4-FA
4-fluoroamphetamine
Studies and references cited across this article, graded by evidence strength.
Data points an editor reviewed and accepted for publication.
Value Provenance
Dosing
oraltrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Threshold | 25 mg | 25 mg | medium |
| Low | 25–75 mg | 25–75 mg | medium |
| Common | 75–130 mg | 75–130 mg | medium |
| Strong | 130–150 mg | 130–150 mg | medium |
| Heavy | 150+ mg | 150+ mg | medium |
| Editorial | Common dose anchored to Phase 1 study at 100 mg oral. 150 mg arm terminated for cardiovascular toxicity. Community dose ranges: threshold 25 mg, light 25-75 mg, common 75-130 mg, strong 130-150 mg, heavy above 150 mg. | ||
ReasoningReasoningCommon dose anchored to Phase 1 study at 100 mg oral. 150 mg arm terminated for cardiovascular toxicity. Community dose ranges: threshold 25 mg, light 25-75 mg, common 75-130 mg, strong 130-150 mg, heavy above 150 mg. Evidence basis: controlled_human_study | |||
Duration
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 45–75 minutes | 45–75 minutes | medium |
| Editorial | Community-reported onset 45-75 min, consistent with controlled study peak at 1 hour post-dose. | ||
ReasoningReasoningCommunity-reported onset 45-75 min, consistent with controlled study peak at 1 hour post-dose. Evidence basis: community_consensus_large | |||
| Come uptrace | 30–75 minutes | 30–75 minutes | medium |
| Editorial | Community-reported come-up 30-75 min, consistent with controlled study timeline. | ||
ReasoningReasoningCommunity-reported come-up 30-75 min, consistent with controlled study timeline. Evidence basis: community_consensus_large | |||
| Peaktrace | 150–210 minutes | 150–210 minutes | medium |
| Editorial | Community-reported peak 2.5-3.5 hours. Consistent with sustained BP elevation of 4-5 hours in controlled study. | ||
ReasoningReasoningCommunity-reported peak 2.5-3.5 hours. Consistent with sustained BP elevation of 4-5 hours in controlled study. Evidence basis: community_consensus_large | |||
| Offsettrace | 2–3 hours | 2–3 hours | medium |
| Editorial | Community-reported offset 2-3 hours, consistent with transition from peak to subacute negative affect phase. | ||
ReasoningReasoningCommunity-reported offset 2-3 hours, consistent with transition from peak to subacute negative affect phase. Evidence basis: community_consensus_large | |||
| Totaltrace | 5–8 hours | 5–8 hours | medium |
| Editorial | Community-reported total 5-8 hours. Consistent with controlled study cardiovascular effects lasting 4-5 hours. | ||
ReasoningReasoningCommunity-reported total 5-8 hours. Consistent with controlled study cardiovascular effects lasting 4-5 hours. Evidence basis: community_consensus_large | |||
| After effectstrace | 6–12 hours | 6–12 hours | medium |
| Editorial | Community-reported aftereffects 6-12 hours, supported by subacute negative affect findings in de Sousa Fernandes Perna 2018. | ||
ReasoningReasoningCommunity-reported aftereffects 6-12 hours, supported by subacute negative affect findings in de Sousa Fernandes Perna 2018. Evidence basis: community_consensus_large | |||
Safety
Toxicity Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Acute | high | high | high |
| Chronic | moderate | moderate | high |
| Organs Affected | cardiovascular, brain, liver | cardiovascular, brain, liver | high |
| Editorial | Acute: classified as high based on multiple independent human case series documenting fatalities, Takotsubo cardiomyopathy (mono-intoxication), hemorrhagic stroke, and the termination of the 150 mg Phase 1 arm for cardiovascular toxicity (Hondebrink 2018, Gresnigt 2022, Aly 2021, Van der Pas 2020, de Sousa Fernandes Perna 2018). Chronic: classified as moderate — in vitro hepatocellular and neuronal mitochondrial toxicity data exist (Luethi 2019, Zhou 2020) but at concentrations well above recreational plasma levels; no human chronic toxicity data published. | ||
