3-FA
3-fluoroamphetamine
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3-FA (3-fluoroamphetamine) — also known as PAL-353 — is a synthetic stimulant of the substituted amphetamine class. It is a fluorinated structural analog of amphetamine, distinguished by strong dopamine-norepinephrine selectivity over serotonin. 3-FA is a monoamine releasing agent, producing its effects by reversing catecholamine transporters to elevate synaptic dopamine and norepinephrine.[1][2]
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amphetamine, methamphetamine, cocaine +1 moreamphetamine, methamphetamine, cocaine, other dopaminergic stimulants show less
3-FA was synthesized at the National Institute on Drug Abuse as part of a systematic library of amphetamine analogs exploring treatments for cocaine use disorder.[1] In preclinical studies it reduced cocaine self-administration in primates,[3][4] but no clinical trials have been initiated. The compound appeared on European research chemical markets around 2009[5] and remains available through unregulated sources.
Subjective effects include wakefulness, cognitive stimulation, physical stimulation, appetite suppression, and motivation enhancement. The experience is purely stimulant — clean, task-oriented focus without the empathogenic warmth of serotonin-releasing agents, placing it closer to prescription amphetamine than to MDMA in character. Compulsive redosing, anxiety, and a pronounced post-use crash of fatigue and low mood are common unsought effects.
3-FA carries significant abuse liability — preclinical data rate its abuse potential comparable to methamphetamine[6] — and its toxic dose in humans is unknown. Cardiovascular strain from potent norepinephrine release is the primary acute risk, compounding with dose escalation as tolerance develops to desired effects but not to cardiac load. The evidence base is almost entirely preclinical — no human pharmacokinetic, metabolic, or clinical safety data have been published.
History[edit]
Discovery
3-FA was synthesized as part of the PAL (Phenylethylamine/amphetamine Library) series at the National Institute on Drug Abuse, led by researchers Richard B. Rothman, Bruce E. Blough, and Michael H. Baumann. The library systematically varied ring substituents on the amphetamine scaffold to map how substitution position controls monoamine releasing selectivity. PAL-353 — the 353rd entry in the series — was first pharmacologically characterized in 2005, when Wee et al. established its in vitro potency profile and evaluated self-administration in rhesus monkeys.[1]
Preclinical therapeutic research
The compound was investigated as a candidate medication for cocaine use disorder. Its preclinical case rested on three findings: it reduced cocaine self-administration in primates under choice paradigms,[3][4][7] it fully substituted for cocaine in drug discrimination assays,[3] and its physicochemical properties supported transdermal delivery — a route that could sustain plasma levels while limiting abuse potential.[8][9] Despite favorable preclinical data, no clinical trials have been registered as of May 2026.
Research chemical market
3-FA appeared on European research chemical markets around January 2009, first notified to the European Early Warning System by Belgian authorities.[5] It followed the earlier establishment of 4-fluoroamphetamine on the European market and is typically distributed as a white crystalline powder in hydrochloride salt form.
The PAL-353 designation reflects the compound's origin as a numbered entry in a systematic research library rather than a substance developed for human consumption. Unlike 4-FA, which gained a distinct recreational identity in Dutch nightlife culture, 3-FA occupies a quieter niche — valued by a small community of research chemical users for functional stimulation rather than recreation. Its reputation as the more utilitarian fluoroamphetamine is consistent with its pharmacology: dopamine without serotonin produces drive without warmth.
Chemistry[edit]
Structural class
3-FA is a ring-fluorinated analog of amphetamine, bearing a fluorine atom at the meta (3-) position of the phenyl ring. The parent scaffold is phenethylamine, with the alpha-methyl group that defines the amphetamine subclass. Three positional isomers of fluoroamphetamine exist: 2-FA (ortho), 3-FA (meta), and 4-FA (para). The position of the fluorine atom determines monoamine releasing selectivity — meta substitution confers the highest dopamine-over-serotonin selectivity in the series.[2]
The systematic name is 1-(3-fluorophenyl)propan-2-amine.
Molecular properties
| Molecular formula | C₉H₁₂FN |
| Molecular weight | 153.20 g/mol |
The molecule consists of a phenyl ring with a fluorine substituent at the 3-position, connected via a methylene bridge to an alpha-methyl aminopropyl chain. Fluorine is a small, highly electronegative atom that modifies the electronic character of the aromatic ring without substantially increasing molecular volume relative to unsubstituted amphetamine.
