generation run 2026-05-08
65 min completedmodel pipeline-v5plan not recordedrun/096abe08…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
9 further caveats recorded as free text — readable on the working page
Reproduce
- inputs
- 27 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
24 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | OpenAlex | synthetic cathinone monoamine transporter substrate releaser (citations sort) | 8 | 2 | Foundational pharmacology papers for cathinone class, provides context for 4-CMC mechanism |
| 2 | ClinicalTrials.gov · absence | clephedrone 4-CMC synthetic cathinone | 0 | 0 | No results - absence of trials is itself a finding |
| 3 | PubChem | clephedrone | 1 | 1 | Primary chemical identity confirmation |
| 4 | PubMed | PMID 41515970 - Poyatos et al. IJMS 2025 | 1 | 1 | Only controlled human study of clephedrone effects and PK |
| 5 | PubMed | 4-CMC cathinone synthetic stimulant | 11 | 4 | Additional relevant papers on behavioral pharmacology, stability, and detection |
| 6 | PubMed/OpenAlex | PMID 29963211 - Tomczak et al. Forensic Toxicology 2018 | 1 | 1 | Only forensic blood concentration dataset for 4-CMC with case data |
| 7 | PubMed | clephedrone 4-chloromethcathinone pharmacology | 14 | 14 | All directly relevant to 4-CMC pharmacology, toxicology, metabolism, or detection |
| 8 | PubMed | PMID 36669877 - Chojnacki et al. JPET 2023 | 1 | 1 | Key pharmacology paper with transporter data |
| 9 | OpenAlex | 4-chloromethcathinone clephedrone pharmacology (citations sort) | 10 | 3 | High-citation review and forensic case data directly relevant to 4-CMC |
| 10 | PubMed | PMID 28657185 - Grifell et al. Human Psychopharmacology 2017 | 1 | 1 | Early systematic review of 4-CMC patterns and toxicity |
| 11 | WebSearch | 4-CMC clephedrone harm reduction drug checking testing | 10 | 1 | Harm reduction context for adulteration risk |
| 12 | PubMed | PMID 25280452 Taschwer 2014 | 1 | 1 | First literature description of clephedrone |
| 13 | PubMed | PMID 37033613 Lopes 2023 metabolic stability cathinones | 1 | 1 | Key pharmacokinetic classification of 4-CMC clearance |
| 14 | WebSearch | 4-chloromethcathinone first appearance drug market 2014 EMCDDA Europe seizures | 10 | 1 | Establishes historical first appearance |
| 15 | WebSearch | clephedrone 4-CMC legal status scheduling UK US EU controlled substance 2026 | 10 | 3 | Core legal status data for major jurisdictions |
| 16 | PubMed | PMID 37698450 postmortem chloromethcathinone isomers | 1 | 1 | Largest postmortem case series for CMC isomers |
| 17 | WebFetch / PMC | Extract specific EC50, Ki values for 4-CMC transporter assays | 1 | 1 | Critical quantitative pharmacology data |
| 18 | WebSearch | DEA Schedule I 4-chloromethcathinone 4-CMC effective date 2025 Federal Register | 10 | 1 | Definitive US scheduling date and justification |
| 19 | WebSearch | clephedrone 4-CMC Australia Canada controlled substance scheduling | 10 | 2 | Australia confirmed; Canada unclear |
| 20 | PubMed | PMID 31425490 Contrucci 2020 cathinone drug interactions | 1 | 1 | Drug interaction profile for synthetic cathinone class |
| 21 | WebFetch | Specific EC50 and transporter data for 4-CMC | 1 | 1 | Critical quantitative pharmacology data for article |
| 22 | Multiple | Cross-reference pharmacological mechanism, seizure data, and legal status | 1 | 0 | Consistency check across sources |
| 23 | WebSearch | DEA Schedule I 4-chloromethcathinone 4-CMC effective date 2025 Federal Register | 10 | 1 | Definitive US scheduling confirmation |
| 24 | WebFetch | Dosage, duration, subjective effects, harm reduction for 4-CMC | 1 | 1 | Only user-report harm reduction data found for onset timing; labeled web_retrieved/low confidence |
92 claims by section — every cited sentence, checked against its source
safety30 · 26 ok
Claim in safety — inconclusiveinconclusiveworking →