ReasoningReasoningAcute: classified as high based on multiple independent human case series documenting fatalities, Takotsubo cardiomyopathy (mono-intoxication), hemorrhagic stroke, and the termination of the 150 mg Phase 1 arm for cardiovascular toxicity (Hondebrink 2018, Gresnigt 2022, Aly 2021, Van der Pas 2020, de Sousa Fernandes Perna 2018). Chronic: classified as moderate — in vitro hepatocellular and neuronal mitochondrial toxicity data exist (Luethi 2019, Zhou 2020) but at concentrations well above recreational plasma levels; no human chronic toxicity data published. Evidence basis: published_case_series | |||
Dependence Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Physical | low | low | medium |
| Psychological | moderate | moderate | medium |
| Compulsive Redosing | moderate | moderate | medium |
| Dose Escalation | moderate | moderate | medium |
| Editorial | Drug liking and wanting significantly increased in controlled human study (Kuypers 2018). Positive reinforcement confirmed in primate self-administration (Wee 2005). Impulsivity not increased, indicating reward-driven rather than impulsivity-driven abuse liability. No human dependence case series exists, but converging evidence supports moderate psychological dependence potential. | ||
ReasoningReasoningDrug liking and wanting significantly increased in controlled human study (Kuypers 2018). Positive reinforcement confirmed in primate self-administration (Wee 2005). Impulsivity not increased, indicating reward-driven rather than impulsivity-driven abuse liability. No human dependence case series exists, but converging evidence supports moderate psychological dependence potential. Evidence basis: controlled_human_study | |||
Withdrawal Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Severity | mild | mild | low |
| Symptoms | fatigue, depressed mood, irritability, cognitive impairment, headache, increased appetite, hypersomnia | fatigue, depressed mood, irritability, cognitive impairment, headache, increased appetite, hypersomnia | low |
| Fatal | No | No | low |
| Medical Supervision | Not required | Not required | low |
| Editorial | No 4-FA-specific withdrawal data published. Withdrawal profile inferred from amphetamine-class pharmacology: stimulant withdrawal syndrome characterized by fatigue, hypersomnia, depressed mood, and increased appetite. Severity expected to be mild given typical intermittent recreational use patterns. | ||
ReasoningReasoningNo 4-FA-specific withdrawal data published. Withdrawal profile inferred from amphetamine-class pharmacology: stimulant withdrawal syndrome characterized by fatigue, hypersomnia, depressed mood, and increased appetite. Severity expected to be mild given typical intermittent recreational use patterns. Evidence basis: controlled_human_study | |||
Tolerance Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Buildup | moderate | moderate | low |
| Half-life | 5 days | 5 days | low |
| Full Reset | 10 days | 10 days | low |
| Cross-tolerances | amphetamine, methamphetamine, MDMA, methylphenidate | amphetamine, methamphetamine, MDMA, methylphenidate | low |
| Editorial | Tolerance values inferred from amphetamine-class pharmacology and community consensus data. No 4-FA-specific tolerance study published. Cross-tolerance with other monoamine releasers expected via shared transporter downregulation mechanism. | ||
ReasoningReasoningTolerance values inferred from amphetamine-class pharmacology and community consensus data. No 4-FA-specific tolerance study published. Cross-tolerance with other monoamine releasers expected via shared transporter downregulation mechanism. Evidence basis: structural_analogy | |||
Effects & Profile
Contraindications
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| cardiovascular cardiovascular diseasetrace | absolute | absolute | high |
