N-Ethylhexedrone
Viewing r1 — May 12, 2026 — CURRENT
Back to HistoryInteractions, related substances, and reports reflect the current entry and are not shown for historical revisions.
N-Ethylhexedrone (2-(ethylamino)-1-phenylhexan-1-one) — hexen, hex-en — is a synthetic stimulant of the cathinone class. It shares cocaine's DAT potency[1] but produces longer-lasting effects. N-Ethylhexedrone is a dopamine-norepinephrine reuptake inhibitor, producing its effects by blocking the clearance of these neurotransmitters from the synapse.[2][3]
Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
Cocaine, Amphetamine, Methylphenidate +2 moreCocaine, Amphetamine, Methylphenidate, Synthetic cathinones, Other DAT/NET inhibitors show less
Synthesized circa 1964 by Boehringer Ingelheim as a candidate appetite suppressant,[4] N-Ethylhexedrone attracted no pharmacological interest for five decades. It appeared on European research chemical markets in late 2015 and by 2017 had become the most frequently seized cathinone in the EU, Norway, and Turkey.[5] It is now Schedule I in the United States and controlled across most European jurisdictions.
Subjective effects include euphoria, psychomotor activation, wakefulness, and appetite suppression. The experience is a focused, driven stimulation — dopamine-dominant and absent the empathogenic warmth of serotonin-releasing cathinones, resembling a longer-acting cocaine.[2] Compulsive redosing,[6] cardiovascular strain, insomnia, and post-use anhedonia are characteristic unsought effects.
N-Ethylhexedrone carries moderate abuse liability[6] and significant acute toxicity risk, with fatalities documented at blood concentrations as low as 145 ng/mL.[7] Its 19–28 hour half-life[8] creates accumulation risk during binge use — subjective effects fade within hours, but the drug persists in plasma for days, compounding cardiovascular and neurotoxic burden with each redose. No controlled human studies existed before 2025,[9] and the current understanding rests primarily on in vitro pharmacology, animal models, and forensic case reports.
History[edit]
Discovery
Synthesized circa 1964 by Boehringer Ingelheim as part of a patent series exploring aminoketone derivatives for appetite suppression,[4] N-Ethylhexedrone emerged from the same research program that produced MDPV — a cathinone that would later become one of the most scrutinized novel psychoactive substances of the 2010s.[4] NEH itself attracted no further pharmacological attention for approximately five decades.
Market emergence
NEH surfaced on European research chemical markets in late 2015, first intercepted by Belgian Customs in November of that year.[4] The EMCDDA issued a formal early warning in February 2016 following notifications from Sweden, the Netherlands, France, Belgium, and Slovenia,[4] and within two years NEH had become the most frequently seized cathinone in the EU, Norway, and Turkey[5] — among the three most common cathinones identified in fatality reports from 2017–2020.[5]
Contemporary status
The United States permanently placed NEH in Schedule I in June 2022,[10] and the WHO Expert Committee on Drug Dependence issued a Critical Review Report at its 47th meeting in 2023.[11] The first prospective human observational study — eight participants self-administering 20–40 mg intranasally — was not published until 2025.[9]
The name hexen — by which N-Ethylhexedrone is most commonly known in drug culture — derives from a phonetic abbreviation of its chemical name (hex- from hexedrone, -en from N-ethyl). The term became standard on research chemical vendor sites and user forums from 2016 onward, largely displacing the clinical abbreviation NEH in informal contexts. The compound's rapid ascent to Europe's most-seized cathinone cemented its reputation as the dominant second-wave stimulant cathinone after the scheduling of mephedrone and MDPV.
Chemistry[edit]
Structural class
N-Ethylhexedrone belongs to the substituted cathinone family, a subset of the phenethylamine and amphetamine structural classes. The cathinone scaffold — a beta-keto-amphetamine — carries a ketone at the beta-carbon of the phenethylamine backbone. NEH extends this with an N-ethyl group on the amino nitrogen and a four-carbon (n-butyl) chain at the alpha-carbon, placing it among the N-alkyl, alpha-chain-extended cathinones rather than the pyrrolidine-ring cathinones (α-PVP, α-PHP).
The compound's systematic name is 2-(ethylamino)-1-phenylhexan-1-one, reflecting the hexanone backbone, the phenyl ring at the carbonyl carbon, and the ethylamino group at the adjacent carbon.
