OBJECTIVE To screen for bioactive compounds in Siwei granules against triple-negative breast cancer （TNBC）， and explore their anti-TNBC effects.METHODS Network pharmacology was applied to screen bioactive compounds of Siwei granules， corresponding targets and TNBC-related targets. A “component-target” interaction regulatory network was constructed， followed by Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analyses. Using MDA-MB-231 and 4T1 cells as subjects， bioactive compounds from Siwei granules against TNBC were screened. Using MDA-MB-231 cells as the subject， the effects of these bioactive compounds， either alone or in combination， on cell apoptosis， migration， cell cycle， reactive oxygen species （ROS） generation， and the expression of proteins related to enriched pathways were explored.RESULTS A total of 67 bioactive compounds were identified by network pharmacology， with 131 overlapping targets between the compound targets and TNBC targets. Six core key targets were identified， including the phosphatidylinositol-4，5-bisphosphate 3-kinase catalytic subunit alpha， etc. The overlapping targets were enriched in GO functions such as proliferation， phosphotransferase complexes， and protein tyrosine kinase activity， as well as in signaling pathways including phosphoinositide 3-kinase （PI3K）/protein kinase B （Akt） and ROS. A total of 4 bioactive compounds were identified by cell experiments. Among them， the half-maximal inhibitory concentration （IC 50 ） of ursolic acid for both cell lines was 25 μmol/L， while that of licochalcone A， luteolin， and aloe-emodin （for 4T1 cells only） was 50 μmol/L for both cell lines. When administered alone （all 20 μmol/L） or in combination （10 μmol/L each）， the four compounds significantly increased the apoptosis rate in MDA-MB-231 cells （only in the combination group only）， relative ROS levels （only in the combination group） and the proportion of cells in the G 2 phase （only in the luteolin group， licochalcone A group， and combination group）， while they significantly reduced the proportion of cells in the G 1 phase （only in the licochalcone A group and the combination group）， scratch healing rate， and the phosphorylation levels of PI3K （except in the aloe-emodin group）， Akt （except in the aloe-emodin group）， and the mammalian target of rapamycin （ P ＜0.05）.CONCLUSIONS The bioactive compounds in Siwei granules responsible for its anti-TNBC activity may be ursolic acid， licochalcone A， luteolin， and aloe-emodin； these compounds can， to varying degrees， inhibit TNBC cell proliferation and migration， promote apoptosis， arrest the cell cycle in the G 2 phase， induce ROS production， and inhibit the phosphorylation the related proteins of the PI3K/Akt signaling pathway.