4-FA
4-fluoroamphetamine
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4-FA (4-fluoroamphetamine) is a synthetic stimulant and entactogen of the substituted Amphetamine class. It sits between amphetamine and MDMA, sharing properties of both but identical to neither. 4-FA is a triple monoamine releasing agent, producing its effects by flooding the brain with dopamine, norepinephrine, and serotonin simultaneously.[1][2][3]
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Synthesized no later than the 1940s as a pharmacological tool compound, 4-FA remained obscure for decades. It emerged on the Dutch research chemical market around 2007 and became one of the most popular new psychoactive substances in the Netherlands by 2016, marketed as "ecstasy light".[4] Following documentation of fatalities and cerebral hemorrhages,[5] it was progressively scheduled internationally — most recently as a US federal Schedule I substance in February 2026.[6]
Subjective effects include stimulant arousal, emotional warmth, enhanced sociability, mood elevation, mild visual distortion, and increased energy.[7] The experience blends amphetamine-like drive with a softer empathogenic glow — more sociable than speed, more clear-headed than MDMA — though cognitive empathy is paradoxically reduced despite elevated oxytocin.[8] Pronounced comedown, headache, bruxism, and next-day cognitive fatigue are characteristic unsought effects.
4-FA carries moderate psychological dependence potential and disproportionate cardiovascular toxicity — blood pressure elevation exceeds that of both MDMA and amphetamine.[9] The sole controlled study terminated its higher-dose arm for cardiovascular concerns;[10] clinical outcomes include stress cardiomyopathy,[11][12] hemorrhagic stroke, and fatalities, with six deaths from 4-FA combined with 25C-NBOMe.[13] All controlled human data derive from a single research program; oral bioavailability, half-life, and lethal dose remain uncharacterized.
History[edit]
Discovery
4-FA was synthesized no later than the 1940s as one of several halogenated amphetamine analogs created for pharmacological research.citation needed It served exclusively as a laboratory tool compound for decades, used to probe how structural modifications to the amphetamine backbone altered monoamine neurotransmission.citation needed The first detailed characterization of its monoamine-releasing properties in the context of abuse liability appeared in 2005.[2]
Market Emergence
4-FA appeared on the Dutch research chemical market around 2007 and, unlike most new psychoactive substances, sustained years of popularity — users positioned it as "ecstasy light," a stimulant perceived to combine the desirable features of Amphetamine and MDMA.[4] By 2016, 4-FA accounted for approximately 10% of all samples submitted to the Dutch Drug Information and Monitoring System,[14] with particular traction in festival and nightlife settings.[15] Purity data from Dutch online and offline markets confirmed 4-FA's position as an established commodity rather than a transient novelty.[16]
Safety Signals & Scheduling
Dutch harm reduction monitoring detected an escalating toxicological signal: increasing emergency presentations,[17] followed by a prospective cohort documenting fatalities, cerebral hemorrhages, and severe cardiovascular events directly attributable to 4-FA.[5] The Netherlands placed 4-FA on List I of the Opium Act in May 2017,[14] triggering a wave of international scheduling that culminated in US federal Schedule I placement effective February 2026.[6] All published controlled human data derive from a single research program at Maastricht University, where a planned 150 mg dose arm was terminated for cardiovascular safety concerns.[10]
The name "para-fluoroamphetamine" carries a historical ambiguity: early publications sometimes applied it to a compound with fluorine at the ethyl group rather than the phenyl ring, while the NPS sold as 4-FA is specifically the phenyl-ring-fluorinated isomer (1-(4-fluorophenyl)propan-2-amine).citation needed The "ecstasy light" label that defined 4-FA's market identity proved misleading on the safety axis — the experience may have felt gentler than MDMA, but the cardiovascular burden was objectively greater.[9]
Chemistry[edit]
Structural Class
4-Fluoroamphetamine belongs to the para-halogenated amphetamine series — compounds in which a halogen atom replaces hydrogen at the 4-position of the Amphetamine phenyl ring. The fluorine substitution is the mildest halogenation in the series, preserving much of amphetamine's stimulant character while introducing meaningful serotonergic activity.[18]
Other members include 4-chloroamphetamine (4-CA), 4-bromoamphetamine (4-BA), and 4-iodoamphetamine (4-IA), with serotonergic potency increasing in the rank order Cl > F > H.[18] Positional isomers within the fluorinated amphetamine family — 2-fluoroamphetamine (2-FA) and 3-fluoroamphetamine (3-FA) — differ substantially in pharmacological profile despite identical molecular formulas.