| Editorial | Blood pressure effects documented in Phase 1 study (de Sousa Fernandes Perna 2018) and comparative ED analysis (Gresnigt 2022). Takotsubo cardiomyopathy confirmed in mono-intoxication cases (Aly 2021, Van der Pas 2020). | ||
ReasoningReasoningBlood pressure effects documented in Phase 1 study (de Sousa Fernandes Perna 2018) and comparative ED analysis (Gresnigt 2022). Takotsubo cardiomyopathy confirmed in mono-intoxication cases (Aly 2021, Van der Pas 2020). | |||
| cardiovascular uncontrolled hypertensiontrace | absolute | absolute | high |
| Editorial | Cerebral hemorrhage documented in Hondebrink 2018 cohort. Hemorrhagic stroke cases in Wijers 2018. Exaggerated BP response confirmed in Gresnigt 2022. | ||
ReasoningReasoningCerebral hemorrhage documented in Hondebrink 2018 cohort. Hemorrhagic stroke cases in Wijers 2018. Exaggerated BP response confirmed in Gresnigt 2022. | |||
| psychiatric psychotic disorderstrace | relative | relative | medium |
| Editorial | Class-level pharmacological inference from amphetamine. No 4-FA-specific psychosis case report found. Mild psychedelic state (Kuypers 2019) adds theoretical risk in vulnerable individuals. | ||
ReasoningReasoningClass-level pharmacological inference from amphetamine. No 4-FA-specific psychosis case report found. Mild psychedelic state (Kuypers 2019) adds theoretical risk in vulnerable individuals. | |||
| other concurrent MAOI usetrace | absolute | absolute | high |
| Editorial | Identified as the primary interaction risk by Inan et al. 2020 systematic review. Mechanistically absolute — MAO inhibition plus monoamine release is a well-established lethal combination class. | ||
ReasoningReasoningIdentified as the primary interaction risk by Inan et al. 2020 systematic review. Mechanistically absolute — MAO inhibition plus monoamine release is a well-established lethal combination class. | |||
| other concurrent serotonergic drug usetrace | relative | relative | high |
| Editorial | Six fatalities from 4-FA + 25C-NBOMe (Gerostamoulos 2023). SSRI/SNRI interaction reviewed by Inan et al. 2020. Tramadol interaction classified as dangerous based on mechanistic inference. | ||
ReasoningReasoningSix fatalities from 4-FA + 25C-NBOMe (Gerostamoulos 2023). SSRI/SNRI interaction reviewed by Inan et al. 2020. Tramadol interaction classified as dangerous based on mechanistic inference. | |||
| other concurrent antiretroviral therapy (CYP2D6 inhibitors)trace | relative | relative | medium |
| Editorial | Specifically identified as a drug interaction risk by Inan et al. 2020 systematic review. CYP2D6 involvement inferred from amphetamine-class metabolism. | ||
ReasoningReasoningSpecifically identified as a drug interaction risk by Inan et al. 2020 systematic review. CYP2D6 involvement inferred from amphetamine-class metabolism. | |||
| pregnancy breastfeeding pregnancytrace | absolute | absolute | medium |
| Editorial | Class-level inference from amphetamine teratogenicity data. No 4-FA-specific reproductive studies. Cardiovascular effects documented in controlled study pose clear pregnancy risk. | ||
ReasoningReasoningClass-level inference from amphetamine teratogenicity data. No 4-FA-specific reproductive studies. Cardiovascular effects documented in controlled study pose clear pregnancy risk. | |||
Timeline Phases
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 2700–4500 sec(i=0.05) | 2700–4500 sec(i=0.05) | medium |
| Editorial | Duration data anchored to community reports (onset 45-75 min, come-up 30-75 min, peak 2.5-3.5 h, offset 2-3 h, aftereffects 6-12 h, total 5-8 h) cross-referenced with controlled study timing (peak subjective effects at ~1 hour post-dose, blood pressure elevation lasting 4-5 hours). The community ranges align well with clinical observations. Aftereffects duration supported by the subacute negative affect findings in de Sousa Fernandes Perna 2018. | ||