Jurowski published the first in silico toxicity assessment, which predicted significant acute toxicity with species-specific variability, moderate genotoxic potential (risk of DNA damage), and notable cardiotoxicity risk via hERG channel inhibitionsupported
First in silico toxicity assessment of 4-CMC. Predicted significant acute toxicity, moderate genotoxic potential, notable cardiotoxicity risk via hERG channel inhibition. ijms25115867
Bassi et al. independently predicted drug-drug interaction potential and cardiotoxicity for CMC compounds including 4-CMC. All LD₅₀, genotoxicity, and hERG inhibition values are computational predictions only — no in vitro or in vivo confirmation has been published.supported
ADMET prediction for 4-CMC compared to 3-CMC analogues. Drug-drug interaction potential and cardiotoxicity predicted for all CMC compounds. ijms262311600
Zhou et al. demonstrated cytotoxicity in SH-SY5Y human neuroblastoma cells: ATP depletion (IC₅₀ ~1.4 mM), decreased mitochondrial membrane potential, impaired electron transport chain function, increased reactive oxygen species (ROS), and induction of apoptosis via the endogenous (mitochondrial) pathwaysupported
4-CMC is cytotoxic in SH-SY5Y cells (IC50 for ATP depletion ~1.4 mM). Decreases mitochondrial membrane potential, impairs electron transport chain, increases ROS, induces apoptosis via endogenous pathway. ijms21082841
The para-chloro substitution specifically increased toxicity compared to unsubstituted methcathinonesupported
Para-chloro substitution increases neurotoxicity. ijms21082841
Critically, the cytotoxic concentration (~1.4 mM) substantially exceeds plasma concentrations observed in living users (1.3–75.3 ng/mL ≈ 0.007–0.38 µM) and even in fatalities (56.2–1870 ng/mL ≈ 0.28–9.5 µM)supported
blood concentrations: nonfatal 1.3-75.3 ng/mL, fatalities 56.2-1870 ng/mL s11419-018-0427-8
Wojcieszak et al. found that 4-CMC cytotoxicity in SH-SY5Y cells emerged and intensified after prolonged incubation, suggesting an indirect mechanism unrelated to acute monoamine transporter interactions — potentially relevant to chronic or repeated-use toxicity.supported
Cytotoxicity vs SH-SY5Y cells intensifies after prolonged incubation, suggesting indirect mechanism unrelated to monoamine transporters. s12640-020-00227-8
In telemetry-implanted rats, clephedrone produced blood pressure and heart rate elevation comparable to mephedrone at equivalent dosessupported
Increased BP, HR, and locomotor activity to similar extent as mephedrone in rats. jpet.122.001478
In silico modeling predicts hERG channel inhibition, suggesting potential QT interval prolongation — though this prediction lacks experimental confirmationsupported
notable cardiotoxicity risk via hERG channel inhibition. ijms25115867
Claim in safety — inconclusiveinconclusiveworking →
Trynda et al. demonstrated that clephedrone at forensically relevant concentrations (170 ng/mL and 2700 ng/mL) alters the surface charge density of erythrocyte and platelet membranessupported
Clephedrone at 170 ng/mL and 2700 ng/mL alters surface charge density of erythrocyte and platelet membranes measured by microelectrophoresis. molecules31020234
Tomczak et al. reported forensic blood concentrations from 15 cases: non-fatal intoxications ranged from 1.3 to 75.3 ng/mL; fatalities ranged from 56.2 to 1870 ng/mLsupported
15 forensic cases; blood concentrations: nonfatal 1.3-75.3 ng/mL, fatalities 56.2-1870 ng/mL s11419-018-0427-8
Romańczuk et al. examined 27 CMC-related deaths in Kraków, Poland (2016–2022), involving primarily 3-CMC and/or 4-CMC isomers. All published fatalities involved polydrug use; no clean 4-CMC monocause fatality has been confirmed in published literaturesupported
27 CMC-related deaths in Kraków 2016-2022. Toxicological interpretation is challenging; unpredictable effects noted. bkad070
A fatal polydrug case reported by Nowak et al. involved 4-CMC alongside U-47700, N-ethylhexedrone, adinazolam, 4-CIC, and sertraline — U-47700 concentration (1470 ng/mL) was consistent with lethal opioid toxicity, and 4-CMC was not the proximate cause of death.supported
