Abstract: The insulin/insulin-like signaling (IIS) pathway is a central regulator of growth, metabolism, and developmental transitions in animals. However, the composition and functional diversification of insulin receptor genes remain insufficiently characterized in many crustacean aquaculture species. The red swamp crayfish, Procambarus clarkii, is an economically important freshwater species that exhibits substantial individual variation in growth rate, yet the molecular basis underlying this variation is still poorly understood. In this study, we systematically identified the insulin receptor gene family (PcInsr) in P. clarkii, characterized its structural and expression features, and investigated growth-related single nucleotide polymorphisms (SNPs) in PcInsr1 through association and functional analyses. A total of six PcInsr genes (PcInsr1 to PcInsr6) were identified from the chromosome-level reference genome. These genes are unevenly distributed on five chromosomes and differ in transcript length, coding sequence length, amino acid number, theoretical molecular weight, and isoelectric point, indicating considerable structural diversity within the family. Structural analyses further showed that most PcInsr members retained the typical features of receptor proteins, whereas PcINSR4 lacked a typical intracellular kinase-related domain and differed markedly from the other members in domain composition. Subcellular localization prediction suggested that PcInsr family members were mainly associated with the plasma membrane, while PcINSR6 was additionally predicted to localize in the cytoplasm. Phylogenetic analysis showed that, except for PcINSR4, the other five PcINSR proteins could be assigned to the RTK1, RTK2, RTK3, and RTK4 clades, with PcINSR1 belonging to RTK1, PcINSR3 to RTK2, PcINSR2 to RTK3, and PcINSR5 and PcINSR6 to RTK4, indicating substantial evolutionary differentiation within the PcInsr family. Quantitative Real-time PCR analysis revealed clear tissue-biased expression patterns across 11 tissues: PcInsr1 and PcInsr6 were highly expressed in the epidermis, PcInsr2 and PcInsr3 were relatively highly expressed in reproductive tissues, PcInsr5 showed its highest expression in the ovary, and PcInsr4 was relatively highly expressed in muscle and the antennal gland. These distinct expression profiles suggest that different PcInsr paralogues may have undergone functional differentiation and may participate in diverse physiological processes related to growth, molting, reproduction, and tissue-specific regulation. To investigate the relationship between PcInsr variation and growth traits, SNPs within PcInsr1 were screened by integrating previous RAD-seq and bulked-segregant resequencing data with phenotypic measurements. Seven highly polymorphic candidate SNPs located in the promoter, 5′ untranslated region, and intronic regions were selected for association analysis in a growth-divergent crayfish population. Four loci were significantly associated with body weight (P<0.05), indicating that non-coding variation in PcInsr1 may contribute to growth regulation. Among these loci, the promoter variant g.-9907 G>A was selected for further functional validation. Dual-luciferase reporter assays showed that the PcInsr1 promoter fragment carrying the G allele drove significantly higher transcriptional activity than the construct carrying the A allele. In silico analysis further suggested that this substitution may alter the binding of transcription factors such as FOXO3, providing a plausible mechanism by which promoter variation in PcInsr1 could influence growth-related regulation. In summary, this study provides a systematic characterization of the PcInsr gene family in P. clarkii at the levels of structure, phylogeny, and tissue expression, and identifies a candidate functional promoter SNP associated with growth traits. These findings improve our understanding of insulin receptor diversification in crayfish and offer candidate loci for future studies on growth regulation and marker-assisted breeding in red swamp crayfish.