NLRP3 and serum lipopolysaccharide activity: To complement the chronic CAPS disease models described above, we next evaluated the potency of MCC950/CRID3 in inhibiting acute Nlrp3-dependent inflammasome responses by subjecting wild-type and CAPS mutant mice to LPS-induced endotoxemia and probing the effect of MCC950/CRID3 on well-documented Nlrp3-dependent readouts such as LPS-induced elevation of serum levels of IL-1β and IL-18 [26].