3-FPM
2-(3-fluorophenyl)-3-methylmorpholine
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3-FPM (3-fluorophenmetrazine) is a synthetic stimulant of the phenylmorpholine class. It is a fluorinated structural analog of phenmetrazine, the appetite suppressant withdrawn from clinical use in the 1980s. 3-FPM is a monoamine releasing agent, producing its effects by forcing dopamine and norepinephrine out of nerve terminals.[1]
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amphetamine, methamphetamine, phenmetrazine +2 moreamphetamine, methamphetamine, phenmetrazine, cocaine, methylphenidate show less
Disclosed in a 2011 patent exploring phenylmorpholine compounds for obesity and addiction treatment,[2] 3-FPM never entered clinical development. It appeared on the recreational new psychoactive substance market in 2014, sold as a research chemical through online vendors. Several European countries have since scheduled it, though it remains uncontrolled at the federal level in the United States.[3]
Subjective effects include euphoria, psychomotor stimulation, increased energy, and enhanced focus.[3] The experience is a moderate, functional stimulation — closer to low-dose amphetamine than to the empathogenic warmth of serotonergic compounds, with oral use producing a gradual build and insufflation a sharper rush. Compulsive redosing, anxiety, and post-use low mood are common unsought effects.
No physical dependence data exist, but 3-FPM's DAT potency — comparable to cocaine — suggests meaningful psychological dependence risk.[1] Cardiovascular toxicity is the primary acute danger: rapid heart rate occurs in nearly half of clinical presentations, and one intravenous case resulted in bilateral limb amputation.[4] The evidence base is extremely thin — one pharmacology study, one single-person pharmacokinetic experiment,[5] and a handful of poisoning case reports constitute the entirety of published data.
History[edit]
Discovery
3-FPM was first described in a 2011 patent filed by Blough and colleagues, covering a series of phenylmorpholine analogs as potential therapeutics for obesity and dependence.[2] No compound in the series advanced to clinical trials. The substance was independently synthesized and analytically confirmed in academic literature by McLaughlin and colleagues after its appearance on the research chemical market — five samples purchased from UK internet vendors all proved authentic.[6]
Parent compound and market emergence
3-FPM derives from phenmetrazine (marketed as Preludin), a catecholamine-releasing stimulant prescribed for weight management in the 1950s and withdrawn following recognition of its abuse potential and cardiovascular risks.[7] Phendimetrazine, a Schedule III prodrug that converts to phenmetrazine in the liver, remains clinically available.[8] 3-FPM first appeared on recreational markets in 2014, detected in Hungary, Sweden, and the United Kingdom,[5][9] sold as a white crystalline powder through online research chemical vendors.
Scheduling and surveillance
Sweden became the first country to control 3-FPM, scheduling it as a narcotic substance on 1 June 2015. The United Kingdom followed under the Psychoactive Substances Act 2016, and Germany under the Neue-psychoaktive-Stoffe-Gesetz later that year. At its 43rd session in 2020, the WHO Expert Committee on Drug Dependence placed 3-FPM under surveillance but did not recommend international scheduling.[3]
The name "3-FPM" follows research chemical convention: the number indicates the fluorine position on the phenyl ring, "F" for fluorine, and "PM" for phenmetrazine. Its laboratory designation PAL-593 derives from the original patent series. 3-FPM's commercial success on the NPS market catalyzed development of further phenmetrazine analogs, including 4-methylphenmetrazine (4-MPM) and 3-methylphenmetrazine (3-MPM).[10]
Chemistry[edit]
Structural class
3-Fluorophenmetrazine belongs to the phenylmorpholine family, sharing the 3-methylmorpholine scaffold with its parent compound phenmetrazine. The core structure is a morpholine ring — a six-membered ring containing one nitrogen and one oxygen — bearing a methyl group at position 3 and a phenyl ring at position 2. 3-FPM is distinguished from phenmetrazine by a single fluorine atom at the meta (3') position of the phenyl ring.
