generation run 2026-05-03
63 min completedmodel pipeline-v5plan not recordedrun/0296e99b…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
- sparse_evidence
- data_gap
Reproduce
- inputs
- 38 source keys (listed under Sources)
- plan
- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
- model
- pipeline-v5
- streams
- none — agent transcripts are persisted from 2026-09 onward
30 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed | methoxetamine conditioned place preference reward reinforcing | 1 | 1 | — |
| 2 | PubMed | methoxetamine death fatality post-mortem toxicology | 2 | 2 | — |
| 3 | PubMed | methoxetamine pharmacology receptor binding | 4 | 3 | — |
| 4 | PubChem | Methoxetamine | 1 | 1 | — |
| 5 | OpenAlex | methoxetamine pharmacology dissociative | 10 | 3 | — |
| 6 | PubMed | methoxetamine metabolism metabolites human | 8 | 4 | — |
| 7 | OpenAlex | methoxetamine MXE abuse toxicity | 10 | 2 | — |
| 8 | ClinicalTrials.gov | methoxetamine | 1 | 0 | — |
| 9 | PubMed | methoxetamine human psychoactive effects subjective survey | 1 | 1 | — |
| 10 | PubMed | methoxetamine antidepressant NMDA ketamine analog | 4 | 3 | — |
| 11 | PubMed | methoxetamine toxicity case report overdose | 2 | 2 | — |
| 12 | PubMed | methoxetamine MXE abuse dependence | 3 | 3 | — |
| 13 | PubMed | methoxetamine rat neurotoxicity dopamine serotonin repeated | 1 | 1 | — |
| 14 | WebSearch | methoxetamine Ki NMDA receptor SERT binding affinity nM Roth 2013 | 10 | 1 | — |
| 15 | WebSearch | methoxetamine MXE fatality 5.8 ug/mL blood death case single substance | 10 | 1 | — |
| 16 | PubMed | methoxetamine cerebellar ataxia acute | 1 | 1 | — |
| 17 | PubMed | methoxetamine acute toxicity hospital emergency intoxication | 2 | 1 | — |
| 18 | WebSearch | methoxetamine MXE melting point physical properties solubility CAS number | 10 | 1 | — |
| 19 | PubMed | get article PMID 23421859 | 1 | 1 | — |
| 20 | WebSearch | methoxetamine MXE synthesis 2010 2011 bladder safe designer drug origin who created | 10 | 1 | — |
| 21 | PubMed | methoxetamine pharmacokinetics tissue distribution animal/Palenicek | 2 | 1 | — |
| 22 | PubMed | methoxetamine death fatality Wikstrom Sweden accidental | 1 | 1 | — |
| 23 | WebSearch | methoxetamine MXE legal status UK US scheduling controlled substance history | 10 | 2 | — |
| 24 | WebSearch | methoxetamine MXE scheduling Australia Canada EU legal status controlled substance date | 10 | 1 | — |
| 25 | PubMed | PMID 25060403 Wiergowski methoxetamine amphetamine fatal polydrug | 1 | 1 | — |
| 26 | PubMed | PMID 25413263 Adamowicz Zuba fatal MXE intoxication | 1 | 1 | — |
| 27 | PubMed/WebSearch | methoxetamine bladder toxicity urinary tract published study evidence | 10 | 2 | Both papers directly refute seed data; must be included in research output as critical correction |
| 28 | PubMed | methoxetamine serotonergic 5-HT2 receptors pharmacological behavioral rat new insights | 1 | 1 | — |
| 29 | Multiple | Bladder toxicity seed data vs published literature | 2 | 2 | — |
| 30 | WebSearch | methoxetamine Ki NMDA receptor SERT binding affinity nM Roth 2013 | 10 | 1 | — |
94 claims by section — every cited sentence, checked against its source
safety35 · 30 ok
Adamowicz & Zuba (2015) reported the first published single-substance MXE fatality, with post-mortem blood concentration of 5.8 µg/mLsupported
Fatal MXE intoxication; blood MXE concentration 5.8 mcg/mL. First confirmed fatal single-substance MXE intoxication published. 1556-4029.12594
Wikström et al. (2013): 26-year-old male, femoral blood MXE 8.6 µg/g, with co-detected synthetic cannabinoids (AM-694, AM-2201, JWH-018, THC). Reference concentrations from four living users: 0.13–0.49 µg/g.supported
26-year-old male found dead; femoral blood MXE 8.6 mcg/g + synthetic cannabinoids AM-694, AM-2201, JWH-018, THC. Reference blood concentrations from living subjects: 0.13-0.49 mcg/g. bks086
