Ephenidine
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Ephenidine (N-ethyl-1,2-diphenylethylamine) — NEDPA, EPE — is a synthetic dissociative of the diarylethylamine class. It is structurally derived from lefetamine, distinguished by longer duration and stimulant-like properties. Ephenidine is an NMDA receptor antagonist, producing its effects by blocking glutamate signaling within the brain's ion channels.[1]
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ketamine, phencyclidine, methoxetamine +3 moreketamine, phencyclidine, methoxetamine, dextromethorphan, diphenidine, methoxphenidine show less
First seized as a designer drug in Germany in 2008,[2] ephenidine emerged from online synthesis communities rather than academic research.[3] It entered wider circulation around 2013 as users sought alternatives to newly scheduled dissociatives like methoxetamine. It is now controlled in the UK, Canada, France, Sweden, and Australia, though it remains unscheduled internationally.
Subjective effects include dissociative anaesthesia, cognitive disruption, euphoria, and hallucinogenic phenomena. The experience combines the disconnection of classical dissociatives with a stimulant-like warmth and activation absent from ketamine, producing a longer, more energizing state closer in character to PCP.[4] Compulsive redosing, cardiovascular stimulation, and confusion are characteristic unsought effects.[5]
Addictive potential is assessed as "highly probable," and no lethal dose has been established.[5]safety citation needed A systematic review identified 48 deaths attributed to the diarylethylamine class globally, one-third involving diarylethylamines alone — suggesting intrinsic toxicity even without polypharmacy.[6] Understanding rests on a single primary pharmacology paper and a handful of case reports; no clinical trials or human pharmacokinetic studies have been conducted.[1]
History[edit]
Discovery
The diarylethylamine scaffold dates to the 1940s, when researchers investigated N-alkylated 1,2-diphenylethylamines as potential analgesics.[7] That work produced lefetamine, an opioid painkiller marketed in Japan and Italy before being controlled for abuse liability.[7] Ephenidine itself was never developed academically — it emerged from online synthesis communities working from lefetamine's structural template, with the specific N-ethyl substitution having no formal research precedent.[3]
Emergence as a designer drug
Ephenidine was first confiscated as a designer drug in Germany in 2008.[2] Recreational use remained limited until around 2013, when it entered the online novel psychoactive substance market alongside diphenidine and methoxphenidine, driven by demand for dissociative alternatives after UK scheduling of arylcyclohexylamines like methoxetamine.[3][1] Clinical complications were first reported to the French Addictovigilance Network in 2013, with case numbers rising substantially through 2015–2016.[5]
Regulation and research
A single primary pharmacology paper — Kang et al. (2017) — established ephenidine's receptor binding profile and NMDA antagonism mechanism.[1] Scheduling actions accelerated from 2015 onward: Sweden controlled it in 2015, the UK enacted the Psychoactive Substances Act in 2016, and the UK classified it as Class B under the Misuse of Drugs Act in March 2024.[8] A 2025 systematic review documented 48 deaths across the diarylethylamine class, cementing the evidence base for regulatory action.[6]
The name ephenidine follows the "-phenidine" suffix convention adopted by the diarylethylamine class, echoing the "-etamine" naming pattern of arylcyclohexylamines. The prefix "e-" derives from the N-ethyl substitution, distinguishing it from the unsubstituted parent compound diphenidine and the methoxy-substituted methoxphenidine. The compound is also referenced by the abbreviations NEDPA and EPE in research literature and online drug discussion forums.[2]
Chemistry[edit]
Structural class
Ephenidine belongs to the 1,2-diarylethylamine chemical class, defined by two phenyl rings attached to adjacent carbons of an ethylamine backbone. The class derives from lefetamine, a pharmaceutical opioid that served as the unintentional structural template for a series of novel psychoactive substances.[7][3] Related compounds include diphenidine (the unsubstituted parent amine), methoxphenidine (2-MeO-diphenidine), and fluorolintane (2'-fluoro-diphenidine).[9]
Molecular identity
| Molecular formula | C₁₆H₁₉N |
| Molecular weight | 225.33 g/mol |
The molecule consists of two unsubstituted phenyl rings — one attached directly to the chirality centre and one via a methylene bridge — with an N-ethyl group on the amine nitrogen. The hydrochloride salt is a solid with a melting point of 236–238°C.
