[PERSON]  
6 Department of Beauty Art, Youngsan University, 142 Bansong Beltway, Busan 48015, Republic of Korea; [EMAIL_ADDRESS] (H.-J.C.); [EMAIL_ADDRESS] (W.-J.B.)  
[PERSON]  
6 Department of Beauty Art, Youngsan University, 142 Bansong Beltway, Busan 48015, Republic of Korea; [EMAIL_ADDRESS] (H.-J.C.); [EMAIL_ADDRESS] (W.-J.B.)  
[PERSON]  
4 Nucleic Acid Therapeutics Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIB), Cheongju 28116, Republic of Korea; [EMAIL_ADDRESS] 4  
[PERSON]  
1 Department of Beauty Art, Youngsan University, 142 Bansong Beltway, Busan 48015, Republic of Korea; [EMAIL_ADDRESS] (H.-J.C.); [EMAIL_ADDRESS] (W.-J.B.)  
[PERSON]  
6 Department of Beauty Art, Youngsan University, 142 Bansong Beltway, Busan 48015, Republic of Korea; [EMAIL_ADDRESS] (H.-J.C.); [EMAIL_ADDRESS] (W.-J.B.)  
[PERSON]  
6 Department of Beauty Art, Youngsan University, 142 Bansong Beltway, Busan 48015, Republic of Korea; rerieved@naver. are complex and involve interactions with host cells and immune responses. Although substantial progress has been made in understanding viral replication and virulence factors, some aspects, such as virus-host interactions, require further investigation. Therefore, understanding the pathogenesis of these viruses and developing effective antiviral strategies is critical. Recently, specific antiviral compounds targeting EV71, CVA16, and CVB3 have shown significant advancements. Preclinical studies have identified various inhibitors that target different stages of the viral replication cycle. One notable example is pleconaril, a broad-spectrum antiviral agent initially developed for enterovirus (EV) and rhinovirus (RV) infections that has demonstrated efficacy against EV71 and CVB3 [6; 7]. Pleconaril inhibits viral attachment and entry into host cells by binding to a hydrophobic pocket of the viral capsid protein, thereby hindering viral replication [8; 9]. Clinical trials and studies have demonstrated the potential of pleconaril in reducing the severity and duration of EV and RV infections, although its development was halted owing to adverse effects [10; 11; 12]. In addition, NITD008, which inhibits RNA polymerase activity; rupintrivir (AG7088), which targets 3 Cpro; and GPP3, which blocks virus entry, have shown antiviral activity against diverse EVs and cossackieviruses [1; 12; 13]. Despite these findings, none of these inhibitors have progressed to clinical use. _Saururus chintensis_, a medicinal herbaceous plant widely distributed in Eastern Asian countries and North America, is traditionally used to treat various medical conditions [14; 15; 16]. Extracts from _S. chinensis_ have diverse pharmacological effects, including antiinflammatory, antioxidant, antiasthmatic, antihypertensive, antiangiogenic, and antiapoptotic properties [17; 18; 19]. Several compounds, including lignans, diterpenes, alkaloids, tannins, flavonoids, steroids, and lipids, have been isolated from _S. chintensis_, and ligament-type compounds, such as sauchinone and manassantin A and B, are considered bioactive [20; 21; 22; 23]. Manassantin B, a compound isolated from _S. chinensis_, activates the stimulator of interferon genes (STING)/TANK-binding kinase-1 (TBK1)/interferon regulatory factor-3 (IRF3) signaling pathway and exhibits antiviral activity against CVB3 [24]. In this study, saucerneol, another compound isolated from _S. chinensis_, displayed significant antiviral activity against EV71, CVA16, and CVB3 infections in Vero cells. The antiviral mechanism of saucerneol involves activation of the STING/TBK-1/IRF3 signaling pathway and an increase in mitochondrial ROS (mROS) generation. Additionally, saucerneol inhibited CVB3 replication in mouse pancreas and mitigated CVB3-induced pancreatitis. These findings emphasize the potential of saucerneol as a natural antiviral agent derived from _S. chinensis_, which is effective against various enteroviral infections, including EV71, CVA16, and CVB3.