Wiergowski et al. (2014): 31-year-old male, serum MXE 0.32 µg/mL with amphetamine 0.06 µg/mL. Clinical course: hyperthermia >39°C, generalized seizures, rhabdomyolysis, hepatic failure, acute renal failure, multi-organ dysfunction, death at 4 weeks.supported
31-year-old male admitted in deep coma after MXE + amphetamine use. MXE serum 0.32 mcg/mL (toxic range), amphetamine 0.06 mcg/mL (non-toxic). Presented with hyperthermia >39C, generalized seizures, massive rhabdomyolysis, hepatic failure, acute renal failure, multi-organ dysfunction. Died 4 weeks post-poisoning. s13382-014-0290-8
Claim in safety — inconclusiveinconclusiveworking →
Chiappini et al. (2015) provided a national overview of UK MXE-related deaths during 2011–2013supported
MXE-related fatalities in UK 2011-2013 documented. Provides mortality overview from UK national data. hup.2422
Elliott & Evans (2014) documented MXE as one of the most frequently detected novel psychoactive substances in UK forensic casework during 2010–2012.supported
2010-2012: 203 NPS cases. MXE in top detected substances. j.forsciint.2014.04.017
Shields et al. (2012) reported three analytically confirmed cases presenting with reversible cerebellar toxicity — a distinctive and potentially diagnostic presentation for high-dose MXE exposuresupported
Three cases of acute neurological toxicity associated with analytically confirmed methoxetamine exposure. Reversible cerebellar toxicity documented. 15563650.2012.683437
Imbert et al. (2014) documented the most detailed cardiovascular presentation in a 21-year-old male after intranasal MXE:supported
21-year-old male: sinus bradycardia (48/min), ST-segment elevation, elevated creatine kinase, hyponatremia after MXE inhalation. bku052
Dargan et al. (2014) administered MXE to mice (30 mg/kg i.p. daily for 3 months) and documented significant bladder inflammation with subsequent fibrosis and renal toxicity at both tubular and glomerular levels.supported
Three months daily MXE (30 mg/kg i.p.) produced significant bladder and renal toxicity in mice: inflammatory changes with subsequent fibrosis in bladder, tubular and glomerular changes in kidney. 15563650.2014.892605
Wang et al. (2017) provided detailed characterization in female rats (30 mg/kg/day i.p. for 4–12 weeks):supported
Female rats: 30 mg/kg MXE i.p. for 4 or 12 weeks caused increased micturition frequency, damaged urothelium, inflammatory cell infiltration. ijms18010117
Costa et al. (2019) demonstrated persistent neurotoxic damage following repeated low-dose MXE in rats (0.1–0.5 mg/kg every other day, 5 doses):supported
Repeated MXE induced persistent anxiety, impaired memory, dopaminergic damage in mPFC/NAcc/caudate-putamen/SNpc/VTA and accumbal serotonergic damage in rats. j.neuropharm.2018.10.031
Extreme agitation, aggression, confusion, hallucinations, amnesia, tachycardia (serum 270 ng/mL, urine 660 ng/mL)partially supported
28-year-old male, intranasal MXE: extreme agitation/aggression, confusion, hallucinations, tachycardia 120/min. MXE serum 270 ng/mL, urine 660 ng/mL. pmid:24466717
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Anxiogenesis: Low doses produce increased anxiety in rodent models (thigmotaxis, decreased centre time); human reports describe dose-dependent anxietysupported
5 and 10 mg/kg induced locomotor stimulation and anxiogenesis. j.brainresbull.2016.05.002
Cognitive impairment: Repeated exposure produces persistent non-spatial memory deficits in animal models (novel object recognition impairment 8 days post-challenge)supported
Repeated MXE induced persistent anxiety, impaired memory, dopaminergic damage. j.neuropharm.2018.10.031
Psychotomimetic effects: PPI disruption at all tested doses indicates psychotomimetic potential consistent with the arylcyclohexylamine classsupported
Behavioral effects in rats: locomotor hyperactivity and disruption of prepulse inhibition confirmed. s00213-016-4203-3
Berquist et al. (2018) demonstrated that MXE substitutes for PCP in drug discrimination and reverses PCP withdrawal signs in rats, confirming cross-tolerance at the NMDA receptor levelsupported
