Juvenile hormone (JH) plays a crucial role in insect development by regulating molting and metamorphosis. Due to its insect-specific functions, JH biosynthesis and signaling have long been attractive targets for insect growth regulators (IGRs). JH analogs, such as methoprene, pyriproxyfen, and fenoxycarb, have been successfully commercialized; however, they often prolong the larval stage in Lepidoptera, which can exacerbate crop damage. In contrast, anti-JH agents, classified as either JH biosynthesis inhibitors or JH antagonists, induce precocious metamorphosis, offering a promising approach for controlling pests in the larval stage. Several JH biosynthesis inhibitors, such as precocene and compactin, have been reported; however, their limited target spectrum and toxicity to mammals hinder their practical applications. Recent advances have clarified the JH signaling pathway, including the JH receptor, methoprene-tolerant (Met). Potential JH antagonists, including N-[2-(4-tert-butyl-2-chlorophenoxy)ethyl]-1H-1,2,4-triazole (JHSI48) and kingidiol (SS5A), were identified using JH receptor–based in vitro screening. Ethyl (E)-3-(4-{[7-(4-methoxycarbonylbenzyloxy)-1,4-benzodioxan-6-yl]methyl}phenyl)-2-propenoate (EMBP) has demonstrated the most potent JH antagonistic activity in vitro and in vivo by specifically suppressing JH-responsive gene expression, thereby inducing precocious metamorphosis.