generation run 2026-04-27
63 min completedmodel pipeline-v5plan not recordedrun/948de6d0…Selection
Verification
- record
- seen / partial
- working
The model's own caveats
- sparse_evidence
Reproduce
- inputs
- 25 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
20 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | CFSRE/WebFetch | DCK legal status and forensic data | 1 | 1 | US legal status and recent forensic detection data |
| 2 | RSC/WebFetch | DCK synthesis and stereochemistry | 1 | 1 | Primary source for DCK synthesis route and stereochemistry |
| 3 | PubMed | DCK new psychoactive substance arylcyclohexylamine forensic case report | 15 | 5 | All contain DCK-specific data in forensic, kinetic, or case report context |
| 4 | WebSearch | deschloroketamine legal status scheduling US UK EU | 10 | 2 | Legal status not available via PubMed API; web fallback necessary |
| 5 | PubMed | deschloroketamine DCK pharmacology | 4 | 4 | All directly relevant to DCK pharmacology, toxicity, or forensic cases |
| 6 | OpenAlex | DCK rat study references | 1 | 1 | Key PK/PD paper - used to trace citation graph |
| 7 | PubChem | deschloroketamine | 1 | 1 | Primary chemical identity verification |
| 8 | Crossref/DOI verify | 10.1039/C8NJ03107J | 1 | 1 | Key synthesis/stereochemistry paper; RSC published |
| 9 | ClinicalTrials.gov · absence | deschloroketamine | 0 | — | Confirms no clinical trial program exists |
| 10 | OpenAlex | deschloroketamine NMDA receptor dissociative | 15 | 2 | Core pharmacology papers with citation context |
| 11 | Erowid/WebFetch | DCK user experience reports | 1 | 1 | Community user report data for phenomenological section |
| 12 | ClinicalTrials.gov · absence | deschloroketamine | 0 | — | Confirms no therapeutic trial program |
| 13 | WebSearch | deschloroketamine original discovery 1962 patent CAS 7063-30-1 | 10 | 2 | Chemical identity and historical context |
| 14 | PubChem CID 437168 (second lookup) | CID 437168 SMILES | 1 | 1 | — |
| 15 | PubMed | PMID 38786747, 32460225, 35445267, 31327332 | 4 | 4 | — |
| 16 | OpenAlex | ketamine analogue NMDA binding Ki dissociative potency SAR arylcyclohexylamine | 9 | 1 | — |
| 17 | Crossref | verify DOI 10.1039/C8NJ03107J | 1 | 1 | DOI verification for key synthesis/stereochemistry paper |
| 18 | WebSearch | deschloroketamine EMCDDA UK Misuse of Drugs Act scheduling | 10 | 1 | Key legal status confirmation |
| 19 | WebSearch | deschloroketamine Australia legal TGA Poisons Standard | 10 | — | — |
| 20 | PsychonautWiki/WebFetch | DCK pharmacology, doses, effects, legal status | 1 | 1 | Community reference for dose verification |
82 claims by section — every cited sentence, checked against its source
safety22 · 18 ok
Zebrafish: DCK produces 100% larval mortality at 2000 µM in the Maximum Tolerated Concentration (MTC) test at 8 days post-fertilisation, with low embryo mortality at equivalent concentrations in early developmental stages — attributed to the absence of NMDA receptors in early zebrafish lifesupported
DCK and 2F-DCK exhibited low embryo mortality even at higher concentrations. In larval stages, ketamine derivatives led to 100% mortality at 2000 µM in the MTC test. Results support absence of NMDA receptors in early zebrafish life stages. j.toxrep.2025.102018
Claim in safety — inconclusiveinconclusiveworking →
Hypertension and tachycardia are reported in clinical presentations involving DCK-containing polydrug exposuressupported
cardiovascular (hypertension, tachycardia) j.forsciint.2020.110327
Claim in safety — inconclusiveinconclusiveworking →
Suicide by fall from height with DCK, 2F-DCK, and methoxpropamine detected post-mortem — cause of death was traumaticsupported
LC-HRMS characterization of DCK, 2F-DCK, and methoxpropamine in post-mortem blood and hair from a forensic suicide case. j.forsciint.2021.110817
DCK detected at 10–350 µg/L across three 2F-DCK cases (two deaths, one self-mutilation)supported
blood levels 8-350 µg/L bkae021
Fatal polydrug intoxication attributed primarily to 2F-DCK (1780 µg/L) with concurrent stimulants and other dissociativessupported
First fatal case involving 2F-DCK and 3-MeO-PCE. Death attributed to respiratory depression in polydrug context. j.forsciint.2021.110852
The arylcyclohexylamine class broadly produces psychotomimetic effects at sub-anaesthetic doses: paranoia, confusion, agitation, and psychosis-like neurocognitive impairmentsupported
Novel ACXs substitute for PCP in discrimination studies...Neurocognitive deficits documented for PCP class. jpet.123.001942
