generation run 2026-05-08
63 min completedmodel pipeline-v5plan not recordedrun/366e18c7…Selection
Verification
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- seen / partial
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The model's own caveats
- sparse_evidence
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- safety_data_unverified
Reproduce
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- 29 source keys (listed under Sources)
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- not recorded — template version, prompt hash and git SHA are written from 2026-09 onward
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- none — agent transcripts are persisted from 2026-09 onward
20 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | PubMed | 3-chloromethcathinone metabolism metabolites urine blood | 1 | 1 | Duplicate of earlier find |
| 2 | PubMed | synthetic cathinone chloromethcathinone pharmacology transporter | 1 | 1 | Directly relevant to chloro-substituted cathinone pharmacology; provides analogy context for 3-CMC |
| 3 | PubMed | mephedrone methcathinone cathinone monoamine releasing agent DAT SERT NET substrate | 1 | 1 | Provides SAR data for meta-substituted cathinones - structural analog context |
| 4 | PubMed | 3-CMC 3-chloromethcathinone clophedrone pharmacology | 6 | 6 | All directly relevant to 3-CMC pharmacology, metabolism, toxicology |
| 5 | ClinicalTrials.gov · absence | 3-CMC chloromethcathinone synthetic cathinone | 0 | 0 | No trials exist |
| 6 | PubChem | 3-chloromethcathinone | 1 | 1 | Primary chemical identity data for 3-CMC |
| 7 | OpenAlex | 3-CMC 3-chloromethcathinone cathinone stimulant | 10 | 4 | These provide class-level context, analytical methods, and cathinone market background relevant to 3-CMC article |
| 8 | PubMed | 3-methylmethcathinone 3-MMC monoamine transporter pharmacology | 1 | 1 | Relevant - covers mephedrone-class cathinone pharmacology with potential 3-MMC data that can be used as structural analog context |
| 9 | WebSearch | 3-CMC clophedrone EMCDDA European drug report seizures 2023 2024 | 8 | 2 | Seizure data context |
| 10 | PubMed | mephedrone synthetic cathinone human cardiovascular subjective effects clinical | 3 | 2 | Mephedrone human pharmacology as closest analog to 3-CMC |
| 11 | EUDA | — | 1 | 1 | Key seizure and market data |
| 12 | PubMed | — | 1 | 1 | Mephedrone CYP2D6 data relevant as 3-CMC analog model |
| 13 | WebSearch | 3-CMC 3-chloromethcathinone legal status scheduling UK US EU countries 2024 2025 | 10 | 5 | Primary legal status sources |
| 14 | EUDA | — | 1 | 1 | EU regulatory history and risk assessment data |
| 15 | WebSearch | 3-CMC first detected Europe year history market 2014 2015 | 10 | 3 | Market history data |
| 16 | ECDD Repository | — | 1 | 1 | Authoritative WHO scheduling and pharmacology summary |
| 17 | OpenAlex | 3-CMC 3-chloromethcathinone human pharmacology effects seizures | 10 | 2 | Fatal chemsex case is critical new evidence; 3-MMC review provides closest analog market/dependence data |
| 18 | WebSearch | 3-chloromethcathinone CAS number structure 3-CMC | 10 | 2 | Chemical identity data |
| 19 | PubChem | CID 50999285 | 1 | 1 | Chemical identity verification |
| 20 | WebSearch | 3-CMC UK Psychoactive Substances Act 2016 Australia Canada scheduling | 10 | 1 | Legal status |
82 claims by section — every cited sentence, checked against its source
safety29 · 26 ok
Romańczuk et al. (2023) reported 27 deaths at one Polish forensic medicine department (2016–2022) involving CMC isomers, of which 13 involved 3-CMCsupported
27 death cases from Department of Forensic Medicine in Kraków, 2016-2022. 52% 4-CMC, 48% 3-CMC. bkad070
Polydrug use was the norm: 82% of cases (22/27) involved co-detected substances including synthetic cannabinoids, synthetic opioids, cocaine, opiates, medications, and/or ethanol.supported
82% polydrug cases. bkad070