Molecular properties
| Molecular formula | C₁₄H₂₁NO |
| Molecular weight | 219.32 g/mol |
Values confirmed via PubChem.[12]
Structure-activity relationships
A systematic comparison of five N-ethyl cathinones differing only in alpha-carbon chain length found that all function as dopamine-selective reuptake inhibitors.[3] Dopamine uptake inhibition follows an inverted U-shaped curve with chain length, peaking in the propyl-to-butyl range where NEH sits, then declining with further elongation. Longer chains also correlate with increased cell toxicity — all five compounds exceeded methamphetamine's toxicity in the same assay.[3]
Stereochemistry
NEH possesses a chirality center at the alpha-aminoketone carbon, producing R- and S-enantiomers.[12] No enantioselective pharmacological studies have been published for NEH; the racemic mixture is presumed to be the form sold on illicit markets. Related cathinones show enantiomer-dependent differences in transporter inhibition,[13] suggesting the individual enantiomers of NEH likely differ in potency — a question that remains unresolved.
Physical properties
No published data exist for the melting point, boiling point, solubility, or partition coefficient of N-Ethylhexedrone. It is typically encountered as a white to off-white crystalline powder.citation needed
Pharmacology[edit]
Mechanism of action
N-Ethylhexedrone blocks the DAT (DAT) and NET (NET), preventing these neurotransmitters from being cleared from the synapse.[2][3][14] This is a blocker mechanism — NEH sits in the transporter and obstructs reuptake without being transported into the nerve terminal itself. The distinction matters: substrate-type releasers like mephedrone or amphetamine force neurotransmitter out of storage, producing a rapid flood. Blockers like NEH instead allow naturally released dopamine and norepinephrine to accumulate, producing a pharmacological profile closer to cocaine.
NEH's selectivity follows DAT > NET > SERT, with dopamine transporter blockade far exceeding serotonin transporter blockade.[1] This dopaminergic dominance explains the compound's pronounced rewarding properties and distinguishes it from serotonin-releasing cathinones like mephedrone, which produce empathogenic warmth alongside stimulation.
Serotonin transporter inhibition is minimal, placing NEH squarely among the dopamine-dominant cathinones — a profile consistently linked to elevated abuse potential.[1]
Pharmacokinetics
The plasma half-life of NEH is estimated at 19–28 hours, derived from serial blood samples in intoxicated patients.[8] This is exceptionally long for a stimulant whose subjective effects last only 2–5 hours by insufflation. The mismatch means the drug remains in the body long after the user feels sober — repeated dosing during this extended tail produces unpredictable accumulation. NEH was still detectable in plasma up to ten days after intoxication.[8]
NEH is metabolized in the liver through reduction of its ketone group, removal of the ethyl group (N-dealkylation), and hydroxylation, followed by conjugation with glucuronic acid.[15][8] The specific liver enzymes responsible have not been identified.
No formal bioavailability studies have been conducted by any route of administration. Peak blood levels, distribution, and protein binding remain entirely uncharacterized.
Neuroscience[edit]
Where it acts
NEH's dopamine reuptake blockade primarily engages the mesolimbic mesolimbic pathway — the projection from the ventral tegmental area to the nucleus accumbens that mediates motivation and reward.[1] Full substitution for both cocaine and methamphetamine in drug discrimination studies[2] confirms that NEH activates the same reward circuitry as established stimulants. The prefrontal cortex, which governs executive function and receives dense dopaminergic input, is also implicated: the focus enhancement and thought acceleration reported by users are consistent with elevated prefrontal dopamine, though no neuroimaging data exist for NEH.
Neurotoxicity and neuroadaptation
In vitro studies reveal neurotoxic properties beyond those of structurally simpler cathinones. NEH causes nerve cell death at concentrations where it also uniquely activates microglia — the brain's immune cells — triggering morphological changes and increased inflammatory activity not seen with buphedrone.[6] All tested N-ethyl cathinones exceed methamphetamine's cell toxicity, with toxicity increasing as the alpha-carbon chain lengthens.[3]
Post-withdrawal depression-like behavior in mice suggests neuroadaptive changes specific to higher-potency cathinones.[6] Repeated dosing of the structural analog NEP upregulates ΔFosB — a molecular marker of addiction-related brain changes — in the striatum,[16] and NEH likely produces similar adaptations. The predictable trajectory of sustained DAT blockade — initial euphoria followed by compensatory downregulation and reduced baseline dopamine signaling — underlies the shift from recreational use to compulsive patterns.
