BPTES inhibits anthrax lethal toxin-induced inflammatory response

•We identified that BPTES was an effective NLRP1b inflammasome inhibitor.•BPTES could effectively and specifically suppress NLRP1b inflammasome activation in macrophages but have no effects on NLRP3, NLRC4 and AIM2 inflammasome activation.•Mechanistically, BPTES alleviated the UBR2 mediated proteasomal degradation pathway of the NRLP1B N terminus, thus blocking the release of the CARD domain for subsequent caspase-1 processing.•Furthermore, BPTES could prevent disease progression in mice challenged with the anthrax lethal toxin.