Pélissier-Alicot et al. (2026) reported a fatal chemsex case: a 62-year-old man found dead with chemsex paraphernalia, with toxic GHB concentrations (330 µg/mL) in combination with 3-CMC (17 ng/mL in frozen blood).supported
62-year-old man found dead with chemsex paraphernalia. GHB toxic (330 µg/mL) + 3-CMC 17 ng/mL in frozen blood. toxics14020131
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Cardiac arrhythmias and thoracic pain are documented in human intoxication casessupported
cardiac arrhythmias, thoracic pain, tachypnea. ijms262311600
Computational ADMET modelling predicts cardiotoxicity risk for 3-CMC and all CMC isomers, including drug–drug interaction potentialpartially supported
Cardiotoxicity risk predicted for all CMC compounds. ijms262311600
The structural analog 4-CMC increases blood pressure and heart rate in rats. No hERG channel binding data or QTc prolongation measurements have been published for 3-CMC.supported
4-CMC increased blood pressure, heart rate, and locomotor activity in rats. jpet.122.001478
Langa et al. (2026) administered 3-CMC (10 or 20 mg/kg i.p.) to Wistar rats with sacrifice at 24 hourssupported
Rats given 10 or 20 mg/kg i.p., sacrificed 24h later. bkaf103
Wojcieszak et al. (2020) demonstrated cytotoxicity of 3-CMC on SH-SY5Y human neuroblastoma cells, with toxicity emerging and intensifying during prolonged incubationsupported
First cytotoxicity data for 3-CMC and 4-CMC on SH-SY5Y neuroblastoma cells — emerges with prolonged incubation, suggesting indirect mechanism. s12640-020-00227-8
Bassi et al. (2025) reported that 3-CMC produces hypothermia in CD-1 mice (0.1–30 mg/kg i.p.), contrasting with the hyperthermia produced by many other synthetic cathinones and MDMAsupported
3-CMC induced locomotor stimulation in CD-1 mice (0.1-30 mg/kg i.p.), tachypnoea and hypothermia. ijms262311600
Willeman et al. (2025) demonstrated that 3-CMC caused false-positive MDMA results at 100 µg/mL and contributed to 17.1% of false-positive MDMA tests in a clinical cohortsupported
3-CMC at 100 µg/mL caused false-positive MDMA assay results. False-positive rate: 16.3% for amphetamine, 17.1% for MDMA assays in 2033 urine samples from 1812 patients. 00045632251331404
Psychosis is documented in human intoxication cases at the Italian Poison Control Centresupported
Human intoxications (Italy, 2014-2025): all non-fatal, male patients, psychomotor agitation, psychosis, aggressiveness ijms262311600
Psychomotor agitation and aggressiveness are reported alongside psychotic symptomssupported
psychomotor agitation, psychosis, aggressiveness, CNS depression ijms262311600
At the cathinone class level, Daziani et al. (2023) documented encephalopathy, coma, convulsions, sympathomimetic and hallucinogenic toxidromes, and excited/agitated delirium syndrome as neurological complications of synthetic cathinone usesupported
Neurotoxic effects include encephalopathy, coma, convulsions, sympathomimetic and hallucinogenic toxidromes, excited delirium syndrome, serotonin syndrome. ijms24076230
Claim in safety — inconclusiveinconclusiveworking →
Van Amsterdam et al. (2025) documented that 3-MMC's shorter duration of action relative to mephedrone leads to increased craving and more frequent redosingsupported
Shorter duration leads to increased craving and redosing. j.drugpo.2025.104971
Treatment-seeking for problematic 3-MMC use in the Netherlands increased from 33 cases in 2021 to 330 cases in 2023, with most cases involving polydrug userssupported
Treatment-seeking increased from 33 to 330 cases 2021-2023. j.drugpo.2025.104971
Pélissier-Alicot et al. (2026) documented a fatal case involving 3-CMC combined with GHB in a chemsex context — a 62-year-old man found dead with a toxic GHB concentration of 330 µg/mL alongside 3-CMC at 17 ng/mLsupported
62-year-old man found dead with chemsex paraphernalia. GHB toxic (330 µg/mL) + 3-CMC 17 ng/mL in frozen blood. toxics14020131
