Wilhelmsen Kevin, Deshpande Aditi, Tronnes Sarah, Mahanta Maitriyee, Banicki Matthew, Cochran Mary, Cowdin Samantha, Fortney Kristen, Hartman George, Hughes Robert E, Montgomery Rusty, Portillo Claudia P, Rubin Paul, Salazar Taiz, Wang Yan, Yan Shijun, Morgan Barry A, Duisembekova Assem, Riou Romane, Marleaux Michael, Hochheiser Inga V, Buthmann Hannes, Ferber Dominic, Torp Jane, Wang Wei, Cranston Melanie, McKee Chloe M, Mawhinney Thea J, McKay Emma C, Eroglu Fehime K, Kümmerle-Deschner Jasmin, Weber Alexander N R, Py Bénédicte F, Geyer Matthias, Coll Rebecca C
BioAge Labs , Emeryville, CA, USA.
HitGen Pharmaceuticals Inc. , Houston, TX, USA.
J Exp Med. 2025 Nov 3;222(11). doi: 10.1084/jem.20242403. Epub 2025 Sep 2.
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.
NLRP3炎性小体是一种细胞内蛋白质复合物,可通过释放白细胞介素-1β和细胞焦亡引发炎症。NLRP3激活与许多年龄相关的炎性疾病有关,抑制NLRP3是一种有前景的治疗策略。我们之前进行了一项DNA编码文库筛选,以鉴定新型NLRP3结合分子。在此,我们描述了BAL-0028作为NLRP3信号传导的强效特异性抑制剂的特性。值得注意的是,BAL-0028对小鼠NLRP3的抑制作用较弱,但对人和灵长类动物NLRP3具有纳摩尔效力的抑制作用。通过细胞和生化分析,我们证明BAL-0028在一个与MCC950结合口袋不同的位点与NLRP3 NACHT结构域结合。使用人源化NLRP3小鼠,我们表明BAL-0028的衍生物BAL-0,598在体内腹膜炎模型中抑制NLRP3激活。最后,我们证明BAL-0028和BAL-0598比MCC950更有效地抑制与自身炎症性疾病相关的某些高活性NLRP3突变。因此,BAL-0028和BAL-059,8代表了炎性疾病中NLRP3抑制的一种新方式。