The innate immune response is started immediately following brain ischemia, resulting in adaptive immunity. More and more experimental evidence has indicated that the immune response caused by cerebral ischemia plays a crucial role during the initial brain damage and subsequent brain injury recovery. Molsidomine, a nitric oxide donor, has been found to reduce schizophrenia-like behavioral abnormalities in rats due to glutamate hypofunction. The current study sought to explore the efficacy of molsidomine versus conventional drugs in cerebral ischemia. This study scavenges literature to retrieve various genes like PI3K, MMP9, COX2, LOX, TLR4, AKT1, mTOR, NLRP3, STAT3, IL1β, NFκB, TNF, IL6, and TP53 involved in cerebral ischemia. A two-step molecular docking revealed significant gene-drug complexes followed by a protein-protein interaction (PPI). Additionally, oncoprint analysis, protein-protein interaction, and functional and pathway enrichment associated with these genes and a circos plot depicting the mutational profile of the genes are incorporated in this study. This comprehensive in-silico approach reveals the efficacy of the potency of the candidate drug, molsidomine in treating cerebral ischemia.