Kevin Wilhelmsen, Aditi Deshpande, Sarah Tronnes, Maitriyee Mahanta, Matthew Banicki, Mary Cochran, Samantha Cowdin, Kristen Fortney, George Hartman, Robert E Hughes, Rusty Montgomery, Claudia P Portillo, Paul Rubin, Taiz Salazar, Yan Wang, Shijun Yan, Barry A Morgan, Assem Duisembekova, Romane Riou, Michael Marleaux, Inga V Hochheiser, Hannes Buthmann, Dominic Ferber, Jane Torp, Wei Wang, Melanie Cranston, Chloe M McKee, Thea J Mawhinney, Emma C McKay, Fehime K Eroglu, Jasmin Kümmerle-Deschner, Alexander N R Weber, Bénédicte F Py, Matthias Geyer, Rebecca C Coll
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We previously performed a DNA-encoded library screen to identify novel NLRP3-binding molecules. Herein we describe the characterization of BAL-0028 as a potent and specific inhibitor of NLRP3 signaling. Notably, BAL-0028 is a poor inhibitor of mouse NLRP3 but inhibits human and primate NLRP3 with nanomolar potency. Using cellular and biochemical analyses, we demonstrate that BAL-0028 binds to the NLRP3 NACHT domain at a site that is distinct from the MCC950-binding pocket. Using humanized NLRP3 mice, we show that a derivative of BAL-0028, BAL-0598, inhibits NLRP3 activation in vivo in a peritonitis model. Finally, we demonstrate that both BAL-0028 and BAL-0598 inhibit select hyperactive NLRP3 mutations associated with autoinflammatory diseases more potently than MCC950. BAL-0028 and BAL-0598 thus represent a new modality for NLRP3 inhibition in inflammatory diseases.</p>","PeriodicalId":15760,"journal":{"name":"Journal of Experimental Medicine","volume":"222 11","pages":""},"PeriodicalIF":10.6000,"publicationDate":"2025-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12404154/pdf/","citationCount":"0","resultStr":"{\"title\":\"Discovery of potent and selective inhibitors of human NLRP3 with a novel mechanism of action.\",\"authors\":\"Kevin Wilhelmsen, Aditi Deshpande, Sarah Tronnes, Maitriyee Mahanta, Matthew Banicki, Mary Cochran, Samantha Cowdin, Kristen Fortney, George Hartman, Robert E Hughes, Rusty Montgomery, Claudia P Portillo, Paul Rubin, Taiz Salazar, Yan Wang, Shijun Yan, Barry A Morgan, Assem Duisembekova, Romane Riou, Michael Marleaux, Inga V Hochheiser, Hannes Buthmann, Dominic Ferber, Jane Torp, Wei Wang, Melanie Cranston, Chloe M McKee, Thea J Mawhinney, Emma C McKay, Fehime K Eroglu, Jasmin Kümmerle-Deschner, Alexander N R Weber, Bénédicte F Py, Matthias Geyer, Rebecca C Coll\",\"doi\":\"10.1084/jem.20242403\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The NLRP3 inflammasome is an intracellular protein complex that causes inflammation via the release of IL-1β and pyroptosis. 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Discovery of potent and selective inhibitors of human NLRP3 with a novel mechanism of action.
The NLRP3 inflammasome is an intracellular protein complex that causes inflammation via the release of IL-1β and pyroptosis. NLRP3 activation is associated with many age-related inflammatory diseases, and NLRP3 inhibition is a promising therapeutic strategy. We previously performed a DNA-encoded library screen to identify novel NLRP3-binding molecules. Herein we describe the characterization of BAL-0028 as a potent and specific inhibitor of NLRP3 signaling. Notably, BAL-0028 is a poor inhibitor of mouse NLRP3 but inhibits human and primate NLRP3 with nanomolar potency. Using cellular and biochemical analyses, we demonstrate that BAL-0028 binds to the NLRP3 NACHT domain at a site that is distinct from the MCC950-binding pocket. Using humanized NLRP3 mice, we show that a derivative of BAL-0028, BAL-0598, inhibits NLRP3 activation in vivo in a peritonitis model. Finally, we demonstrate that both BAL-0028 and BAL-0598 inhibit select hyperactive NLRP3 mutations associated with autoinflammatory diseases more potently than MCC950. BAL-0028 and BAL-0598 thus represent a new modality for NLRP3 inhibition in inflammatory diseases.
期刊介绍:
Since its establishment in 1896, the Journal of Experimental Medicine (JEM) has steadfastly pursued the publication of enduring and exceptional studies in medical biology. In an era where numerous publishing groups are introducing specialized journals, we recognize the importance of offering a distinguished platform for studies that seamlessly integrate various disciplines within the pathogenesis field.
Our unique editorial system, driven by a commitment to exceptional author service, involves two collaborative groups of editors: professional editors with robust scientific backgrounds and full-time practicing scientists. Each paper undergoes evaluation by at least one editor from both groups before external review. Weekly editorial meetings facilitate comprehensive discussions on papers, incorporating external referee comments, and ensure swift decisions without unnecessary demands for extensive revisions.
Encompassing human studies and diverse in vivo experimental models of human disease, our focus within medical biology spans genetics, inflammation, immunity, infectious disease, cancer, vascular biology, metabolic disorders, neuroscience, and stem cell biology. We eagerly welcome reports ranging from atomic-level analyses to clinical interventions that unveil new mechanistic insights.