Carboxylesterase 3 (CES3) is a member of the mammalian carboxylesterase family, a group of serine hydrolases that catalyze the hydrolysis of ester-, thioester-, and amide-containing endogenous compounds and xenobiotics involved in drug and lipid metabolism
[1][2]. CES3 belongs to one of the five recognized human carboxylesterase families and shares conserved catalytic and structural features with other CES enzymes, supporting its role in metabolic biotransformation pathways
[1][3]. Mechanistically, carboxylesterases participate in the metabolism of lipid esters and contribute to energy homeostasis and lipid-related biological processes, providing a functional framework for investigating CES3 in metabolic regulation
[4]. CES3 is expressed in multiple tissues, including the brain, colon, and trachea, and has been implicated in neural and colon drug metabolism, suggesting potential relevance to tissue-specific xenobiotic processing
[5]. In disease-related research, the broader carboxylesterase family has been linked to metabolic disorders and fatty liver disease, making CES3 a candidate for studies examining esterase-mediated metabolic regulation
[4]. Compared with the extensively characterized CES1 and CES2 isoforms, CES3 remains less well understood, and available evidence indicates that it may exhibit lower catalytic efficiency toward selected substrates
[3]. Structural analyses have identified sequence insertions and deletions in CES3 relative to CES1, which may influence enzymatic properties and substrate recognition
[3]. Therefore, CES3 provides a useful experimental model for studying carboxylesterase isoform diversity, substrate specificity, and mechanisms of xenobiotic and lipid metabolism
[1][3].