4μ8C blocks substrate(RIDD) access to the active site of IRE1 and selectively inactivates both Xbp1 splicing and IRE1-mediated mRNA degradation. IRE1 inhibition subsequently induces ER stress without measureable acute toxicity. 4μ8C, as an IRE1 inhibitor, blocks IL-4, IL-5, and IL-13 production from CD4+ T cells.