Molecular Properties
| Molecular formula | C₉H₁₂FN |
| Molecular weight | 153.20 g/mol |
The molecule consists of a phenyl ring bearing a fluorine atom at the 4-position, connected via a methylene bridge to an aminopropyl chain. The carbon–fluorine bond is among the strongest single bonds in organic chemistry, conferring metabolic stability at the substituted position — the compound resists enzymatic hydroxylation at that carbon, redirecting metabolism toward other sites on the ring and the side chain.[20]
Stereochemistry
4-FA contains one chirality center at the alpha-carbon of the propylamine chain, producing R- and S-enantiomers. Commercially available material is typically sold as the racemic mixture. The enantiospecific pharmacology has not been characterized — by analogy with Amphetamine, the S-(+)-enantiomer is expected to be more potent at catecholamine transporters, but this remains unconfirmed for 4-FA.citation needed
Physical Properties
4-FA is commonly encountered as a white crystalline powder, typically as the hydrochloride salt. No peer-reviewed data on melting point, solubility, or partition coefficient have been published.
Pharmacology[edit]
Mechanism of Action
4-FA functions as a triple monoamine releasing agent: it enters nerve terminals via the norepinephrine (NET), dopamine (DAT), and serotonin (SERT) transporters, displaces stored neurotransmitter, and reverses transporter directionality to flood the synaptic cleft with all three monoamines.[3]
The para-fluorine substitution shifts the balance between dopamine and serotonin release compared to unsubstituted amphetamine. 4-FA retains amphetamine-like potency at dopamine and norepinephrine transporters but gains meaningful serotonin-releasing activity[1][2] — enough to produce entactogenic effects, though considerably less than MDMA.[18]
Beyond transporter-mediated release, 4-FA binds the 5-HT₂A receptor,[3] consistent with the mild psychedelic features observed in controlled studies.[7] The compound may also inhibit monoamine oxidase to a degree, a property relevant to drug interaction risk.[21]
In animal models, para-substituted amphetamines with greater serotonin-releasing activity produce less stimulant-driven locomotion[1] — a serotonergic brake that explains why users describe 4-FA as less "wired" than amphetamine despite comparable dopamine release.
Pharmacokinetics
Controlled human data from oral doses of 100 mg and 150 mg show peak blood concentrations approximately 1–2 hours after ingestion,[22] consistent with the timing of peak subjective effects. Absolute bioavailability has not been formally determined but is presumed high based on the amphetamine class.
Two primary metabolic pathways were identified in human urine: beta-hydroxylation (producing a norephedrine structural analog) and ring hydroxylation (heavily conjugated via glucuronidation).[20] Parent 4-FA predominates in urine, with metabolites appearing at low concentrations. The specific liver enzymes involved have not been identified, though CYP2D6 involvement is plausible by analogy with Amphetamine.[21]
A formal half-life has not been published. Based on urinary excretion peaking at approximately 4 hours and total subjective duration of 5–8 hours, the half-life is estimated in the 5–8 hour range but remains unconfirmed. Some secondary sources report a "half-life" of approximately 5 days — this refers to tolerance half-life (the rate of functional tolerance decay), not pharmacokinetic elimination.
Neuroscience[edit]
Where It Acts
4-FA's stimulant effects originate in the mesolimbic pathway — the projection from the ventral tegmental area to the nucleus accumbens — where massive dopamine release drives the increased drug liking and wanting documented in controlled studies.[23] Concurrent norepinephrine release amplifies sympathetic activation, producing the sustained blood pressure and heart rate elevation that dominates the cardiovascular risk profile.[10]
The serotonergic component modulates this stimulant drive in two ways: it dampens motor activation (explaining why 4-FA feels less "speedy" than amphetamine despite comparable dopamine release[1]) and engages 5-HT₂A receptors to produce mild psychedelic features.[3][7]
Why It Matters
4-FA exemplifies how the dopamine-to-serotonin release ratio shapes both subjective experience and abuse potential. Compounds with greater serotonergic activity are less compulsively reinforcing in animal self-administration models[2] — 4-FA sits in the middle, more reinforcing than MDMA but potentially less so than pure dopaminergic stimulants.
The disproportionate cardiovascular toxicity[9] has a clear neurochemical basis: massive catecholamine release produces sustained sympathetic activation sufficient to cause stress cardiomyopathy[11][12] and, through severe blood pressure elevation, hemorrhagic stroke.[24]
Several fundamental questions remain unanswered. Whether 4-FA produces lasting serotonergic neurotoxicity at recreational doses is unknown — its close relative 4-chloroamphetamine is an established serotonin neurotoxin, but whether the milder fluorine structural analog carries similar risk has not been studied.
