Intraperitoneal injection of 4μ8c (IRE1 Inhibitor III), at a dosage of 10 mg/kg/day for an additional four weeks, results in a marked decrease (45.2%) in the atherosclerotic lesion area in en face aorta samples, demonstrating 4μ8c's capacity to effectively impede plaque formation in mice^[4].

Oral administration of 4μ8C at doses of 10, 50, or 100 mg/kg efficiently curtails passive cutaneous anaphylaxis (PCA) in mice, with an effective dose 50 (ED50) of 25.1 mg/kg^[5].

Additionally, 4μ8C counteracts the ER stress-induced depletion of several recognized RIDD targets, showcasing an EC50 roughly equivalent to that for the inhibition of XBP1 target gene activation, approximately 4 μM^[1].

4μ8C (IRE1 Inhibitor III) is a small-molecule inhibitor of IRE1α^[1].

Additionally impedes Xbp1 mRNA splicing in a dose-responsive manner when added to the culture media of ER-stressed cells. This inhibitor's binding to IRE1 is characterized by a slow dissociation rate, although removal of the inhibitor allows for a quick resumption of Xbp1 splicing in the cells^[1].

The mechanism by which 4μ8C operates, especially in preventing the splicing of XBP1 mRNA under ER stress conditions, such as those induced by mutant proinsulin production, provides insight into its potential application in managing ER stress-related cellular dysfunctions^[2].

Treatment with 4μ8C significantly reduces IL-4 production by CD4+ T cells under Th0 conditions, as evidenced by decreased IL-4 levels in culture supernatants and a lower percentage of IL-4 positive cells. The production of IL-5 and IL-13 is also notably diminished following 4μ8C administration^[3].