Deschloroketamine

Pre-existing hypertension, particularly uncontrolled or poorly managed. Hypertension and tachycardia documented in clinical presentations involving DCK co-exposure (Tang et al. 2020). Risk of hypertensive crisis or cardiac arrhythmia.

Epilepsy or seizure disorders. Convulsions reported in 5/20 patients in a clinical case series involving DCK co-exposure (Tang et al. 2020). NMDA antagonists may lower seizure threshold in susceptible individuals.

Personal or family history of schizophrenia, schizoaffective disorder, or other psychotic spectrum conditions. NMDA antagonists produce PCP-like psychotomimetic effects documented in rodent models (Shaw et al. 2024) and human clinical presentations (Tang et al. 2020). Risk of prolonged psychotic episode or decompensation.

Bipolar I or II disorder. Dissociative experiences and mood elevation from NMDA blockade may precipitate manic switching, particularly in unmedicated or undertreated individuals.

Moderate to severe hepatic impairment. DCK is extensively metabolised via N-demethylation, hydroxylation, and glucuronidation (Hájková et al. 2020; Frankenfeld et al. 2024). Reduced clearance in hepatic impairment may produce prolonged and intensified effects.

Pre-existing urological conditions including interstitial cystitis, bladder dysfunction, or hydronephrosis. No DCK-specific uropathy data exist, but ketamine uropathy is a well-documented class risk. DCK's longer duration may increase per-session bladder exposure.

Pregnancy at any stage. No reproductive or developmental toxicity studies have been conducted for DCK. NMDA receptor signalling is essential for fetal brain development. Zebrafish data show 100% larval mortality at high concentrations (Rodrigues et al. 2025).