Objective: This study was designed to search for candidate drugs that act on IL-33 and ST2, which was carried out using a bioinformatics approach. Methods: We first analyzed Network Electronic Cigarette Smokes Predictions of therapeutic targets by Cytoscape. We collected from the Swiss TargetPrediction database [http://www. swisstargetprediction. ch/] by inputting each compound structure of the electronic cigarette smoke in SDF format. The target protein data is then supplemented with UniProt ID data to uniform protein identity. We then identified COPD Related Targets in Humans by Cytoscape. Subsequently, we identified key receptors in the pathogenesis of COPD. All target proteins that have a significant role in the pathogenesis of COPD exposed to cigarette smoke will be known from the combination of this network. Results: Based on the validation results of the protein receptor for ST2, a protein is used as a receptor with PDB ID: 1IRA. After analyzed by PyMol software, a protein with PDB ID 1IRA it has no missing residue in its sequenceDrug candidates analyzed by the structural similarity with the native ligand using PubChem and DRUGBANK analysis are follow: N-acetylmannosamine, Aceneuramic acid, Ceramide AP, Ceramide NP, Hg9a-9, Nonanoyl-N-hydroxyethylglucamide, N-Acetyl-2-deoxy-2-amino-galactose, N-Acetyllactosamine, MLi/2,6-dimethyl-4-[6-[5-[1-methylcyclopropyl] oxy-1H-indazol-3-yl] pyrimidin-4-yl] morpholine, Terazosin, BMS-911543, NAG Inhibitor, FGFR Inhibitor/sodium; 2-amino-5-[1-methoxy-2-methylindolizine-3-carbonyl] benzoate. After docking, the smallest or more negative binding affinity values are obtained. The stronger the FGFR Inhibitor ligand showed the interaction with the Receptor with a binding affinity value of-9.0 kcal/mol with mode/position 0, and RMSD 0.0. The second smallest binding affinity value is the NAG ligand with a-8.5 kcal/mol with mode/position 0 and RMSD 0.0. Conclusion: The findings revealed that FGFR Inhibitor was a suitable repurposing medication for anti-COPD development via the IL-33/ST-2 signaling pathway.