Fatal polydrug intoxication (Poland 2017). Blood: 4-CMC 1.7 ng/mL, U-47700 1470 ng/mL. s11419-020-00568-1
Klavž et al. reported the first clinical identification of 4-CMC in Slovenia: a 38-year-old male presented after ingesting a mixture including AB-CHMINACA, AB-FUBINACA, alpha-PHP, alpha-PVP, and 4-CMC in a suicide attemptsupported
Case report: 38-year-old male, non-fatal intoxication with 5 NPS including 4-CMC. First positive identification of these 5 drugs by a clinical laboratory in Slovenia. j.forsciint.2016.01.018
Claim in safety — inconclusiveinconclusiveworking →
Compulsive redosing is driven by the dopaminergic component (DAT release EC₅₀ = 91 nM). The compound's low clearance means each subsequent dose compounds existing plasma concentration, escalating both cardiovascular and psychological risksupported
4-CMC is a LOW clearance compound (unlike most other cathinones which are intermediate clearance). fphar.2023.1145140
Sensitization rather than tolerance: Wojcieszak et al. found that 7-day intermittent 4-CMC treatment produced behavioral sensitization in DBA/2J mice — locomotor activity increased with repeated exposuresupported
4-CMC increases locomotor activity and produces behavioral sensitization after 7-day intermittent treatment. s12640-021-00329-x
Conditioned place preference: 4-CMC produced no conditioned place preference in DBA/2J mice at tested doses, contrasting with the more dopamine-selective 4-MeO-PVPsupported
4-CMC did NOT produce conditioned place preference (unlike 4-MeO-PVP). s12640-021-00329-x
Withdrawal: No significant withdrawal symptoms were detected in mice following 14-day intermittent treatment, as assessed by tail suspension test, forced swim test, and sucrose preference testsupported
No significant withdrawal symptoms after 14-day treatment. s12640-021-00329-x
Abuse liability framework: The balanced DAT/SERT activity theoretically reduces abuse liability relative to purely dopamine-selective agents, though clephedrone's DAT release EC₅₀ of 91 nM is sufficient to produce robust reinforcement.supported
DAT>SERT selectivity associated with high abuse potential. 7854_2016_18
Clephedrone releases large quantities of serotonin, dopamine, and norepinephrine; MAOIs prevent their metabolic degradation, producing potentially fatal monoamine accumulation.supported
Serotonin syndrome risk with MAOIs and serotonergic medications. ftd.0000000000000682
Claim in safety — inconclusiveinconclusiveworking →
Opioids: While not a direct pharmacodynamic interaction with clephedrone's mechanism, the fatal case reported by Nowak et al. — involving U-47700 (a synthetic opioid) alongside 4-CMC — demonstrates the extreme fatality risk of stimulant-opioid polydrug combinations.supported
Fatal polydrug intoxication (Poland 2017). Blood: 4-CMC 1.7 ng/mL, U-47700 1470 ng/mL. s11419-020-00568-1
Antihypertensives: Clephedrone's robust α₁-adrenergic-mediated hypertension may overcome antihypertensive medications, producing unpredictable blood pressure effects.supported
Increased BP, HR, and locomotor activity to similar extent as mephedrone in rats. jpet.122.001478
Given its low-clearance classification, CYP inhibitors that further reduce clephedrone clearance could significantly increase plasma concentrations — a potentially dangerous interaction that cannot currently be predicted or quantified.supported
4-CMC is a LOW clearance compound. Keto reduction and hydroxylation are main Phase I reactions; glucuronide conjugation as Phase II. fphar.2023.1145140
Concurrent MAOI therapy (including moclobemide, phenelzine, tranylcypromine, selegiline at antidepressant doses) — risk of fatal serotonin syndrome and hypertensive crisissupported
Serotonin syndrome risk with MAOIs and serotonergic medications; cardiovascular interactions with antihypertensives. ftd.0000000000000682
Severe cardiovascular disease (uncontrolled hypertension, recent myocardial infarction, decompensated heart failure, known arrhythmias) — clephedrone produces significant blood pressure and heart rate elevation with predicted hERG channel inhibitionsupported