Stereochemistry
Ephenidine possesses one chiral centre and is distributed as a racemic mixture. No study has evaluated ephenidine's enantioselective pharmacology. However, the structural analog diphenidine displays dramatic enantioselectivity at the NMDA: the (S)-enantiomer has approximately 40-fold higher affinity than the (R)-enantiomer.[10] Whether ephenidine shows a similar enantioselective profile remains unknown.inferred
Structure-activity relationships
Within the diarylethylamine series, NMDA receptor affinity varies with N-alkyl chain length and ring substitution. Ephenidine's N-ethyl group places it between the unsubstituted diphenidine and longer-chain analogues in the structural progression. Ring modifications — such as the 2-methoxy group in methoxphenidine or the 2'-fluoro in fluorolintane — modulate both potency and selectivity across the series.[9]
Pharmacology[edit]
Mechanism of action
Ephenidine blocks the NMDA by lodging in the open ion channel at the same binding site used by ketamine and PCP.[1] This block is voltage-dependent — the channel must be open for the drug to enter — and produces the core dissociative state by disrupting glutamate signaling across the brain. In laboratory preparations, ephenidine selectively inhibited NMDA receptor activity without affecting AMPA receptors, confirming its specificity for the NMDA channel.[1]
Beyond NMDA antagonism, ephenidine inhibits the reuptake of dopamine and norepinephrine.[1][3] This secondary activity accounts for the stimulant-like dimension of the experience — euphoria, elevated heart rate, and blood pressure increases — that distinguishes ephenidine from purer NMDA blockers.
Modest affinity at sigma receptors has been measured, though what this contributes to the subjective experience is unknown.[1] No data exist for human receptor binding, in vivo receptor occupancy, or opioid receptor affinity — the last of which is notable given the opioid activity of the parent compound lefetamine.[1]
Pharmacokinetics
No human pharmacokinetic studies have been published. All metabolic data come from rat urine and human liver microsome experiments.
The primary metabolic pathway strips the N-ethyl group to yield diphenidine — itself an active NMDA antagonist — meaning the drug produces a pharmacologically active metabolite.[2][10] Secondary pathways include hydroxylation of the ring systems and Phase II conjugation.[2] In rats, the parent compound was undetectable in urine at low doses, with only metabolites recovered, suggesting extensive first-pass metabolism.[2]
Multiple liver enzymes contribute to the primary metabolic step, which predicts a low risk of significant drug interactions at this pathway.[11] Oral bioavailability, time to peak effect, half-life, and other standard pharmacokinetic parameters remain entirely uncharacterised in humans.
Neuroscience[edit]
Where it acts
Ephenidine's NMDA blockade disrupts glutamate signaling across cortical and subcortical circuits. Based on the extensive literature for ketamine — which shares the same blocking mechanism — this produces a characteristic disconnection between the cortex and deeper brain structures: reduced information flow through the thalamus, paradoxical increases in cortical excitation, and disruption of the synchronised neural oscillations that underlie normal conscious experience. The secondary dopamine reuptake inhibitor additionally potentiates reward-circuit activity, contributing to the euphoric and potentially reinforcing qualities that set ephenidine apart from pure NMDA antagonists.[1]
Why it matters
The leading theoretical framework — cortical disinhibition — proposes that NMDA blockers preferentially silence inhibitory interneurons (which fire more frequently and thus have more open channels), releasing excitatory neurons from their normal restraint.citation needed This net increase in cortical excitability explains both the psychotomimetic effects and the paradoxical brain activation seen with dissociatives.
Ephenidine's confirmed blockade of long-term potentiation in hippocampal tissue[1] directly implicates disruption of the neuroplasticity mechanisms underlying memory formation — a cellular explanation for the cognitive impairment characteristic of NMDA antagonist dissociation.
Whether ephenidine's higher NMDA affinity translates to greater cortical disruption than ketamine remains untested — binding strength in a dish does not predict brain penetration or receptor occupancy in vivo. The active metabolite diphenidine may prolong or alter the dissociative experience as it forms, but the time course and extent of metabolite production in humans are unknown.