For the structural analog mephedrone, Papaseit et al. (2019) demonstrated in a randomised crossover trial that mephedrone combined with alcohol (0.8 g/kg) produced significantly increased cardiovascular effects and greater euphoria than either drug alone, with mephedrone reducing alcohol's perceived sedationsupported
Mephedrone 200 mg + alcohol 0.8 g/kg. Combination increased cardiovascular effects and euphoria vs either drug alone. Mephedrone reduced alcohol sedation. fphar.2019.01588
If CYP2D6 is the primary metabolising enzyme for 3-CMC — as established for mephedrone — co-administration with CYP2D6 inhibitors (fluoxetine, paroxetine, bupropion, quinidine) could reduce 3-CMC metabolism, elevating plasma exposure and toxicity risksupported
Mephedrone metabolic disposition mediated by CYP2D6. Low CYP2D6 functionality increases toxicity risk. cpt.1417
Daziani et al. (2023) documented serotonin syndrome within the broader synthetic cathinone classsupported
Neurotoxic effects include encephalopathy, coma, convulsions, sympathomimetic and hallucinogenic toxidromes, excited delirium syndrome, serotonin syndrome. ijms24076230
Romańczuk et al. (2023) found that 82% of fatal CMC-related cases (22/27) involved co-detected substances, including synthetic cannabinoids, synthetic opioids, cocaine, opiates, medications, and/or ethanolsupported
27 death cases... 82% polydrug cases. bkad070
Cardiac arrhythmias and thoracic pain are documented in human intoxication cases, and ADMET modelling predicts cardiotoxicity across CMC isomerssupported
cardiac arrhythmias, thoracic pain... Cardiotoxicity risk predicted for all CMC compounds. ijms262311600
Nephrotoxicity signals (histopathological kidney changes at high dose, elevated urea) were observed in acute rat exposuresupported
increased glucose and urea... Histopathological changes in brain, liver, lungs (both doses), kidneys (high dose). bkaf103
Liver histopathological changes were observed at both doses in the rat studysupported
Histopathological changes in brain, liver, lungs (both doses), kidneys (high dose). bkaf103
If CYP2D6 mediates 3-CMC metabolism as predicted, CYP2D6 poor-metaboliser phenotype represents an additional risk factor for elevated exposure.supported
Low CYP2D6 functionality increases toxicity risk. cpt.1417
Class-level seizure threshold reduction is documented for synthetic cathinones.supported
Neurotoxic effects include encephalopathy, coma, convulsions, sympathomimetic and hallucinogenic toxidromes ijms24076230
Psychosis is documented in intoxication casessupported
psychomotor agitation, psychosis, aggressiveness ijms262311600
pharmacology11 · 11 ok
This classification places it in the same mechanistic category as mephedrone and other ring-substituted methcathinone analogs, which act as transporter substrates rather than reuptake inhibitors.supported
Ring-substituted cathinones like mephedrone are transporter substrates (releasers) that evoke neurotransmitter release via reversed transporter flux 164_2018_178
Direct evidence for 3-CMC's releaser activity comes from Wojcieszak et al. (2020), who demonstrated that chloromethcathinones including 3-CMC and 4-CMC enhance non-selective dopamine and serotonin release, consistent with substrate-type activity at DAT and SERTsupported
Chloromethcathinones enhance non-selective DA/5-HT release. s12640-020-00227-8
The positional isomer 4-CMC has been directly characterised at monoamine transporters in rats, where it functions as a substrate at DAT, NET, and SERT with comparable potency across all three transporters, similar to mephedronesupported
4-CMC functions as substrate (releaser) at DAT, NET, SERT with similar potency at all three transporters, comparable to mephedrone. jpet.122.001478