MXE produced PCP-lever selection in drug discrimination without behavioral disruption. MXE partially reversed PCP withdrawal. j.neuropharm.2017.08.028
Conditioned place preference: MXE (2.5–5 mg/kg) induces CPP comparable to ketamine (5 mg/kg)supported
MXE (2.5 and 5 mg/kg) induced CPP comparable to ketamine. j.pbb.2015.03.007
Self-administration: Rats self-administer MXE (0.25–1.0 mg/kg/infusion), though MXE is a less effective reinforcer than PCPpartially supported
Modest self-administration rates. j.pbb.2015.03.007
Self-administration: Rats self-administer MXE (0.25–1.0 mg/kg/infusion), though MXE is a less effective reinforcer than PCPsupported
MXE was less effective reinforcer than PCP. j.neuropharm.2017.08.028
Mesolimbic dopamine: MXE substitutes for ketamine in self-administration and enhances dopaminergic transmissionsupported
MXE substitutes for ketamine in self-administration. MXE enhances mesolimbic dopaminergic transmission. s00213-016-4275-0
The confirmed SERT inhibition (Ki = 479 nM) means any co-administration with serotonergic agents carries serotonin syndrome risksupported
MXE showed appreciable affinity for serotonin transporter. journal.pone.0059334
Claim in safety — inconclusiveinconclusiveworking →
Synthetic cannabinoids: Documented in a polydrug fatality (MXE 8.6 µg/g with AM-694, AM-2201, JWH-018)supported
femoral blood MXE 8.6 mcg/g + synthetic cannabinoids AM-694, AM-2201, JWH-018, THC. bks086
The single documented MXE + amphetamine fatality (Wiergowski et al. 2014) produced hyperthermia, rhabdomyolysis, and multi-organ failuresupported
Presented with hyperthermia >39C, generalized seizures, massive rhabdomyolysis, hepatic failure, acute renal failure, multi-organ dysfunction. s13382-014-0290-8
Cardiovascular disease: ST-segment changes and bradycardia documented; pre-existing cardiac conduction abnormalities may be exacerbatedsupported
sinus bradycardia (48/min), ST-segment elevation... after MXE inhalation. bku052
Seizure disorders: New seizure activity documented in casessupported
Seizures during hospitalization. bku052
Claim in safety — not_supportednot supportedworking →
Hepatic impairment: CYP2B6/CYP3A4-dependent metabolism — impaired clearance in hepatic diseasesupported
CYP2B6 and CYP3A4 catalyze initial N-deethylation. s00216-013-7051-6
Renal impairment: Documented renal toxicity in animals; impaired excretionsupported
tubular and glomerular changes in kidney. 15563650.2014.892605
Concurrent serotonergic medications: SERT inhibition at Ki = 479 nM creates serotonin syndrome risksupported
MXE showed appreciable affinity for serotonin transporter. journal.pone.0059334
History of urological disease: Animal data demonstrate bladder toxicitysupported
inflammatory changes with subsequent fibrosis in bladder. 15563650.2014.892605
History of urological disease: Animal data demonstrate bladder toxicitysupported
damaged urothelium, inflammatory cell infiltration, elevated IL-1beta/IL-6... interstitial fibrosis. ijms18010117
Psychotic disorders: Psychotomimetic effects (PPI disruption at all doses) may precipitate episodessupported
disruption of prepulse inhibition confirmed. s00213-016-4203-3
pharmacology13 · 8 ok
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
In vivo microdialysis confirmed MXE (0.25–0.5 mg/kg i.v.) significantly elevated serotonin in the medial prefrontal cortex and nucleus accumbens.supported
In vivo microdialysis: MXE (0.25-0.5 mg/kg i.v.) significantly altered serotonin levels in rat mPFC and NAcc. j.expneurol.2021.113836
Claim in pharmacology — inconclusiveinconclusiveworking →
The antidepressant mechanism parallels ketamine's: NMDA blockade triggers downstream AMPA receptor activation (confirmed by NBQX blockade of antidepressant effects), which in turn activates mTOR phosphorylation and upregulates GluA1 and GluA2 AMPA subunit protein levels in hippocampus and prefrontal cortexpartially supported