Subjective Effects[edit]
Ephenidine delivers a dissociative experience coloured by stimulant warmth — a dual character that emerges from its combined NMDA blockade and dopamine-norepinephrine reuptake activity. At lower doses, the stimulant component dominates: mood lift, physical energy, and mild perceptual shifts. As dose increases, the dissociative dimension deepens — cognitive disconnection, hallucinogenic phenomena, and anaesthetic numbness progressively overtake the stimulant tone. Set and setting strongly modulate the emotional and hallucinogenic dimensions, as with all dissociatives acting at the PCP site.
The experience is most often compared to PCP in qualitative character rather than ketamine — longer, more activating, with a documented tendency toward compulsive redosing that ketamine does not typically produce.[5] Among diarylethylamines, ephenidine is reported as more stimulating than methoxphenidine and qualitatively distinct from diphenidine, though direct comparison data from controlled settings do not exist.
Effect Grid
At common doses (70–100 mg oral), the full dissociative experience manifests: pronounced cognitive disconnection from the external environment, significant distortion of spatial and temporal perception, and marked analgesia. Hallucinogenic effects emerge — internal imagery, environmental distortion, and a dreamlike quality to perception. Euphoria is more prominent at this range, consistent with DAT/NET activity at pharmacologically relevant concentrations.
Cardiovascular stimulation becomes significant — tachycardia and hypertension are documented at these doses. Numbness, ataxia, and nausea may occur. Motor coordination is substantially impaired.
Duration is 5–7 hours. Functional impairment persists well beyond the subjective peak. Compulsive redosing urges are reported at this range.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Sensory deprivation · Sleep-transition hallucinations · Visual acuity suppression · Perspective distortion · Music enhancement · Touch suppression · Visual haze / noise · Visual drifting · Auditory distortion · Auditory suppression · Tracers · Visual breathing · Peripheral vision distortion · Dreaming enhancement · Color alteration · Auditory enhancement · Visual morphing · Tinnitus · Visual processing suppression · Internal hallucinations · Environmental orbism / cubism · Visual scenery slicing · Auditory hallucinations · External hallucinations · Object transformations
Music enhancement · Touch suppression · Visual haze / noise · Visual drifting · Auditory distortion · Auditory suppression · Tracers · Visual breathing · Peripheral vision distortion · Dreaming enhancement · Color alteration · Auditory enhancement · Visual morphing · Tinnitus · Visual processing suppression · Internal hallucinations · Environmental orbism / cubism · Visual scenery slicing · Auditory hallucinations · External hallucinations · Object transformations
Bodily lightness · Bodily heaviness · Stimulation · Appetite suppression · Nausea · Spontaneous body sensations · Sedation · Wakefulness · Laughter fits · Pupil dilation · Dry mouth · Physical fatigue · Heart rate perception changes · Body schema distortion · Sexual arousal suppression · Muscle relaxation · Muscle tension · Vasoconstriction · Tingling / electric sensations · Insomnia · Restlessness · Headache · Bruxism · Excessive sweating · Respiratory depression · Abnormal heartbeat · Vomiting · Trembling · Involuntary body movements · Bodily dissociation
Appetite suppression · Nausea · Spontaneous body sensations · Sedation · Wakefulness · Laughter fits · Pupil dilation · Dry mouth · Physical fatigue · Heart rate perception changes · Body schema distortion · Sexual arousal suppression · Muscle relaxation · Muscle tension · Tingling / electric sensations · Insomnia · Restlessness · Headache · Bruxism · Excessive sweating · Respiratory depression · Abnormal heartbeat · Vomiting · Trembling · Involuntary body movements · Bodily dissociation
Analysis suppression · Cognitive euphoria · Thought disorganization · Information processing suppression · Focus suppression · Pattern recognition suppression · Novelty enhancement · Introspection enhancement · Memory fragmentation · Delusions of sobriety · Cognitive fatigue · Humor enhancement · Conceptual thinking · Compulsive redosing urge · Thought loops · Thought deceleration · Language suppression · Immersion enhancement · Openness enhancement · Aesthetic enhancement · Creativity enhancement · Motivation enhancement · Amnesia · Delirium · Delusions
Information processing suppression · Focus suppression · Pattern recognition suppression · Novelty enhancement · Introspection enhancement · Memory fragmentation · Cognitive fatigue · Humor enhancement · Conceptual thinking · Compulsive redosing urge · Thought loops · Thought deceleration · Language suppression · Immersion enhancement · Openness enhancement · Aesthetic enhancement · Creativity enhancement · Motivation enhancement · Amnesia · Delirium · Delusions
Emotional suppression · Emotional lability · Dysphoria · Empathy suppression · Irritability · Anhedonia
Irritability · Anhedonia
Automaticity · Sociability suppression · Communication suppression · Craving · Emotional susceptibility · Ego inflation · Cognitive disconnection · Boundary dissolution · Identity alteration · Ego dissolution
Emotional susceptibility · Ego inflation · Cognitive disconnection · Boundary dissolution · Identity alteration · Ego dissolution
Timeline
First alerts appear as subtle cognitive slowing and a faint sense of spatial detachment. Mild stimulation from monoamine reuptake inhibition may precede dissociative effects.