Increased BP, HR, and locomotor activity to similar extent as mephedrone in rats. jpet.122.001478
Severe cardiovascular disease (uncontrolled hypertension, recent myocardial infarction, decompensated heart failure, known arrhythmias) — clephedrone produces significant blood pressure and heart rate elevation with predicted hERG channel inhibitionsupported
notable cardiotoxicity risk via hERG channel inhibition. ijms25115867
Hepatic impairment — low-clearance compound; impaired hepatic metabolism could produce dangerous accumulationsupported
4-CMC is a LOW clearance compound. Keto reduction and hydroxylation are main Phase I reactions; glucuronide conjugation as Phase II. fphar.2023.1145140
pharmacokinetic-detail13 · 13 ok
Oral fluid concentration peaked within the first 3 hours after 100 mg oral dosing — a substantially delayed profile compared to methylone under similar conditionssupported
delayed onset and peak compared to methylone. ijms27010089
Human pharmacokinetic data are limited to observational studies using oral doses of 100–150 mg in small cohortssupported
Human observational study: 8 volunteers self-administered 100 or 150 mg oral clephedrone. Oral fluid PK data collected over 5 h. ijms27010089
Human pharmacokinetic data are limited to observational studies using oral doses of 100–150 mg in small cohortssupported
4-CMC (100 mg oral) in 6 consumers. ijms24119387
Human pharmacokinetic data are limited to observational studies using oral doses of 100–150 mg in small cohortssupported
4-CMC administered orally (100-150 mg) to volunteers. j.jpba.2024.115994
Oral fluid concentration peaked within the first 3 hours after 100 mg oral dosing — a substantially delayed profile compared to methylone under similar conditionssupported
peak oral fluid concentration in first 3 hours. ijms24119387
No intranasal pharmacokinetic data exist for 4-CMC; intranasal data reported in the same studies pertain to N-ethylpentedrone and N-ethylhexedrone, not clephedrone.supported
4-CMC administered orally (100-150 mg) to volunteers. j.jpba.2024.115994
No intranasal pharmacokinetic data exist for 4-CMC; intranasal data reported in the same studies pertain to N-ethylpentedrone and N-ethylhexedrone, not clephedrone.supported
4-CMC (100 mg oral) in 6 consumers. ijms24119387
Berardinelli et al. conducted the most comprehensive metabolic profiling of clephedrone using human hepatocyte incubation combined with LC-HRMS/MS, validated against clinical and forensic urine samplessupported
Identified 10 metabolites for 4-CMC via human hepatocyte incubation. s12248-024-00940-8
Massano et al. confirmed Phase I metabolites (ketoreduction, hydroxylation, dealkylation) and identified 4-CMC-glucuronide as a relevant Phase II metabolite in urinesupported
Phase-I and glucuronide metabolites identified. 4-CMC detected at high concentrations in original form up to 5h post-administration. j.jpba.2024.115994
Lopes et al. identified ketoreduction and hydroxylation as common metabolic pathways, with glucuronic acid conjugation to ketoreduced metabolites as the sole Phase II transformation.supported
Keto reduction and hydroxylation are main Phase I reactions; glucuronide conjugation as Phase II. fphar.2023.1145140
Lopes et al. formally classified 4-CMC as a low-clearance compound based on human hepatocyte incubation — distinct from the intermediate-clearance classification of most other synthetic cathinones studiedsupported
4-CMC is a LOW clearance compound (unlike most other cathinones which are intermediate clearance). fphar.2023.1145140
Romańczuk et al. detected dihydro-CMC in blood in all 27 CMC-related deaths examined, even when the parent compound was absent due to degradation.supported
Stability problems in biological matrices; dihydro-CMC is better biomarker of intake. bkad070
Adamowicz documented degradation in blood and urine at room temperature and at +4°Cpartially supported