MXE produced antidepressant effects at 30 min sustained 24 h via AMPA and 5-HT2 receptor mechanisms. Blocked by NBQX and ketanserin. j.neuropharm.2017.08.038
Claim in pharmacology — inconclusiveinconclusiveworking →
Ketanserin blockade of antidepressant effects confirms 5-HT₂ receptor involvement in this cascade.supported
Blocked by NBQX and ketanserin. j.neuropharm.2017.08.038
MXE enhances mesolimbic dopaminergic transmission and substitutes for ketamine in self-administration paradigmssupported
MXE substitutes for ketamine in self-administration. MXE enhances mesolimbic dopaminergic transmission. s00213-016-4275-0
Coppola & Mondola (2012) hypothesized MXE activity at dopamine D₂, sigma-1, opioid mu and kappa, and muscarinic cholinergic receptorspartially supported
Hypothesis: MXE as NMDA antagonist, dopamine reuptake inhibitor, D2/5HT2/sigma-1/opioid mu and kappa agonist. j.mehy.2012.07.002
Claim in pharmacology — inconclusiveinconclusiveworking →
Horsley et al. (2016) provide the most detailed PK characterization (Wistar rats, 10 mg/kg s.c.):supported
Behavioural PK and metabolic characterization in rats. 5 and 10 mg/kg induced locomotor stimulation and anxiogenesis. j.brainresbull.2016.05.002
Meyer et al. (2013) identified CYP enzyme involvement via in vitro human liver microsomal studies:supported
CYP2B6 and CYP3A4 catalyze initial N-deethylation. Eight metabolites identified. s00216-013-7051-6
Menzies et al. (2014) confirmed phase I and II metabolites in urine from three patients with acute MXE toxicitysupported
Phase I and II metabolites characterized by LC-HRMS. Major metabolites confirmed in urine from 3 acute MXE toxicity patients. dta.1541
summary12 · 10 ok
The modification produces a longer-acting dissociative profile (4–6 hours oral) at lower weight-based doses than ketamine, with substantial brain tissue accumulation (brain:serum ratio 2.06–2.93).partially supported
Brain:serum ratio 2.06-2.93 throughout observation. Duration exceeds ketamine. j.brainresbull.2016.05.002
Claim in summary — inconclusiveinconclusiveworking →
Despite early commercial framing as a research chemical, its pharmacological profile attracted scientific investigation into antidepressant mechanisms paralleling ketamine's NMDA–AMPA–mTOR cascadesupported
MXE produced antidepressant effects at 30 min sustained 24 h via AMPA and 5-HT2 receptor mechanisms. j.neuropharm.2017.08.038
Claim in summary — inconclusiveinconclusiveworking →
This dual mechanism — absent in ketamine — engages 5-HT₂ receptor signalling as a critical mediator of both motor and sensory effectssupported
5-HT2 receptors confirmed as key mediators of MXE sensorimotor effects. j.expneurol.2021.113836
A single-substance fatality has been documented (post-mortem blood 5.8 µg/mL)supported
Fatal MXE intoxication; blood MXE concentration 5.8 mcg/mL. First confirmed fatal single-substance MXE intoxication published. 1556-4029.12594
Acute toxicity presentations include reversible cerebellar dysfunction, cardiovascular compromise (bradycardia, ST-segment elevation), and rhabdomyolysis in polydrug contextssupported
Reversible cerebellar toxicity documented. 15563650.2012.683437
Acute toxicity presentations include reversible cerebellar dysfunction, cardiovascular compromise (bradycardia, ST-segment elevation), and rhabdomyolysis in polydrug contextssupported
21-year-old male: sinus bradycardia (48/min), ST-segment elevation... after MXE inhalation. bku052
Acute toxicity presentations include reversible cerebellar dysfunction, cardiovascular compromise (bradycardia, ST-segment elevation), and rhabdomyolysis in polydrug contextssupported
Presented with hyperthermia >39C, generalized seizures, massive rhabdomyolysis, hepatic failure, acute renal failure, multi-organ dysfunction. s13382-014-0290-8
Chronic animal studies demonstrate bladder inflammation, fibrosis, and renal damage — directly contradicting marketing claims of urological safetysupported
