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Sources
32
16 strong · 10 moderate · 6 weak

Studies and references cited across this article, graded by evidence strength.

Values approved
142/145 (98%)

Data points an editor reviewed and accepted for publication.

01

Value Provenance

Dosing

oraltrace

FieldPublishedAI ProposedConfidence
Threshold25 mg25 mgmedium
Low25–75 mg25–75 mgmedium
Common75–130 mg75–130 mgmedium
Strong130–150 mg130–150 mgmedium
Heavy150+ mg150+ mgmedium
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.

Reasoning

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.

Evidence basis: controlled_human_study

Duration

oral

FieldPublishedAI ProposedConfidence
Onsettrace45–75 minutes45–75 minutesmedium
Editorial

Community-reported onset 45-75 min, consistent with controlled study peak at 1 hour post-dose.

Reasoning

Community-reported onset 45-75 min, consistent with controlled study peak at 1 hour post-dose.

Evidence basis: community_consensus_large

Come uptrace30–75 minutes30–75 minutesmedium
Editorial

Community-reported come-up 30-75 min, consistent with controlled study timeline.

Reasoning

Community-reported come-up 30-75 min, consistent with controlled study timeline.

Evidence basis: community_consensus_large

Peaktrace150–210 minutes150–210 minutesmedium
Editorial

Community-reported peak 2.5-3.5 hours. Consistent with sustained BP elevation of 4-5 hours in controlled study.

Reasoning

Community-reported peak 2.5-3.5 hours. Consistent with sustained BP elevation of 4-5 hours in controlled study.

Evidence basis: community_consensus_large

Offsettrace2–3 hours2–3 hoursmedium
Editorial

Community-reported offset 2-3 hours, consistent with transition from peak to subacute negative affect phase.

Reasoning

Community-reported offset 2-3 hours, consistent with transition from peak to subacute negative affect phase.

Evidence basis: community_consensus_large

Totaltrace5–8 hours5–8 hoursmedium
Editorial

Community-reported total 5-8 hours. Consistent with controlled study cardiovascular effects lasting 4-5 hours.

Reasoning

Community-reported total 5-8 hours. Consistent with controlled study cardiovascular effects lasting 4-5 hours.

Evidence basis: community_consensus_large

After effectstrace6–12 hours6–12 hoursmedium
Editorial

Community-reported aftereffects 6-12 hours, supported by subacute negative affect findings in de Sousa Fernandes Perna 2018.

Reasoning

Community-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

FieldPublishedAI ProposedConfidence
Acutehighhighhigh
Chronicmoderatemoderatehigh
Organs Affectedcardiovascular, brain, livercardiovascular, brain, liverhigh
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.

Reasoning

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.

Evidence basis: published_case_series

Dependence Profiletrace

FieldPublishedAI ProposedConfidence
Physicallowlowmedium
Psychologicalmoderatemoderatemedium
Compulsive Redosingmoderatemoderatemedium
Dose Escalationmoderatemoderatemedium
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.

Reasoning

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.

Evidence basis: controlled_human_study

Withdrawal Profiletrace

FieldPublishedAI ProposedConfidence
Severitymildmildlow
Symptomsfatigue, depressed mood, irritability, cognitive impairment, headache, increased appetite, hypersomniafatigue, depressed mood, irritability, cognitive impairment, headache, increased appetite, hypersomnialow
FatalNoNolow
Medical SupervisionNot requiredNot requiredlow
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.

Reasoning

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.

Evidence basis: controlled_human_study

Tolerance Profiletrace

FieldPublishedAI ProposedConfidence
Buildupmoderatemoderatelow
Half-life5 days5 dayslow
Full Reset10 days10 dayslow
Cross-tolerancesamphetamine, methamphetamine, MDMA, methylphenidateamphetamine, methamphetamine, MDMA, methylphenidatelow
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.

Reasoning

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.