Structure-activity relationship data from meta-substituted trifluoromethyl methcathinone analogs indicate that meta-ring substitution increases SERT potency relative to DAT compared to unsubstituted analogs, suggesting 3-CMC may exhibit relatively greater serotonergic activity than its para-substituted isomersupported
Meta-substituted (3-position) ring substituents on methcathinone analogs increase SERT potency but decrease NET/DAT activity. j.ejphar.2012.11.008
The most direct human data come from Di Trana et al. (2026), who conducted an observational naturalistic study in 16 regular psychostimulant users who self-administered 3-CMC orally (100–150 mg) or intranasally (60–80 mg)supported
16 regular psychostimulant users self-administered 3-CMC orally (100-150 mg) or intranasally (60-80 mg). s12248-025-01200-z
N-glucuronidation of 3-CMC was hypothesised for the first time in this study.supported
3-CMC N-glucuronidation hypothesized for first time. s12248-025-01200-z
Berardinelli et al. (2024) conducted the most comprehensive metabolite profiling, identifying 12 metabolites via human hepatocyte incubation with LC-HRMS/MS confirmation in clinical and forensic specimens (blood, urine, oral fluid)supported
12 metabolites identified for 3-CMC via human hepatocyte incubation + LC-HRMS/MS... 3-CMC-positive blood, urine, and oral fluid analyzed from clinical/forensic casework. s12248-024-00940-8
Major metabolic reactions included β-keto reduction (producing dihydro-3-CMC), N-demethylation, and a combined N-demethylation plus ω-carboxylation pathway that produced the predominant urinary metabolite — a pathway previously unreported for any methcathinone analog.supported
Major reactions: ketoreduction, N-demethylation. Predominant urinary metabolite: N-demethylation + ω-carboxylation combination. s12248-024-00940-8
M3 (dihydro-3-CMC) was the predominant metabolite in postmortem samplessupported
M3 (beta-keto reduction). M3 was predominant metabolite in postmortem samples. j.forsciint.2025.112364
Mestria et al. (2025) confirmed dihydro-CMC stereoisomers and N-demethyl-CMC as key metabolites in a murine dried blood spot model.supported
DBS technique in murine model. Main metabolites: dihydro-CMC stereoisomers, N-demethyl-CMC, dihydro-N-demethyl-CMC. dta.3782
By structural analogy to mephedrone, CYP2D6 is the probable primary metabolising enzyme: Olesti et al. (2019) demonstrated in a Phase I clinical trial that mephedrone metabolism is CYP2D6-mediated, with individuals carrying low or absent CYP2D6 activity at elevated risk of toxicity. This CYP2D6 involvement has not been directly confirmed for 3-CMC.supported
Mephedrone metabolic disposition mediated by CYP2D6. Low CYP2D6 functionality increases toxicity risk. cpt.1417
neuroscience10 · 8 ok
Claim in neuroscience — inconclusiveinconclusiveworking →
Langa et al. (2026) reported oxidative stress and energy biomarker alterations in brain, lung, and kidney tissue of Wistar rats following acute 3-CMC exposure (10 or 20 mg/kg i.p.), with histopathological changes observed in the brain at both doses.supported
Oxidative stress in brain, lungs, kidneys. Histopathological changes in brain, liver, lungs (both doses), kidneys (high dose). bkaf103
What is the dose-response curve for cardiovascular toxicity? Cardiac arrhythmias are documented in clinical intoxication but the dose threshold, exposure duration, and individual risk factors (e.g., pre-existing cardiac conditions, CYP2D6 status) have not been characterised.supported
Human intoxications (Italy, 2014-2025): all non-fatal, male patients... cardiac arrhythmias, thoracic pain, tachypnea. ijms262311600
Dopaminergic reward pathway. Substrate-type monoamine releasers increase extracellular dopamine concentrations in the mesolimbic pathway (ventral tegmental area → nucleus accumbens), producing the reinforcing and euphoric effects characteristic of psychostimulantssupported
transporter substrates (releasers) that evoke neurotransmitter release via reversed transporter flux... All increase extracellular monoamines. 164_2018_178