inflammatory changes with subsequent fibrosis in bladder, tubular and glomerular changes in kidney. MXE marketed as 'bladder friendly' but no data supports this claim. 15563650.2014.892605
Chronic animal studies demonstrate bladder inflammation, fibrosis, and renal damage — directly contradicting marketing claims of urological safetysupported
damaged urothelium, inflammatory cell infiltration... interstitial fibrosis. Direct toxic and pro-inflammatory effects on human urothelial cells. ijms18010117
Repeated low-dose exposure in rats produces persistent dopaminergic and serotonergic neurotoxicitysupported
dopaminergic damage in mPFC/NAcc/caudate-putamen/SNpc/VTA and accumbal serotonergic damage in rats. j.neuropharm.2018.10.031
history7 · 3 ok
Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
Corazza et al. coined the street name "Special M" — a deliberate parallel to ketamine's "Special K" — in documenting MXE's recreational trajectory from online markets to nightlife environments.supported
Reviews ketamine and MXE recreational use. MXE emerged as bladder-friendly KET alternative. cns.12063
The compound was actively marketed as a "bladder-friendly" and safer alternative to ketaminesupported
MXE marketed as 'bladder friendly' but no data supports this claim. 15563650.2014.892605
Corazza et al. (2012) characterized MXE's rapid internet dissemination as a public health challenge requiring coordinated international regulatory response, documenting the compound's availability across multiple online vendor platforms during the 2010–2012 period.supported
Critical discussion of online availability as public health challenge. hup.1242
Claim in history — inconclusiveinconclusiveworking →
pharmacokinetic-detail6 · 5 ok
Horsley et al. (2016) conducted the most comprehensive pharmacokinetic evaluation in Wistar rats (10 mg/kg s.c.):supported
Behavioural PK and metabolic characterization in rats. 5 and 10 mg/kg induced locomotor stimulation and anxiogenesis. j.brainresbull.2016.05.002
Meyer et al. (2013) characterized the metabolic pathway using in vitro human liver microsomes and recombinant CYP enzymes:supported
Phase I and II metabolites in rat and human urine. CYP2B6 and CYP3A4 catalyze initial N-deethylation. s00216-013-7051-6
Menzies et al. (2014) confirmed these pathways in human clinical specimens from three MXE-intoxicated patients, identifying normethoxetamine, O-desmethylmethoxetamine, dihydromethoxetamine, dehydromethoxetamine, hydroxymethoxetamine isomers, and hydroxynormethoxetamine as phase I products.supported
Major metabolites confirmed in urine from 3 acute MXE toxicity patients: normethoxetamine, O-desmethylmethoxetamine, dihydromethoxetamine, glucuronide conjugates. dta.1541
Immunoassay cross-reactivity: MXE may produce false-positive results on amphetamine immunoassayssupported
Initial immunoassay gave false positive for amphetamines. pmid:27339480
Confirmatory methods: GC-MS and LC-MS/MS validated for blood, urine, and hair matricespartially supported
Phase I and II metabolites in rat and human urine. s00216-013-7051-6
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
receptor-pharmacology6 · 2 ok
The comprehensive receptor binding profile derives from Roth et al. (2013), who screened MXE against 57 molecular targets through the NIMH Psychoactive Drug Screening Program:supported
Pharmacological profiles of ketamine and PCP analogues via NIMH PDSP. journal.pone.0059334
Notably, the PDSP screen found no significant affinity at dopamine D₂, sigma-1, opioid mu/kappa, muscarinic cholinergic, or norepinephrine transporter (NET) sites — contradicting earlier hypotheses.supported
Hypothesis: MXE as NMDA antagonist, dopamine reuptake inhibitor, D2/5HT2/sigma-1/opioid mu and kappa agonist. j.mehy.2012.07.002
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
effects-overview4 · 4 ok
MXE's subjective character is shaped by its dual pharmacology — NMDA antagonism producing classical dissociative disconnection, overlaid with serotonergic modulation that lends a warmer, more emotionally coloured quality absent from ketaminesupported
