Toxicology
January 5, 2005
Helena Carmo, Jan G Hengstler, Douwe De Boer et al.
85 citations
The psychoactive designer drug 2C-B is broken down by liver cells from humans, monkeys, dogs, rabbits, rats, and mice through oxidative deamination and demethylation, producing several metabolites. A previously unknown metabolite, 4-bromo-2,5-dimethoxy-phenol (BDMP), appeared only in mouse cells, while another metabolite, 2-(4-bromo-2-hydroxy-5-methoxyphenyl)-ethanol (B-2-HMPE), formed in human, monkey, and rabbit cells but not in dog, rat, or mouse cells. Toxic effects on liver cells varied little across species but showed large differences among cells from three human donors, indicating that individual human variation may be more important than species differences in determining 2C-B toxicity.
Toxicology
March 1, 2024
Arthur L de Oliveira, Raul G Miranda, Daniel J Dorta
1 citation
MDMA (ecstasy) at recreational doses does not cause liver cell damage in a 3D human liver cell model, even under hyperthermia. The study used HepG2 spheroids to test MDMA's hepatotoxicity and found no significant reduction in cell viability, no increase in reactive oxygen species, no loss of mitochondrial membrane potential, no cell cycle arrest, and no apoptotic cell death. These results support further preclinical research into MDMA's safety for both harm reduction and therapeutic use, as non-abusive recreational and therapeutic doses overlap.
Toxicology
March 1, 2026
Lea Wagmann, Simon D Brandt, Pierce V Kavanagh et al.
Three recently identified psychedelics and entactogens—3-APBT, 5-APBT, and 6-APBT—activate serotonin 2 receptor subtypes and cause head-twitch responses in mice. Their toxicokinetics, metabolism, and monoamine oxidase (MAO) inhibition were characterized using liquid chromatography-high-resolution tandem mass spectrometry. Metabolites were identified in urine from male Wistar rats over 24 hours after oral administration (2 mg/kg) and in incubations with pooled human liver S9 fraction (25 µM). Hydroxylation, primarily catalyzed by CYP1A2, CYP2D6, CYP3A4, and CYP3A5, was the main phase I biotransformation; phase II reactions included N-acetylation, glucuronidation, and sulfation. All three isomers strongly inhibited MAO-A (IC50: 5-APBT 0.4 µM, 6-APBT 0.6 µM, 3-APBT 4 µM) but only weakly inhibited MAO-B (IC50 23-49 µM). Clinically relevant MAO-A inhibition and associated interaction risks cannot be excluded.