The dose-dependent locomotor stimulation observed with 3-CMC in mice is a standard behavioural correlate of mesolimbic dopamine releasesupported
3-CMC and 4-CMC stimulate horizontal locomotor activity dose-dependently in mice. Chloromethcathinones enhance non-selective DA/5-HT release. s12640-020-00227-8
Claim in neuroscience — inconclusiveinconclusiveworking →
Noradrenergic activation. NET substrate activity produces the sympathomimetic effects documented in human intoxication cases: tachycardia, hypertension, tachypnoea, and psychomotor agitationpartially supported
Human intoxications (Italy, 2014-2025): all non-fatal, male patients, psychomotor agitation, psychosis, aggressiveness, CNS depression, cardiac arrhythmias, thoracic pain, tachypnea. ijms262311600
The parallel with 3-MMC's documented compulsive redosing pattern supports this framework.supported
Shorter duration leads to increased craving and redosing. j.drugpo.2025.104971
What is the DAT/SERT selectivity ratio of 3-CMC? The meta-chloro substitution is predicted to shift selectivity toward SERT based on trifluoromethyl SAR data, but no direct measurement exists. This ratio determines whether 3-CMC's profile is more stimulant-like (DAT-preferring) or entactogen-like (balanced/SERT-preferring).supported
Meta-substituted (3-position) ring substituents on methcathinone analogs increase SERT potency but decrease NET/DAT activity. j.ejphar.2012.11.008
Does 3-CMC produce enantioselective pharmacological effects? Enantioselective metabolism is confirmed, but whether the (R)- or (S)-enantiomer drives the primary pharmacological effects — as demonstrated for mephedrone — is unknown.supported
Mephedrone has chiral centre, exists as R and S enantiomers. Enantiomer-specific effects at monoamine transporters demonstrated. bph.12951
pharmacokinetic-detail8 · 7 ok
Langa et al. (2026) administered racemic 3-CMC (10 or 20 mg/kg i.p.) to Wistar rats and demonstrated enantioselective metabolismsupported
Sold as racemate, exhibits enantioselective metabolism. Rats given 10 or 20 mg/kg i.p. bkaf103
Di Trana et al. (2026) enrolled 16 regular psychostimulant users who self-administered 3-CMC at the following doses:supported
16 regular psychostimulant users self-administered 3-CMC orally (100-150 mg) or intranasally (60-80 mg). s12248-025-01200-z
Berardinelli et al. (2024) identified 12 metabolites via human hepatocyte incubation confirmed by LC-HRMS/MS in clinical and forensic specimenssupported
12 metabolites identified for 3-CMC via human hepatocyte incubation + LC-HRMS/MS. s12248-024-00940-8
Feliu et al. (2025) confirmed four primary HLM metabolites: M1 (aliphatic hydroxylation), M2 (N-demethylation), M3 (β-keto reduction), and M4 (M1 + β-keto reduction)supported
Four primary metabolites: M1 (hydroxylation of aliphatic group), M4 (M1 + beta-keto reduction), M2 (N-demethylation), M3 (beta-keto reduction). j.forsciint.2025.112364
A notable finding from Di Trana et al. (2026) is route-dependent metabolic divergence: oral administration produced three exclusive metabolites absent after intranasal dosing, while the β-hydroxylated metabolite (β-OH-3-CMC) accumulated preferentially after intranasal administrationpartially supported
N-acetylation occurs primarily via oral route; β-OH-3-CMC accumulates more after intranasal use. s12248-025-01200-z
Olesti et al. (2019) demonstrated in a double-blind, randomised, Phase I clinical trial that mephedrone metabolism is CYP2D6-mediatedsupported
Randomized crossover Phase I clinical trial of mephedrone 50-200 mg... Mephedrone metabolic disposition mediated by CYP2D6. cpt.1417
Claim in pharmacokinetic-detail — inconclusiveinconclusiveworking →
Dihydro-3-CMC is therefore the recommended forensic biomarker for documenting 3-CMC intake, particularly in cases where specimen collection is delayed or storage conditions are suboptimalsupported