Whether NEH's R- and S-enantiomers differ in potency or neurotoxicity remains untested. The in vitro finding of unique microglial activation has not been confirmed in living animals — if replicated, it would suggest a neuroinflammatory risk distinct from other cathinones. No dose-response relationship has been characterized for any pharmacological effect, and no longitudinal data exist on cognitive or structural brain changes following repeated use.
Subjective Effects[edit]
N-Ethylhexedrone delivers a focused, driven stimulation shaped by strong dopamine reuptake blockade with negligible serotonergic contribution. The experience is one of clean energy and euphoria without the empathogenic warmth or perceptual shifts of serotonin-active cathinones. At higher doses, stimulation intensifies and compulsive redosing becomes a defining feature — the drive to take more persists even as subjective pleasure plateaus, a pattern characteristic of potent DAT blockers. Set and setting modulate intensity but not the fundamental character: this is a stimulant that amplifies drive and focus, not one that reshapes mood or perception.
Among cathinones, NEH occupies a middle ground between the ultra-potent pyrrolidine-ring compounds (α-PVP, α-PHP) and the serotonin-releasing entactogens (mephedrone, methylone). The subjective profile most closely resembles a longer-acting cocaine — comparable reward-circuit engagement[2] with a peak stimulant duration roughly twice that of an insufflated cocaine line.
Effect Grid
Clear stimulant effects establish themselves — euphoria, psychomotor activation, and pronounced wakefulness define the experience. Thought acceleration and focus enhancement are prominent, and motivation enhancement creates a driven, task-oriented mental state. Compulsive redosing urges begin to manifest at this level, reflecting NEH's high DAT selectivity.
Physical effects include noticeable increases in heart rate and blood pressure, appetite suppression, bruxism, and dry mouth. Excessive sweating and muscle tension may appear. Temperature dysregulation is possible but typically mild at this range.
This is the dose range used in the only published human observational study (20–40 mg insufflated spans common-to-strong). Subjective effects last 2–5 hours insufflated, but the 19–28 hour half-life means redosing accumulates unpredictably — each subsequent dose adds to a still-elevated baseline. Insomnia is likely for many hours after dosing.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Tinnitus · Auditory hallucinations · External hallucinations · Shadow people
Dry mouth · Insomnia · Pupil dilation · Body high · Excessive sweating · Heart rate perception changes · Muscle tension · Physical fatigue · Restlessness · Bruxism · Dehydration sensation · Respiratory stimulation · Spontaneous body sensations · Tactile euphoria · Bodily lightness · Breathing alteration · Headache · Nasal congestion · Nausea · Sexual arousal enhancement · Tingling / electric sensations · Trembling · Vibrations / buzzing · Constipation · Dizziness · Involuntary body movements · Nystagmus (eye wobbles) · Vomiting · Tactile hallucination
Excessive sweating · Heart rate perception changes · Muscle tension · Physical fatigue · Restlessness · Bruxism · Dehydration sensation · Respiratory stimulation · Spontaneous body sensations · Tactile euphoria · Bodily lightness · Breathing alteration · Headache · Nasal congestion · Nausea · Sexual arousal enhancement · Tingling / electric sensations · Trembling · Vibrations / buzzing · Constipation · Dizziness · Involuntary body movements · Nystagmus (eye wobbles) · Vomiting · Tactile hallucination
Motivation enhancement · Motivation suppression · Focus enhancement · Analysis enhancement · Cognitive dysphoria · Cognitive flexibility · Information processing enhancement · Multiple thought streams · Pattern recognition enhancement · Thought loops · Thought organization · Creativity enhancement · Language enhancement · Memory enhancement · Cognitive impairment · Confusion · Thought disorganization · Delusions · Delirium
Analysis enhancement · Cognitive dysphoria · Cognitive flexibility · Information processing enhancement · Multiple thought streams · Pattern recognition enhancement · Thought loops · Thought organization · Creativity enhancement · Language enhancement · Memory enhancement · Cognitive impairment · Confusion · Thought disorganization · Delirium
Dysphoria · Anhedonia · Emotional lability · Mania
Disinhibition · Social connection · Flow state · Ego inflation · Depersonalization · Derealization
Depersonalization · Derealization
Timeline
Mild stimulation begins as alertness increases and attention sharpens. A faint body energy may be noticed.
