Docking is not enough: 17-trifluoromethylphenyl trinor PGF2α is only a very weak ligand of neurokinin-1 receptor

Joanna Matalińska; Piotr F J Lipiński

doi:10.1016/j.yexmp.2022.104849

Docking is not enough: 17-trifluoromethylphenyl trinor PGF2α is only a very weak ligand of neurokinin-1 receptor

Exp Mol Pathol. 2023 Feb:129:104849. doi: 10.1016/j.yexmp.2022.104849. Epub 2022 Dec 14.

Authors

Joanna Matalińska¹, Piotr F J Lipiński²

Affiliations

¹ Department of Neuropeptides, Mossakowski Medical Research Institute Polish Academy of Sciences, 5 Pawińskiego Street, PL 02-106, Warsaw, Poland. Electronic address: jmatalinska@imdik.pan.pl.
² Department of Neuropeptides, Mossakowski Medical Research Institute Polish Academy of Sciences, 5 Pawińskiego Street, PL 02-106, Warsaw, Poland. Electronic address: plipinski@imdik.pan.pl.

PMID: 36526011
DOI: 10.1016/j.yexmp.2022.104849

Abstract

17-trifluoromethylphenyl trinor prostaglandin F_2α (17-CF₃PTPGF_2α) was reported recently to exhibit in vitro and in vivo anticancer activity. Based solely on the results of in silico molecular docking, it was claimed that this compound is NK1 receptor (NK1R) antagonist and that its activity is through this receptor. In this contribution we show that 17-CF₃PTPGF_2α is only a very weak NK1R ligand (IC₅₀ > 200 μM). In connection with that we discuss the issue of this compound's molecular target. Finally, we briefly narrate on the proper use of molecular docking in biomedical research.

Keywords: Docking; In silico methods; Prostaglandins.

MeSH terms

Dinoprost*
Ligands
Molecular Docking Simulation
Receptors, Neurokinin-1*

Substances

Dinoprost
Receptors, Neurokinin-1
Ligands