Dihydrometabolites more stable. All detectable to 90 days. dta.3782
comparative-pharmacology6 · 6 ok
Mephedrone's pharmacokinetics have been characterised in a Phase I clinical trial: CYP2D6 mediates its primary metabolism, and poor metabolisers face elevated plasma concentrations and toxicity risksupported
Randomized crossover Phase I clinical trial of mephedrone 50-200 mg... Mephedrone metabolic disposition mediated by CYP2D6. Low CYP2D6 functionality increases toxicity risk. cpt.1417
Structure-activity relationship data from trifluoromethyl methcathinone analogs demonstrate that meta-ring substitution increases SERT release potency relative to DAT compared to para- and unsubstituted analogssupported
Meta-substituted (3-position) ring substituents on methcathinone analogs increase SERT potency but decrease NET/DAT activity. j.ejphar.2012.11.008
4-CMC has been characterised in standardised in vitro assays: Chojnacki et al. (2023) demonstrated that it functions as a substrate at DAT, NET, and SERT with comparable potency, increasing blood pressure, heart rate, and locomotor activity in ratssupported
4-CMC functions as substrate (releaser) at DAT, NET, SERT with similar potency at all three transporters... 4-CMC increased blood pressure, heart rate, and locomotor activity in rats. jpet.122.001478
Its acute pharmacological effects have been studied in controlled human settings, including route comparison (oral vs intranasal) and alcohol interactionpartially supported
10 subjects self-administered mephedrone orally (100-200 mg) or intranasally (50-100 mg). Both routes enhanced euphoria and cardiovascular effects. ph14020100
Van Amsterdam et al. (2025) documented a systematic pattern with 3-MMC: its shorter duration of action relative to mephedrone leads to increased craving and more frequent redosingsupported
Shorter duration leads to increased craving and redosing. j.drugpo.2025.104971
This distinction, established by Baumann et al. (2018), separates compounds like 3-CMC, 4-CMC, and mephedrone (releasers) from α-pyrrolidinophenone cathinones such as α-PVP and MDPV (DAT blockers)supported
Ring-substituted cathinones like mephedrone are transporter substrates (releasers)... whereas pyrrolidine cathinones are blockers. 164_2018_178
receptor-pharmacology6 · 5 ok
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
The same study confirmed enhanced non-selective dopamine/serotonin release for chloromethcathinone analogs.supported
Chloromethcathinones enhance non-selective DA/5-HT release. s12640-020-00227-8
Structure-activity relationships. Cozzi et al. (2013) demonstrated that meta-ring substitution on the methcathinone scaffold (using trifluoromethyl probes) increases SERT release potency relative to DAT compared to unsubstituted analogssupported
Meta-substituted (3-position) ring substituents on methcathinone analogs increase SERT potency but decrease NET/DAT activity. j.ejphar.2012.11.008
Saha et al. (2015) demonstrated differential monoamine transporter effects among second-generation mephedrone analogs, confirming that minor structural modifications significantly alter the DAT/SERT selectivity ratio.supported
4-MEC is SERT substrate + DAT blocker; 4-MePPP is DAT/NET blocker. Structural modifications govern DAT vs SERT selectivity in cathinone class. npp.2014.325
Baumann et al. (2018) established the canonical framework: ring-substituted cathinones are transporter substrates (releasers), not blockers, and all cathinones in this structural class increase extracellular monoamine concentrations in the brain.supported
Ring-substituted cathinones like mephedrone are transporter substrates (releasers)... All increase extracellular monoamines. 164_2018_178
Enantioselective metabolism is confirmed: Langa et al. (2026) demonstrated that enantiomeric fractions of both parent compound and three metabolite pairs deviated significantly from 0.5 in Wistar ratssupported
