Abstract: Stroke is a common disease with complex and diverse clinical manifestations. Fufang Longmai Ningfang has been found to exhibit therapeutic effect on stroke, but its molecular mechanism for treating stroke remains unclear. The aim of this study was to investigate the molecular mechanism of Fufang Longmai Ningfang in the treatment of ischemic stroke by using the method of network pharmacology to define the active ingredients, target and molecular pathway of Fufang Longmai Ningfang. The TCMSP database was used to obtain the potential active components of Fufang Longmai Ningfang in the treatment of stroke. The CNKI database was used to verify the literature. The target was predicted and screened by PharmMapper and UniProt database. The target protein group was collected by TTD database. The Cytoscape software was used to construct a "component-target" network map, "component-target-disease" network map, and "target protein interaction" network map. The EAGLE algorithm was used for cluster analysis, the KEGG database was used for pathway analysis, and the SYBYL software was used for molecular docking for bioactivity verification. We found 39 potential active ingredients and 17 potential effective targets related to stroke. The representative active ingredients were ligustrazine, dioscin, and puerarin, and the related targets were MMP9, NOS3, NOS2, KDR, ALB, IL2, TGFB2, and CPB among others. The study found that carbon metabolism and HIF-1 signaling pathway are the main molecular pathways for treatment of stroke by Fufang Longmai Ningfang. The treatment of ischemic stroke by Fufang Longmai Ningfang may involve reduction of inflammatory response, enhancement of vascular permeability and inhibition of cerebral ischemia-reperfusion injury, providing a theoretical basis for their clinical use.