Subjective Effects[edit]
4-FA's experiential character is defined by the tension between its stimulant and entactogenic components — a balance that shifts substantially with set, setting, and social context. In high-energy environments (clubs, festivals), the stimulant dimension dominates: energy, arousal, and motor drive. In intimate social settings, empathogenic warmth and emotional openness become more prominent.[4] The dose-response curve shifts gradually from mild stimulation at lower doses toward a fuller empathogenic state with increasing amounts, without the sharp perceptual break seen in classical psychedelics.
Compared to MDMA, 4-FA is more stimulating, longer-lasting, and more cognitively clear — but it lacks the deep interpersonal attunement that defines the MDMA experience. Cognitive empathy is paradoxically reduced during intoxication despite elevated oxytocin,[8] producing a state that feels warm and sociable without the characteristic emotional merger of MDMA. The "ecstasy light" framing common among users captures the experiential quality but not the risk — the cardiovascular burden is objectively greater than either MDMA or amphetamine.[9]
Effect Grid
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.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Visual acuity enhancement · Visual processing acceleration · Color enhancement · Auditory enhancement · Sleep-transition hallucinations · Visual haze / noise · Tinnitus
Sleep-transition hallucinations · Visual haze / noise · Tinnitus
Wakefulness · Dry mouth · Insomnia · Dehydration sensation · Body high · Heart rate perception changes · Physical fatigue · Restlessness · Spontaneous body sensations · Headache · Muscle tension · Excessive sweating · Tactile euphoria · Bruxism · Dizziness · Nausea · Respiratory stimulation · Tingling / electric sensations · Sexual arousal enhancement · Motor control enhancement · Bodily lightness · Breathing alteration · Constipation · Laughter fits · Pain suppression · Vibrations / buzzing · Increased urination · Abnormal heartbeat · Sexual arousal suppression · Motor control impairment · Nystagmus (eye wobbles) · Trembling · Brain zaps · Vomiting · Seizure threshold reduction
Dehydration sensation · Body high · Heart rate perception changes · Physical fatigue · Restlessness · Spontaneous body sensations · Headache · Muscle tension · Excessive sweating · Tactile euphoria · Bruxism · Dizziness · Nausea · Respiratory stimulation · Tingling / electric sensations · Sexual arousal enhancement · Motor control enhancement · Bodily lightness · Breathing alteration · Constipation · Laughter fits · Pain suppression · Vibrations / buzzing · Increased urination · Sexual arousal suppression · Motor control impairment · Nystagmus (eye wobbles) · Trembling · Brain zaps · Vomiting · Seizure threshold reduction
Motivation enhancement · Aesthetic enhancement · Introspection enhancement · Openness enhancement · Pattern recognition enhancement · Novelty enhancement · Immersion enhancement · Motivation suppression · Information processing enhancement · Focus enhancement · Analysis enhancement · Cognitive dysphoria · Cognitive flexibility · Creativity enhancement · Multiple thought streams · Thought connectivity · Humor enhancement · Language enhancement · Thought organization · Thought disorganization · Memory enhancement · Cognitive impairment · Confusion · Focus suppression · Thought loops · Thought deceleration · Delirium
Openness enhancement · Pattern recognition enhancement · Novelty enhancement · Immersion enhancement · Motivation suppression · Information processing enhancement · Focus enhancement · Analysis enhancement · Cognitive dysphoria · Cognitive flexibility · Creativity enhancement · Multiple thought streams · Thought connectivity · Humor enhancement · Language enhancement · Thought organization · Thought disorganization · Memory enhancement · Cognitive impairment · Confusion · Focus suppression · Thought loops · Thought deceleration
Empathy enhancement · Anhedonia · Dysphoria · Irritability · Anxiety suppression · Catharsis · Emotional lability · Simultaneous emotions · Mania · Suicidal ideation
Irritability · Anxiety suppression · Catharsis · Emotional lability · Simultaneous emotions · Suicidal ideation
Trust enhancement · Disinhibition · Communication enhancement · Ego inflation · Flow state · Boundary dissolution
Flow state · Boundary dissolution
Timeline
First alerts appear 45–75 minutes after ingestion: a subtle shift in alertness, mild mood brightening, and faint physical warmth. Effects may be mistaken for anticipation at this stage.
