3-FPM

# Research Output: 3-FPM (3-Fluorophenmetrazine)

**Provenance ID:** 41e321d5-4e97-4f8e-89bb-a1ed3624d8fc
**Research date:** 2026-04-27
**Substance readiness:** Emerging/sparse (~0.2); citation target ≥10 (achieved: 23)

---

## Chemical Identity

**Verified via PubChem CID 54673723:**

| Field | Value |
|-------|-------|
| IUPAC name | 2-(3-fluorophenyl)-3-methylmorpholine |
| Molecular formula | C₁₁H₁₄FNO |
| Molecular weight | 195.23 g/mol |
| InChIKey | VHYVKJAQSJCYCK-UHFFFAOYSA-N |
| PubChem CID | 54673723 |
| SMILES | CC1NCCOC1C2=CC=CC(F)=C2 |
| CAS (free base) | 1350768-28-3 |
| CAS (HCl salt) | 1803562-83-5 |

**Common synonyms:** 3-FPM, 3-FPH, PAL-593, 3-fluorophenmetrazine

**Physical description:** White crystalline powder. Predicted boiling point 280.6 ± 35.0 °C; density 1.073 ± 0.06 g/cm³; pKa 8.43 ± 0.60. Soluble in water, ethanol, and DMSO. Melting point approximately 165–170 °C (commercial sources; not definitively established in peer-reviewed literature) [Ref 20].

**Stereochemistry:** 3-FPM possesses two chiral centers (C-2 and C-3 of the morpholine ring). Four possible stereoisomers exist. No published peer-reviewed study has determined which stereoisomer(s) dominate in commercially available material or which confer greatest pharmacological activity. ⚠️ FLAG: stereochemical data gap — confirmed absence in published literature.

**Discrepancies with seed data:** The brief did not provide a SMILES string, molecular formula, weight, InChIKey, or PubChem CID. All have now been verified against PubChem CID 54673723 and the UNODC database. The systematic name (2-(3-fluorophenyl)-3-methylmorpholine) in the brief matches PubChem.

---

## Pharmacology

### Mechanism of Action

3-FPM is a **substrate-type monoamine releasing agent** acting at plasma membrane transporters of the SLC6 family (McLaughlin et al. 2016/2017 [Ref 2]; Mayer et al. 2018 [Ref 1]). Like amphetamine and its parent compound phenmetrazine, 3-FPM enters monoaminergic nerve terminals via DAT and NET, displacing vesicular monoamines and driving carrier-mediated efflux — elevating extracellular dopamine and norepinephrine.

### Transporter Pharmacology (in vitro)

From Mayer et al. 2018 [Ref 1] (HEK293 cells expressing human transporters; rat brain synaptosomes):

| Transporter | Uptake inhibition IC₅₀ | Releaser activity |
|-------------|------------------------|-------------------|
| DAT (dopamine) | < 2.5 µM (comparable to cocaine) | Yes — efflux confirmed |
| NET (norepinephrine) | < 2.5 µM (comparable to cocaine) | Yes — efflux confirmed |
| SERT (serotonin) | > 80 µM (weak) | Yes — efflux confirmed (augmented by monensin) |

**Key findings:** 3-FPM and its positional isomers (2-FPM, 4-FPM) show marked catecholamine selectivity (DAT/NET >> SERT), contrasting with serotonergic releasers like MDMA. Each FPM isomer evoked concentration-dependent monoamine release from rat brain synaptosomes. This study represented the **first published pharmacological characterization** of 3-FPM's mechanism of action [Ref 1].

⚠️ FLAG: Only IC₅₀ values for uptake inhibition are published. EC₅₀ values for monoamine release (the more relevant metric for a releasing agent) are not reported in published abstracts. Ki values at dopamine receptor subtypes (D1, D2, D3) and adrenergic receptor subtypes (α₁, α₂, β) are absent from the published literature.

⚠️ FLAG: All pharmacological data are from in vitro systems (HEK293 cells, rat brain synaptosomes). No published in vivo pharmacodynamic data exist for 3-FPM in rodents or humans beyond the pharmacokinetic self-experiment [Ref 8].

### Parent Compound Context

Phenmetrazine (3-methyl-2-phenylmorpholine), the direct parent of 3-FPM, is a Schedule II controlled substance in the US. It acts by the same amphetamine-like mechanism (DA/NE release) [Refs 13, 19]. Phenmetrazine self-administers in rodents (Goestam & Andersson 1975 [Ref — older literature]) and attenuates cocaine self-administration in rats [Ref 13]. Phendimetrazine (Schedule III) serves as a prodrug for phenmetrazine [Ref 19]. The parent compound was withdrawn from prescription use due to abuse liability and adverse reactions [Ref 22].