Stimulation builds rapidly; euphoria emerges alongside rising heart rate and focus enhancement. Appetite suppression begins.
Full stimulant effects — euphoria, thought acceleration, wakefulness, and cardiovascular stimulation at maximum. Compulsive redosing urges are strongest here.
Gradual decline in euphoria and stimulation. Residual wakefulness, cardiovascular effects, and appetite suppression persist. Irritability or mild anxiety may emerge.
Residual insomnia, appetite suppression, and mild dysphoria. Cardiovascular effects may persist due to the 19–28 hour elimination half-life.
⚠ Do not drive or operate machinery for at least 8 hours after last dose — residual impairment from cardiovascular effects, fatigue, and potential anxiety may persist well beyond subjective offset.
Safety[edit]
- Acute toxicity
- High
- Chronic toxicity
- Moderate
- Withdrawal
- Moderate
- Tolerance buildup
- moderate
- Tolerance reset
- 10.5 days
- Physical
- Moderate
- Psychological
- Moderate
- Compulsive redosing
- High
- Dose escalation
- Moderate
- Cross-tol.
- Cocaine · Amphetamine · Methylphenidate
Toxicity
Lethal dose
No lethal dose has been established for N-Ethylhexedrone in any species.[12] The lowest postmortem blood concentration in a confirmed fatality was 145 ng/mL.[7]
Fatal cases
Three analytically confirmed deaths involving NEH appear in published literature. A 21-year-old male who purchased NEH believing it was cocaine presented with disorientation, aggression, body temperature exceeding 41°C, heart rate above 160 bpm, and kidney failure, dying within hours (postmortem blood NEH: 145 ng/mL).[7] A second fatality involved combined NEH and synthetic cannabinoid (ADB-FUBINACA) use.[17] A third was a polydrug death attributed primarily to the synthetic opioid U-47700, with NEH present at 58 ng/mL alongside multiple other substances.[18]
A review of cathinone-related fatalities from 2017–2020 identified NEH among the three most frequently occurring substances in 75 reported deaths.[5]
Severe non-fatal toxicity
Three confirmed single-substance NEH intoxications required hospitalization: two patients needed mechanical ventilation, and one developed dangerously low blood sodium levels (SIADH).[8] NEH remained detectable in one patient for ten days. An additional case of severe toxicity from combined dissociative (3-HO-PCP) and NEH use has been confirmed.[19]
Cardiovascular toxicity
The stimulant toxidrome includes severe rapid heart rate (>160 bpm), high blood pressure, and dangerously elevated body temperature.[7] As with cocaine and amphetamines, heart rhythm disturbances, heart attack, and stroke are mechanistically expected risks.inferred
Neurotoxicity
In laboratory cell studies, NEH causes nerve cell death and uniquely activates brain immune cells (microglia) at lower concentrations than structurally simpler cathinones.[6] It exceeds methamphetamine's cell toxicity,[3] and animals show depression-like behavior after withdrawal.[6] Whether these laboratory findings translate directly to human brain damage at typical doses is unknown.
Psychological risks
Paranoia, feelings of persecution, anxiety, and anhedonia have been documented during and after NEH intoxication.[8] Post-use depression is supported by both clinical observations — fatigue, lack of motivation, thought deceleration[8] — and animal models.[6]
As a potent DAT blocker with confirmed rewarding properties, NEH carries substantial risk for compulsive redosing and binge use patterns. Animal studies show it produces reward responses comparable to cocaine and methamphetamine.[6][2] Agitation and aggression occur in severe intoxication.[7]
No published data exist on longer-term psychological consequences of repeated NEH use in humans.
Tolerance & dependence
No controlled human studies have measured tolerance development for NEH. Community reports suggest tolerance builds with repeated use, with an estimated reset period of approximately 1.5 weeks.safety citation needed These estimates are unverified and distinct from the pharmacokinetic half-life of 19–28 hours.[8]
Evidence supporting clinically relevant abuse liability includes: reward-seeking behavior in mice,[6] full substitution for cocaine and methamphetamine in drug discrimination tests,[2] addiction-related molecular changes (ΔFosB) in the brain following repeated dosing of the structural analog NEP,[16] and post-withdrawal depression-like behavior specific to NEH.[6]
Cross-tolerance is expected with other dopamine/norepinephrine reuptake inhibitors including cocaine, amphetamine, methylphenidate, and other synthetic cathinones.[2] Physical withdrawal has not been formally characterized in humans.
