Chronic myeloid leukemia is a clonal myeloproliferative disorder that is characterized by high levels of immature white blood cells. The reciprocal CTEP translocation between your 9 and 22 produces a fusion gene known, and results in the Ph chromosome as Bcr Abl. This fusion gene encodes a protein which turns on the dysregulated tyrosine kinase activity and drives CML. In CML, a Bcr Abl isoform is initially expressed in haematopoietic stem cells with the capacity of giving rise to both separated lymphoid and myeloid progeny. The biology of CML has permitted preclinical and clinical oncology experiments with targeted therapies. Imatinib is the first available Bcr Abl focused treatment and produces full cytogenetic responses in 70 85% of patients with CML in early chronic stage. However, inspite of the efficacy with this agent, resistance or intolerance to imatinib may become increasingly important. Furthermore, imatinib does not com-pletely eradicate residual leukemic stem cells and progenitors, which provide a risk of disease relapse. Consequently, there’s a clear importance of CML Eumycetoma research to concentrate on novel targets and targeted drugs. Various systems may possibly subscribe to imatinib resistance, and it could be categorized into two broad groups: Bcr Abldependent and Bcr Abl independent. The key cause in Bcr Abl dependent imatinib opposition requires point mutations in the Abl kinase domain of the fusion protein and over expression of Bcr Abl kinase through gene amplification. In addition, the Src family of kinase people Hck and Lyn are overexpressed in certain mobile lines and imatinib resistant patient remote, suggesting that SFKs could be associated with Bcr Abl independent imatinib resistance. Abl shares significant sequence homology and remarkable structural resemblance in its active state with Src family supplier Dizocilpine members. Several Src inhibitors from various chemical courses, including bosutinib, dasatinib and INNO 406 have been produced. These agents are far more effective than imatinib in stopping Bcr Abl tyrosine kinase autophosphorylation, and these effects extend to point mutations of Bcr Abl. FB2 is just a novel N pyrimidin 4 amine derivative, and we had found that FB2 inhibited imatinib resistance CML and painful and sensitive cell lines with the wild typ-e Bcr Abl fusion gene. In this report, we sought to identify this novel compound for treating Ph+ chronic myeloid leukemia that’s effective in blocking Bcr Abl kinase activity, including point mutations in the kinase domain, and inhibits src kinase activity. To evaluate its potential as a agent, we investigated the influence of FB2 on Ba/F3 cells expressing various isoforms of Bcr Abl, and survival of mice inoculated with K562 cells.