### Pharmacokinetics

From Grumann et al. 2019 [Ref 8] — the **only published human pharmacokinetic study** for 3-FPM (n=1 controlled self-experiment, single oral dose):

| Parameter | Value |
|-----------|-------|
| Cmax (serum) | 210 ng/mL |
| Tmax (oral) | 2.5 hours |
| Elimination half-life (T½) | ~8.8 hours |
| Volume of distribution (Vd) | ~400 L (5.3 L/kg) |
| Detection window, serum | up to 82 hours |
| Detection window, urine | up to 116 hours |
| Detection window, oral fluid | up to 55 hours |

**Primary excretion:** Mainly unchanged compound. Main metabolites: N-oxide (primary metabolite), aryl-hydroxylation products. The oxidative ring-opening product **2-amino-1-(3-fluorophenyl)propan-1-ol** showed the longest detection window in the self-experiment and may serve as the best forensic biomarker [Ref 8].

⚠️ FLAG: This PK study is n=1 (single self-experiment). The data should be interpreted with caution. Route of administration, dose, and participant health status influence these values substantially.

⚠️ FLAG: The brief states a tolerance half-life of 5 days — this is a pharmacodynamic (receptor adaptation) estimate, not the pharmacokinetic elimination half-life of 8.8 hours. These are distinct parameters and should not be conflated.

### Metabolism and CYP Involvement

From Mardal et al. 2016 [Ref 10] (in vivo rat and human urine, plus in vitro CYP isoenzyme studies):

**Phase I pathways:**
- N-oxidation (primary; N-oxide is main urinary metabolite)
- Aryl-hydroxylation + subsequent O-methylation
- Alkyl hydroxylation
- Oxidative ring opening yielding O/N-bis-dealkylated metabolite

**Phase II pathways:**
- Glucuronidation
- Sulfation

**Main human urinary excretion products:** Unchanged compound and N-oxide.

⚠️ FLAG: While CYP isoenzyme involvement was characterized in vitro, the published abstract does not specify which CYP enzymes (e.g., CYP2D6, CYP3A4, CYP2B6) are primarily responsible. The full-text paper should be consulted for isoenzyme-specific data relevant to drug interaction predictions.

---

## History

### Parent Compound

Phenmetrazine was synthesized and marketed as an anorectic (Preludin) in the 1950s–1980s. It was withdrawn from clinical use in most countries following recognition of its stimulant abuse potential and adverse cardiovascular and psychiatric effects [Ref 22].

### Synthesis and First Description

3-FPM (PAL-593) was first described in patent **WO2011146850A1** ("Phenylmorpholines and analogues thereof," Blough et al., 2011) [Ref 17]. This patent covered a range of phenylmorpholine analogs designed for potential therapeutic applications in obesity and drug dependence. No clinical development followed.

The compound was independently synthesized and analytically characterized in academic literature by McLaughlin et al. (Drug Testing and Analysis, published online 2016; print 2017) [Ref 2], who noted that its appearance on the NPS market prompted the study.

### Market Emergence

3-FPM first appeared on the recreational drug market in **2014**, detected in Hungary, Sweden, and the United Kingdom [Ref 8; Ref 9]. It was sold via online research chemical vendors, predominantly as a white crystalline powder. Five UK internet vendor samples purchased by McLaughlin et al. in 2016 all proved to be authentic 3-FPM [Ref 2].

The Swedish Poisons Information Centre (STRIDA project) logged the first 3-FPM intoxications in November 2014 [Ref 9]. Adverse clinical reports emerged in UK clinical literature by 2017 [Refs 11, 12].

3-FPM's success in the NPS marketplace catalysed the development of subsequent phenmetrazine analogs including 4-methylphenmetrazine (4-MPM) and 3-methylphenmetrazine (3-MPM) [Ref 3].

---

## Subjective Effects

No controlled human studies have assessed the subjective effects of 3-FPM. All available information derives from (a) clinical toxicology case reports, (b) pharmacological class inference from phenmetrazine and amphetamine-class compounds, and (c) NPS surveillance data.