Three positional isomers exist: 2-FPM (ortho-fluorine), 3-FPM (meta-fluorine), and 4-FPM (para-fluorine). All three display catecholamine-selective releasing activity, though they differ in transporter potency.[1] The isomers are distinguishable by standard analytical methods including NMR, mass spectrometry, and chromatography.[6]
Molecular properties
| Molecular formula | C₁₁H₁₄FNO |
| Molecular weight | 195.23 g/mol |
The morpholine ring carries a phenyl substituent at C-2 and a methyl group at C-3. The fluorine atom sits at the meta position of the aryl ring. The free base has a predicted pKa of approximately 8.4.[11]
Stereochemistry
3-FPM possesses two chirality centers at C-2 and C-3 of the morpholine ring, producing four possible stereoisomers (two pairs of enantiomers). No published study has determined which stereoisomer(s) predominate in commercially available material or which carry the greatest pharmacological activity. Commercial 3-FPM is presumed racemic mixture.citation needed
The gap is significant: phenmetrazine's activity is stereoselective, and the same is expected for 3-FPM. Until stereoselective pharmacology data are published, the contribution of individual isomers to the racemic mixture's effects remains unknown.
Physical properties
3-FPM free base is a white crystalline powder. Available physical data derive from computational prediction and commercial sources rather than peer-reviewed studies:
| Melting point | ~165–170 °C (commercial source; not peer-reviewed)[11] |
| Solubility | Water, ethanol, DMSO |
No peer-reviewed melting point, boiling point, or solubility data have been published. Stability and degradation pathways under storage conditions have not been characterized.
Pharmacology[edit]
Mechanism of action
3-FPM is a substrate-type monoamine releasing agent acting at the DAT (DAT) and NET (NET).[6][1] Like amphetamine and its parent compound phenmetrazine, it enters nerve terminals through these transporters and forces stored dopamine and norepinephrine out into the synapse — a mechanism distinct from simple reuptake inhibitor.
Activity at both the dopamine and norepinephrine transporters is potent (comparable to cocaine), while SERT activity is negligible.[1] Each fluorinated phenmetrazine isomer (2-FPM, 3-FPM, 4-FPM) evokes concentration-dependent monoamine release, confirming true releasing activity rather than uptake blockade alone.[1]
This catecholamine-selective profile (DAT/NET with negligible SERT) distinguishes 3-FPM sharply from serotonergic releasers such as MDMA. The Mayer et al. study represented the first published pharmacological characterization of 3-FPM.[1] No in vivo pharmacodynamic data exist beyond a single pharmacokinetic self-experiment.[5]
Pharmacokinetics
The only published human pharmacokinetic data come from a single-person self-experiment using one oral dose.[5] Peak blood concentration occurred at 2.5 hours, with an half-life of approximately 8.8 hours. The large volume of distribution (5.3 L/kg) indicates extensive penetration into body tissues, meaning the drug distributes widely beyond the bloodstream.
3-FPM remained detectable in blood for up to 82 hours, in urine for up to 116 hours, and in oral fluid for up to 55 hours.[5] These values derive from a single participant; route, dose, and individual metabolism substantially affect pharmacokinetic parameters.
Metabolism
Mardal et al. characterized 3-FPM metabolism using rat and human urine samples and in vitro liver enzyme studies.[12] The primary metabolic pathway is N-oxidation, producing the N-oxide as the main urinary metabolite. Additional routes include hydroxylation of the aromatic ring, alkyl hydroxylation, and oxidative ring opening. Phase II metabolism involves glucuronidation and sulfation.
The parent compound is excreted largely unchanged alongside its N-oxide. An oxidative ring-opening product — 2-amino-1-(3-fluorophenyl)propan-1-ol — showed the longest detection window across all sample types and may serve as the optimal forensic marker.[5] The specific liver enzymes responsible for 3-FPM's breakdown have not been fully identified,[12] limiting predictions about individual variation and interaction risk with drugs that affect those enzymes.
Neuroscience[edit]
Where it acts
3-FPM's dopamine release targets the mesolimbic mesolimbic pathway — the projection from the ventral tegmental area to the nucleus accumbens — producing the euphoric and motivational effects reported in clinical surveillance.[3] Norepinephrine release in the prefrontal cortex underlies the cognitive stimulation (focus enhancement, thought acceleration), while peripheral norepinephrine drives the cardiovascular activation seen in 47% of clinical presentations.[9]
Why it matters
The incentive salience framework distinguishes "wanting" (dopamine-driven craving) from "liking" (hedonic pleasure). 3-FPM's potent DAT activity suggests strong engagement of the wanting system, consistent with compulsive redosing behavior. Tolerance to euphoria may develop faster than tolerance to craving — a pattern well-documented for amphetamine-class stimulants.