exhibits enantioselective metabolism... three enantiomeric metabolite pairs. Enantiomeric enrichment observed. bkaf103
summary6 · 6 ok
It emerged as a successive replacement following international control of mephedrone (2010) and 4-CMC (2020), and by 2024 accounted for over 63% of all new psychoactive substance seizures in Europepartially supported
In 2024, 3-Chloromethcathinone (3-CMC) accounted for over 63% of all New Psychoactive Substances seized in Europe s12248-025-01200-z
3-CMC functions as a substrate-type releaser, increasing extracellular concentrations of dopamine, serotonin, and norepinephrinepartially supported
Chloromethcathinones enhance non-selective DA/5-HT release. s12640-020-00227-8
Structural analogy with 4-CMC and structure-activity relationship data for meta-substituted cathinones suggest relatively greater serotonergic activity compared to para-substituted analogs, though this has not been confirmed with direct binding assayssupported
Meta-substituted (3-position) ring substituents on methcathinone analogs increase SERT potency but decrease NET/DAT activity. j.ejphar.2012.11.008
Cardiovascular toxicity is the primary safety concern: cardiac arrhythmias and thoracic pain are documented in human intoxication cases, and computational ADMET modelling predicts cardiotoxicity risk across all CMC isomerssupported
cardiac arrhythmias, thoracic pain, tachypnea. Main predicted metabolism: N-dealkylation, N-hydroxylation, phenyl hydroxylation. Cardiotoxicity risk predicted for all CMC compounds. ijms262311600
Fatal cases involving 3-CMC have been reported, including cases where it was the sole identified substance, though the majority of fatalities involve polydrug usesupported
27 death cases from Department of Forensic Medicine in Kraków, 2016-2022. 52% 4-CMC, 48% 3-CMC. 82% polydrug cases. bkad070
The compound's short duration of action is associated with compulsive redosing and elevated dependence liability, mirroring patterns documented for the structural analog 3-MMCsupported
Shorter duration leads to increased craving and redosing. j.drugpo.2025.104971
chemistry4 · 3 ok
Enantioselective metabolism has been confirmed in Wistar rats: both the parent drug and its three pairs of enantiomeric metabolites exhibited enantiomeric fractions significantly different from 0.5 following acute intraperitoneal exposure at 10 and 20 mg/kgsupported
exhibits enantioselective metabolism. Rats given 10 or 20 mg/kg i.p., sacrificed 24h later. 3-CMC detected exclusively in urine with three enantiomeric metabolite pairs. Enantiomeric enrichment observed. bkaf103
Meta-substitution on the cathinone scaffold has been associated with increased serotonin transporter potency relative to dopamine transporter potency compared to para-substituted analogs.supported
Meta-substituted (3-position) ring substituents on methcathinone analogs increase SERT potency but decrease NET/DAT activity. j.ejphar.2012.11.008
For the structural analog mephedrone, enantioselective neurochemical and behavioural effects have been demonstrated in rats, suggesting that enantiomer-specific pharmacology may be clinically relevant for 3-CMC as well.supported
Mephedrone has chiral centre, exists as R and S enantiomers. Enantiomer-specific effects at monoamine transporters demonstrated. bph.12951
Claim in chemistry — inconclusiveinconclusiveworking →
clinical-evidence1 · 1 ok
The most direct human pharmacological data come from Di Trana et al. (2026), an observational, uncontrolled, naturalistic study in 16 regular psychostimulant users who self-administered 3-CMCsupported
16 regular psychostimulant users self-administered 3-CMC orally (100-150 mg) or intranasally (60-80 mg). s12248-025-01200-z
history1 · 1 ok
2023: 3-CMC accounted for more than 46% of all NPS-related seizures in Europesupported
3-CMC accounts for over 46% of NPS-related seizures in 2023. bkaf103