Stimulant activation builds steadily over 30–75 minutes. Energy, sociability, and mood elevation increase noticeably. Heart rate and blood pressure begin rising.
Peak effects last approximately 2. 5–3. 5 hours.
Effects decline over 2–3 hours. Stimulant activation fades gradually, and the entactogenic warmth dissipates. Negative affect begins to emerge — irritability, low mood, and fatigue replace the positive subjective state.
A prolonged aftereffect period of 6–12 hours follows, characterized by headache, cognitive fatigue, negative mood, and sometimes "brain zaps. " Physical exhaustion and appetite changes are common. This is not a positive afterglow — it is a recovery phase dominated by monoamine depletion effects.
Safety[edit]
- Acute toxicity
- High
- Chronic toxicity
- Moderate
- Withdrawal
- Mild
- Tolerance buildup
- moderate
- Tolerance reset
- 10 days
- Physical
- Low
- Psychological
- Moderate
- Compulsive redosing
- Moderate
- Dose escalation
- Moderate
- Cross-tol.
- amphetamine · methamphetamine · MDMA
Toxicity
4-FA produces exaggerated cardiovascular effects compared to both MDMA and amphetamine. The 150 mg dose arm of the sole controlled human study was terminated for cardiovascular safety concerns.[10]
Heart & Circulation
In controlled settings (100 mg oral), blood pressure elevation persisted 4–5 hours and heart rate remained elevated beyond the blood pressure peak.[10] Emergency department data confirm that 4-FA produces more severe blood pressure elevation than both MDMA and amphetamine.[9]
Two cases of Takotsubo (stress) cardiomyopathy — one classic, one reverse-type — have been confirmed in 4-FA mono-intoxications in otherwise healthy individuals.[11][12] This is a dose-independent risk driven by the catecholamine surge. Additional documented cardiac outcomes include heart attack and acute heart failure.[5]
Stroke
A Dutch prospective cohort documented four patients with cerebral hemorrhage (one fatal),[5] and two additional hemorrhagic stroke cases were independently confirmed.[24] The mechanism is sustained severe blood pressure elevation rupturing cerebral blood vessels.[9]
Cellular Toxicity
In laboratory cell models, 4-FA depleted cellular energy stores and increased oxidative stress at high concentrations.[25] Similar effects were observed in liver cells.[18] Cardiac cell models showed decreased electrical activity and increased markers associated with abnormal heart rhythm risk at high concentrations.[26]
These concentrations likely exceed typical recreational blood levels but may be relevant at overdose. In brain cell models, 4-FA inhibited neuronal activity at concentrations far above pharmacologically active levels,[27] suggesting lower acute brain toxicity compared to some other new psychoactive substances.
Fatalities
Fatalities from 4-FA mono-intoxication have been documented in the Dutch cohort.[5] Six deaths over 9 months in Australia resulted from capsules containing premixed 4-FA and 25C-NBOMe[13] — neither substance alone at the measured concentrations explained death; the combined serotonergic and serotonin 2A receptor agonist activity produced fatal outcomes. No published LD₅₀ data exist.
Psychological Risks
Controlled studies document a pronounced comedown following 4-FA — low mood, irritability, headache, and cognitive fatigue in the hours and day after use.[10] Users commonly report "brain zaps" and impaired thinking the following day.[15]
No published case reports link 4-FA specifically to psychosis or persistent perceptual disturbances. Given the mild psychedelic state at standard doses,[7] triggering psychotic episodes in predisposed individuals is pharmacologically plausible but undocumented. Anxiety during peak effects, paranoid thoughts at high doses, and post-use depressive symptoms from monoamine depletion are expected from the pharmacological class.
