We examined the results of the agent on Ba/F3 cell lines carrying the Y253F and T315I mutations that confer resistance to imatinib, to further assess the effective chemotherapy of FB2. FB2 was found here to be a potent antiproliferative agent against Ba/F3 p210 cells in culture except Ba/F3 p210 T315I cells in MTT assays, which can be shown by its activity in vivo against CML xenografts. The survival time of NOD/SCID mice bearing Balb/c mice and K562 cells bearing Ba/F3 p210 Chk1 inhibitor cells was prolonged over that of controls when FB2 was given orally once-a day. All those effects were just like those seen in dasatinib. The Abl/Src inhibitory activity of FB2 is probably the major contributor for the activity of FB2 againstCMLcells. The amount of Bcr Abl tyrosine phosphorylation was considerably downregulated in Ba/F3 p210 cells except Ba/F3 p210 T315I cells. According to some docking model, there’s little room around T315I which is problematic for an competitive inhibitor of Bcr Abl to inhibit the mutant. FB2 is the ATP competitive inhibitor as dasatinib same, its inhibition is bound in the phosphorylation of T315I Bcr Abl which can be probably because the agent binding site is blocked by T315I mutation. So we’re looking for new element to conquer the mutation. Only inhibition of Bcr Abl kinase activity by kinase inhibitors is inadequate to power down all Bcr Abl downstream Metastatic carcinoma signaling pathways. There are many facts that indicate the relationship between Bcr Abl and Src kinases, and activation of Src kinases by Bcr Abl is not dependent on its kinase activity. Clinical evidence and Increasing preclinical implicates that SFKs play important roles in CML advancement and imatinib resistance. In today’s research, FB2 showed livlier inhibition on Src kinase activity than dasatinib in equally Ba/F3 WT cells and Ba/F3 cells expressing variations of Bcr Abl. FB2 is therefore a great candidate for that antileukemia Cabozantinib FLt inhibitor representative, nonetheless it is restricted to inhibit the phosphorylation of Bcr Abl with T315I point mutation. To find out whether FB2 can be used to deal with imatinibresistant CML, we further characterised the molecular mechanism of the agent by watching the effect on cell cycle progression in Ba/F3 p210 cells. It’s been recognized that get a grip on of cell cycle progression in cancer cells is an effective strategy to stop tumor growth. And many anti-cancer drugs show activities by inhibiting cell cycle progression and have cell cycle specificity, as an example, taxol blocks cell cycle at G2/M. Flow cytometric cell cycle analysis demonstrated marked increase of cells in G0/G1 cycle after treatment, which shows that certain of the systems by FB2 may be the inhibition of cell cycle progression.