The parent compound phenmetrazine self-administers in rodents[13] and produces effects in primates that generalize to Amphetamine,[8] confirming that the phenylmorpholine scaffold engages the same reward circuitry as classical stimulants.
No neurotoxicity, self-administration, or neuroimaging studies have been conducted for 3-FPM. Whether it produces the dopaminergic terminal damage seen with high-dose methamphetamine, engages TAAR1 (TAAR1), or causes lasting brain changes with chronic use remains unknown.
Subjective Effects[edit]
The 3-FPM experience is one of clean, moderate stimulation — increased energy, mental clarity, and mood elevation without the empathogenic warmth of serotonin-active compounds. At lower doses the character is functional and focused; higher doses shift toward stronger euphoria with mounting physical activation and greater compulsive redosing potential. Set and setting modulate the experience, though less dramatically than for psychedelics — the pharmacological character is largely dose- and route-dependent, with insufflation producing a sharper onset and stronger rush than oral administration.
Within the stimulant landscape, 3-FPM sits between amphetamine and milder phenylethylamine stimulants in perceived potency. Users frequently compare it to low-dose amphetamine with a gentler onset and more moderate duration. Its phenylmorpholine scaffold distinguishes it structurally, but the subjective profile overlaps substantially with other catecholamine-selective releasers — the absence of serotonergic activity keeps the experience firmly in the "stimulant" rather than "empathogen" domain.
Effect Grid
At common doses (~30–60 mg oral), the full stimulant profile manifests: pronounced euphoria, significant psychomotor stimulation, increased energy and wakefulness, and marked thought acceleration. Focus enhancement peaks in this range, with sustained concentration and heightened motivation for both cognitive and physical tasks. Sociability and talkativeness increase substantially. Music enhancement may become apparent.
Physical effects become more prominent: appetite suppression is strong, heart rate is noticeably elevated, jaw tension (bruxism) may emerge, and vasoconstriction can produce cool extremities. Insomnia is expected for 4–6 hours following ingestion, potentially longer given the 8.8-hour elimination half-life.
This range represents the most commonly reported recreational dose window. Functional impairment varies with task complexity — simple tasks may benefit from enhanced focus, while complex judgment and risk assessment are diminished.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Brightness alteration
Pupil dilation · Insomnia · Dry mouth · Heart rate perception changes · Muscle tension · Physical fatigue · Restlessness · Dehydration sensation · Headache · Nasal congestion · Temperature dysregulation · Excessive sweating · Constipation · Dizziness · Nausea · Respiratory stimulation · Trembling · Increased urination · Sexual arousal enhancement · Bruxism · Motor control enhancement · Vomiting · Sexual arousal suppression
Heart rate perception changes · Muscle tension · Physical fatigue · Restlessness · Dehydration sensation · Headache · Nasal congestion · Excessive sweating · Constipation · Dizziness · Nausea · Respiratory stimulation · Trembling · Increased urination · Sexual arousal enhancement · Bruxism · Motor control enhancement · Vomiting · Sexual arousal suppression
Motivation enhancement · Cognitive flexibility · Information processing enhancement · Analysis enhancement · Immersion enhancement · Motivation suppression · Memory enhancement · Thought organization · Aesthetic enhancement · Pattern recognition enhancement · Thought deceleration
Immersion enhancement · Motivation suppression · Memory enhancement · Thought organization · Aesthetic enhancement · Pattern recognition enhancement · Thought deceleration
Irritability · Dysphoria
Ego inflation · Self-control enhancement · Derealization
Timeline
First alerts appear as subtle mood lift and mild increase in alertness. A slight quickening of thought and faint energy increase mark the transition from baseline.
Stimulation builds steadily. Euphoria, focus enhancement, and increased motivation become clearly perceptible. Heart rate begins to rise and appetite diminishes.
Maximum stimulation and euphoria, peaking around 2. 5 hours post-ingestion (consistent with the published Tmax). Pronounced focus, energy, and talkativeness.
Intensity diminishes from peak but functional stimulation persists. Focus and motivation remain elevated. Appetite suppression and mild cardiovascular activation continue.
Gradual return toward baseline. Stimulation fades to residual wakefulness. Emerging fatigue and irritability may appear as dopamine stores deplete.