The arylcyclohexylamine class broadly produces psychotomimetic effects at sub-anaesthetic doses: paranoia, confusion, agitation, and psychosis-like neurocognitive impairmentsupported
Review covering NPS pharmacodynamics, pharmacokinetics, and psychopathological risks; discusses dissociative NPS class. s0033291719001727
Clinical case series report impaired consciousness, agitation, and abnormal behaviour in presentations involving DCK.supported
neurological (impaired consciousness, agitation) j.forsciint.2020.110327
Convulsions occurred in a subset of the 20-patient case series reported by Tang et al. The longer duration of DCK relative to ketamine may prolong the period of psychological vulnerability and disorientation.supported
5 patients lost consciousness or had convulsions. All recovered. j.forsciint.2020.110327
Animal data support meaningful dependence liability: DCK produces both conditioned place preference (rewarding) and intravenous self-administration (reinforcing) in mice, with concurrent dopaminergic activationsupported
DCK (10 mg/kg) produced CPP and increased SA lever presses/infusions in mice. Both DCK and diphenidine increased dopamine in PC-12 cells. DCK has both rewarding and reinforcing effects. j.pbb.2022.173333
Rat behavioural studies confirm addictive profiles similar to ketamine.supported
DCK showed similar behavioural and addictive profiles and pharmacodynamics to ketamine bph.15680
Tang et al. found that in 19 of 20 analytically confirmed 2F-DCK cases, at least one additional ketamine-type drug was detected, with DCK present in 50%supported
20 cases of 2F-DCK exposure; DCK co-detected in 50% of cases. j.forsciint.2020.110327
Matey et al. documented DCK in hair alongside ketamine, 3-MeO-PCP, and methoxetaminesupported
DCK detected alongside 3-MeO-PCP and methoxetamine in hair of defendants positive for ketamine. j.forsciint.2021.111080
Ketamine combined with fentanyl produces greater brain oxygen depletion than either drug alone, while also causing peripheral vasoconstriction that may mask clinical signs of respiratory depressionpartially supported
Ketamine increases brain oxygenation but potentiates brain hypoxia from fentanyl co-administration. j.neuropharm.2023.109465
Synergistic CNS and respiratory depression is anticipated when DCK is combined with alcohol, benzodiazepines, or other sedative-hypnoticssupported
Dissociative designer drugs primarily act as NMDA receptor antagonists; pose similar risks to ketamine. s00204-020-02693-7
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Absolute: Personal or family history of psychotic disorders — NMDA antagonists are established psychotomimetics that can precipitate or exacerbate psychosissupported
Novel ACXs substitute for PCP in discrimination studies...Neurocognitive deficits documented for PCP class. jpet.123.001942
Relative: Cardiovascular disease (hypertension and tachycardia reported in clinical cases); epilepsy or seizure disorders (convulsions observed in a subset of clinical presentations); hepatic impairment (metabolic processing may be compromised); urological conditions (ketamine uropathy risk by class analogy); concurrent use of CNS depressants, opioids, or MAOIs.partially supported
cardiovascular (hypertension, tachycardia); 5 patients lost consciousness or had convulsions. j.forsciint.2020.110327
Relative: Cardiovascular disease (hypertension and tachycardia reported in clinical cases); epilepsy or seizure disorders (convulsions observed in a subset of clinical presentations); hepatic impairment (metabolic processing may be compromised); urological conditions (ketamine uropathy risk by class analogy); concurrent use of CNS depressants, opioids, or MAOIs.partially supported
cardiovascular (hypertension, tachycardia); 5 patients lost consciousness or had convulsions. j.forsciint.2020.110327
pharmacology20 · 18 ok
Claim in pharmacology — inconclusiveinconclusiveworking →
Deschloroketamine functions as an uncompetitive antagonist at the NMDA (N-methyl-D-aspartate) receptor, blocking the ion channel in an open-state-dependent mannersupported
Dissociative designer drugs primarily act as NMDA receptor antagonists; pose similar risks to ketamine. s00204-020-02693-7
No substance-specific binding affinity data (Ki, IC₅₀, or functional potency) for DCK at the NMDA receptor or any other target has been published. The designation as an NMDA antagonist rests on structural analogy with ketamine, confirmatory behavioural pharmacology in rats, and the compound's production of the characteristic dissociative phenotype in both animals and human users.supported
