The intervention of rheumatoid arthritis gene and compound Q-1 screening based on transcriptomics combined with N6-Methyladenosine (m6A) was investigated. A collagen-induced arthritis model was replicated in rats, and the levels of interleukin1β（IL-1β), interleukin 6(IL-6), and tumour necrosis factor-alpha(TNF-α) in the serum of each group of rats were detected. Transcriptome sequencing analysis was performed on the differential genes in ankle joint tissue, and signal pathway analysis of differential genes was conducted. Intersection analysis between RA differentially expressed genes and 26 m6A system genes was performed, receiveroperating characteristic curve (ROC) analysis was carried out on zinc finger CCCH domain-containing protein 13(ZC3H13) and insulin-like growth factor binding protein 2 (IGFBP2), and molecular docking was used to analyze the binding of compound Q-1 to ZC3H13 and IGFBP2. The levels of TNF-α, IL-6, and IL-1β in the serum of the model group rats were found to be significantly increased compared to the normal control group (P <0.01). A total of 1 300 differentially expressed genes were identified in the model group compared to the normal control group, of which 805 differentially expressed genes were upregulated and 495 differentially expressed genes were downregulated. Intersection with 26 m6A system genes resulted in the obtaining of 2 m6A genes (ZC3H13, IGFBP2). Through molecular docking, it was found that compound Q-1 has strong binding to ZC3H13 (total score > 7) and good binding to IGFBP2 (total score > 5). Compound Q-1 forms four hydrogen bonds (Asp1054, Arg999, Glu1057, Gln99) with ZC3H13 and two hydrogen bonds(Arg201, Leu217) with IGFBP2. ZC3H13 and IGFBP2 may be involved in the regulation of biological metabolism through m6A modification and serve as targets for the diagnosis and treatment of RA. Compound Q-1 was found to have a good binding affinity with ZC3H13 and IGFBP2.