Residual wakefulness, mild fatigue, and reduced appetite may persist for 4–12 hours beyond subjective offset, consistent with the 8. 8-hour elimination half-life. Mild dysphoria or anhedonia is common.
Safety[edit]
- Acute toxicity
- Moderate
- 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 · phenmetrazine
Toxicity
Acute toxicity
No lethal dose has been established for 3-FPM in any species.[3] In the first documented fatality, blood concentration was 2.4 mg/L — a value the authors noted is similar to concentrations seen in non-fatal poisonings.[14] This overlap between intoxicating and potentially fatal blood levels suggests a narrow safety margin when 3-FPM is combined with other substances.
All documented deaths involved polysubstance use. No published case attributes death to 3-FPM alone.safety citation needed
Heart and circulation
Cardiovascular toxicity is the most consistently documented adverse effect. Rapid heart rate occurred in 47% of clinical presentations.[9][15]
One intravenous use case caused severe blood vessel spasm in all four limbs, resulting in bilateral below-knee amputation and finger tissue death.[4] Heart rhythm abnormalities (widespread T-wave inversions) indicating electrical disturbance were observed in a 3-FPM/etizolam overdose and resolved on their own.[16]
Kidney damage
Acute kidney failure requiring 26 days of continuous blood filtration was documented in the intravenous use case, likely caused by blood vessel spasm restricting flow to the kidneys and triggering immune complement activation.[4]
Neurological effects
Seizures occurred in 16% of presentations, confusion with agitation in 37%, and reduced consciousness in 42%.[9][15] All cases involved multiple substances, so the specific contribution of 3-FPM to neurological toxicity cannot be isolated.
Psychological Risks
No controlled studies have assessed 3-FPM's psychological adverse effects. By class inference from amphetamine and other catecholamine releasers:
- Acute anxiety and agitation — reported in 37% of clinical presentations,[9] consistent with norepinephrine overstimulation
- Stimulant psychosis — a recognized risk with all potent dopamine releasers at high doses or with sustained use; confusion with psychotic features occurred in 37% of cases
- Post-use low mood — dopamine depletion following sustained use produces depressive symptoms and anhedonia
- Compulsive redosing — inherent to potent DAT substrates; 3-FPM's cocaine-comparable potency suggests significant risk
Tolerance & Dependence
No published data exist on tolerance, physical dependence, or psychological dependence specific to 3-FPM. All inference derives from the phenmetrazine and amphetamine pharmacological class.
Phenmetrazine self-administers in rodents at reinforcing doses[13] and produces effects in primates that generalize to Amphetamine.[8] Chronic phenmetrazine treatment reduces cocaine self-administration in rats,[13] consistent with cross-tolerance at shared dopamine transporter targets.
For catecholamine releasers as a class, tolerance develops through transporter upregulation, downregulation, and depletion of neurotransmitter stores. Cross-tolerance is expected with other dopaminergic stimulants. Physical dependence is typically mild compared to opioids or sedatives, but psychological dependence — driven by craving and incentive salience — can be substantial, particularly with compounds showing cocaine-comparable dopamine transporter potency.
Drug Interactions
Tramadol
3-FPM combined with tramadol carries severe risk of seizures and potential serotonin syndrome. Tramadol lowers the seizure threshold on its own; stimulant-induced excitation compounds this risk. Sympathomimetics pharmacologically analogous to 3-FPM should be discontinued before surgery due to potential interactions with tramadol and antidepressants.[17] This interaction extends to 3-FPM by structural and mechanistic analogy.inferred
CNS depressants (opioids, benzodiazepines)
Multiple fatalities and near-fatalities involved 3-FPM co-administered with opioids and/or benzodiazepines.[14][18][16] 3-FPM's stimulant effects mask the sedation and respiratory depression that normally warn of depressant overdose. When 3-FPM wears off (half-life ~8.8 hours), unopposed depressant effects can emerge, producing delayed breathing failure.