Dissociative effects build progressively — increasing detachment, emerging numbness, and growing perceptual distortion. Cardiovascular stimulation (increased heart rate) becomes noticeable.
Maximum dissociation with pronounced cognitive disconnection, hallucinogenic phenomena, analgesia, and euphoria. Tachycardia and hypertension are most prominent. Memory suppression is marked at common doses and above.
Intensity gradually diminishes but significant dissociation persists. Motor coordination remains impaired. Compulsive redosing urges are most likely during this phase as acute tolerance develops.
Progressive return of normal sensory processing and cognitive function. Residual numbness, mild confusion, and fatigue are common. Some users report a stimulant-like residual alertness from noradrenergic activity.
Subtle cognitive effects may persist for 6–12 hours after resolution — mild dissociative aftereffects, emotional blunting, and difficulty concentrating. Sleep may be disrupted.
⚠ Do not drive or operate heavy machinery for at least 12 hours after the last dose, or until the following day after a full night of sleep.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- moderate
- Tolerance reset
- 10 days
- Physical
- Low
- Psychological
- Moderate
- Compulsive redosing
- High
- Dose escalation
- Moderate
- Cross-tol.
- ketamine · phencyclidine · methoxetamine
Toxicity
Acute toxicity
No lethal dose has been established for ephenidine.safety citation needed No controlled toxicity studies — animal or human — have been published.
Acute toxic effects documented across the diarylethylamine class include elevated blood pressure, rapid heart rate, hallucinations, confusion, and muscle breakdown (rhabdomyolysis).[4] Muscle breakdown carries secondary risk of acute kidney damage.
The French Addictovigilance Network reported four ephenidine-specific cases between 2012 and 2016, all involving multiple substances.[5] Complications spanned psychiatric, neurological, and cardiovascular symptoms, with two cases classified as probably caused by ephenidine.[5]
Class-level mortality
A systematic review identified 48 deaths globally attributed to the diarylethylamine class, with 37 in the United Kingdom between 2014 and 2019.[6] Decedents were predominantly male (91%), with a mean age of 37 years and a history of drug use (72%). Accidental overdose was the cause in 89–92% of cases.
Two-thirds of deaths involved co-administration of opioids, benzodiazepines, or stimulants — but one-third involved diarylethylamines alone, suggesting the class carries intrinsic lethal potential even without polypharmacy.[6] Ephenidine is not separately enumerated in available mortality data; the figures cover the diarylethylamine class collectively.safety citation needed
Psychological risks
Acute psychological adverse effects include agitation, confusion, hallucinations, and psychiatric decompensation.[5][4] As an NMDA antagonist acting at the PCP site, ephenidine carries the class-level risk of triggering or worsening psychotic episodes, particularly in individuals with pre-existing psychotic or bipolar spectrum conditions.inferred
No data on persistent perceptual disturbances, long-term psychiatric consequences, or prevalence of adverse psychological outcomes have been published.
Tolerance and dependence
Tolerance to ephenidine's dissociative effects develops with repeated use, consistent with NMDA receptor adaptation documented for ketamine and other NMDA antagonists. How quickly tolerance builds, how long it persists, and how long full reset takes have not been measured.