ReasoningReasoningDuration data anchored to community reports (onset 45-75 min, come-up 30-75 min, peak 2.5-3.5 h, offset 2-3 h, aftereffects 6-12 h, total 5-8 h) cross-referenced with controlled study timing (peak subjective effects at ~1 hour post-dose, blood pressure elevation lasting 4-5 hours). The community ranges align well with clinical observations. Aftereffects duration supported by the subacute negative affect findings in de Sousa Fernandes Perna 2018. | |||
| Come uptrace | 1800–4500 sec(i=0.35) | 1800–4500 sec(i=0.35) | medium |
| Editorial | Duration data anchored to community reports (onset 45-75 min, come-up 30-75 min, peak 2.5-3.5 h, offset 2-3 h, aftereffects 6-12 h, total 5-8 h) cross-referenced with controlled study timing (peak subjective effects at ~1 hour post-dose, blood pressure elevation lasting 4-5 hours). The community ranges align well with clinical observations. Aftereffects duration supported by the subacute negative affect findings in de Sousa Fernandes Perna 2018. | ||
ReasoningReasoningDuration data anchored to community reports (onset 45-75 min, come-up 30-75 min, peak 2.5-3.5 h, offset 2-3 h, aftereffects 6-12 h, total 5-8 h) cross-referenced with controlled study timing (peak subjective effects at ~1 hour post-dose, blood pressure elevation lasting 4-5 hours). The community ranges align well with clinical observations. Aftereffects duration supported by the subacute negative affect findings in de Sousa Fernandes Perna 2018. | |||
| Peaktrace | 9000–12600 sec(i=1.00) | 9000–12600 sec(i=1.00) | medium |
| Editorial | Duration data anchored to community reports (onset 45-75 min, come-up 30-75 min, peak 2.5-3.5 h, offset 2-3 h, aftereffects 6-12 h, total 5-8 h) cross-referenced with controlled study timing (peak subjective effects at ~1 hour post-dose, blood pressure elevation lasting 4-5 hours). The community ranges align well with clinical observations. Aftereffects duration supported by the subacute negative affect findings in de Sousa Fernandes Perna 2018. | ||
ReasoningReasoningDuration data anchored to community reports (onset 45-75 min, come-up 30-75 min, peak 2.5-3.5 h, offset 2-3 h, aftereffects 6-12 h, total 5-8 h) cross-referenced with controlled study timing (peak subjective effects at ~1 hour post-dose, blood pressure elevation lasting 4-5 hours). The community ranges align well with clinical observations. Aftereffects duration supported by the subacute negative affect findings in de Sousa Fernandes Perna 2018. | |||
| Resolutiontrace | 7200–10800 sec(i=0.30) | 7200–10800 sec(i=0.30) | medium |
| Editorial | Duration data anchored to community reports (onset 45-75 min, come-up 30-75 min, peak 2.5-3.5 h, offset 2-3 h, aftereffects 6-12 h, total 5-8 h) cross-referenced with controlled study timing (peak subjective effects at ~1 hour post-dose, blood pressure elevation lasting 4-5 hours). The community ranges align well with clinical observations. Aftereffects duration supported by the subacute negative affect findings in de Sousa Fernandes Perna 2018. | ||
ReasoningReasoningDuration data anchored to community reports (onset 45-75 min, come-up 30-75 min, peak 2.5-3.5 h, offset 2-3 h, aftereffects 6-12 h, total 5-8 h) cross-referenced with controlled study timing (peak subjective effects at ~1 hour post-dose, blood pressure elevation lasting 4-5 hours). The community ranges align well with clinical observations. Aftereffects duration supported by the subacute negative affect findings in de Sousa Fernandes Perna 2018. | |||
| Afterglowtrace | 21600–43200 sec(i=0.10) | 21600–43200 sec(i=0.10) | medium |
| Editorial | Duration data anchored to community reports (onset 45-75 min, come-up 30-75 min, peak 2.5-3.5 h, offset 2-3 h, aftereffects 6-12 h, total 5-8 h) cross-referenced with controlled study timing (peak subjective effects at ~1 hour post-dose, blood pressure elevation lasting 4-5 hours). The community ranges align well with clinical observations. Aftereffects duration supported by the subacute negative affect findings in de Sousa Fernandes Perna 2018. | ||