Monoamine oxidase inhibitors (MAOIs)
Monoamine oxidase inhibitors combined with any monoamine releasing agent risk severe blood pressure crisis and serotonin syndrome. No published 3-FPM + MAOI cases exist, but the combination is contraindicated on pharmacological grounds.inferred
MDMA and serotonergic stimulants
Combined use of 3-FPM with MDMA or other serotonergic releasers risks dangerous body temperature, high blood pressure, and rapid heart rate. While 3-FPM itself has weak serotonin activity, the additive stimulant burden and combined monoamine release pose the primary danger.inferred
Alcohol
No published data exist on the 3-FPM–alcohol interaction. Class-level evidence suggests alcohol may increase stimulant blood concentrations.citation needed The combination increases cardiovascular strain and impairs risk judgment.
Contraindications
- Pre-existing heart conditions (high blood pressure, abnormal heart rhythms, coronary artery disease, structural heart disease) — rapid heart rate occurred in 47% of presentations and abnormal rhythms are documented[9][4]
- Seizure disorders — stimulants lower the seizure threshold; seizures occurred in 16% of presentations (polysubstance context)[9]
- Concurrent MAOI use — risk of blood pressure crisis and serotonin syndrome
- Concurrent tramadol use — seizure and serotonin syndrome risk[17]
- Pregnancy — catecholamine releasers carry established risks of restricted fetal growth and reduced placental blood flowinferred
- Peripheral vascular disease — the documented case of catastrophic limb loss following intravenous 3-FPM indicates dramatically increased risk with pre-existing vascular compromise[4]
Harm Reduction[edit]
Forms & Identification
3-FPM is most commonly encountered as a white crystalline powder, though pressed pills and capsules circulate. The three positional isomers (2-FPM, 3-FPM, 4-FPM) are visually indistinguishable, and mislabeling between them is plausible. Standard reagent testing can confirm the presence of a phenylmorpholine but cannot reliably distinguish between positional isomers — analytical services or mass spectrometry are required for definitive identification.
Purity in the research chemical market is variable and unregulated. The single analytical study that tested five vendor samples found all to be authentic 3-FPM,[6] but this does not guarantee consistency across sources or over time.
Guidelines
- Test material with reagent kits before use; consider analytical testing services for definitive identification
- Use the oral route to reduce compulsive redosing risk and cardiovascular strain
- Pre-measure a single dose and put remaining material out of easy reach
- Stay hydrated but avoid overhydration — normal water intake is sufficient
- Eat a light meal before use; stimulants suppress appetite, and skipping food worsens the comedown
- Set a hard cutoff time to protect sleep — the 8.8-hour half-life means late-day use will disrupt rest
- Avoid redosing; if the effects feel insufficient, the dose was too low rather than too few
- Do not use alone if trying 3-FPM for the first time
- Keep a log of dose, time, and route for each session to detect escalation patterns early
Set & Setting
3-FPM is a functional stimulant, and its effects are strongly route-dependent. Oral administration produces a gradual onset over 1–2 hours with a moderate, manageable plateau; insufflation delivers a faster, sharper peak with greater euphoria and substantially higher compulsive redosing risk. Choosing the oral route and pre-measuring a single dose before beginning reduces the likelihood of unplanned escalation.
A calm, familiar environment with access to water and food supports a smoother experience. Avoid using when sleep-deprived, dehydrated, or in a state of high anxiety — norepinephrine release amplifies existing stress responses.
Aftercare & integration. The stimulant comedown from 3-FPM typically involves fatigue, low mood, irritability, and difficulty concentrating. These effects reflect temporary dopamine depletion and resolve within 24–48 hours for single-use episodes.
Prioritize sleep as the primary recovery tool — the long half-life (8.8 hours) means residual stimulation may delay sleep onset. Eat nutrient-dense meals even if appetite is suppressed. Avoid caffeine and other stimulants during the recovery period. Light physical activity and social contact support mood restoration.
If low mood or anhedonia persists beyond 3–4 days after a single use, or if you notice a pattern of using to escape baseline mood states, consider speaking with a healthcare provider.
Recovery & Support
3-FPM's cocaine-comparable DAT potency creates real psychological dependence risk, particularly with frequent use. Warning signs include needing higher doses for the same effect, using more frequently than planned, continued use despite negative consequences, and difficulty functioning without the substance.
Stimulant dependence responds well to behavioral interventions. Cognitive behavioral therapy and contingency management have the strongest evidence base for stimulant use disorders. There is no medication specifically approved for stimulant dependence, but professional support significantly improves outcomes.
