Background　Lung　cancer　remains　a　leading　cause　of　cancer-related　mortality　worldwide,　primarily　due　to　late-stage　diagnosis　and　resistance　to　conventional　therapies.　Recent　studies　have　highlighted　the　potential　of　natural　compounds　in　enhancing　the　efficacy　and　reducing　the　side　effects　of　conventional　cancer　treatments.　Baicalin,　a　bioactive　compound　from　Scutellaria　baicalensis,　exhibits　significant　anticancer　properties.Objectives　This　study　aimed　to　investigate　the　role　of　baicalin　in　modulating　lung　cancer　cell　behavior　through　the　arachidonate　12-lipoxygenase　(ALOX12)-mediated　ferroptosis　pathway.Methods　We　employed　cyber　pharmacology　and　molecular　docking　techniques　to　predict　and　validate　the　interaction　between　baicalin　and　ALOX12.　In　vitro　experiments　were　conducted　on　A549　lung　cancer　cells　to　assess　the　effects　of　baicalin　on　cell　proliferation,　migration,　and　invasion.　The　expression　levels　of　ALOX12,　reactive　oxygen　species　(ROS),　and　ferroptosis　markers,　such　as　Glutathione　Peroxidase　4　(GPX4)　and　Acyl-CoA　Synthetase　Long-Chain　Family　Member　4　(ACSL4),　were　measured.Results　Baicalin　treatment　significantly　upregulated　ALOX12　expression　in　lung　cancer　cells,　and　this　upregulation　was　associated　with　a　reduction　in　cell　proliferation,　migration,　and　invasion.　Furthermore,　baicalin-induced　ferroptosis　was　characterized　by　increased　ROS　levels,　iron　accumulation,　and　elevated　expression　of　GPX4　and　ACSL4.　These　findings　suggest　that　baicalin　enhances　ferroptosis　through　ALOX12　activation,　synergistically　inhibiting　cancer　cell　growth.Conclusion　Baicalin　significantly　upregulated　ALOX12　expression,　promoted　ferroptosis,　and　inhibited　the　proliferation　and　migration　of　A549　lung　cancer　cells.　This　finding　provides　evidence　for　the　potential　use　of　baicalin　as　a　therapeutic　agent　for　lung　cancer　and　highlights　the　importance　of　ALOX12　in　lung　cancer　treatment　strategies.