ReasoningReasoningDuration data anchored to community reports (onset 45-75 min, come-up 30-75 min, peak 2.5-3.5 h, offset 2-3 h, aftereffects 6-12 h, total 5-8 h) cross-referenced with controlled study timing (peak subjective effects at ~1 hour post-dose, blood pressure elevation lasting 4-5 hours). The community ranges align well with clinical observations. Aftereffects duration supported by the subacute negative affect findings in de Sousa Fernandes Perna 2018. | |||
Dose Tier Summaries
Doses exceeding 150 mg oral carry substantially elevated risk with no controlled human safety data. The sole clinical study terminated its 150 mg arm due to cardiovascular toxicity — doses above this threshold have no safety characterization whatsoever. Clinical case series document Takotsubo cardiomyopathy, hemorrhagic stroke, myocardial infarction, and fatalities at recreational doses, though specific dose-outcome relationships are not established. At these doses, stimulant effects may become dysphoric: anxiety, agitation, paranoid ideation, and overwhelming physical discomfort from sustained hypertension and tachycardia. The entactogenic quality may be overshadowed by sympathomimetic toxicity. The aftereffect period is prolonged and severe. Negative affect, cognitive impairment, and physical exhaustion may persist for 24–48 hours. This dose range approaches documented fatality concentrations.
No controlled data above 150 mg. The 150 mg arm was terminated for cardiovascular toxicity. Clinical case series document severe outcomes including fatalities. Community reports describe increasing dysphoria and physical distress at high doses.
ReasoningReasoning
No controlled data above 150 mg. The 150 mg arm was terminated for cardiovascular toxicity. Clinical case series document severe outcomes including fatalities. Community reports describe increasing dysphoria and physical distress at high doses.
Evidence basis: published_case_series
At threshold doses, effects are subtle and may be attributed to placebo or expectation. A faint increase in alertness and sociability emerges, with mild mood brightening that does not reach full stimulant activation. Physical signs are minimal — slight pupil dilation may be noticeable to an observer. These doses do not produce the entactogenic or psychedelic components of the 4-FA experience. The effect is closer to a mild caffeine-like stimulation than to the full pharmacological profile. Sleep may be mildly delayed but is generally achievable within a few hours.
No published threshold dose data for 4-FA. Inferred from community reports and amphetamine-class pharmacology. The Phase 1 study used 100 mg as the lowest dose.
ReasoningReasoning
No published threshold dose data for 4-FA. Inferred from community reports and amphetamine-class pharmacology. The Phase 1 study used 100 mg as the lowest dose.
Evidence basis: community_consensus_large
At light doses, a clear stimulant effect emerges: increased energy, enhanced focus, mild mood elevation, and greater conversational fluency. The entactogenic component begins to appear as a subtle warmth and increased sociability, though it does not reach the pronounced empathogenic character seen at higher doses. Physically, heart rate and blood pressure begin to rise noticeably. Mild jaw tension and appetite suppression are common. Pupil dilation becomes more apparent. The total experience lasts approximately 4–6 hours, with a mild aftereffect period of fatigue and low mood the following day. Sleep is difficult for 4–6 hours after ingestion. Functional impairment is mild — many users report being able to engage in structured tasks.
Inferred from community dose-response reports and the pharmacological profile. No published clinical data exist below 100 mg.
ReasoningReasoning
Inferred from community dose-response reports and the pharmacological profile. No published clinical data exist below 100 mg.