SMART Recovery, local harm reduction organizations, and substance use helplines provide anonymous, judgment-free support for anyone concerned about their use patterns.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Uncomfortable but manageable effects include mild anxiety, elevated heart rate, and restlessness. Seek immediate medical help if any of the following occur: chest pain or pressure, seizure or convulsions, loss of consciousness, body temperature that feels dangerously hot to the touch, severe confusion or inability to communicate, or blue/grey discoloration of fingers or toes (indicating blood vessel spasm).
Immediate steps:
- 1. Call emergency services immediately if any red-flag symptoms are present
- 2. Keep the person calm and in a cool, quiet environment
- 3. If unconscious but breathing, place in the recovery position (on their side)
- 4. Do not restrain the person unless they are in immediate danger of harming themselves
- 5. Do not induce vomiting
- 6. Monitor breathing continuously while waiting for help
What to tell the dispatcher: Name the substance (3-FPM / 3-fluorophenmetrazine), the amount taken if known, the route of administration, the time of ingestion, and current symptoms. Many jurisdictions have Good Samaritan laws that protect people who call for help during a drug emergency.
Legal Status[edit]
3-FPM occupies a fragmented international legal position. It is specifically controlled in several European jurisdictions but is not federally scheduled in the United States. The WHO Expert Committee on Drug Dependence reviewed 3-FPM at its 43rd session in 2020 and placed it under surveillance without recommending international scheduling.[3]
In the United States, 3-FPM is not listed in the Controlled Substances Act schedules. As a structural and pharmacological structural analog of Schedule II phenmetrazine, it may fall under the Federal Analogue Act (21 U.S.C. § 813) when intended for human consumption. Virginia has independently classified 3-FPM as Schedule I (effective 16 November 2016).
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| Sweden | Narcotic substance | First country to control 3-FPM; effective 1 June 2015 |
| United Kingdom | Controlled (blanket) | Psychoactive Substances Act 2016, effective 26 May 2016; covers all psychoactive substances except specified exemptions |
| Germany | Controlled (NpSG) | Neue-psychoaktive-Stoffe-Gesetz, effective 26 November 2016 |
| Hungary | Controlled | NPS legislation; 3-FPM detected in country from 2014 |
| Finland | Controlled | NPS/analog legislation |
| Estonia | Controlled | NPS/analog legislation |
| Switzerland | Controlled | NPS legislation |
| United States (federal) | Not explicitly scheduled | Potential Federal Analogue Act coverage as analog of Schedule II phenmetrazine |
| Virginia (US) | Schedule I | State-level scheduling effective 16 November 2016 |
| International (WHO) | Under surveillance | ECDD 43rd session (2020): not recommended for scheduling[3] |
Legal status for Canada and Australia could not be confirmed from published or authoritative governmental sources.citation needed 3-FPM is not specifically listed in Canada's Controlled Drugs and Substances Act or Australia's Standard for the Uniform Scheduling of Medicines and Poisons, though analog or blanket provisions may apply in both jurisdictions.
Analog Act considerations
The US Federal Analogue Act extends Schedule I/II control to substances "substantially similar" in chemical structure or pharmacological effect to a scheduled compound when intended for human consumption. 3-FPM meets both criteria with respect to phenmetrazine: it shares the 3-methylmorpholine scaffold (differing only by a meta-fluorine on the phenyl ring) and acts by the same monoamine-releasing mechanism.[1] Prosecution under the Analogue Act requires proof of intent for human consumption, making 3-FPM's legal status in the US context-dependent rather than absolute.
references
- [1] ^abcdefghMayer FP, Burchardt NV, Decker AM, Partilla JS, Li Y, McLaughlin G, Kavanagh PV, Sandtner W, Blough BE, Brandt SD, Baumann MH, Sitte HH (2018) Fluorinated phenmetrazine "legal highs" act as substrates for high-affinity monoamine transporters of the SLC6 family — Neuropharmacology doi:10.1016/j.neuropharm.2017.10.006
- [2]
- [3]
- [4]
- [5]
- [6] ^abcdMcLaughlin G, Morris N, Kavanagh PV, Dowling G, Power JD, Twamley B, O'Brien J, Talbot B, Sitte HH, Brandt SD (2017) Test purchase, synthesis and characterization of 3-fluorophenmetrazine (3-FPM) and differentiation from its ortho- and para-substituted isomers — Drug Testing and Analysis doi:10.1002/dta.1945