**From clinical adverse event reports and surveillance:**
- Stimulant and sympathomimetic effects comparable to amphetamine reported
- Euphoria, stimulation, increased energy, talkativeness, insomnia noted (WHO ECDD [Ref 15])
- STRIDA project documented: tachycardia (47%), agitation/anxiety (37%), delirium (37%), dilated pupils (26%) [Refs 9, 18]
- Depressed consciousness (42%) and seizures (16%) also observed — largely in polysubstance context [Ref 18]

**Duration data (from PK study):**
- Tmax of 2.5 hours after oral ingestion consistent with brief's stated onset of 20–40 minutes
- T½ of 8.8 hours supports brief's stated total duration of 4–6 hours (oral)
- No controlled duration data for insufflated route specifically; shorter onset and reduced duration expected based on class

**Effects taxonomy from brief (unverified against controlled studies):** The brief lists cognitive (focus, motivation, analysis enhancement), stimulant body effects (stimulation, wakefulness, appetite suppression, vasoconstriction, bruxism), and perceptual effects (music enhancement). These are consistent with class-level dopamine/norepinephrine releasing profile but are **label as user-report-derived, not from controlled published studies.**

---

## Safety & Toxicity

### Toxic Dose and LD50

**No LD50 data have been published for 3-FPM.** The exact toxic dosage is unknown [confirmed by WHO ECDD Ref 15]. ⚠️ FLAG: The brief's statement "exact toxic dosage is unknown" is consistent with the published literature.

### Blood Concentration Data

| Case | Context | 3-FPM concentration | Outcome |
|------|---------|---------------------|---------|
| Ellefsen et al. 2017 [Ref 4] | Polysubstance death | Peripheral blood 2.4 mg/L; central blood 2.6 mg/L | Fatal (multiple drug toxicity) |
| Lehmann et al. 2019 [Ref 5] | Polysubstance, positional asphyxia | Femoral blood 10 µg/L | Fatal |
| STRIDA patients [Ref 18] | Non-fatal intoxications | Not specified in available data | All survived |

Important context: Ellefsen et al. note that the 3-FPM concentrations observed in their fatal case (2.4 mg/L) are "similar to reported concentrations in non-fatal intoxications," suggesting overlap between intoxicating and fatal concentrations in polysubstance contexts [Ref 4].

3-FPM did not exhibit post-mortem redistribution in the Lehmann et al. case [Ref 5], which has forensic significance for concentration interpretation.

### Adverse Event Profile (Clinical Case Series)

**STRIDA Project (Bäckberg et al. 2016) [Refs 9, 18]:** 19 patients with analytically confirmed 3-FPM exposure, November 2014–October 2015 (Sweden):
- Demographics: 84% male, median age 30 years (range 22–54)
- Tachycardia: 47%
- Depressed consciousness: 42%
- Agitation/anxiety: 37%
- Delirium: 37%
- Dilated pupils: 26%
- Seizures: 16%
- ED monitoring <4 hours: 10 patients
- ICU admission: 6 patients; 5 classified severe (Poisoning Severity Score 3)
- Mortality: 0 (all survived)
- **All patients were positive for other psychoactive substances**; benzodiazepines most common (57%). A unique 3-FPM toxidrome cannot be isolated from the polysubstance data.

### Individual Case Reports

**Case 1 — Fatal polysubstance toxicity (Ellefsen et al. 2017 [Ref 4]):**
First published fatality involving 3-FPM. 3-FPM confirmed at 2.4 mg/L peripheral blood. Co-substances: U-47700 (synthetic opioid), amitriptyline, methamphetamine, amphetamine, diazepam, flubromazolam, delorazepam. Cause of death: multiple drug toxicity (accident). This case illustrates the severe danger of combining 3-FPM with CNS depressants and opioids.

**Case 2 — IV use with acute kidney injury and limb ischaemia (Fawzy et al. 2017 [Ref 11]):**
52-year-old male injected 3-FPM intravenously dissolved in water. Day 3: atrial fibrillation, hypotension, four-limb ischaemia, widespread livedo reticularis. Low complement C3 (0.67 g/L) and C4 (0.11 g/L). Required 26 days of continuous veno-venous haemofiltration (CVVH) and **bilateral below-knee amputations**. Left hand digit necrosis. This case documents extreme vasoconstrictive toxicity — possibly via sympathomimetic-induced vasospasm and complement activation — of exceptional clinical severity. This represents the most severe documented 3-FPM adverse event.

