Hinokitiol, derived from Chamaecyparis taiwanensis wood, has gained attention for its broad therapeutic applications, particularly its antiinflammatory effects. Traditionally known for antimicrobial properties in Japan, hinokitiol inhibits the NF-κB pathway, preventing IκBα degradation, thereby reducing the transcription of proinflammatory cytokines such as TNF-α, IL-6, and IL-1β. It also downregulates COX-2 expression. In the TLR4 signaling, hinokitiol inhibits LPS binding to TLR4, reducing downstream cytokine production. Additionally, hinokitiol modulates the Wnt/β-catenin pathway by preventing β-catenin nuclear translocation and attenuating inflammation. Hinokitiol's antioxidant properties are crucial in mitigating oxidative stress and inflammation, especially in gentamicin-induced nephrotoxicity. By scavenging ROS and modulating inflammatory pathways, hinokitiol protects renal tubular cells from oxidative damage. Moreover, it activates the Keap1/Nrf2/HO-1 pathway, enhancing cellular defenses against oxidative stress and ferroptosis, particularly in neuronal cells with posttraumatic brain injury. Hinokitiol inhibits melanogenesis by targeting the AKT/mTOR signaling pathway, reducing the expression of MITF and tyrosinase, key regulators of melanin synthesis. This inhibition is accompanied by increased autophagy, contributing to its antimelanogenic effects. The multifaceted actions of hinokitiol across various signaling pathways highlight its therapeutic potential in managing a wide range of inflammatory and oxidative stress-related conditions. Further research is needed to fully elucidate hinokitiol's mechanisms and explore its clinical applications in inflammation, oxidative stress, and related disorders