Evidence basis: community_consensus_large
At common doses (100–130 mg oral), the full stimulant-entactogen profile manifests. Vigor, elation, arousal, and friendliness are significantly elevated — findings confirmed in the controlled Phase 1 study at 100 mg. A mild psychedelic state emerges, with enhanced color perception and subtle perceptual brightening, though without the geometric visual distortions characteristic of classical psychedelics. Emotional openness and sociability increase substantially. Cardiovascular effects become prominent: blood pressure elevation persists 4–5 hours, and heart rate remains elevated beyond the subjective peak. Jaw tension, appetite suppression, and mild bruxism are typical. Sweating and temperature dysregulation may occur in warm environments. The total experience lasts 5–8 hours. A pronounced aftereffect period follows, characterized by negative affect, headache, and cognitive fatigue lasting 6–12 hours. Sleep is impossible for approximately 6–8 hours after ingestion.
The 100 mg dose was used in the controlled Phase 1 study (de Sousa Fernandes Perna 2018), providing direct clinical evidence for effects at this dose. Community reports extend the common range to 130 mg.
ReasoningReasoning
The 100 mg dose was used in the controlled Phase 1 study (de Sousa Fernandes Perna 2018), providing direct clinical evidence for effects at this dose. Community reports extend the common range to 130 mg.
Evidence basis: controlled_human_study
At strong doses (130–150 mg oral), stimulant and entactogenic effects intensify substantially. The psychedelic component becomes more noticeable — enhanced sensory perception, mild visual brightening, and a more pronounced sense of emotional connection. Euphoria and sociability peak in intensity. However, the 150 mg arm of the sole controlled human study was terminated after 5 participants due to severe cardiovascular effects. Cardiovascular risk escalates markedly at this range. Blood pressure elevation is pronounced and sustained, with documented cases of clinical concern in the Phase 1 trial. Jaw clenching, bruxism, and muscle tension increase. Sweating becomes more prominent. The comedown period is more severe than at common doses, with pronounced negative affect, headache, and fatigue. Full functional recovery may take 24 hours or more. Sleep is impossible for 8+ hours.
The 150 mg arm of the Phase 1 study was terminated for cardiovascular safety (de Sousa Fernandes Perna 2018). Community reports describe intensified effects at 130-150 mg. This dose range carries documented clinical risk.
ReasoningReasoning
The 150 mg arm of the Phase 1 study was terminated for cardiovascular safety (de Sousa Fernandes Perna 2018). Community reports describe intensified effects at 130-150 mg. This dose range carries documented clinical risk.
Evidence basis: controlled_human_study
History
publish Oct 2, 2026 · by agent-psx
backfill Jun 4, 2026
Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.
Sources
- [1]moderate4-Fluoroamphetamine in the Netherlands: more than a one-night standLinsen F, Koning RP, van Laar M, Niesink RJ, Koeter MW, Brunt TM · 2015 · Addiction
- [2]moderateFatalities, Cerebral Hemorrhage, and Severe Cardiovascular Toxicity After Exposure to the New Psychoactive Substance 4-Fluoroamphetamine: A Prospective Cohort StudyHondebrink L, Nugteren-van Lonkhuyzen JJ, Rietjens SJ, Brunt TM, Venhuis B, Soerdjbalie-Maikoe V, Smink BE, van Riel AJHP, de Vries I · 2018 · Annals of Emergency Medicine