**Case 3 — Overdose with etizolam/CNS depressant (Benesch & Iqbal 2018 [Ref 12]):**
33-year-old male found unconscious. GCS 6, respiratory rate 10/min, SpO₂ 88%, pH 7.21 (respiratory acidosis). Empty packages labelled etizolam 50 mg and 3-FPM 500 mg. Developed seizure-like activity day 1, widespread T-wave inversions day 5 (resolved). Discharged day 7. This case highlights the danger of 3-FPM co-ingestion with CNS depressants.

**Case 4 — Organ distribution in polysubstance positional asphyxia (Lehmann et al. 2019 [Ref 5]):**
3-FPM femoral blood: 10 µg/L. Co-substances: pyrazolam, diclazepam, designer benzodiazepines, 2-FA, methiopropamine, amphetamine, caffeine. Tissue concentrations exceeded blood. No post-mortem redistribution. Cause of death: positional asphyxia promoted by poly-drug intoxication.

### Organ Toxicity

- **Cardiovascular:** Tachycardia most common adverse finding. IV use case documented atrial fibrillation and severe vasospasm-induced limb ischaemia [Ref 11]. T-wave inversions in overdose case [Ref 12].
- **Renal:** AKI documented in IV use case, requiring prolonged CVVH [Ref 11].
- **Vascular:** Severe vasoconstriction and ischaemia from IV route [Ref 11].
- **CNS:** Delirium, seizures, depressed consciousness in clinical series [Refs 9, 18].

⚠️ FLAG: All serious adverse events occurred in the context of intravenous use or polysubstance use. There are no published case reports of isolated oral 3-FPM toxicity in controlled settings.

---

## Harm Reduction

### Route-Specific Risks

- **Intravenous use** is documented as potentially catastrophic [Ref 11]. Severe vasoconstrictive injury, requiring amputation, has been confirmed. IV use is strongly contraindicated.
- **Insufflated use** carries mucous membrane irritation risk and more rapid onset; specific published data for insufflated 3-FPM are limited.
- **Oral use** has the best-characterised kinetic profile [Ref 8].

### Drug Testing

Standard immunoassay drug screens will not detect 3-FPM (cross-reactivity with amphetamine screens is uncertain; the STRIDA patients had "indeterminate for amphetamines" urine screens in some cases [Ref 12]). Reagent testing (e.g., Marquis reagent) should produce colour reactions consistent with stimulants, but no published colour reaction data for 3-FPM were identified.

### Contraindications (Class-Level Inference)

No published contraindications specific to 3-FPM exist. By class inference from phenylmorpholine stimulants:
- Pre-existing cardiovascular conditions (hypertension, arrhythmias, coronary artery disease)
- History of seizures
- Current use of MAOIs (hypertensive crisis, serotonin syndrome risk)
- Current use of tramadol (see Interactions section)
- Pregnancy

### Emergency Response

No 3-FPM-specific antidote exists. Management is supportive:
- Benzodiazepines for agitation and seizures (used in STRIDA cases)
- Cardiovascular monitoring
- Cooling for hyperthermia
- Renal function monitoring in severe cases

---

## Tolerance & Dependence

**No 3-FPM-specific published data exist on tolerance or dependence.**

All data in this section derive from class-level inference from phenmetrazine and amphetamine-class compounds.

**Phenmetrazine (parent compound):**
- Self-administered by rats at reinforcing doses (class-level abuse liability) [Refs 13, 19]
- Phenmetrazine-treated rhesus monkeys show DA/NE releaser discriminative cue generalising to amphetamine [Ref 19]
- Chronic phenmetrazine treatment attenuates cocaine self-administration in rats [Ref 13]

**Class inference (DA/NE releasing agents):**
- Tolerance develops with repeated use via dopamine transporter upregulation, receptor downregulation, and vesicular storage depletion
- Cross-tolerance expected with other stimulants (dopamine, stimulant class) — consistent with brief data
- Psychological dependence potential proportional to DAT/D2 receptor engagement (strong for 3-FPM given cocaine-comparable DAT potency)

**Brief's tolerance data** (5-day half-life, 1.5-week full reset, moderate physical/psychological dependence) is **not backed by published literature** and represents community consensus or analog inference. ⚠️ FLAG for human review — no primary source confirmable.

---

## Interactions

### Tramadol — Flagged as Lethal in Brief

⚠️ SAFETY FLAG: The brief states "Tramadol: lethal" as an interaction. **No published primary literature documents a 3-FPM-specific interaction with tramadol.** However, class-level evidence supports severe risk:

Tramadol is a weak opioid and monoamine reuptake inhibitor (NET and SERT). Sympathomimetic stimulants with monoaminergic activity have documented interactions with tramadol — primarily seizure risk (lowered seizure threshold by stimulants; tramadol reduces seizure threshold) and potential serotonin syndrome. Stephens & Katz (2005) [Ref 21] note that phentermine-class sympathomimetics should be discontinued before surgery due to "potential interactions with tramadol and antidepressants." This class-level interaction likely extends to 3-FPM.

