We found that down-regulation of Notch 1 by small interfering RNA or, secretase inhibitors before TW 37 treatment triggered improved cell growth inhibition and apoptosis. Our data suggest that the observed Lenalidomide molecular weight anti-tumor action of TW 37i s mediated via a novel pathway concerning inactivation of Notch 1 and Jagged 1. Pancreatic cancer remains one of the most aggressive cancers having a very poor prognosis. Over 33,000 people die with this deadly disease each year in the United States. A large proportion of individuals present with gross metastases or micrometastases requiring effective drug therapies. Nevertheless, traditional chemotherapy shows only a little survival advantage when coupled with surgical resection. This outcome shows that new and alternative ways to the control of cancer are critically needed. Pancreatic cancer has been proven to overexpress Bcl 2 and its family members. Consequently, blockade of Bcl 2 exercise must turn into a new therapeutic technique for pancreatic cancer. Several groups have already been trying to develop anticancer drugs that block the function of Bcl 2 people. TW 37, a recently created small molecule inhibitor of Bcl 2, goals Posttranslational modification (PTM) multiple members of the Bcl 2 family and attenuates activation of Bcl 2. TW 37 was designed to target the groove of anti-apoptotic proteins that normally bind the BH3 domain of proapoptotic effectors including Bid, Bax, Bim, and others. We’ve discovered that TW 37 inhibits the development of a number of cancer cells, including breast, prostate, lymphoma, and pancreatic cancer. But, the precise mechanism of action of TW 37 as an anti-tumor agent hasn’t yet been fully established. It is well documented that Bcl 2 features through heterodimerization with proapoptotic members of the Bcl 2 household to prevent mitochondrial pore formation and prevent cytochrome c release and initiation of apoptosis. But, there are more purchase Imatinib evidences showing that Bcl 2 might play an oncogenic role through survival paths other than its purpose in the mitochondrial membrane. . It has been reported that Bcl 2 activates nuclear factor nB by a signaling system that requires Raf 1/MEKK 1 mediated activation of IKKh. Mortenson and colleagues demonstrate that overexpression of Bcl 2 enhanced the activity of IKK and AKT along with NF nB transcriptional activity in pancreatic cancer. Kumar and colleagues found that Bcl 2 induced tumor cell invasion and tumor cell proliferation were somewhat mediated by interleukin 8. Lately, Tucker and colleagues reported that Bcl 2 over-expression ultimately causing preservation of cyclin D1a expression may occur through p38 mitogen-activated protein kinase mediated signaling pathways in human lymphoma cell lines. Moreover, down-regulation of Bcl 2 pAkt in prostate cancer cell lines, vascular endothelial growth factor, and also could regulate the expression of anhydrase IX.