DCK showed similar behavioural and addictive profiles and pharmacodynamics to ketamine, with S-DCK being in general more active. bph.15680
S-DCK is approximately twice as cytotoxic as R-DCK across human cell lines (IC₅₀ in HEK 293T: S-DCK < 0.99 mM, R-DCK ~1.82 mM)supported
(S)-DCK ~2x more cytotoxic than (R)-DCK in HEK293T. c8nj03107j
Rat pharmacodynamic studies confirm S-DCK as "in general more active" across behavioural and pharmacodynamic measuressupported
S-DCK being in general more active bph.15680
The only systematic pharmacological study of DCK in rodents found that it produces behavioural and addictive profiles similar to ketamine in Wistar rats, with a slightly slower pharmacokinetic profile consistent with the longer duration of action reported by users.supported
DCK showed similar behavioural and addictive profiles and pharmacodynamics to ketamine...slightly slower pharmacokinetic profile than ketamine, which is consistent with its reported longer duration of action. bph.15680
At 1 mg/kg/infusion, DCK significantly increases active lever presses and infusions in a self-administration (SA) paradigm, demonstrating reinforcing effectssupported
increased SA lever presses/infusions in mice. DCK has both rewarding and reinforcing effects. j.pbb.2022.173333
DCK also increases dopamine levels in PC-12 cellssupported
Both DCK and diphenidine increased dopamine in PC-12 cells. j.pbb.2022.173333
Novel arylcyclohexylamines as a class produce phencyclidine-like abuse liability and psychosis-like neurocognitive effects in rodent models.supported
Novel ACXs substitute for PCP in discrimination studies...Neurocognitive deficits documented for PCP class. jpet.123.001942
DCK exhibits an unbound fraction (fu) of 0.54–0.84 in pooled human liver microsomes — the lowest protein binding of all ketamine analogues testedsupported
DCK had lowest protein binding (fu 0.54-0.84) j.jpba.2019.113049
The in vitro-in vivo extrapolation (IVIVE) of hepatic clearance for DCK was disregarded by the authors due to low drug elimination under experimental conditions, suggesting a lower hepatic clearance rate than ketamine and 2F-DCKsupported
DCK IVIVE hepatic clearance was disregarded due to low drug elimination under experimental conditions. j.jpba.2019.113049
In rats, DCK and its primary metabolite nordeschloroketamine (NDCK) achieve concentrations of 0.5–860 ng/mL in serum and 0.5–4700 ng/g in brain tissuesupported
DCK concentrations in brain up to 4700 ng/g; serum 0.5-860 ng/mL. dta.2726
Claim in pharmacology — inconclusiveinconclusiveworking →
N-demethylation producing nordeschloroketamine (NDCK), the primary metabolitesupported
Major metabolites: trans-dihydrodeschloroketamine, cis/trans-dihydronordeschloroketamine, nordeschloroketamine. dta.2726
Reduction producing trans-dihydrodeschloroketaminesupported
Major metabolites: trans-dihydrodeschloroketamine... dta.2726
Combined N-demethylation and reduction producing cis- and trans-dihydronordeschloroketaminesupported
cis/trans-dihydronordeschloroketamine dta.2726
Hydroxylation and oxidation producing additional Phase I productssupported
Main pathways: N-dealkylation, hydroxylation, oxidation, glucuronidation, N-acetylation. metabo14050270
Phase II conjugation via glucuronidation and N-acetylation; glucuronide conjugates are unstable in wastewaterpartially supported
Main pathways: N-dealkylation, hydroxylation, oxidation, glucuronidation, N-acetylation. metabo14050270
Phase II conjugation via glucuronidation and N-acetylation; glucuronide conjugates are unstable in wastewatersupported
Phase II glucuronides unstable in WW. All parent compounds detectable after 24h WW incubation. dta.3839
DCK has been confirmed as a metabolite of 2-fluorodeschloroketamine (2F-DCK) in pooled human liver microsomessupported
DCK confirmed as a 2F-DCK metabolite in human liver microsomes. bkad030
history10 · 6 ok
Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
Claim in history — inconclusiveinconclusiveworking →
The first published scientific analytical characterisation of DCK from seized drug material appeared in 2016, when Frison et al. described GC/MS, LC-HRMS, MS/MS, and NMR identification of DCK in seized powders.supported
Analytical characterization of DCK as a new ketamine derivative in seized powders. GC/MS, LC-HRMS, MS/MS, and NMR characterization provided. rcm.7425