Significant instability observed, particularly at room temperature. j.forsciint.2018.12.001
pharmacology13 · 12 ok
Chojnacki et al. characterized the transporter pharmacology in rat synaptosomes using both uptake inhibition and substrate release assayssupported
4-CMC functions as substrate at DAT, NET, and SERT with potency similar to mephedrone. jpet.122.001478
The DAT/SERT release potency ratio of approximately 1.85:1 places clephedrone in an intermediate selectivity range: modestly dopamine-preferring relative to MDMA but substantially less DAT-selective than purely dopaminergic cathinones such as α-PVP.supported
QSAR analysis of 4-substituted methcathinone series. DAT>SERT selectivity associated with high abuse potential. Volume of 4-position substituent is key determinant of DAT vs SERT selectivity. 7854_2016_18
As a β-keto amphetamine, clephedrone does not appear to be a TAAR1 (trace amine-associated receptor 1) ligand — a class distinction between cathinones and non-β-keto amphetaminessupported
Cathinones not TAAR1 ligands. j.1476-5381.2012.02145.x
Claim in pharmacology — inconclusiveinconclusiveworking →
In telemetry-implanted rats, clephedrone (1, 3, and 10 mg/kg i.p.) produced dose-dependent cardiovascular and locomotor effects:supported
Increased BP, HR, and locomotor activity to similar extent as mephedrone in rats. jpet.122.001478
Wojcieszak et al. confirmed dose-dependent horizontal locomotor stimulation in mice, with a locomotor profile consistent with monoamine releasing agents — enhanced horizontal but not vertical locomotion, contrasting with dopamine-selective cathinones.supported
4-CMC stimulates horizontal locomotor activity in mice dose-dependently. s12640-020-00227-8
Human pharmacokinetic data for clephedrone derive from small observational studies using oral administration at 100–150 mgsupported
Human observational study: 8 volunteers self-administered 100 or 150 mg oral clephedrone. ijms27010089
Human pharmacokinetic data for clephedrone derive from small observational studies using oral administration at 100–150 mgsupported
4-CMC administered orally (100-150 mg) to volunteers; urine collected. j.jpba.2024.115994
Human pharmacokinetic data for clephedrone derive from small observational studies using oral administration at 100–150 mgsupported
4-CMC (100 mg oral) in 6 consumers; peak oral fluid concentration in first 3 hours. ijms24119387
After 100 mg oral administration, 4-CMC reached maximum oral fluid concentration within the first 3 hours — substantially later than intranasally administered cathinones (NEP and NEH), which peaked within the first hoursupported
4-CMC (100 mg oral) in 6 consumers; peak oral fluid concentration in first 3 hours. ijms24119387
High concentrations of unchanged parent compound persisted in urine 5 hours after oral administration, attributed to a long half-life and low intrinsic clearancesupported
4-CMC detected at high concentrations in original form up to 5h post-administration, suggesting long half-life and low intrinsic clearance. j.jpba.2024.115994
Lopes et al. formally classified 4-CMC as a low-clearance compound using human hepatocyte incubation — in contrast to most other cathinones tested, which were classified as intermediate clearancesupported
4-CMC is a LOW clearance compound (unlike most other cathinones which are intermediate clearance). fphar.2023.1145140
Approximately 0.3% of an orally administered dose was recovered in sweat over 4 hours.supported
Excreted in sweat ~0.3% of administered dose. ijms24119387
summary12 · 6 ok
Claim in summary — not_supportednot supportedworking →
Claim in summary — not_supportednot supportedworking →
Clephedrone (4-chloromethcathinone, 4-CMC) is a synthetic substituted cathinone and non-selective monoamine releasing agent that acts as a full substrate at the dopamine, norepinephrine, and serotonin transporters with potency virtually identical to mephedronesupported
