ArticleJournal of Crohn's & colitis2021
Suppressing Kv1.3 Ion Channel Activity with a Novel Small Molecule Inhibitor Ameliorates Inflammation in a Humanised Mouse Model of Ulcerative Colitis.
Article in Journal of Crohn's & colitis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Wuji Wan ameliorates ulcerative colitis by restoring impaired membrane transport.Frontiers in pharmacology · 2026Article
- Validation of a model of rheumatoid arthritis using mice reconstituted with patient peripheral blood mononuclear cells.Disease models & mechanisms · 2025Article
- Selective inhibition of mitochondrial Kv1.3 prevents and alleviates multiple sclerosis in vivo.EMBO molecular medicine · 2025Article
- Recent advances in the pharmacology of voltage-gated ion channels.Pharmacological reviews · 2025Review
- NOD/Scid IL2RγJID innovations : skin science from molecules to population health · 2024Article
- Structure of the voltage-gated potassium channel KChannels (Austin, Tex.) · 2023Review
- Humanized NSG Mouse Models as a Preclinical Tool for Translational Research in Inflammatory Bowel Diseases.International journal of molecular sciences · 2023Article
- Tofacitinib fails to prevent T cell transfer colitis in mice but ameliorates disease activity.Scientific reports · 2023Article
- Ion channel regulation of gut immunity.The Journal of general physiology · 2023Article
- The potassium channel Kv1.3 as a therapeutic target for immunocytoprotection after reperfusion.Annals of clinical and translational neurology · 2021Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimsThe potassium channel Kv1.3 is a potentially attractive therapeutic target in T cell-mediated inflammatory diseases, as the activity of antigen-activated T cells is selectively impeded by Kv1.3 inhibition. In this study, we examined Kv1.3 as a potential therapeutic intervention point for ulcerative colitis [UC], and studied the efficacy of DES1, a small-molecule inhibitor of Kv1.3, in vitro and in vivo.
methodsKv1.3 expression on T cells in peripheral blood mononuclear cells [PBMCs] isolated from donors with and without UC was examined by flow cytometry. In biopsies from UC patients, Kv1.3-expressing CD4+ T cells were detected by flow cytometry and immunohistochemistry. In vitro, we determined the ability of DES1 to inhibit anti-CD3-driven activation of T cells. In vivo, the efficacy of DES1 was determined in a humanised mouse model of UC and compared with infliximab and tofacitinib in head-to-head studies.
resultsKv1.3 expression was elevated in PBMCs from UC patients and correlated with the prevalence of TH1 and TH2 T cells. Kv1.3 expression was also detected on T cells from biopsies of UC patients. In vitro, DES1 suppressed anti-CD3-driven activation of T cells in a concentration-dependent manner. In vivo, DES1 significantly ameliorated inflammation in the UC model and most effectively so when PBMCs from donors with higher levels of activated T cells were selected for reconstitution. The efficacy of DES1 was comparable to that of either infliximab or tofacitinib.
conclusionInhibition of Kv1.3 [by DES1, for instance] appears to be a potential therapeutic intervention strategy for UC patients.
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