MXE inhibits NMDA-mediated field potentials and GABA-mediated spontaneous currents. 5-HT2 receptors confirmed as key mediators of MXE sensorimotor effects. j.expneurol.2021.113836
Set and setting exert strong modulatory influence across all dose ranges — anxiogenic environments amplify the dysphoric potential that rodent models confirm at low doses.supported
5 and 10 mg/kg induced locomotor stimulation and anxiogenesis. j.brainresbull.2016.05.002
MXE occupies a position between ketamine and phencyclidine in the dissociative landscape — longer-acting and more potent by weight than ketamine, but less stimulating and less reinforcing than PCPsupported
MXE was less effective reinforcer than PCP. MXE produced hypothermia but not locomotor stimulation. j.neuropharm.2017.08.028
The serotonergic dimension distinguishes MXE from both, contributing perceptual and emotional textures that users describe as qualitatively distinct from pure NMDA antagonists.supported
Survey of UK polydrug users on MXE prevalence, subjective effects, motivations for use. dar.12259
neuroscience4 · 3 ok
Marti et al. (2021) demonstrated via in vivo microdialysis that MXE (0.25–0.5 mg/kg i.v.) significantly elevates extracellular serotonin in medial prefrontal cortex and nucleus accumbenssupported
In vivo microdialysis: MXE (0.25-0.5 mg/kg i.v.) significantly altered serotonin levels in rat mPFC and NAcc. j.expneurol.2021.113836
Costa et al. (2019) documented persistent damage following repeated low-dose MXE (0.1–0.5 mg/kg every other day, 5 doses, i.p., rats):supported
Repeated MXE induced persistent anxiety, impaired memory, dopaminergic damage in mPFC/NAcc/caudate-putamen/SNpc/VTA and accumbal serotonergic damage in rats. j.neuropharm.2018.10.031
This mechanism is confirmed indirectly by the PPI disruption observed at all tested doses, which reflects impaired sensorimotor gating mediated by cortico-striato-pallido-thalamic circuits.supported
disruption of prepulse inhibition confirmed. s00213-016-4203-3
Claim in neuroscience — inconclusiveinconclusiveworking →
clinical-evidence3 · 3 ok
Botanas et al. (2021) provided the stereochemistry-resolved comparison:supported
R(-)-MXE and S(+)-MXE both show NMDA receptor affinity and SERT inhibition. R-MXE showed fewer behavioral side effects. j.neuropharm.2021.108619
These effects were blocked by NBQX (AMPA antagonist) and ketanserin (5-HT₂ antagonist), establishing the glutamatergic–serotonergic dual mechanism.supported
Blocked by NBQX and ketanserin. j.neuropharm.2017.08.038
The R(−)-MXE enantiomer has been identified as a potential development candidate given its reduced abuse liability profile while retaining full antidepressant efficacy.supported
R-MXE showed fewer behavioral side effects (no CPP, no hyperlocomotion, no PPI deficits) compared to S-MXE. j.neuropharm.2021.108619
comparative-pharmacology3 · 2 ok
The duration difference is explained by MXE's sustained brain tissue accumulation — peak brain levels at 30 minutes with slow release over 6 hours — versus ketamine's rapid redistribution out of CNS tissue.supported
Brain levels peaked at 30 min, declined to near-zero at 6h. Duration exceeds ketamine. j.brainresbull.2016.05.002
Berquist et al. (2018) characterized MXE's relationship to PCP through drug discrimination and self-administration:supported
MXE produced PCP-lever selection in drug discrimination without behavioral disruption. MXE was less effective reinforcer than PCP. j.neuropharm.2017.08.028
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
chemistry1 · 1 ok
De Paoli et al. (2013) confirmed the structural identity of street-sourced MXE samples via GC-MS and NMR spectroscopy, verifying the compound as 2-(ethylamino)-2-(3-methoxyphenyl)cyclohexanone.supported
MXE obtained from online retailer and characterized by GC-MS, NMR, DAD. Confirmed structure as 2-(ethylamino)-2-(3-methoxyphenyl)cyclohexanone. bkt023