- [3]weakSchedules of Controlled Substances: Placement of 4-Fluoroamphetamine in Schedule IDrug Enforcement Administration (DEA) · 2026linkno claims checked
- [4]moderateIn vivo effects of amphetamine analogs reveal evidence for serotonergic inhibition of mesolimbic dopamine transmission in the ratBaumann MH, Clark RD, Woolverton WL, Wee S, Blough BE, Rothman RB · 2011 · Journal of Pharmacology and Experimental Therapeutics
- [5]strongRelationship between the serotonergic activity and reinforcing effects of a series of amphetamine analogsWee S, Anderson KG, Baumann MH, Rothman RB, Blough BE, Woolverton WL · 2005 · Journal of Pharmacology and Experimental Therapeuticspubmed 15677348no claims checked
- [6]strongMonoamine transporter and receptor interaction profiles of novel psychoactive substances: para-halogenated amphetamines and pyrovalerone cathinonesRickli A, Hoener MC, Liechti ME · 2015 · European Neuropsychopharmacology
- [7]strongA First-in-Man Study with 4-Fluoroamphetamine Demonstrates it Produces a Mild Psychedelic StateKuypers KPC, De Sousa Fernandes Perna EB, Theunissen EL, Toennes SW, Mason NL, Hutten NRPW, Ramaekers JG · 2019 · Journal of Psychoactive Drugs
- [8]strongIndependent elevation of peripheral oxytocin concentrations and reduction in cognitive empathy during 4-fluoroamphetamine intoxicationDolder PC, de Sousa Fernandes Perna EB, Mason NL, Hutten NRPW, Toennes SW, Theunissen EL, Ramaekers JG, Kuypers KPC · 2018 · Human Psychopharmacology
- [9]moderate4-Fluoroamphetamine (4-FA) intoxication results in exaggerated blood pressure effects compared to MDMA and amphetamine: A retrospective analysisGresnigt FMJ, Snik A, Franssen EJF, Vanhommerig JW, de Lange DW, Riezebos RK · 2022 · Journal of the American College of Emergency Physicians Open
- [10]strongSafety Profile and Neurocognitive Function Following Acute 4-Fluoroamphetamine (4-FA) Administration in Humansde Sousa Fernandes Perna EB, Theunissen EL, Dolder PC, Mason NL, Hutten NRPW, Toennes SW, Kuypers KPC, Ramaekers JG · 2018 · Frontiers in Pharmacology
- [11]weakFatal Intoxications from a Combination of 4-Fluoroamphetamine and 25C-NBOMeGerostamoulos D, Glowacki L, Pricone M, Crump K, Di Rago M, Joubert S, Lynch MJ, Woodford NW, Drummer OH · 2023 · Journal of Analytical Toxicology
- [12]weakTakotsubo cardiomyopathy as a consequence of 4-fluoroamphetamine Mono-intoxication documented by toxicological analysesAly SM, Deheul S, Puymirat E, Richeval C, Allorge D, Gaulier JM · 2021 · Clinical Toxicology
- [13]weakAcute onset heart failure due to reverse type Takotsubo cardiomyopathy caused by a single dose of 4-Fluoroamphetamine in a healthy young individualvan der Pas RSD, Gresnigt FMJ, Wansink L, Franssen EJF, Riezebos RK · 2020 · Toxicology Reports
- [14]weak
- [15]moderatePharmacokinetics, pharmacodynamics and toxicology of new psychoactive substances (NPS): 2C-B, 4-fluoroamphetamine and benzofuransNugteren-van Lonkhuyzen JJ, van Riel AJ, Brunt TM, Hondebrink L · 2015 · Drug and Alcohol Dependence
- [16]moderateMonitoring new psychoactive substances (NPS) in The Netherlands: data from the drug market and the Poisons Information CentreHondebrink L, Nugteren-van Lonkhuyzen JJ, Van Der Gouwe D, Brunt TM · 2015 · Drug and Alcohol Dependence
- [17]moderatePurity, adulteration and price of drugs bought on-line versus off-line in the Netherlandsvan der Gouwe D, Brunt TM, van Laar M, van der Pol P · 2017 · Addiction