Compulsive redosing during sessions is documented across multiple sources[5][4][6] and is consistent with rapid tolerance developing within a single session. The French Addictovigilance Network assessed the addictive potential of diarylethylamine dissociatives as "highly probable".[5] The first formal substance use disorder diagnosis in the class was documented for methoxphenidine,[12] confirming that prolonged compulsive use can produce clinically diagnosable dependence.
No physical withdrawal has been described for ephenidine or any diarylethylamine.
Drug interactions
No published interaction studies exist for ephenidine. All interaction data derive from class-level evidence and mechanistic reasoning.
CNS depressants pose the highest risk. In class-level mortality data, 66% of diarylethylamine fatalities involved co-administration of opioids, benzodiazepines, or stimulants.[6] Opioid co-use carries the greatest danger through combined respiratory depression. Stimulant co-use compounds cardiovascular strain — ephenidine's own dopamine and norepinephrine reuptake activity stacks with exogenous stimulant effects.
MAO inhibitors represent a high-risk combination: ephenidine's noradrenaline and dopamine reuptake inhibitor, combined with monoamine oxidase blockade, could trigger dangerously elevated blood pressure.inferred
Combination with other NMDA antagonists (ketamine, PCP, MXE, DXM) produces additive dissociative effects and toxicity.
Multiple liver enzymes metabolise ephenidine, suggesting low overall susceptibility to metabolism-based drug interactions.[11] However, potent inhibitors of specific enzymes — particularly fluvoxamine or fluconazole — could slow metabolism and elevate blood levels.[11]
Contraindications
No clinical data establish specific contraindications. The following are inferred from pharmacology and class-level evidence:
Heart conditions and high blood pressure: Elevated heart rate and blood pressure are documented toxic effects.[4] Pre-existing cardiovascular disease or concurrent use of stimulants substantially increases risk.
Psychotic disorders: NMDA antagonists acting at the PCP site are established psychotomimetics. Personal or family history of psychotic spectrum disorders is a strong relative contraindication.inferred
MAO inhibitor therapy: The combination of reuptake inhibition with MAO blockade creates risk of dangerously elevated blood pressure.inferred
Kidney impairment: Muscle breakdown is a documented complication.[4] Pre-existing kidney impairment heightens the risk of acute kidney damage.
Pregnancy and breastfeeding: No reproductive safety data exist. NMDA receptor signaling is critical to neurodevelopment; exposure during pregnancy is a theoretical concern for all compounds in this class.inferred
Harm Reduction[edit]
Forms & Identification
Ephenidine typically circulates as a white to off-white powder or pressed into tablets. Reagent testing cannot confirm identity alone but can help rule out dangerous substitutions — particularly confusion with more potent dissociatives or stimulants. Quantitative analysis via a drug checking service is the most reliable method of confirming substance identity and purity, especially given the variable quality of novel psychoactive substance supply chains.
Guidelines
- Use reagent testing and, where available, a drug checking service to verify substance identity before use
- Start with a low dose and wait at least 90 minutes before considering redosing — onset can be slow and gradual
- Resist the urge to redose. Compulsive redosing is widely documented with this substance and is the most common route to dangerous cumulative doses[5]
- Measure doses with a milligram-precision scale — never estimate by eye
- Ensure adequate hydration, but avoid excessive water intake
- Have a sober, trusted companion present throughout the experience
- Clear the environment of hazards — sharp objects, open water, stairs, and balconies all pose elevated risk during dissociation
- Avoid physical activity that requires coordination
- Do not drive or operate machinery for at least 12 hours after ingestion
Set & Setting
Dissociative experiences are strongly shaped by environment and mental state. Ephenidine's long duration demands more advance planning than shorter-acting dissociatives like ketamine. A calm, familiar, physically safe environment reduces the risk of injury during periods of impaired coordination and spatial awareness. A sober companion who understands dissociative effects is strongly recommended, particularly at higher doses where communication may become difficult or impossible.
Aftercare & integration. The extended duration of ephenidine means residual cognitive dulling and physical fatigue may persist well beyond the primary experience. Plan for a full rest day afterward — prioritise sleep, light nutrition, and low-demand activity. Avoid making important decisions or returning to demanding work until mental clarity fully returns.