Stereochemistry
3-FA has a chirality center at the alpha-carbon and exists as two enantiomers: R-(−) and S-(+). The compound is typically encountered as the racemic mixture. Enantioseparation has been demonstrated using sulfated β-cyclodextrin HPLC and GC-MS derivatization methods.[10] No data on the differential activity of individual enantiomers have been published.
By class analogy with amphetamine, the S-(+) enantiomer is expected to be more potent at releasing dopamine, but this remains unconfirmed for 3-FA.inferred
Physical properties
No published melting point, solubility, or crystallographic data exist. The free base is highly lipophilic — approximately 70% of drug permeated through human epidermis in vitro,[9] indicating strong passive transdermal penetration. On the research chemical market, 3-FA is encountered as a white crystalline powder in hydrochloride salt form.
Pharmacology[edit]
Mechanism of action
3-FA enters neurons through monoamine transporters and reverses their function, driving dopamine, norepinephrine, and serotonin out of presynaptic terminals and into the synapse — the same fundamental mechanism as amphetamine.[1][2]
The defining feature of 3-FA is its pronounced selectivity for catecholamine release over serotonin release. It releases norepinephrine and dopamine at concentrations roughly 80–120 times lower than those required to release serotonin.[1][2] This makes it pharmacologically closer to d-amphetamine than to entactogenic agents like MDMA, which preferentially releases serotonin.
Amphetamine-class compounds also activate TAAR1 (TAAR1), which partially self-limits stimulant effects.[11][12] No substance-specific TAAR1 data exist for 3-FA, but activation is inferred from structural class membership.inferred
In vivo effects
Rat microdialysis confirmed the in vitro profile: 3-FA produced the greatest dopamine elevation (5–14-fold above baseline) and the lowest serotonin elevation of four tested fluorinated amphetamine analogs, along with the strongest forward locomotion.[2] In squirrel monkeys, it increased nucleus accumbens dopamine and produced behavioral stimulation where more serotonergic analogs did not.[13]
In mice and rats, 3-FA produces locomotor stimulation comparable to methamphetamine and fully substitutes for methamphetamine in drug discrimination tests.[6] It also suppresses food intake at a rate similar to amphetamine.[14]
Pharmacokinetics
No human pharmacokinetic data exist for 3-FA. In rats receiving an intravenous dose of 5 mg/kg, the plasma half-life was approximately 2.3 hours.[8]
Transdermal delivery has been investigated as a potential clinical route. A 10% gel formulation achieved approximately 70% permeation through human epidermis in vitro, and iontophoresis enhanced permeation 548-fold over passive diffusion.[8][9]
Metabolism
No published data on 3-FA metabolism exist in any species. By analogy with 4-fluoroamphetamine, fluoroamphetamines are expected to undergo beta-hydroxylation and aromatic ring hydroxylation followed by conjugation.[15] The specific enzymes involved have not been identified for 3-FA.inferred
Neuroscience[edit]
Where it acts
3-FA's primary neural target is the mesolimbic pathway — the projection from the ventral tegmental area to the nucleus accumbens that assigns motivational value to stimuli. Rat microdialysis shows 3-FA elevates nucleus accumbens dopamine 5–14-fold above baseline, the greatest elevation among tested fluorinated amphetamine analogs.[2][13] This massive dopamine surge underlies the wakefulness, goal-directed motivation, and reinforcing properties of the compound.
Potent norepinephrine release simultaneously activates the peripheral sympathetic nervous system — producing the elevated heart rate, blood pressure, and alertness that accompany the subjective stimulation — and is expected to enhance prefrontal cortical function at moderate doses via an inverted-U dose-response curve characteristic of catecholaminergic stimulants.inferred
Why it matters
Robinson and Berridge's incentive salience framework distinguishes wanting (dopamine-mediated motivational drive) from liking (hedonic pleasure mediated by opioid and GABAergic circuits). 3-FA, as a potent dopamine releaser with minimal serotonergic activity, strongly amplifies wanting — the urgent drive to pursue rewards — more than hedonic satisfaction. This explains the compulsive redosing and task-focused stimulation reported with dopamine-selective stimulants: the experience is defined by motivation rather than pleasure.