- [18]weakHaemorrhagic stroke related to the use of 4-fluoroamphetamineWijers CHW, Visser MC, van Litsenburg RTH, Niesink RJM, Willemse RB, Croes EA · 2018 · Journal of Neurology
- [19]strongPara-Halogenation Affects Monoamine Transporter Inhibition Properties and Hepatocellular Toxicity of Amphetamines and MethcathinonesLuethi D, Walter M, Zhou X, Rudin D, Krähenbuhl S, Liechti ME · 2019 · Frontiers in Pharmacology
- [20]moderate
- [21]strongExcretion of 4-fluoroamphetamine and three metabolites in urine after controlled oral ingestionToennes SW, Schneider D, Pogoda W, Paulke A, Wunder C, Theunissen EL, de Sousa Fernandes Perna EB, Ramaekers JG · 2020 · Journal of Pharmaceutical and Biomedical Analysis
- [22]strongNovel Phenethylamines and Their Potential Interactions With Prescription Drugs: A Systematic Critical ReviewInan F, Brunt TM, Contrucci RR, Hondebrink L, Franssen EJF · 2020 · Therapeutic Drug Monitoring
- [23]strongPharmacokinetic properties of 4-fluoroamphetamine in serum and oral fluid after oral ingestionToennes SW, Schneider D, Pogoda W, Paulke A, Wunder C, Theunissen EL, Kuypers KPC, de Sousa Fernandes Perna E, Ramaekers JG · 2019 · Drug Testing and Analysis
- [24]strongDrug liking and wanting, not impulsive action or reflection is increased by 4-fluoroamphetamineKuypers KPC, de Sousa Fernandes Perna EB, Dolder PC, Toennes SW, Theunissen EL, Mason NL, Hutten NRPW, Ramaekers JG · 2018 · Psychopharmacology
- [25]strongDifferential effects of psychoactive substances on human wildtype and polymorphic T356M dopamine transporters (DAT)Zwartsen A, Litjens CHC, Hondebrink L, van den Heuvel JJMW, Greupink R, Russel FGM, de Lange DW, Legler J, Koenderink JB, Westerink RHS · 2019 · Toxicology
- [26]strongAnalysis of 4-fluoroamphetamine in cerumen after controlled oral applicationMeier SI, Petzel-Witt S, Schubert-Zsilavecz M, de Sousa Fernandes Perna EB, Theunissen EL, Ramaekers JG, Toennes SW · 2020 · Drug Testing and Analysis
- [27]moderatePrevalence and concentrations of new designer stimulants, synthetic opioids, benzodiazepines, and hallucinogens in postmortem hair samples: A 13-year retrospective studyNiebel A, Westendorf L, Krumbiegel F, Hartwig S, Parr MK, Tsokos M · 2022 · Drug Testing and Analysis
- [28]strongDesigner drugs: mechanism of action and adverse effectsLuethi D, Liechti ME · 2020 · Archives of Toxicology
- [29]strongPara-Halogenation of Amphetamine and Methcathinone Increases the Mitochondrial Toxicity in Undifferentiated and Differentiated SH-SY5Y CellsZhou X, Bouitbir J, Liechti ME, Krähenbuhl S, Mancuso RV · 2020 · International Journal of Molecular Sciences
- [30]strongCardiotoxicity screening of illicit drugs and new psychoactive substances (NPS) in human iPSC-derived cardiomyocytes using microelectrode array (MEA) recordingsZwartsen A, de Korte T, Nacken P, de Lange DW, Westerink RHS, Hondebrink L · 2019 · Journal of Molecular and Cellular Cardiology
- [31]strongNeurotoxicity screening of (illicit) drugs using novel methods for analysis of microelectrode array (MEA) recordingsHondebrink L, Verboven AHA, Drega WS, Schmeink S, de Groot MWGDM, van Kleef RGDM, Wijnolts FMJ, de Groot A, Meulenbelt J, Westerink RHS · 2016 · Neurotoxicology
- [32]moderateMonoamine Transporter and Receptor Interaction Profiles in Vitro Predict Reported Human Doses of Novel Psychoactive Stimulants and PsychedelicsLuethi D, Liechti ME · 2018 · International Journal of Neuropsychopharmacology
Claim Verification
No claim verification has run for this version.