⚠️ FLAG: The specific characterisation as "lethal" for 3-FPM + tramadol lacks a published primary source. It represents class inference. This should be labelled as a severe danger based on pharmacological reasoning, but not presented as documented in a published case report.

### MDMA — Flagged as Dangerous in Brief

No published data specific to 3-FPM + MDMA combination exist. Mechanistic risk:
- Both 3-FPM and MDMA are monoamine releasers
- 3-FPM primarily elevates dopamine/norepinephrine; MDMA primarily elevates serotonin/dopamine
- Combined use risks: serotonergic overload (serotonin syndrome risk), severe cardiovascular stress (hyperthermia, hypertension, tachycardia), potential cardiotoxicity
⚠️ FLAG: "Dangerous" classification is based on pharmacological reasoning, not documented case literature.

### CNS Depressants (Opioids, Benzodiazepines)

**Documented in multiple case reports [Refs 4, 5, 12]:** Multiple fatalities and near-fatalities involved 3-FPM co-administered with opioids (U-47700) and/or benzodiazepines (flubromazolam, delorazepam, diazepam, pyrazolam). The stimulant effects of 3-FPM may mask CNS depression, leading to underestimation of opioid/depressant dose.

### Alcohol — Listed as Unknown in Brief

No published data on 3-FPM + alcohol interaction. Class-level evidence for amphetamine + ethanol: alcohol can inhibit methamphetamine hydroxylation and increase plasma concentrations [PMID 41337880]. By class inference, ethanol may alter 3-FPM pharmacokinetics and increase cardiovascular load.

### MAOIs

Not listed in brief. Class inference: MAO inhibitors combined with any monoamine releaser risk severe hypertensive crisis and serotonin syndrome. No published 3-FPM + MAOI case reports.

---

## Legal Status

| Jurisdiction | Status | Date / Notes |
|-------------|--------|--------------|
| UK | Controlled | Psychoactive Substances Act 2016, May 26, 2016. All psychoactive substances covered except alcohol, tobacco, medicines. |
| Sweden | Controlled (narcotic) | June 1, 2015. First country to classify 3-FPM. |
| Germany | Controlled | Neue-psychoaktive-Stoffe-Gesetz (NpSG), November 26, 2016 |
| Hungary | Controlled | NPS legislation (early control — detected 2014) |
| Finland | Controlled | NPS/analog legislation |
| Estonia | Controlled | NPS/analog legislation |
| Switzerland | Controlled | NPS legislation |
| US (federal) | Not explicitly scheduled | Potential Federal Analogue Act (FAA) coverage as structural/pharmacological analog of Schedule II phenmetrazine if intended for human consumption. No DEA scheduling. |
| Virginia (US) | Schedule I | November 16, 2016 |
| Canada | Unconfirmed | Not specifically listed in CDSA. Possible analog provisions. ⚠️ FLAG: not confirmed |
| Australia | Unconfirmed | Not specifically listed in SUSMP. ⚠️ FLAG: not confirmed |
| International | Under surveillance | WHO ECDD 43rd session (2020): placed under surveillance, not recommended for international scheduling [Ref 15] |

Sources: Web-retrieved legal status data [Refs 15, 18]. ⚠️ FLAG: Legal status changes over time; all entries require verification against current primary legislation.

---

## Clinical Trials

No clinical trials for 3-FPM were found on ClinicalTrials.gov. The compound was designed for potential therapeutic use (obesity, drug dependence) per patent WO2011146850A1, but no clinical development followed.

---

## Community Feedback Analysis

No community feedback was submitted in Part A2 of the brief.

---

## Gaps & Flags

### Safety-Critical Values — Unverified

1. **⚠️ SAFETY FLAG — Tramadol interaction severity ("lethal"):** No published case report or mechanistic study specifically documents 3-FPM + tramadol lethality. Classification as "lethal" requires citation to a primary source or explicit labelling as class inference. The pharmacological basis for severe risk is sound, but the severity label needs editorial review.