Evidence basis: structural_analogy

Effects & Profile

Contraindications

FieldPublishedAI ProposedConfidence
cardiovascular cardiovascular diseasetraceabsoluteabsolutehigh
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).

Reasoning

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).

cardiovascular uncontrolled hypertensiontraceabsoluteabsolutehigh
Editorial

Cerebral hemorrhage documented in Hondebrink 2018 cohort. Hemorrhagic stroke cases in Wijers 2018. Exaggerated BP response confirmed in Gresnigt 2022.

Reasoning

Cerebral hemorrhage documented in Hondebrink 2018 cohort. Hemorrhagic stroke cases in Wijers 2018. Exaggerated BP response confirmed in Gresnigt 2022.

psychiatric psychotic disorderstracerelativerelativemedium
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.

Reasoning

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.

other concurrent MAOI usetraceabsoluteabsolutehigh
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.

Reasoning

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.

other concurrent serotonergic drug usetracerelativerelativehigh
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.

Reasoning

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.

other concurrent antiretroviral therapy (CYP2D6 inhibitors)tracerelativerelativemedium
Editorial

Specifically identified as a drug interaction risk by Inan et al. 2020 systematic review. CYP2D6 involvement inferred from amphetamine-class metabolism.

Reasoning

Specifically identified as a drug interaction risk by Inan et al. 2020 systematic review. CYP2D6 involvement inferred from amphetamine-class metabolism.

pregnancy breastfeeding pregnancytraceabsoluteabsolutemedium
Editorial

Class-level inference from amphetamine teratogenicity data. No 4-FA-specific reproductive studies. Cardiovascular effects documented in controlled study pose clear pregnancy risk.

Reasoning

Class-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

FieldPublishedAI ProposedConfidence
Onsettrace2700–4500 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.

Reasoning

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.

Come uptrace1800–4500 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.

Reasoning

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.

Peaktrace9000–12600 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.

Reasoning

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.

Resolutiontrace7200–10800 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.

Reasoning

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.

Afterglowtrace21600–43200 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.

Reasoning

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.

Dose Tier Summaries

heavytrace
medium

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.

Editorial

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.

Reasoning

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

thresholdtrace
low

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.

Editorial

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.

Reasoning

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

lighttrace
low

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.

Editorial

Inferred from community dose-response reports and the pharmacological profile. No published clinical data exist below 100 mg.

Reasoning

Inferred from community dose-response reports and the pharmacological profile. No published clinical data exist below 100 mg.

Evidence basis: community_consensus_large

commontrace
medium

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.

Editorial

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.

Reasoning

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

strongtrace
medium

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.

Editorial

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.

Reasoning

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

02

History

current version
published Oct 2, 2026system—
versions
2 total · since previous: +0 / −0 citations
publication ledger

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.