2016 — First analytical characterisation from seized materialsupported
Analytical characterization of DCK as a new ketamine derivative in seized powders. rcm.7425
2020 — First metabolite identification and quantification in rat serum and brain tissue; first comparative toxicokinetic study with other ketamine analoguespartially supported
DCK concentrations in brain up to 4700 ng/g; serum 0.5-860 ng/mL. dta.2726
2020 — First metabolite identification and quantification in rat serum and brain tissue; first comparative toxicokinetic study with other ketamine analoguespartially supported
Toxicokinetic comparison of ketamine, norketamine, 2FDCK, methoxetamine, and deschloroketamine. j.jpba.2019.113049
2021 — First post-mortem forensic case with DCK detected in biological matricessupported
LC-HRMS characterization of DCK, 2F-DCK, and methoxpropamine in post-mortem blood and hair from a forensic suicide case. j.forsciint.2021.110817
2022 — First systematic rat pharmacokinetic, pharmacodynamic, and behavioural study; first demonstration of conditioned place preference and self-administration in micepartially supported
DCK showed similar behavioural and addictive profiles and pharmacodynamics to ketamine bph.15680
comparative-pharmacology8 · 8 ok
Potency: User reports cited in the pharmacological literature estimate DCK at approximately 3× the weight-potency of ketamine and ~1.5× that of methoxetamine. These figures derive from community sources, not controlled dose-response studies.supported
reported ~3x more potent than ketamine c8nj03107j
Duration: DCK's oral duration (4–6 hours, community consensus) substantially exceeds ketamine's (1–2 hours), consistent with DCK's lower hepatic clearance observed in vitro and its slower pharmacokinetic profile in rats.supported
DCK IVIVE hepatic clearance was disregarded due to low drug elimination under experimental conditions. j.jpba.2019.113049
Duration: DCK's oral duration (4–6 hours, community consensus) substantially exceeds ketamine's (1–2 hours), consistent with DCK's lower hepatic clearance observed in vitro and its slower pharmacokinetic profile in rats.supported
slightly slower pharmacokinetic profile than ketamine, which is consistent with its reported longer duration of action. bph.15680
Protein binding: DCK shows lower protein binding (fu 0.54–0.84) than ketamine in pooled human liver microsomes, consistent with reduced lipophilicity from dechlorination.supported
DCK had lowest protein binding (fu 0.54-0.84) j.jpba.2019.113049
Enantiomeric pattern: Both compounds follow the S > R potency relationship.supported
S-DCK being in general more active bph.15680
Data from Kim et al. 2022supported
DCK (10 mg/kg) produced CPP and increased SA lever presses/infusions in mice. Both DCK and diphenidine increased dopamine in PC-12 cells. j.pbb.2022.173333
2-Fluorodeschloroketamine (2F-DCK) replaces DCK's unsubstituted phenyl hydrogen at the ortho position with fluorine. 2F-DCK is metabolised to DCK via defluorination in human liver microsomessupported
DCK confirmed as a 2F-DCK metabolite in human liver microsomes. bkad030
The two compounds frequently co-occur in forensic casework: Tang et al. found DCK in 50% of analytically confirmed 2F-DCK intoxication presentations, and Matey et al. detected DCK in hair of individuals testing positive for ketamine alongside other arylcyclohexylamines.supported
20 cases of 2F-DCK exposure; DCK co-detected in 50% of cases. j.forsciint.2020.110327
summary7 · 6 ok
User reports cited in the pharmacological literature place DCK at approximately three times the weight-potency of ketamine, with a substantially longer duration of action: 4–6 hours oral versus ketamine's typical 1–2 hours.partially supported
reported ~3x more potent than ketamine c8nj03107j
Originally proposed as a candidate immunomodulatory and anti-infective agent during the 1960s arylcyclohexylamine structure-activity relationship program, DCK never entered clinical developmentsupported
DCK originally proposed as immunomodulation agent; reported ~3x more potent than ketamine c8nj03107j
It re-emerged on research chemical markets circa 2015 and received its first analytical characterisation from seized material in 2016supported
Analytical characterization of DCK as a new ketamine derivative in seized powders. GC/MS, LC-HRMS, MS/MS, and NMR characterization provided. rcm.7425
Claim in summary — inconclusiveinconclusiveworking →
