The construction of the active compound was established as chlorogenic acid, C16H18O9, melting point 205?206 8C, aD 33.25. Its identification was established by comparing its physical data as well as its infra-red, nuclear magnetic resonance, selective FAAH inhibitor, and mass spectral data with those of an authentic sample. Antibodies were purchased from the next suppliers: Antibodies to h Abl, Bax, cIAP1, Bcl XL, Bcl 2, phospho STAT5, phospho JNK, phospho p38, actin, SMAC, Bad, Bim, Bid, Mcl 1, survivin, XIAP, DR4, DR5, JNK2 and p38 were purchased from Santa Cruz Biotechnology. Antibody to DR5 was also obtained from eBioscience. Antibodies to poly ADP ribose polymerase, cytochrome h, caspase 3, caspase 9, TNFR1 and TNFR2 were purchased from BD Biosciences. Antibodies to phospho c Abl, caspase 8, cleaved caspase 8 and phospho CrkL were procured from Cell Signaling Technology. Deborah acetyl L cysteine, JNK specific chemical, tetrachloro tetraethylbenzimidazolylcarbocyanineiodide, dichlorodihydrofluorescein diacetate, dihydroethidium, Z VAD FMK, Z IETD FMK and LEHD CHO were from Calbiochem. Polyethylene glycol conjugated catalase was bought from Sigma?Aldrich. Bcr Abl cell lines K562, KU812 and KCL 22 and Bcr Abl cell lines THP 1, U937 and MOLT 4 were cultured in RPMI 1640 medium containing ten percent fetal bovine serum and 100 U/ml penicillin?streptomycin. Clean peripheral blood samples from three CML patients and two healthier donors were collected and mononuclear cells were separated by HISTOPAQUE density gradient centrifugation. All studies with human blood were performed under an accepted institutional Human Ethics Committee Infectious causes of cancer project. Informed consent was provided in line with the Declaration of Helsinki. Cells in triplicate were incubated in 0. 2 ml RPMI 1640?? 10 % fetal bovine serum containing different concentrations of Chl in the presence and absence of NAC or specific inhibitors of different caspases. Cell viability was dependant on the Trypan blue exclusion assay. Possibility of major CML cells was determined in the same way except that recombinant human granulocyte macrophage colony stimulating factor was included. To gauge the role of ROS in Chl mediated killing of Bcr Abl cells in vivo, K562 xenografts were produced in nude mice as described. Chl was applied once a day for 15 days andNAC wasadministered on alternate days via intra peritoneal route. Tumefaction Decitabine solubility volumes were monitored and after 15 days of therapy, animals were sacrificed and images of the dissected tumors were taken all through postmortem with Olympus CAMEDIA D 4000 Zoom digital camera. Animal studies were conducted under an accepted institutional Animal Care and Use Committee protocol. Cells seeded at a density of 1. 5 105 cells/ml were possibly pretreated with NAC or left alone for 1 h accompanied by incubation with Chl at different concentrations for 24 h.