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The rate of pancreatic cancer has increased to a large extent. Almost 90 % of cases have a K-ras mutation in them and hence express Ras oncoprotein constitutively. It is normally treated by radiochemotherapy. To reduce metastasis gemcitabine based treatment is the only effective treatment present. Tipifarnib has been identified as a good choice against such type of cancer preventions. It inhibits the over expressed Ras oncoprotein by inhibiting its anchorage through the cell membrane which is a very important step in its activity. As opposed to many other antitumor agents which have mostly kinase inhibitor activity tipifarnib has a quite different mechanism of action. A number of cellular proteins contain a CAAX-box and a cysteine residue at their C-terminal region. This cysteine gets farnesylated by the help of an enzyme known as FTP (farnesyl protein transferase). During this process of farnesylation a 15 carbon compound farnesyl isoprenoid is transferred to C-terminal cysteine residue and the protein is then attached to the membrane. This anchoragement of Ras is very important for its activity; therefore inhibition of FTP enzyme may inhibit the action of Ras proteins. Tipifarnib was known to inhibit FTP enzyme. It is also known to be angiogenesis inhibitor in case of pancreatic cancer [1]. It has shown a significant antiproliferative activity in the cancers which have this pathway over efficient in them. Its inhibitory activity ranges in concentration from 9.5 – 500 nmol/L. Tipifarnib in combination with gemcitabine has shown quite efficient inhibition and hence efficient cure against cancer. Under physiological conditions the combination is safe having no adverse side effects on the body. Myeloid leukemias are caused by different reasons and cytotoxic drugs normally used are inefficient against them. The use of tipifarnib against secondary AML patients was studied in clinical trial phase II. It showed efficiency in the patients of secondary AML or patients having adverse cytogenetics. IFN-? was used in therapy against tumor and tipifarnib has been seen to enhance its activity. It was experimented both in vivo and in vitro conditions. IFN-? is one of the apoptosis inhibitors present inside the body that promotes growth and inhibit apoptosis after binding EGFR i.e., a cell surface receptor and afterwards stimulates Ras dependent MAP kinase pathway. Tipifarnib and IFN-? were administered in combination and complete reversal of Ras and Eek1/2 activation was seen. The combination suspended the growth of tumor cells by inhibiting the proliferation of cells and reducing the Akt activity. It promoted the apoptosis of tumor cells. It also enhanced the formation of immunoconjugate between Raf-1/bcl-2. Tipifarnib was selected after screening of a huge compound library of Farnesyl transferase inhibitors. In case of acute myeloid leukemia (AML) it modulates a variety of genetic pathways which may be the genes involved in the cellular immunity, cytoskeletal organization and the genes having a role in cell signaling. Tipifarnib is an inhibitory molecule that acts against MAPK pathway via a different mechanism and checks the FTP enzyme involved in activatio0n of regulatory protein. As one of the world leading suppliers of high-performance life-science products. We have over 8,000 products which consist of inhibitors, antibodies, RNAis, proteins and peptides those which focus on signaling pathways such as Neratinib, osi-906, AZD2171 & so on. Furthermore, compound libraries for high-throughput screening and high-content screening are also available.
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