Identification of Kir2.1 Inhibitors from a High-Throughput Screen
The inward-rectifier potassium channel (Kir) 2.x family is an important family of ion channels in the context of human health. These potassium channels are involved in processes such as cardiac action potential, formation of skeletal muscle, bone development, vasodilation, and neuronal activity and are expressed centrally and peripherally. Given their importance, they are an attractive target for the development of tool compounds. The high homology between the members of the Kir family has made isoform selectivity challenging. In an effort to discover novel chemical matter related to this intriguing target, we performed a high-throughput screen utilizing compounds from the Vanderbilt Institute of Chemical Biology Discovery Collection. This screen of over 20,000 compounds resulted in 48 verified hits consisting of six novel chemical scaffolds. Of these hits, VU0523203 and VU0606851 were selected as promising starting points for initial medicinal chemistry optimization to improve potency and distribution, metabolism, and pharmacokinetic (DMPK) properties. These efforts resulted in the discovery of VU6073995, a compound with modest potency at Kir2.1 and improved DMPK properties compared with ML133.
Authors
- Emily Days
- Jerod S. Denton (ORCID: https://orcid.org/0000-0003-0032-8586)
- Snehal Sant (ORCID: https://orcid.org/0000-0003-0426-4057)
- Jacob L. Bouchard (ORCID: https://orcid.org/0000-0002-5936-1244)
- Masahito Abe (ORCID: https://orcid.org/0000-0001-8686-7139)
- Roman M. Lazarenko (ORCID: https://orcid.org/0000-0003-0177-2961)
- Olivier G. Boutaud (ORCID: https://orcid.org/0000-0002-8910-0598)
- Patricia Van Horn
- Sichen Chang
- Yu Nishio
- Joshua A. Bauer
- Liangping Li
- Craig W. Lindsley
Institutions
- Vanderbilt University (US)
- Vanderbilt University Medical Center (US)
Publication Details
- Journal
- Assay and Drug Development Technologies
- Published
- 2026-02-17
- DOI
- https://doi.org/10.1177/1540658x261415763
- Primary Topic
- Ion channel regulation and function
- Type
- article
- Field-Weighted Citation Impact
- 0.00