Extended Data Fig. 9: SK56 protects against sepsis induced by CLP.

a, Kaplan–Meier analysis of survival rates in WT and Gsdmd^−/− mice challenged with CLP surgery and treated with SK56 (i.v. 1 mg/kg, 16 hours after CLP surgery) (n = 10 mice per group). b-c, Histopathology assay showing H&E-stained lung tissues (b) and pathological scores (c, n = 15 samples) in SK56-treated WT and Gsdmd^−/− mice 2 days after CLP. Scale bars, 1 mm (whole section) and 50 µm (zoomed-in). d, Cytokine assay showing plasma cytokines level in SK56 treated or untreated CLP wild-type or Gsdmd^−/− mice (n = 10 mice). e, Biochemistry assay indicating blood levels of organ damage markers in SK56 treated or untreated CLP mice (n = 6 mice). f, Body weight changes were monitored in mice subjected to LPS or CLP surgery with or without SK56 (n = 10 mice per group). g-h, SK56 and three GSDMD-NT pore formation inhibitors (DSF, disulfiram; DMF, dimethyl fumarate; NSA, necrosulfonamide) were evaluated for their impact on IL-1β levels (g) and biochemical markers (h) in LPS-treated mice blood (n = 10 mice). Data in c-e and g-h were analyzed using two-tailed paired Student’s t-test; NS (P > 0.05, not significant); means ± s.d. Data in a was analyzed by log-rank (Mantel-Cox) test.