Repeated use produces opposing neuroadaptations — sensitization of motivational circuits alongside tolerance through downregulation — contributing to escalating use patterns and a withdrawal state marked by anhedonia and fatigue.inferred
Several critical questions remain unanswered. Whether 3-FA shares the dopaminergic neurotoxicity of methamphetamine — damage to dopamine terminals via oxidative stress — is entirely unknown, with no neurotoxicity studies conducted despite comparable dopamine-releasing potency.safety citation needed
Subjective Effects[edit]
3-FA produces an experience defined by clean dopaminergic stimulation — focused wakefulness, heightened motivation, and appetite suppression without empathogenic warmth or perceptual alteration. The qualitative character remains consistent across the dose range, with intensity scaling linearly rather than introducing new experiential dimensions at higher doses. Set and setting shape the cognitive direction: task-oriented environments channel stimulation toward productivity, while social contexts may amplify sociability without the emotional openness characteristic of serotonin-releasing compounds.
In comparative terms, 3-FA sits closest to d-amphetamine — a purely functional stimulant. Community reports consistently describe it as less recreational and more utilitarian than its para-substituted isomer 4-FA, consistent with its dramatically lower serotonergic potency. Where 4-FA offers a hybrid stimulant-entactogen experience, 3-FA delivers drive without euphoric warmth.
Effect Grid
Clear stimulant effects with pronounced wakefulness, cognitive euphoria, focus enhancement, and motivation enhancement. Thought acceleration is noticeable — mental processing feels faster and more directed. Appetite suppression becomes significant, often eliminating hunger awareness entirely during the peak period. This is the typical functional and recreational dose range.
Physical stimulation is evident: elevated heart rate, possible bruxism, and mild excessive sweating. Body high is present but secondary to cognitive effects. The experience is characterized more by driven motivation than by hedonic pleasure — consistent with 3-FA's dopamine-selective, non-entactogenic profile.
Peak effects last approximately 2–3 hours, with a total subjective duration of 4–6 hours. Insomnia is likely if taken within 6 hours of intended sleep.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Dry mouth · Insomnia · Pupil dilation · Restlessness · Physical fatigue · Muscle tension · Excessive sweating · Heart rate perception changes · Tingling / electric sensations · Dehydration sensation · Tactile euphoria · Bodily lightness · Body high · Constipation · Headache · Nausea · Sexual arousal enhancement · Trembling · Bruxism · Motor control enhancement · Spontaneous body sensations · Vibrations / buzzing · Abnormal heartbeat
Restlessness · Physical fatigue · Muscle tension · Excessive sweating · Heart rate perception changes · Tingling / electric sensations · Dehydration sensation · Tactile euphoria · Bodily lightness · Body high · Constipation · Headache · Nausea · Sexual arousal enhancement · Trembling · Bruxism · Motor control enhancement · Spontaneous body sensations · Vibrations / buzzing
Motivation enhancement · Analysis enhancement · Information processing enhancement · Motivation suppression · Aesthetic enhancement · Cognitive flexibility · Immersion enhancement · Thought organization · Language enhancement · Memory enhancement · Creativity enhancement · Thought deceleration
Aesthetic enhancement · Cognitive flexibility · Immersion enhancement · Thought organization · Language enhancement · Memory enhancement · Creativity enhancement · Thought deceleration
Irritability · Anhedonia · Emotional enhancement · Anxiety suppression
Social connection · Flow state
Timeline
Gradual awareness of increased alertness and mild appetite changes. Effects emerge subtly — a slight sharpening of attention without a distinct perceptual shift.
Building stimulation with focus sharpening and mood elevation beginning. Heart rate increases noticeably. Wakefulness intensifies and appetite suppression becomes evident.
Full stimulant effects — pronounced wakefulness, cognitive euphoria, focus enhancement, appetite suppression, and physical stimulation. Motivation and thought acceleration are at maximum intensity. Bruxism and sweating may be present at higher doses.
Gradual decline in stimulation with onset of fatigue. Irritability and restlessness may emerge as catecholamine levels fall. Focus and motivation begin to wane.
Residual wakefulness or insomnia, mild physical fatigue, and possible depressed mood. Appetite gradually returns. Cognitive fatigue and motivation suppression may persist for several hours.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Moderate
- Withdrawal
- Moderate
- Tolerance buildup
- moderate
- Tolerance reset
- 5.5 days
- Physical
- Moderate
- Psychological
- High
- Compulsive redosing
- High
- Dose escalation
- Moderate
- Cross-tol.
