule I under the synthetic Drug Abuse Prevention Act of 2012.[5] The United Kingdom classified it as Class A under the Misuse of Drugs Act 1971 as early as 2002, via a phenethylamine catch-all provision.[22] Prior to formal scheduling in the US, the Federal Analogue Act could be applied — the arrest in the 2011 Minnesota incident was made under this provision.[7]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I | Scheduled 9 July 2012 under SDAPA; DEA drug codes established 4 January 2013[5] |
| United Kingdom | Class A | Controlled since 2002 under phenethylamine catch-all amendment to Misuse of Drugs Act 1971[22] |
| Sweden | Controlled | Scheduled 1 October 2004[22] |
| Denmark | Schedule I | Scheduled 8 April 2007[22] |
| Israel | Controlled | Scheduled December 2007[22] |
| China | Category I psychotropic | Scheduled September 2010[22] |
| Germany | Anlage I (BtMG) | Scheduled 13 December 2014[22] |
| Brazil | Controlled | Scheduled 18 February 2014[22] |
| Finland | Banned | Scheduled 19 December 2014[22] |
| Japan | Designated substance | Under designated substances law; specific date unconfirmed[22] |
| New Zealand | Schedule 3 / Class C | Controlled under analogues provision[22] |
| Canada | Unconfirmed (possibly Schedule III) | Erowid notes potential Schedule III status but marks as unconfirmed[22] |
| Australia | Likely Schedule 9 (unconfirmed) | By analogy with other 2C compounds; not independently verifiedcitation needed |
references
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- [5] ^abcdDEA (2013) Establishment of drug codes for 26 substances. Final rule — Federal Register PMID:23289157
- [6] ^abcdde la Fuente Revenga M, Jaster AM, McGinn J, Silva G, Saha S, Gonzalez-Maeso J (2022) Tolerance and Cross-Tolerance among Psychedelic and Nonpsychedelic 5-HT2A Receptor Agonists in Mice — ACS Chemical Neuroscience doi:10.1021/acschemneuro.2c00170