{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T11:47:29Z","timestamp":1791978449746,"version":"4.4.0"},"reference-count":47,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2022,10,2]],"date-time":"2022-10-02T00:00:00Z","timestamp":1664668800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100005564","name":"Gilead Sciences","doi-asserted-by":"publisher","award":["Mucus in CF"],"award-info":[{"award-number":["Mucus in CF"]}],"id":[{"id":"10.13039\/100005564","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2022,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The solute carrier 26 family member A9 (SLC26A9) is an epithelial anion transporter that is assumed to contribute to airway chloride secretion and surface hydration. Whether SLC26A9 or CFTR is responsible for airway Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    transport under basal conditions is still unclear, due to the lack of a specific inhibitor for SLC26A9. In the present study, we report a novel potent and specific inhibitor for SLC26A9, identified by screening of a drug\u2010like molecule library and subsequent chemical modifications. The most potent compound S9\u2010A13 inhibited SLC26A9 with an IC\n                    <jats:sub>50<\/jats:sub>\n                    of 90.9\u2009\u00b1\u200913.4\u2009nM. S9\u2010A13 did not inhibit other members of the SLC26 family and had no effects on Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    channels such as CFTR, TMEM16A, or VRAC. S9\u2010A13 inhibited SLC26A9 Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    currents in cells that lack expression of CFTR. It also inhibited proton secretion by HGT\u20101 human gastric cells. In contrast, S9\u2010A13 had minimal effects on ion transport in human airway epithelia and mouse trachea, despite clear expression of SLC26A9 in the apical membrane of ciliated cells. In both tissues, basal and stimulated Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    secretion was due to CFTR, while acidification of airway surface liquid by S9\u2010A13 suggests a role of SLC26A9 for airway bicarbonate secretion.\n                  <\/jats:p>","DOI":"10.1096\/fj.202200313rr","type":"journal-article","created":{"date-parts":[[2022,10,2]],"date-time":"2022-10-02T08:55:40Z","timestamp":1664700940000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["The\n                    <scp>SLC26A9<\/scp>\n                    inhibitor\n                    <scp>S9\u2010A13<\/scp>\n                    provides no evidence for a role of\n                    <scp>SLC26A9<\/scp>\n                    in airway chloride secretion but suggests a contribution to regulation of\n                    <scp>ASL pH<\/scp>\n                    and gastric proton secretion"],"prefix":"10.1096","volume":"36","author":[{"given":"Sungwoo","family":"Jo","sequence":"first","affiliation":[{"name":"College of Pharmacy, Yonsei Institute of Pharmaceutical Sciences Yonsei University  Incheon South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raquel","family":"Centeio","sequence":"additional","affiliation":[{"name":"Physiological Institute, University of Regensburg  Regensburg Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinhong","family":"Park","sequence":"additional","affiliation":[{"name":"College of Pharmacy, Yonsei Institute of Pharmaceutical Sciences Yonsei University  Incheon South Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiraporn","family":"Ousingsawat","sequence":"additional","affiliation":[{"name":"Physiological Institute, University of Regensburg  Regensburg 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