The apoptotic effects of celecoxib were complete with imatinib. To explore the mechanisms of celecoxib induced apoptosis in IR K562 cells, we examined the cytoplasmic release of cytochrome. As shown in Fig. 7, cytochrome was seen in the cytoplasmic portion of IR K562 cells treated with imatinib or celecoxib alone for 2-4 h. But, the release of cytochrome was greater in IR K562 cells treated with both imatinib and celecoxib. More over, a higher amount of the form of PARP, Dovitinib PDGFR inhibitor a more developed substrate for caspase 3, was observed in IR K562 cells treated with both celecoxib and imatinib. An important decline in the Bcl2 Bax rate, with down-regulation of Bcl2 and no change in Bax expression,was noticed in IR K562 cells treated with celecoxib and imatinib compared to cells treated with imatinib or celecoxib alone. Ear-lier studies have shown that celecoxib induces apoptosis of cancer cells by blocking Akt activation. So, we next examined the possible contribution of Akt in the induction of apoptosis by celecoxib. Fig. 7 shows the Western blot analysis of p and Akt Akt in IR K562 cells treated with imatinib and/or celecoxib. The amount of phosphorylated Akt decreased in cells treated with imatinib or celecoxib alone. The decrease is a lot higher in cells treated with both celecoxib and imatinib. The quantities of Akt, on the other hand, were unaltered in all the solutions compared to the control. Take-n Ribonucleic acid (RNA) together, these results indicate that celecoxib induced apoptosis in IR K562 cells is by inhibiting the Akt cell survival signaling pathway and the effects are complete with imatinib. Today’s study demonstrates that COX 2 and MDR1 over expression, but not the variations in the Abl kinase domain, may play a role in the development of resistance to Ima tinib in K562 cells. Celecoxib, a COX 2 particular inhibitor induces apoptosis of IR K562 cells by inhibiting MDR 1 and COX 2 through Akt pathway. Also, celecoxib at 1 M concentration dramatically enhanced the cytotoxic effects of imatinib o-n IR K562 cells by decreasing the IC50 of imatinib from 1-0 Canagliflozin concentration to 6 M. The outcome from ugly tiny analysis, DNA fragmentation and move cytometer analysis of IR K562 cells treated with imatinib and celecoxib alone or in combination linked with the complete induction of apoptosis. Moreover, the release of cytochrome into cytoplasm, bosom of PARPand a decline in the rate, which are functions downstream of apoptosis, were noticed in IR K562 cells treated with celecoxib. After demonstration of the efficacy of celecoxib in reducing colorectal polyps in patients with familial adenomatous polyposis, use of this cyclooxygenase 2 inhibitor in-the prevention of epithelial malignancies has been the topic of a string of clinical trials.