Drug interactions
No substance-specific interaction studies have been published for NEH. The following are based on pharmacological mechanism and class-level evidence.[20]
Monoamine oxidase inhibitors
Combining NEH with MAOIs risks dangerous blood pressure spikes and potentially serotonin syndrome. NEH's norepinephrine reuptake blockade combined with MAOI-mediated prevention of monoamine breakdown produces dangerously elevated neurotransmitter levels.[20]
Serotonergic drugs
SSRIs, SNRIs, triptans, and tramadol combined with NEH create risk of serotonin syndrome, particularly at higher NEH doses.[20] The tramadol–NEH combination is designated lethal and the MDMA–NEH combination dangerous; no published case reports confirm these specific designations,safety citation needed though both are mechanistically plausible.
Opioids
A fatal polydrug case documents the lethal potential of cathinone-opioid-benzodiazepine combinations: NEH (58 ng/mL) with U-47700 (1470 ng/mL) and adinazolam.[18]
Other stimulants
Combination with cocaine, amphetamines, or other cathinones produces additive cardiovascular burden. A fatal combination of NEH with the synthetic cannabinoid ADB-FUBINACA has been reported.[17]
Dissociatives
Severe acute toxicity from combined 3-HO-PCP and NEH has been analytically confirmed.[19]
Cardiovascular and psychiatric medications
NEH's stimulant effects may overwhelm blood pressure medications.[20] Combination with antipsychotics carries risk of competing dopamine effects and heart rhythm prolongation.[20]
Contraindications
No substance-specific contraindication studies exist. The following are inferred from NEH's pharmacological profile and clinical adverse events.inferred
Pre-existing heart conditions, high blood pressure, or rhythm abnormalities are absolute contraindications — NEH produces heart rates exceeding 160 bpm and blood pressure spikes in severe cases.[7] Kidney impairment compromises clearance of the drug (half-life 19–28 hours) and increases susceptibility to kidney damage.[7] Liver impairment may prolong drug exposure due to reduced metabolic processing.[8]
Seizure disorders represent elevated risk, as synthetic cathinones lower seizure threshold.[21] Psychiatric conditions including psychotic disorders, severe anxiety, and bipolar disorder are contraindicated given NEH's documented ability to produce paranoia and agitation.[8] Major depressive disorder compounds the risk of post-use depressive episodes.[6]
No reproductive toxicity data exist; as a potent stimulant with documented hyperthermia, use during pregnancy carries presumed fetal risk.inferred The report of SIADH following NEH intoxication[8] indicates particular danger for individuals with pre-existing low sodium levels or electrolyte disorders.
Harm Reduction[edit]
Forms & Identification
N-Ethylhexedrone is typically sold as a white to off-white crystalline powder, often marketed as "hexen" or "hex-en." As a cathinone-class compound, it lacks a distinctive reagent color pattern that would reliably distinguish it from other cathinones — reagent testing confirms the broad chemical class but cannot verify the specific compound. Quantitative analysis through an energy control or drug checking service provides the only reliable identification.
The powder form introduces significant dosing variability. Volumetric measurement (scooping) is unreliable — a milligram-capable scale (0.001 g) is essential, as active doses are measured in tens of milligrams and the margin between desired and dangerous effects is poorly characterized.
Guidelines
- Weigh every dose on a milligram-capable scale — never estimate by eye or volume
- Start with the lowest reported active dose and wait at least 90 minutes before considering redosing
- Pre-set a firm dose limit before the session begins; compulsive redosing is the compound's defining behavioral risk
- Keep the total session supply limited — having more available is the strongest predictor of binge use
- Ensure access to water and a cool environment; body temperature regulation is impaired under stimulant load
- Do not use alone for the first time; have a sober person present or informed of your plans
- Avoid use within 24 hours of a previous session — the long half-life means the previous dose has not fully cleared
Set & Setting
NEH's dopamine-dominant stimulation amplifies existing mood states and environmental pressures. Anxious or paranoid baseline states can escalate rapidly under stimulant activation. Use in unfamiliar or high-stress environments increases the risk of agitation and paranoid ideation documented in clinical cases.
The 19–28 hour half-life means physiological stimulation persists far beyond perceived effects. Planning for extended inability to sleep, eat, or relax is essential — NEH is not a substance compatible with next-day obligations.