4-CMC functions as substrate at DAT, NET, and SERT with potency similar to mephedrone. jpet.122.001478
Claim in summary — inconclusiveinconclusiveworking →
First characterized in 2014 from a commercially available online research chemical sample, clephedrone rapidly became one of the most frequently seized synthetic cathinones in Europe by the mid-2020spartially supported
First characterization of clephedrone. Confirmed identity by GC-MS and NMR. Sold via Internet from deboralabs.com. j.forsciint.2014.09.007
Claim in summary — inconclusiveinconclusiveworking →
Claim in summary — inconclusiveinconclusiveworking →
Subjective effects have been broadly described as stimulant-like in the single controlled human observation, with pharmacological modeling predicting both psychostimulant and empathogenic qualities based on the balanced monoamine release profile.supported
Stimulant-like subjective effects; delayed onset and peak compared to methylone. ijms27010089
Claim in summary — inconclusiveinconclusiveworking →
No in vivo LD₅₀ data exist; in silico modeling predicts significant acute toxicity and hERG channel inhibitionsupported
First in silico toxicity assessment of 4-CMC. Predicted significant acute toxicity, moderate genotoxic potential, notable cardiotoxicity risk via hERG channel inhibition. ijms25115867
All published fatalities involving clephedrone are polydrug cases, and forensic blood concentrations in non-fatal and fatal cases overlap substantially (1.3–75.3 ng/mL vs 56.2–1870 ng/mL), precluding any concentration-based lethality thresholdsupported
15 forensic cases; blood concentrations: nonfatal 1.3-75.3 ng/mL, fatalities 56.2-1870 ng/mL s11419-018-0427-8
The compound's low intrinsic clearance raises the risk of accumulation with repeated dosingsupported
4-CMC is a LOW clearance compound (unlike most other cathinones which are intermediate clearance). fphar.2023.1145140
chemistry6 · 3 ok
Claim in chemistry — inconclusiveinconclusiveworking →
Within the quantitative structure-activity framework established for 4-substituted methcathinones, the chloro substituent — a large, moderately electronegative halogen — produces a balanced DAT/SERT selectivity profile intermediate between the fluorine analogue (flephedrone, SERT-preferring) and the methyl analogue (mephedrone, slightly DAT-preferring).supported
Volume of 4-position substituent is key determinant of DAT vs SERT selectivity. 7854_2016_18
Claim in chemistry — inconclusiveinconclusiveworking →
Commercially available material is a racemic mixture, as confirmed by Taschwer et al. using enantioselective gas chromatography and capillary electrophoresissupported
Racemic mixture confirmed; chiral separation by GC and CE developed. j.forsciint.2014.09.007
Claim in chemistry — inconclusiveinconclusiveworking →
The compound is notably unstable in biological matrices: degradation occurs at room temperature and even at +4°C over extended storage periodspartially supported
Significant instability observed, particularly at room temperature. j.forsciint.2018.12.001
history6 · 4 ok
Clephedrone was first described in the scientific literature in 2014 by Taschwer et al. at Karl-Franzens-University Graz, who characterized a commercially available sample obtained from an online vendorsupported
First characterization of clephedrone. Confirmed identity by GC-MS and NMR. Sold via Internet from deboralabs.com. j.forsciint.2014.09.007
The compound was first detected on the European drug market in June 2014, placing it among a wave of para-halogenated cathinones that emerged following the scheduling of earlier cathinones — particularly mephedrone and flephedrone — in several European jurisdictions.supported
Systematic review of clephedrone (4-CMC), 4-CEC, and 4-BMC on recreational drug markets. Analysis of market samples and available information on these para-halogenated cathinones. hup.2621
Majchrzak et al. identified 4-CMC as part of a broader wave of ring-substituted methcathinone analogues designed to circumvent scheduling laws during 2014–2017supported
