〔Abstract〕 Objective To investigate the mechanism of Jixueteng and Puhuangtan (JXT-PHT), two components of the Anzi Tiaochong Fang (ATF) with a harmonizing effect on blood, in the treatment of immune-related recurrent pregnancy losses (IRRPL) based on network pharmacology and molecular docking techniques to lay the foundation for further dissection of the ATF. Methods Using the TCMSP and HERB databases for component retrieval, the Swiss Target Prediction database was used to predict drug targets. The Genecards and ImmPort databases were used to obtain IRRPL targets. A Venn diagram was drawn using jvenn. A protein-protein interaction (PPI) network was constructed in the STRING database, and key targets were analyzed. A "herb for harmonizing blood-component-target-disease" network was constructed, and the core components were analyzed using Cytoscape 3.10.0 for visualization. The DAVID (v2023q1) database was used for gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis of potential targets. Finally, molecular docking was performed using AutoDock-Vina (v1.2.5), and PyMOL 2.5 was used for visualization. Results The screening identified 31 active components in JXT-PHT that have a harmonizing effect on blood in the ATF. 586 potential targets were predicted and 226 IRRPL targets were screened. After constructing a protein-protein interaction (PPI) network and analysis, 38 potential targets were identified. Four core targets were identified through PPI network analysis. A "herbs for harmonizing blood-component-target-disease" network was constructed, and three core components were identified through analysis. The potential targets were enriched in 277 GO terms and 86 KEGG terms. Conclusion Based on the results of this study, it can be concluded that the Chinese herbal medicine JXT and PHT, which have a harmonizing effect on blood in ATF, may be closely related to inflammatory responses, positive regulation of transcription from ribonucleic acid (RNA) polymerase II promoter, positive regulation of cell migration, and positive regulation of MAPK cascade. They exert their therapeutic effects on IRRPL through signaling pathways such as PI3K-AKT, Th17 cell differentiation, interleukin–17 (IL–17), Rap1, and tumor necrosis factor (TNF).