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Background: A common oral inflammatory disease known as apical periodontitis (AP) is caused by the intrusion of microorganisms into the dental pulp, resulting in an inflammatory response and bone degradation in periapical tissues. A growing body of evidence indicates that the receptor-interacting serine-threonine kinase 3 (RIPK3) is closely associated with AP. Objectives: This study sought to address the requirement for effective RIPK3 inhibitors by examining the potential of cinnamic acid natural metabolites capable of inhibiting RIPK3. Methods: The binding affinity of 20 cinnamic acids to the RIPK3 active site was evaluated by using AutoDock 4.0 software. The most favorable scores were assigned to the highest-ranking cinnamic acids based on their ΔGbinding values to the RIPK3 catalytic domain. A 100-nanosecond (ns) computer simulation was performed using molecular dynamics for the most efficacious inhibitor of RIPK3, and the findings were contrasted with those obtained for free RIPK3. The Discovery Studio Visualizer tool was employed to showcase the interactions between the RIPK3 active site and the highest-ranking metabolites. Results: The binding affinity of cynarin, rosmarinic acid (RosA), and chlorogenic acid (CGA) to the RIPK3 active site was noteworthy, as the ΔGbinding values were