Dissociative experiences can surface unexpected emotional or perceptual material. Journaling observations in the days following use can help process unusual thoughts or feelings. If distressing psychological effects persist beyond 48 hours — particularly derealization, persistent confusion, or mood disturbance — consult a healthcare professional.
Recovery & Support
Compulsive redosing and escalating use patterns are documented for ephenidine and the diarylethylamine class.[5] If use has become difficult to control, support is available. SMART Recovery and other evidence-based programmes offer structured approaches to substance use concerns. A healthcare provider familiar with dissociative substances can help assess dependence and develop a cessation or reduction plan. No established withdrawal protocol exists for diarylethylamines, but professional support reduces risk during discontinuation.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognising an emergency: Uncomfortable but manageable effects include mild confusion, nausea, and elevated heart rate. Seek immediate help if any of the following occur: chest pain, seizure, loss of consciousness, severe muscle rigidity, inability to communicate or respond, or extreme agitation with self-harm risk.
Immediate steps:
- Call emergency services without delay if the person is unconscious, seizing, or showing signs of severe distress
- Place an unconscious but breathing person in the recovery position (on their side, airway clear)
- Do not restrain an agitated person unless they are in immediate danger of harming themselves — restraint can worsen agitation and increase risk of muscle breakdown
- Do not induce vomiting
- Monitor breathing and heart rate continuously while waiting for help
What to tell the dispatcher: State the substance name (ephenidine / diarylethylamine dissociative), the approximate amount taken, the time of ingestion, and current symptoms. Mention any other substances taken. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
No specific reversal agent exists for ephenidine or any NMDA antagonist. Treatment is supportive.
Legal Status[edit]
Ephenidine is not scheduled at the international level under the UN 1971 Convention, though its structural analog diphenidine was added to Schedule II following the 43rd WHO ECDD review in 2020.[13] Ephenidine has not been independently reviewed by the WHO ECDD. Scheduling actions have accelerated since 2015 in response to adverse events and deaths across the diarylethylamine class.
The UK Advisory Council on the Misuse of Drugs recommended scheduling ephenidine alongside diphenidine and methoxphenidine, citing pharmacological similarity to ketamine, 37 UK deaths in the compound class between 2014 and 2019, and documented addictive potential.[4]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Not specifically scheduled (federal) | Possible coverage under the Federal Analogue Act if intended for human consumption; legal status untested in courtcitation needed |
| United Kingdom | Class B (Misuse of Drugs Act 1971) | Scheduled 20 March 2024 via SI 2024/190;[8] previously covered by Psychoactive Substances Act 2016[14] |
| Canada | Schedule I (Controlled Drugs and Substances Act) | Controlled since March 2016 |
| Sweden | Controlled hazardous substance | Scheduled 18 August 2015 |
| France | Narcotic (Annex IV) | Scheduled following 2015–2016 adverse event surge[5] |
| Germany | Controlled under narcotics legislation | First confiscation 2008;[2] specific scheduling date unconfirmed |
| Australia | Schedule 9 (Prohibited substance) | Scheduled October 2024 |
| International (UN) | Not separately scheduled | Parent compound diphenidine added to Schedule II, UN 1971 Convention (April 2021)[13] |
references
- [1]
- [2] ^abcdefgWink CS, Meyer GM, Wissenbach DK, Jacobsen-Bauer A, Meyer MR, Maurer HH (2014) Lefetamine-derived designer drugs N-ethyl-1,2-diphenylethylamine (NEDPA) and N-iso-propyl-1,2-diphenylethylamine (NPDPA): metabolism and detectability in rat urine using GC-MS, LC-MSn and LC-HR-MS/MS — Drug Testing and Analysis doi:10.1002/dta.1621
- [3]
- [4]
- [5] ^abcdefghijklEiden C, Leone-Burgos S, Serre A, Carton L, Gerardin M, Le Boisselier R, Gibaja V, Monzon E, Fouilhe N, Boucher A, Peyriere H (2018) Ephenidine, diphenidine, and methoxphenidine complications reported to the French Addictovigilance Network — Fundamental & Clinical Pharmacology doi:10.1111/fcp.12395
- [6]