- amphetamine · methamphetamine · cocaine
Toxicity
Acute toxicity
No lethal dose has been established for 3-FA in any species, and no human overdose reports or postmortem cases have been published.safety citation needed Acute toxicity from amphetamine-type releasing agents produces a characteristic pattern: dangerous body temperature elevation, rapid heart rate, high blood pressure, agitation, sweating, dilated pupils, and seizure risk.[16] Body temperature elevation is the single greatest predictor of death in stimulant overdose.
First-line management centers on benzodiazepines for agitation and seizure prevention, active cooling for temperature elevation, and avoidance of beta-blockers (which risk dangerous vasoconstriction). Antipsychotics carry seizure and heart rhythm risks and are not preferred.[17]
Cardiovascular effects
3-FA's potent norepinephrine release drives rapid heart rate, elevated blood pressure, and increased cardiac workload. Heart rhythm disturbances are possible at high doses.[16] Fluorinated amphetamine analogs as a class have been associated with heart failure, brain hemorrhage, and death,[6] though these events have been documented primarily for 4-FA — including fatalities involving 4-FA in combination with other substances.[18]
No cardiovascular adverse events have been specifically attributed to 3-FA in published literature.safety citation needed
Neurotoxicity
Methamphetamine damages dopamine-producing nerve terminals through oxidative stress. Whether 3-FA shares this liability is unknown — no neurotoxicity studies have been conducted. Given comparable dopamine-releasing potency, the possibility cannot be excluded.safety citation needed
Psychological risks
No published data on psychological adverse effects of 3-FA in humans exist. By mechanism and class:
- Stimulant psychosis: Extended high-dose use of dopamine-releasing stimulants produces paranoid delusions, auditory hallucinations, and thought disorganization. Risk increases with dose, duration, and sleep deprivation. 3-FA's potent dopamine release places it in the same risk category as amphetamine and methamphetamine.inferred
- Anxiety and paranoia: Elevated catecholamine levels produce acute anxiety, agitation, and paranoia, particularly at higher doses or during extended use.
- Compulsive redosing: The dopamine-selective profile and absence of serotonergic self-limitation make 3-FA prone to compulsive redosing — a well-documented pattern with dopamine-selective stimulants.
- Post-use crash: Catecholamine depletion produces depressed mood, anhedonia, fatigue, and irritability. Severity scales with dose and duration of use.
Tolerance & dependence
No substance-specific tolerance or dependence studies have been published for 3-FA.
Tolerance develops as the brain downregulates dopamine receptors and upregulates transporters in response to repeated supraphysiological stimulation, requiring higher doses for the same effect. Cross-tolerance with other dopaminergic stimulants (amphetamine, methamphetamine, cocaine) is expected.inferred
Dependence liability is confirmed by preclinical data. Rhesus monkeys self-administer 3-FA at rates comparable to other dopamine-selective amphetamine analogs.[1] The compound lacks the serotonergic brake that reduces reinforcing efficacy in MDMA-like compounds — elevated serotonin attenuates dopaminergic reinforcement, and this mechanism is absent in 3-FA.[1] Its abuse potential has been assessed as comparable to methamphetamine.[6]
Physical withdrawal has not been characterized but is anticipated at moderate levels. Amphetamine withdrawal produces fatigue, excessive sleep, appetite enhancement, and depressed mood but is not life-threatening.inferred
Drug interactions
Combination of 3-FA with any monoamine oxidase inhibitor (MAOI) is potentially lethal. Monoamine oxidase inhibitors block the breakdown of dopamine, norepinephrine, and serotonin inside neurons; co-administration with a monoamine releasing agent causes massive accumulation of these neurotransmitters, producing dangerously high blood pressure and body temperature.[19] This applies to irreversible MAOIs (phenelzine, tranylcypromine), reversible MAO-A inhibitors (moclobemide), and selegiline at higher doses.