Aftercare & integration. The comedown from NEH can include fatigue, depressed mood, difficulty concentrating, and lack of motivation — effects consistent with temporary dopamine depletion after sustained reuptake blockade. These effects may persist for several days given the drug's long elimination half-life.
Prioritize sleep, hydration, and regular meals in the 48–72 hours following use. Avoid caffeine and other stimulants during recovery, as they stress the same cardiovascular and neurochemical systems. If depressed mood or anhedonia persists beyond one week, consider consulting a healthcare professional — post-withdrawal depressive symptoms are documented in animal models of NEH use.
Recovery & Support
NEH's pharmacological profile — high DAT potency, confirmed reward-circuit engagement, and compulsive redosing patterns — places it among the cathinones with the highest dependence risk. Users who find themselves unable to limit sessions, who escalate doses, or who experience significant post-use depression should consider these warning signs.
Professional support options include addiction counseling, cognitive-behavioral therapy, and peer support groups experienced with stimulant dependence (such as SMART Recovery or stimulant-focused 12-step programs). Medical evaluation is recommended for anyone experiencing cardiovascular symptoms, persistent mood changes, or cognitive difficulties following repeated use.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: chest pain, seizures, loss of consciousness, body temperature hot enough to feel through clothing, uncontrollable agitation, or confusion that prevents communication all require immediate medical attention. These signs distinguish a medical emergency from ordinary stimulant discomfort.
Immediate steps:
- 1. Call emergency services immediately if any of the above signs are present
- 2. Move the person to a cool, quiet space
- 3. Remove excess clothing and apply cool (not ice-cold) water to the skin if body temperature is elevated
- 4. Place an unconscious person in the recovery position (on their side, airway clear)
- 5. Do not restrain a person unless they are in immediate danger of harming themselves — restraint can worsen hyperthermia
- 6. Do not induce vomiting
What to tell the dispatcher: Name the substance (N-Ethylhexedrone / hexen), the approximate amount taken, the time of last dose, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
N-Ethylhexedrone is controlled in most major jurisdictions, either through specific scheduling or through broad novel psychoactive substance legislation targeting the cathinone class. The WHO Expert Committee on Drug Dependence issued a Critical Review Report on NEH at its 47th meeting in 2023;[11] the scheduling recommendation outcome from that review was not confirmed during research for this article.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | Temporarily scheduled July 2019;[22] permanently placed in Schedule I effective June 2022[10] |
| United Kingdom | Controlled under Psychoactive Substances Act 2016 | Blanket prohibition on substances producing psychoactive effects by stimulating or depressing the CNS; effective May 26, 2016citation needed |
| Germany | Controlled under Neue-psychoaktive-Stoffe-Gesetz (NpSG) | Controlled since November 26, 2016; production, import for market placement, and commercial trading are criminal offences; simple possession prohibited but not criminally punishablecitation needed |
| Canada | Schedule I (Controlled Drugs and Substances Act) | All cathinones encompassed under broad chemical class schedulingcitation needed |
| Australia | Controlled substance (Office of Drug Control) | Listed by ODC; exact schedule not confirmed — likely Schedule 9 based on cathinone class controlscitation needed |
| European Union | Subject to EMCDDA early warning (February 2016) | Sweden, France, Belgium, Netherlands, and Slovenia among first to notify; most EU member states have enacted controls through national NPS legislation or analogue provisions[4] |
references
- [1] ^abcdPersson M, Vikingsson S, Kronstrand R, Green H (2024) Characterization of neurotransmitter inhibition for seven cathinones by a proprietary fluorescent dye method. — Drug Testing and Analysis doi:10.1002/dta.3547
- [2]
- [3]
- [4]
- [5] ^abcdLa Maida N, Di Trana A, Giorgetti R, Tagliabracci A, Busardò FP, Huestis MA (2021) A Review of Synthetic Cathinone-Related Fatalities From 2017 to 2020 — Therapeutic Drug Monitoring doi:10.1097/ftd.0000000000000808
- [6] ^abcdefghijkde Mello-Sampayo C, Vaz AR, Henriques SC, Fernandes A, Paradinha F, Florindo P, Faria P, Moreira R, Brites D, Lopes A (2021) Designer Cathinones N-Ethylhexedrone and Buphedrone Show Different In Vitro Neurotoxicity and Mice Behaviour Impairment — Neurotoxicity Research doi:10.1007/s12640-020-00229-6