03

Sources

16 strong · 10 moderate · 6 weak
  1. [1]
    moderate
    4-Fluoroamphetamine in the Netherlands: more than a one-night stand
    Linsen F, Koning RP, van Laar M, Niesink RJ, Koeter MW, Brunt TM · 2015 · Addiction
  2. [2]
    moderate
    Fatalities, Cerebral Hemorrhage, and Severe Cardiovascular Toxicity After Exposure to the New Psychoactive Substance 4-Fluoroamphetamine: A Prospective Cohort Study
    Hondebrink 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
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    weak
    Schedules of Controlled Substances: Placement of 4-Fluoroamphetamine in Schedule I
    Drug Enforcement Administration (DEA) · 2026
    linkno claims checked
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    moderate
    In vivo effects of amphetamine analogs reveal evidence for serotonergic inhibition of mesolimbic dopamine transmission in the rat
    Baumann MH, Clark RD, Woolverton WL, Wee S, Blough BE, Rothman RB · 2011 · Journal of Pharmacology and Experimental Therapeutics
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    strong
    Relationship between the serotonergic activity and reinforcing effects of a series of amphetamine analogs
    Wee S, Anderson KG, Baumann MH, Rothman RB, Blough BE, Woolverton WL · 2005 · Journal of Pharmacology and Experimental Therapeutics
    pubmed 15677348no claims checked
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    strong
    Monoamine transporter and receptor interaction profiles of novel psychoactive substances: para-halogenated amphetamines and pyrovalerone cathinones
    Rickli A, Hoener MC, Liechti ME · 2015 · European Neuropsychopharmacology
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    strong
    A First-in-Man Study with 4-Fluoroamphetamine Demonstrates it Produces a Mild Psychedelic State
    Kuypers KPC, De Sousa Fernandes Perna EB, Theunissen EL, Toennes SW, Mason NL, Hutten NRPW, Ramaekers JG · 2019 · Journal of Psychoactive Drugs
  8. [8]
    strong
    Independent elevation of peripheral oxytocin concentrations and reduction in cognitive empathy during 4-fluoroamphetamine intoxication
    Dolder PC, de Sousa Fernandes Perna EB, Mason NL, Hutten NRPW, Toennes SW, Theunissen EL, Ramaekers JG, Kuypers KPC · 2018 · Human Psychopharmacology
  9. [9]
    moderate
    4-Fluoroamphetamine (4-FA) intoxication results in exaggerated blood pressure effects compared to MDMA and amphetamine: A retrospective analysis
    Gresnigt FMJ, Snik A, Franssen EJF, Vanhommerig JW, de Lange DW, Riezebos RK · 2022 · Journal of the American College of Emergency Physicians Open
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    strong
    Safety Profile and Neurocognitive Function Following Acute 4-Fluoroamphetamine (4-FA) Administration in Humans
    de Sousa Fernandes Perna EB, Theunissen EL, Dolder PC, Mason NL, Hutten NRPW, Toennes SW, Kuypers KPC, Ramaekers JG · 2018 · Frontiers in Pharmacology
  11. [11]
    weak
    Fatal Intoxications from a Combination of 4-Fluoroamphetamine and 25C-NBOMe
    Gerostamoulos D, Glowacki L, Pricone M, Crump K, Di Rago M, Joubert S, Lynch MJ, Woodford NW, Drummer OH · 2023 · Journal of Analytical Toxicology
  12. [12]
    weak
    Takotsubo cardiomyopathy as a consequence of 4-fluoroamphetamine Mono-intoxication documented by toxicological analyses
    Aly SM, Deheul S, Puymirat E, Richeval C, Allorge D, Gaulier JM · 2021 · Clinical Toxicology
  13. [13]
    weak
    Acute onset heart failure due to reverse type Takotsubo cardiomyopathy caused by a single dose of 4-Fluoroamphetamine in a healthy young individual
    van der Pas RSD, Gresnigt FMJ, Wansink L, Franssen EJF, Riezebos RK · 2020 · Toxicology Reports
  14. [14]
    weak
    Legal Status of 4-Fluoroamphetamine by Jurisdiction
    Erowid · 2017
    linkno claims checked
  15. [15]
    moderate
    Pharmacokinetics, pharmacodynamics and toxicology of new psychoactive substances (NPS): 2C-B, 4-fluoroamphetamine and benzofurans
    Nugteren-van Lonkhuyzen JJ, van Riel AJ, Brunt TM, Hondebrink L · 2015 · Drug and Alcohol Dependence
  16. [16]
    moderate
    Monitoring new psychoactive substances (NPS) in The Netherlands: data from the drug market and the Poisons Information Centre
