Interleukin-33 (IL-33) is a key cytokine driving Type 2 immune responses in allergic diseases . This study aimed to characterize the drug metabolism and pharmacokinetic properties of a novel small molecule IL-33 inhibitor, IAC-1, in support of its preclinical development. Following a single oral dose in mice, IAC-1 exhibited moderate systemic clearance (3.6 L/hr/kg) and a high volume of distribution (V_ss = 9.8 L/kg). However, after repeated oral dosing (30 mg/kg for 17 days), its plasma exposure (AUC_inf) decreased by approximately 1.6-fold, suggesting auto-induction of its clearance. This was supported by increased hepatic mRNA expression of Cyp1a2 and Cyp2b10 enzymes in IAC-1-treated mice. Reaction phenotyping subsequently identified Cyp1a2 and Cyp2b10 as the primary enzymes responsible for IAC-1 metabolism. In vitro-in vivo extrapolation (IVIVE) based on liver microsomal stability data predicted a moderate clearance in mice, consistent with the in vivo results, and low clearance in humans. A total of seven metabolites, formed by hydroxylation, dehydrogenation, and N-dealkylation, were identified in vitro in both mouse and human liver microsomes. Notably, a metabolite resulting from both hydroxylation and N-dealkylation was detected only in mouse liver microsomes. This study characterized the drug metabolism and pharmacokinetics of the novel IL-33 inhibitor IAC-1, providing key data for further optimization and future therapeutic development.