Review of new synthetic cathinones 2014-2017. Para-substituted methcathinone derivatives including 4-CMC discussed. s11419-017-0385-6
Claim in history — not_supportednot supportedworking →
Spanish drug checking services (Energy Control) identified clephedrone in 29 samples between 2014 and 2016, often sold misrepresented as 3-MMC, MDMA, ketamine, or other cathinonessupported
Systematic review of clephedrone (4-CMC), 4-CEC, and 4-BMC on recreational drug markets. Analysis of market samples. hup.2621
Claim in history — not_supportednot supportedworking →
neuroscience5 · 3 ok
What is the dose-response relationship for cardiovascular toxicity in humans? Animal data confirm dose-dependent hypertension and tachycardia, but no human dose-response data exist for any cardiovascular endpoint.supported
Increased BP, HR, and locomotor activity to similar extent as mephedrone in rats. jpet.122.001478
Claim in neuroscience — inconclusiveinconclusiveworking →
Claim in neuroscience — inconclusiveinconclusiveworking →
The absence of conditioned place preference in DBA/2J mice is consistent with this framework, though species-specific factors limit extrapolation.supported
4-CMC did NOT produce conditioned place preference (unlike 4-MeO-PVP). s12640-021-00329-x
The low-clearance profile of clephedrone may extend both the acute pharmacodynamic window and the subsequent recovery phase relative to faster-metabolized cathinones.supported
4-CMC is a LOW clearance compound (unlike most other cathinones which are intermediate clearance). fphar.2023.1145140
comparative-pharmacology3 · 3 ok
Clephedrone and mephedrone differ by a single structural modification — chlorine versus methyl at the para-position of the phenyl ring — and display virtually identical transporter potency in the same assay system:supported
4-CMC functions as substrate at DAT, NET, and SERT with potency similar to mephedrone. jpet.122.001478
Cardiovascular effects (blood pressure and heart rate elevation) in telemetry-implanted rats were comparable between the two compounds at equivalent dosessupported
Increased BP, HR, and locomotor activity to similar extent as mephedrone in rats. jpet.122.001478
Negus and Banks established a quantitative structure-activity relationship (QSAR) framework demonstrating that the volume and electronic character of the para-substituent on 4-substituted methcathinones determines the DAT/SERT selectivity ratio and, consequently, abuse potentialsupported
QSAR analysis of 4-substituted methcathinone series. DAT>SERT selectivity associated with high abuse potential. Volume of 4-position substituent is key determinant of DAT vs SERT selectivity. 7854_2016_18
effects-overview2 · 2 ok
Pharmacologically, clephedrone is the nearest analogue to mephedrone among widely circulated synthetic cathinones — near-identical transporter potency but slower metabolic clearancesupported
4-CMC functions as substrate at DAT, NET, and SERT with potency similar to mephedrone. jpet.122.001478
Pharmacologically, clephedrone is the nearest analogue to mephedrone among widely circulated synthetic cathinones — near-identical transporter potency but slower metabolic clearancesupported
4-CMC is a LOW clearance compound (unlike most other cathinones which are intermediate clearance). fphar.2023.1145140
clinical-evidence1 · 1 ok
The sole controlled human pharmacological study was an observational investigation in which 8 healthy volunteers (6 women) self-administered a single oral dose of 100 or 150 mg, with oral fluid sampling and vital sign monitoring over 5 hourssupported
Human observational study: 8 volunteers self-administered 100 or 150 mg oral clephedrone. Oral fluid PK data collected over 5 h. ijms27010089
receptor-pharmacology1 · 1 ok
The definitive quantitative dataset for clephedrone's transporter interactions was established by Chojnacki et al. in rat synaptosomes:supported
4-CMC functions as substrate at DAT, NET, and SERT with potency similar to mephedrone. jpet.122.001478