The hallmark genetic abnormality of CML is named Philadelphia chromosome. Philadelphia chromosome occurs as a result of recombination of two genes, namely the cellular ABL gene on chromosome 9 and BCR gene located on chromosome 22. The Philadelphia chromosomal translocation is responsible for the ABL and BCR fusion. The ABL and BCR proteins play a central role in the pathogenesis of CML. The malignant transformation by BCR-ABL is critically dependent on its protein tyrosine kinase activity. It makes ABL kinase is an attractive target for therapeutic intervention. In this research, about 653,214 leadlike compounds were obtained from MOE database. The compounds were screened using Data Warrior v.4.6.1 and also docked to predict their binding affinity to BCR-ABL1 tyrosine kinase protein using MOE 2014.09 software. Fragment-based drug design was applied to find a new drug candidate. Finally, five new compounds were generated from this method. The compound LUT-1 has the highest potential due to the low ΔG binding score, acceptable RMSD score, and ADME-Tox result.