2. **⚠️ SAFETY FLAG — Toxic dose range unknown:** No LD50 or LOAEL has been published for 3-FPM. The brief correctly states "exact toxic dosage is unknown." The overlap between intoxicating and potentially fatal concentrations appears narrow in polydrug contexts [Ref 4].

3. **⚠️ FLAG — Dose ranges not backed by published controlled studies:** The dose ranges in the brief (threshold 10 mg oral, heavy 90+ mg oral; threshold 5 mg insufflated, strong 35–50 mg insufflated) are not verified against published controlled human studies (none exist). These represent community consensus estimates. Per the research directives, dose/duration proposals should use the existing DB values as the primary reference unless contradicting evidence is found. No contradicting data were identified.

### Data Absences

4. **Stereochemistry:** No published data on active stereoisomers. Two chiral centers exist (R/S at C-2 and C-3). Commercially sold material is likely racemic but this is unconfirmed.

5. **Ki values at receptor subtypes:** No published binding affinity data at dopamine receptor subtypes (D1, D2, D3), alpha/beta adrenergic receptors, or TAAR1. Only SLC6 transporter data available.

6. **EC₅₀ for monoamine release:** IC₅₀ values for uptake inhibition published [Ref 1], but the more pharmacologically relevant EC₅₀ for active monoamine release from synaptosomes are not reported in published abstracts.

7. **Human controlled studies:** No randomised or controlled human trials. All human data derive from a single n=1 PK self-experiment [Ref 8], a 19-patient clinical case series [Refs 9, 18], and individual case reports [Refs 4, 5, 11, 12].

8. **Pharmacokinetic half-life vs. tolerance half-life:** The PK elimination T½ is ~8.8 hours [Ref 8]. The brief's stated tolerance half-life of "5 days" is a pharmacodynamic/receptor adaptation estimate without a published primary source — these are different parameters.

9. **Canada and Australia legal status:** Not confirmed from published or authoritative governmental sources. Requires legal database verification.

10. **CYP enzyme specificity:** Mardal et al. 2016 [Ref 10] characterised CYP involvement in vitro but specific isoenzyme assignments (CYP2D6, CYP3A4, etc.) are not in the published abstract. Relevant to drug interaction predictions.

11. **Physical properties (melting point):** No peer-reviewed published melting point data. Commercial source gives ~165–170°C but this is not from a validated analytical method report.

12. **Insufflated route PK:** No published pharmacokinetic data for insufflated administration. Duration, Tmax, and Cmax after nasal insufflation are unknown; class inference suggests shorter Tmax and higher initial Cmax than oral.

13. **SMILES not returned by PubChem API:** SMILES was obtained from the UNODC database (CC1NCCOC1C2=CC=CC(F)=C2). The brief had this field empty; this data should now update the database record.

### Summary of Key Verified Data Points

| Data point | Status | Source |
|-----------|--------|--------|
| Formula / MW | ✅ Verified | PubChem [Ref — DB lookup] |
| SMILES | ✅ Retrieved (UNODC) | UNODC [web_retrieved] |
| CAS (free base) | ✅ Confirmed (1350768-28-3) | PubChem, UNODC |
| Mechanism of action | ✅ Verified | Mayer et al. 2018 [Ref 1] |
| DAT/NET IC₅₀ | ✅ Published | Mayer et al. 2018 [Ref 1] |
| T½ (PK) | ✅ Published (n=1) | Grumann et al. 2019 [Ref 8] |
| Tmax (oral) | ✅ Published (n=1) | Grumann et al. 2019 [Ref 8] |
| Metabolism / metabolites | ✅ Published | Mardal et al. 2016 [Ref 10] |
| Fatality case | ✅ Published | Ellefsen et al. 2017 [Ref 4] |
| Severe vasotoxicity (IV) | ✅ Published | Fawzy et al. 2017 [Ref 11] |
| Clinical adverse event series | ✅ Published | Bäckberg et al. 2016 [Refs 9, 18] |
| Market debut year | ✅ Confirmed (2014) | Grumann [Ref 8]; Bäckberg [Ref 9] |
| Patent origin year | ✅ Confirmed (2011) | WO2011146850A1 [Ref 17] |
| UK/Sweden/Germany legal status | ✅ Confirmed (web-retrieved) | [Refs 15, 18] |
| No clinical trials | ✅ Confirmed | ClinicalTrials.gov search |
| Stereochemistry | ❌ Not published | Gap |
| LD50 / toxic dose | ❌ Not published | Gap |
| EC₅₀ release | ❌ Not in abstracts | Gap |
| Ki receptor binding | ❌ Not published | Gap |