    Hondebrink L, Nugteren-van Lonkhuyzen JJ, Van Der Gouwe D, Brunt TM · 2015 · Drug and Alcohol Dependence
  17. [17]
    moderate
    Purity, adulteration and price of drugs bought on-line versus off-line in the Netherlands
    van der Gouwe D, Brunt TM, van Laar M, van der Pol P · 2017 · Addiction
  18. [18]
    weak
    Haemorrhagic stroke related to the use of 4-fluoroamphetamine
    Wijers CHW, Visser MC, van Litsenburg RTH, Niesink RJM, Willemse RB, Croes EA · 2018 · Journal of Neurology
  19. [19]
    strong
    Para-Halogenation Affects Monoamine Transporter Inhibition Properties and Hepatocellular Toxicity of Amphetamines and Methcathinones
    Luethi D, Walter M, Zhou X, Rudin D, Krähenbuhl S, Liechti ME · 2019 · Frontiers in Pharmacology
  20. [20]
    moderate
    PubChem Compound Summary: 4-Fluoroamphetamine (CID 9986)
    PubChem · 2024
    linkno claims checked
  21. [21]
    strong
    Excretion of 4-fluoroamphetamine and three metabolites in urine after controlled oral ingestion
    Toennes 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
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    strong
    Novel Phenethylamines and Their Potential Interactions With Prescription Drugs: A Systematic Critical Review
    Inan F, Brunt TM, Contrucci RR, Hondebrink L, Franssen EJF · 2020 · Therapeutic Drug Monitoring
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    strong
    Pharmacokinetic properties of 4-fluoroamphetamine in serum and oral fluid after oral ingestion
    Toennes 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
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    strong
    Drug liking and wanting, not impulsive action or reflection is increased by 4-fluoroamphetamine
    Kuypers KPC, de Sousa Fernandes Perna EB, Dolder PC, Toennes SW, Theunissen EL, Mason NL, Hutten NRPW, Ramaekers JG · 2018 · Psychopharmacology
  25. [25]
    strong
    Differential 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. [26]
    strong
    Analysis of 4-fluoroamphetamine in cerumen after controlled oral application
    Meier SI, Petzel-Witt S, Schubert-Zsilavecz M, de Sousa Fernandes Perna EB, Theunissen EL, Ramaekers JG, Toennes SW · 2020 · Drug Testing and Analysis
  27. [27]
    moderate
    Prevalence and concentrations of new designer stimulants, synthetic opioids, benzodiazepines, and hallucinogens in postmortem hair samples: A 13-year retrospective study
    Niebel A, Westendorf L, Krumbiegel F, Hartwig S, Parr MK, Tsokos M · 2022 · Drug Testing and Analysis
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    Designer drugs: mechanism of action and adverse effects
    Luethi D, Liechti ME · 2020 · Archives of Toxicology
  29. [29]
    strong
    Para-Halogenation of Amphetamine and Methcathinone Increases the Mitochondrial Toxicity in Undifferentiated and Differentiated SH-SY5Y Cells
    Zhou X, Bouitbir J, Liechti ME, Krähenbuhl S, Mancuso RV · 2020 · International Journal of Molecular Sciences
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    strong
    Cardiotoxicity screening of illicit drugs and new psychoactive substances (NPS) in human iPSC-derived cardiomyocytes using microelectrode array (MEA) recordings
    Zwartsen A, de Korte T, Nacken P, de Lange DW, Westerink RHS, Hondebrink L · 2019 · Journal of Molecular and Cellular Cardiology
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    strong
    Neurotoxicity screening of (illicit) drugs using novel methods for analysis of microelectrode array (MEA) recordings
    Hondebrink L, Verboven AHA, Drega WS, Schmeink S, de Groot MWGDM, van Kleef RGDM, Wijnolts FMJ, de Groot A, Meulenbelt J, Westerink RHS · 2016 · Neurotoxicology
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    Monoamine Transporter and Receptor Interaction Profiles in Vitro Predict Reported Human Doses of Novel Psychoactive Stimulants and Psychedelics
    Luethi D, Liechti ME · 2018 · International Journal of Neuropsychopharmacology
04

Claim Verification

No claim verification has run for this version.

05

Coverage & Gaps

effect links
117 links · 114 approved · 44 audited3/117 with evidence basis
interactions
10 approved pairs0/10 graded