Tolerance & Dependence
No 4-FA-specific tolerance study has been published. Cross-tolerance with other monoamine releasers (Amphetamine, MDMA) is expected via transporter downregulation and monoamine depletion.inferred
4-FA demonstrates moderate abuse potential: controlled studies found significant increases in drug liking and wanting,[23] and primates will self-administer the compound.[2] Physical dependence potential is low, consistent with the amphetamine class. Psychological dependence potential is moderate, driven by mesolimbic pathway activation.[23]
Drug Interactions
Serotonergic Combinations
The most clearly documented lethal combination involves 4-FA with other serotonergic agents. Six deaths from 4-FA combined with 25C-NBOMe confirmed that dual serotonergic stimulation — transporter-mediated release plus direct receptor activation — can be fatal at individually survivable concentrations.[13]
MAOIs are an absolute contraindication. 4-FA releases massive monoamine quantities; blocking the enzyme that breaks them down creates convergent risk of dangerously high blood pressure, overheating, and serotonin syndrome.[21]
SSRIs and SNRIs compete with 4-FA at the SERT. Combined use may reduce 4-FA's empathogenic effects or, depending on the regimen, increase serotonin syndrome risk.[21]
Tramadol blocks serotonin and norepinephrine reuptake and activates opioid receptors; combined with 4-FA's monoamine release, serotonin syndrome risk is substantially elevated.[21]
Cardiovascular Combinations
Stimulant medications (methylphenidate, amphetamine salts) produce additive effects — combined blood pressure elevation, rapid heart rate, and irregular heart rhythm risk.[21]
Metabolic Interactions
Antiretrovirals (particularly ritonavir and other CYP2D6 inhibitors) may slow 4-FA metabolism, producing elevated blood levels and intensified, prolonged effects.[21]
Uncharacterized Combinations
Interactions with cannabis, cocaine, GHB/GBL, and ketamine lack published data specific to 4-FA. Cannabis plus 4-FA carries additive rapid heart rate risk; cocaine plus 4-FA carries additive cardiovascular risk from combined catecholamine elevation.
Contraindications
Heart conditions and high blood pressure are absolute contraindications based on the documented severe and prolonged blood pressure elevation[10][9] and the occurrence of stress cardiomyopathy, heart attack, and hemorrhagic stroke in the clinical record.
Concurrent MAOI use is an absolute contraindication due to risk of dangerously high blood pressure and serotonin syndrome.[21]
Concurrent serotonergic drug use (SSRIs, SNRIs, tramadol, serotonergic psychedelics) is a relative-to-absolute contraindication depending on the agent, with documented fatality risk for the combination with 25C-NBOMe.[13]
Antiretroviral therapy involving CYP2D6 inhibitors carries pharmacokinetic risk of intensified 4-FA effects.[21]
Personal or family history of psychotic disorders is a relative contraindication based on class-level pharmacology.inferred
Harm Reduction[edit]
Forms & Identification
4-FA belongs to the fluorinated amphetamine family, where positional isomers (2-FA, 3-FA) have distinct pharmacological profiles but may produce similar reagent reactions. A positive result for "fluoroamphetamine" does not specify which isomer is present. Mass spectrometry-based drug checking services, where available, provide definitive identification.
Because 4-FA's cardiovascular toxicity is dose-dependent and the controlled study's 150 mg arm was terminated for safety,[10] accurate dosing is critical. Weigh doses with a milligram-precision scale rather than estimating by volume or appearance.
Guidelines
- Test the substance with reagent kits and, where possible, a drug checking service to confirm identity and rule out substitution
- Weigh doses with a milligram scale — do not estimate
- Start at the low end of the dose range; cardiovascular risk escalated sharply at 150 mg in the sole controlled study[10]
- Allow at least 2 hours before considering any redose — peak effects arrive 1–2 hours after ingestion[22]
- Stay hydrated but do not overhydrate — moderate, regular water intake
- Avoid strenuous physical exertion during peak effects to reduce cardiovascular strain
- Have a sober companion aware of the substance taken and its cardiovascular risk profile
Set & Setting
4-FA's experiential character shifts significantly with context.[4] In high-energy environments (clubs, festivals), the stimulant drive dominates, which can mask awareness of cardiovascular strain — elevated heart rate and blood pressure may go unnoticed during physical exertion.
Social settings bring out the empathogenic warmth. Choosing a low-exertion, temperature-controlled environment with access to water reduces the cardiovascular burden that represents 4-FA's primary danger.
Aftercare & integration. The comedown from 4-FA commonly includes low mood, headache, irritability, and cognitive fatigue lasting 12–24 hours.[10] "brain zaps" and difficulty concentrating the following day are frequently reported.[15]
Prioritize sleep — the stimulant effects may delay sleep onset even after subjective effects fade. Eat nutritious food, hydrate, and avoid additional stimulants (including caffeine) during the recovery window. Physical and cognitive performance may be impaired the day after use; plan accordingly. If low mood persists beyond 48–72 hours, this may indicate significant monoamine depletion and warrants attention.
Recovery & Support
4-FA's moderate psychological dependence potential means that patterns of escalating use can develop, particularly among people drawn to its combination of stimulant productivity and social warmth. If use has become regular — weekly or more frequent — tolerance will have reduced the desired effects while cardiovascular risk remains unchanged or increases.
