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K. S. Yoon

4 papers in the library · publishing 2019-2021

Papers

2-((2-(4-Iodo-2,5-dimethoxyphenyl)ethylamino)methyl)phenol (25I-NBOH) and 2-(((2-(4-chloro-2,5-dimethoxyphenyl)ethyl)amino)methyl)phenol (25C-NBOH) induce adverse effects on the cardiovascular system.

Toxicology Letters November 1, 2021 K. S. Yoon, Hye Jin Cha, S. Choi et al.

Two new psychoactive substances, 25I-NBOH and 25C-NBOH, abused as recreational hallucinogens, were evaluated for cardiotoxicity. In cell and animal tests, both compounds decreased viability of rat heart cells and prolonged QT and RR intervals in rat electrocardiography, indicating potential heart rhythm disturbances. 25I-NBOH reduced PAK1 protein expression in heart cells and inhibited potassium channels in a hERG assay, while 25C-NBOH did not affect PAK1 expression. Neither substance altered the pumping function or heart rate of isolated rat hearts. The findings suggest both substances may pose cardiovascular risks, with further research needed on the role of PAK1.

25I-NBOMe, a phenethylamine derivative, induces adverse cardiovascular effects in rodents: possible involvement of p21 (CDC42/RAC)-activated kinase 1

Drug and chemical toxicology (New York, N.Y. 1978) June 29, 2020 K. S. Yoon, Sun Mi Gu, Hye Jin Cha et al.

The psychoactive substance 25I-NBOMe, a phenethylamine analog, is toxic to heart muscle cells and can disrupt normal heart electrical activity in rats. In laboratory tests, the compound reduced the viability of rat heart cells in a dose-dependent manner, with a half-maximal toxic concentration of 70.4 μM. It also lowered the activity of the protein PAK1, which plays a key role in cardiovascular function. When injected into rats at doses of 1.0 and 3.0 mg/kg, 25I-NBOMe prolonged the QTc interval on electrocardiograms, an abnormal pattern linked to risk of dangerous heart rhythms. The findings suggest that 25I-NBOMe's cardiotoxicity involves PAK1-related pathways.

Cardiotoxic effects of [3-[2-(diethylamino)ethyl]-1H-indol-4-yl] acetate and 3-[2-[ethyl(methyl)amino]ethyl]-1H-indol-4-ol: Short title: QT prolongation by 4-acetoxy-DET and 4-hydroxy-MET.

Toxicology Letters November 6, 2019 K. S. Yoon, Jin-Moo Lee, Young-Hoon Kim et al.

Two synthetic tryptamines, 4-AcO-DET and 4-HO-MET, are abused as recreational hallucinogens and may pose unknown health risks. In laboratory tests, both substances increased the proliferation of rat heart cells in a concentration-dependent manner, prolonged QT intervals in rats, and inhibited potassium channels in hamster cells, indicating potential cardiotoxicity. Expression of the PAK1 protein, involved in cardiovascular function, did not change. The findings suggest these new psychoactive substances could cause adverse cardiovascular effects, supporting evidence for their legal scheduling.

2-(2,5-Dimethoxy-4-methylphenyl)-N-(2-methoxybenzyl)ethanamine (25D-NBOMe) and N-(2-methoxybenzyl)-2,5-dimethoxy-4-chlorophenethylamine (25C-NBOMe) induce adverse cardiac effects in vitro and in vivo.

Toxicology Letters April 1, 2019 K. S. Yoon, Jaesuk Yun, Young-Hoon Kim et al.

Two emerging psychoactive substances, 25D-NBOMe and 25C-NBOMe, show potential for disrupting heart rhythm, based on laboratory and animal tests. At 100 μM, both compounds reduced cell viability in a cell-based assay. In rats, doses of 2.0 mg/kg and 0.75 mg/kg prolonged QT intervals on electrocardiography, a marker of altered cardiac repolarization. The compounds also decreased levels of PAK1, a protein linked to cardiotoxicity, and 25D-NBOMe inhibited potassium channels in a hERG assay. The findings suggest these substances may pose a risk for cardiac arrhythmias, but further research is needed to clarify the role of PAK1 down-regulation.