DCK acts as an uncompetitive NMDA receptor antagonist, blocking the ion channel in an open-state-dependent manner consistent with its arylcyclohexylamine classsupported
Dissociative designer drugs primarily act as NMDA receptor antagonists; pose similar risks to ketamine. s00204-020-02693-7
No substance-specific binding affinity (Ki or IC₅₀) has been published; the NMDA antagonist designation rests on structural analogy with ketamine and confirmatory behavioural evidence in ratssupported
DCK showed similar behavioural and addictive profiles and pharmacodynamics to ketamine bph.15680
Animal studies demonstrate both rewarding (conditioned place preference) and reinforcing (self-administration) properties comparable to ketamine, indicating meaningful dependence liabilitysupported
DCK (10 mg/kg) produced CPP and increased SA lever presses/infusions in mice. DCK has both rewarding and reinforcing effects. j.pbb.2022.173333
clinical-evidence4 · 4 ok
DCK detected at 10, 8, and 350 µg/L in blood across three 2F-DCK cases (two deaths and one self-mutilation)supported
DCK detected in biological fluids of 2F-DCK cases; blood levels 8-350 µg/L. bkae021
A fatal polydrug intoxication primarily attributed to 2F-DCK (1780 µg/L blood) with concurrent 3-MeO-PCE, 5-MeO-DMT, amphetamine, and cocaine — respiratory depression was the attributed causesupported
First fatal case involving 2F-DCK and 3-MeO-PCE. Death attributed to respiratory depression in polydrug context. j.forsciint.2021.110852
Tang et al. reported a case series of 20 patients presenting with analytically confirmed 2F-DCK exposure, of whom 50% had DCK co-detectedsupported
20 cases of 2F-DCK exposure; DCK co-detected in 50% of cases. j.forsciint.2020.110327
A suicide by fall from height in which DCK, 2F-DCK, and methoxpropamine were detected in post-mortem blood and hair — cause of death was traumatic, not toxicologicalsupported
LC-HRMS characterization of DCK, 2F-DCK, and methoxpropamine in post-mortem blood and hair from a forensic suicide case. j.forsciint.2021.110817
receptor-pharmacology4 · 3 ok
The NMDA receptor antagonist classification rests entirely on structural analogy with ketamine and behavioural confirmation in rodent models.supported
DCK showed similar behavioural and addictive profiles and pharmacodynamics to ketamine bph.15680
Claim in receptor-pharmacology — inconclusiveinconclusiveworking →
For contextual comparison, Ebert et al. measured NMDA receptor binding affinities for ketamine enantiomers and their primary metabolites via radioligand displacement:supported
S-ketamine Ki 0.3 uM, R-ketamine Ki 1.4 uM at NMDA receptor. S-norketamine Ki 1.7 uM; R-norketamine 13 uM. pmid:9311667
Given the structural similarity between DCK and ketamine and the conserved S > R enantiomeric potency pattern observed for both compounds, DCK's NMDA binding affinity is hypothesised to fall in a comparable or slightly higher affinity range — but this remains inference, not measurement.supported
(S)-DCK ~2x more cytotoxic than (R)-DCK in HEK293T. DCK originally proposed as immunomodulation agent; reported ~3x more potent than ketamine. c8nj03107j
chemistry3 · 2 ok
The absolute configuration of both enantiomers was determined by Jurásek et al. using vibrational circular dichroism (VCD), electronic circular dichroism (ECD), and X-ray crystallographysupported
Absolute configuration determined via VCD, ECD and X-ray crystallography. c8nj03107j
S-DCK is approximately twice as cytotoxic as R-DCK in HEK 293T cells (IC₅₀ < 0.99 mM vs. ~1.82 mM)supported
(S)-DCK ~2x more cytotoxic than (R)-DCK in HEK293T. c8nj03107j
Claim in chemistry — inconclusiveinconclusiveworking →
pharmacokinetic-detail3 · 3 ok
Data from Hájková et al. 2020supported
DCK concentrations in brain up to 4700 ng/g; serum 0.5-860 ng/mL. dta.2726
DCK undergoes extensive Phase I metabolism via N-demethylation, hydroxylation, oxidation, and ketone reduction, followed by Phase II glucuronidation and N-acetylationsupported
Main pathways: N-dealkylation, hydroxylation, oxidation, glucuronidation, N-acetylation. 29 phase I and 10 phase II metabolites detected total. metabo14050270
Glucuronide conjugates are unstable in wastewater, complicating population-level epidemiological monitoring.supported
Phase II glucuronides unstable in WW. dta.3839
neuroscience1 · 1 ok
DCK increases dopamine levels in PC-12 cells, consistent with the mesolimbic dopaminergic activation observed with ketamine at sub-anaesthetic dosessupported
Both DCK and diphenidine increased dopamine in PC-12 cells. j.pbb.2022.173333