Tramadol: tramadol inhibits serotonin reuptake and lowers the seizure threshold. Combined with a monoamine releaser — even one with low serotonergic potency — serotonin syndrome risk exists, compounded by seizure risk. This combination is classified as potentially lethal.safety citation needed
Other stimulants: Combining 3-FA with cocaine, other amphetamines, or sympathomimetic agents produces additive cardiovascular stress — rapid heart rate, high blood pressure, blood vessel constriction, and heart rhythm disturbance risk increase multiplicatively. PCP compounds these risks with additional brain excitotoxicity, temperature elevation, and psychosis risk.safety citation needed
CNS depressants: alcohol and GHB/GBL may mask subjective signs of stimulant intoxication without reducing cardiovascular risk, creating a dangerous gap between how a person feels and how their body is actually responding.
Caffeine: Mild additional cardiovascular stimulation at typical doses. Generally low-risk but may worsen rapid heart rate and anxiety in sensitive individuals.
Contraindications
No substance-specific contraindication data exist. The following are derived from 3-FA's mechanism as a potent catecholamine-releasing agent.inferred
- Heart conditions (absolute): Pre-existing cardiac disease — including coronary artery disease, cardiomyopathy, irregular heart rhythms, and structural heart defects — is an absolute contraindication. The combination of rapid heart rate, elevated blood pressure, and increased heart oxygen demand can trigger acute cardiac events.
- High blood pressure (absolute): Catecholamine release produces acute blood pressure spikes that compound pre-existing hypertension, increasing stroke and aortic dissection risk.
- Concurrent MAOI use (absolute): Potentially lethal via dangerously high blood pressure, as detailed above.
- Seizure disorders (relative): Stimulant-induced sympathetic activation lowers the seizure threshold.
- Overactive thyroid (relative): Excess thyroid hormone amplifies sensitivity to catecholamines; 3-FA compounds this effect.
- Pregnancy (absolute): Catecholamine-releasing agents constrict uterine blood vessels and cause fetal rapid heart rate. No reproductive toxicity data exist for 3-FA.inferred
- Psychotic disorders (relative): Dopaminergic stimulation can trigger or worsen psychotic episodes in individuals with schizophrenia spectrum disorders or a history of stimulant-induced psychosis.
Harm Reduction[edit]
Forms & Identification
The structured data module above displays reagent test results, physical forms, and common substitution risks for 3-FA. Because 3-FA is distributed exclusively through unregulated research chemical channels, batch composition and purity are unverified by default. Reagent testing confirms the presence of an amphetamine-class compound but cannot distinguish between positional isomers (2-FA, 3-FA, 4-FA) — this matters because the isomers differ substantially in pharmacological profile and risk. Where possible, confirm identity with an analytical testing service that provides quantitative results.
Guidelines
- Weigh doses with a milligram-precision analytical scale — never estimate by eye.
- Reagent test every batch before use. A Marquis test will confirm an amphetamine-class compound but cannot distinguish positional isomers.
- Start with the lowest reported active dose and wait at least 90 minutes before considering redosing — oral onset is gradual and premature redosing is a common path to overdose.
- Set a firm redosing limit before the session begins. 3-FA's dopaminergic profile promotes compulsive redosing — decisions made while stimulated are unreliable.
- Stay hydrated but do not overdrink — stimulants suppress thirst cues, but forced water intake can cause electrolyte imbalance.
- Eat a balanced meal before use. Appetite suppression will persist throughout the experience and into the following day.
- Plan for the comedown: have sleep aids (melatonin, magnesium), nutritious food, and a low-demand schedule for the day after.
Set & Setting
3-FA's dopaminergic profile produces sustained, task-oriented stimulation without euphoric warmth. A structured environment with clear activities channels the stimulation productively; unstructured settings risk restless agitation. Avoid use during periods of sleep deprivation — stimulant psychosis risk scales directly with time without sleep. Ensure access to water, food, and a calm space to rest during the comedown.
Aftercare & integration. The stimulant comedown following 3-FA use typically involves fatigue, low mood, irritability, and difficulty concentrating. These effects reflect temporary catecholamine depletion and generally resolve within 24–72 hours.
Recovery priorities: Sleep is the single most important recovery tool — use melatonin or magnesium if needed, avoid further stimulant use (including excess caffeine), and allow the body to rest. Eat nutrient-dense meals even if appetite remains suppressed. Gentle physical activity (walking, stretching) can help restore normal mood more quickly than sedentary recovery.
If depressed mood, anhedonia, or fatigue persist beyond one week, or if you notice escalating use patterns between sessions, seek professional support.