Reducing frequency gradually is preferable to abrupt cessation, though physical withdrawal is minimal. If 4-FA use has become entangled with social or occupational functioning, professional support through a substance use counselor or peer support group can help establish alternative patterns.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: chest pain or tightness, severe headache with sudden onset, seizures, loss of consciousness, or body temperature hot to the touch through clothing. Given 4-FA's documented risk of stroke and heart complications, do not wait to see if these symptoms resolve.
Immediate steps:
- 1. Call emergency services immediately if any of the above signs appear
- 2. Keep the person still and calm — physical exertion worsens cardiovascular strain
- 3. Move to a cool environment if overheating
- 4. If unconscious but breathing, place in the recovery position (on their side, airway clear)
- 5. Do not induce vomiting
- 6. Do not restrain unless there is immediate danger of self-harm
What to tell the dispatcher: Name the substance (4-fluoroamphetamine / 4-FA), the estimated amount taken, the time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
No reversal agent exists for 4-FA. Treatment is supportive — managing blood pressure, temperature, and cardiac symptoms.
Legal Status[edit]
4-FA is controlled in most major jurisdictions as of 2026. The regulatory trajectory followed a common NPS pattern: initial uncontrolled status, progressive scheduling in individual European and Asian nations during 2007–2015, accelerated action following documentation of fatalities and hemorrhagic strokes in the Netherlands, and US federal scheduling in 2026. The WHO reviewed 4-FA under the Convention on Psychotropic Substances prior to US scheduling.[6]
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (Controlled Substances Act) | DEA Final Rule effective February 17, 2026; prior state-level scheduling in FL (2017), VA (2012), LA (2013), AZ (2014)[6] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled under phenethylamine analog provisions[14] |
| Netherlands | Opium Act List I | Scheduled May 25, 2017 following fatality and stroke cluster[5][14] |
| Canada | Schedule III (Food and Drugs Act) | Controlled as amphetamine analog[14] |
| Germany | Anlage I (BtMG) | Controlled since January 2012[14] |
| France | Annexe IV (narcotic list) | Controlled since January 2012[14] |
| China | Category I psychotropic | Controlled since September 2010; illegal to sell, buy, import, export, or manufacture[14] |
| Israel | Controlled substance | Controlled since December 2007[14] |
| Brazil | Lista F2 | Controlled since July 2015[14] |
| Australia | Schedule 9 (inferred) | Amphetamine analog under TGA Poisons Standard; direct confirmation pendingcitation needed |
| Belgium, Italy, Poland, Hungary, Serbia, Slovakia | Controlled | Various dates 2011–2013[14] |
Analog Act Considerations
Prior to February 2026, 4-FA was unscheduled at the US federal level. The Federal Analogue Act could theoretically have applied if 4-FA was marketed for human consumption as a structural analog of amphetamine, but no prosecuted cases under this provision were documented.[14] The DEA Final Rule placing 4-FA directly in Schedule I rendered this question moot.[6]
references
- [1] ^abcdBaumann MH, Clark RD, Woolverton WL, Wee S, Blough BE, Rothman RB (2011) In vivo effects of amphetamine analogs reveal evidence for serotonergic inhibition of mesolimbic dopamine transmission in the rat — Journal of Pharmacology and Experimental Therapeutics doi:10.1124/jpet.110.176271
- [2]
- [3] ^abcdRickli A, Hoener MC, Liechti ME (2015) Monoamine transporter and receptor interaction profiles of novel psychoactive substances: para-halogenated amphetamines and pyrovalerone cathinones — European Neuropsychopharmacology doi:10.1016/j.euroneuro.2014.12.012
- [4] ^abcdLinsen F, Koning RP, van Laar M, Niesink RJ, Koeter MW, Brunt TM (2015) 4-Fluoroamphetamine in the Netherlands: more than a one-night stand — Addiction doi:10.1111/add.12932
- [5] ^abcdefHondebrink L, Nugteren-van Lonkhuyzen JJ, Rietjens SJ, Brunt TM, Venhuis B, Soerdjbalie-Maikoe V, Smink BE, van Riel AJHP, de Vries I (2018) Fatalities, Cerebral Hemorrhage, and Severe Cardiovascular Toxicity After Exposure to the New Psychoactive Substance 4-Fluoroamphetamine: A Prospective Cohort Study — Annals of Emergency Medicine doi:10.1016/j.annemergmed.2017.07.482
- [6]