Recovery & Support
Stimulant use disorders develop gradually — the transition from occasional use to compulsive redosing often occurs before the person recognizes a pattern. Warning signs include using more frequently or at higher doses than intended, neglecting responsibilities during or after use, and continuing despite negative consequences.
Evidence-based treatments for stimulant use disorders include cognitive behavioral therapy, contingency management, and motivational interviewing. No approved pharmacological treatment exists specifically for amphetamine-type stimulant dependence, but clinical support significantly improves outcomes. SAMHSA's National Helpline (1-800-662-4357) provides free, confidential treatment referrals. SMART Recovery and mutual aid groups offer peer-based support.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Uncomfortable stimulation (jitteriness, mild anxiety, fast heart rate) is distinct from a medical emergency. Seek immediate help for: chest pain or pressure, seizure activity, loss of consciousness, body temperature so high it can be felt through clothing, severe confusion or paranoid psychosis, or inability to stop repetitive movements.
Immediate steps:
- 1. Call emergency services immediately if any of the above signs are present.
- 2. Move the person to a cool, quiet environment.
- 3. Remove excess clothing and apply cool water to the skin if overheating.
- 4. Do not restrain the person unless they are in immediate danger of harming themselves or others.
- 5. Place an unconscious person in the recovery position (on their side, airway clear).
- 6. Do not induce vomiting.
What to tell the dispatcher: Name the substance (3-FA / 3-fluoroamphetamine), approximate amount taken, time of ingestion, and current symptoms. Many jurisdictions have Good Samaritan laws that protect people who call for help during a drug emergency.
No specific reversal agent exists for amphetamine-type stimulant overdose. Hospital treatment focuses on sedation with benzodiazepines, active cooling, and cardiovascular monitoring.
Legal Status[edit]
3-FA occupies an ambiguous legal position in most jurisdictions. It is not listed under any United Nations convention schedule and has not been assessed by the WHO Expert Committee on Drug Dependence as of May 2026. Several countries control it through amphetamine structural analog provisions or novel psychoactive substance legislation.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled under the amphetamine analogue clause; maximum penalties equivalent to amphetamine[5] |
| Germany | NpSG (Neue-psychoaktive-Stoffe-Gesetz) | Controlled since November 26, 2016. Production, import for market placement, and trade are punishable; possession is prohibited but not separately penalized under NpSG[5] |
| United States | Not specifically scheduled | No permanent or emergency DEA scheduling as of May 2026. May be prosecuted as a controlled substance analogue under the Federal Analogue Act based on structural and pharmacological similarity to amphetamine; enforcement is case-dependentsafety citation needed |
| Canada | Likely Schedule III (CDSA) | Amphetamine analogues are controlled under Schedule III of the Controlled Drugs and Substances Act; 3-FA would likely fall under this provision, though no specific scheduling decision has been publicly confirmedcitation needed |
| Australia | Status unconfirmed | Amphetamine is listed in the SUSMP; analogues may fall under this provision depending on TGA interpretationcitation needed |
| New Zealand | Schedule 3 controlled substance | Classified as an amphetamine analoguecitation needed |
Analogue act considerations
3-FA's structural relationship to amphetamine — differing only by a fluorine atom at the meta ring position — and its pharmacological similarity (potent dopamine/norepinephrine releaser with methamphetamine-comparable behavioral effects[6]) make it a strong candidate for prosecution under analogue provisions. The United States Federal Analogue Act requires that a substance be substantially similar in both chemical structure and pharmacological effect to a Schedule I or II controlled substance — criteria 3-FA plausibly meets.
However, analogue act prosecutions require case-by-case determination and are not equivalent to explicit scheduling.
references
- [1]
- [2]
- [3] ^abcNegus SS, Mello NK, Blough BE, Baumann MH, Rothman RB (2007) Monoamine releasers with varying selectivity for dopamine/norepinephrine versus serotonin release as candidate agonist medications for cocaine dependence — The Journal of Pharmacology and Experimental Therapeutics PMID:17071819
- [4] ^abBanks ML, Blough BE, Negus SS (2011) Effects of monoamine releasers with varying selectivity for releasing dopamine/norepinephrine versus serotonin on choice between cocaine and food in rhesus monkeys — Behavioural Pharmacology doi:10.1097/fbp.0b013e32834d63ac
- [5]
- [6]