GFR based activation strategies such as insulin growth factor receptor BRL-15572 1 by IGF  and IGF Plays an r Essential role in cell proliferation and tumor dissemination through F Promotion cell cycle progression and presence of apoptosis prevention and control and maintenance of the metastatic tumor-Ph Genotype. A wide variety of tumors show abnormal expression or increased Hte IGF IGF and 1R, which leads correlated with yourself and paracrine growth stimulation, which was obtained Hter proliferation of tumor differentiation, stage of disease, the development of metastasis and survival of patients reduced. Obtained Hte expression of IGF 1R was also demonstrated in the BTC System and IGF / IGFR was shown that one play r Central role in the proliferation and suppression of apoptosis in cholangiocarcinoma cells, making the system IGF / IGFR signaling an attractive target for the treatment of BTC.
Thus blocking Antique 1R body IGF, IGF 1R antisense oligonucleotides, siRNA or IGF 1R showed all his F Ability, with IGF 1R mediated signaling in vitro and tumor growth in vivo and interfere dissemination. We validated and other selective IGF 1R tyrosine kinase NVP AEW541 as a promising new drug for the treatment of certain cancers. Moreover, we have shown that the combination of IGF 1R inhibitors sorafenib multikinase inhibitor offer cholangiocarcinoma additive antitumor activity in vitro. The anti-cancer properties and related compounds as NVPAEW541 NVPADW742 were in pr Ewing sarcoma clinical trials M S nozzles, fibrosarcoma, breast cancer and sarcomas demonstrated the musculoskeletal system.
Antique Body that specifically removes IGFR powerfully from the prostate and the growth of cancer cells in vitro. The antique IGFR body clinically most advanced the fight against CP 751,871, currently tested in three phase  Trials for advanced breast cancer, NSCLC and prostate cancer. It is important to show vorl INDICATIVE clinical data that inhibition IGFR is well tolerated. Security is important, since the inhibition IGFRbased long been a high-risk intervention associated due to the high homology of the receptors for IGF 1R with the insulin receptor, and the fear has been recognized that the IGF 1R tyrosine kinase inhibitors k can lead to insulin resistance and overt diabetes. However, should the current in vivo data support this hypothesis, which then causes a growing interest in therapies anti-IGFR base.
crosstalk between IGF signaling system / IGFR and other growth factor receptors capable of the antitumor effect of monotherapy Ans PageSever, the combination of IGF / IGFRtargeting require with other therapeutic treatments to improve efficiency reduce. This may be achieved through dual targeting and IGF 1R EGFR, EGFR, as the system by IGF / IGFR leads to tyrosine kinase oncogene mito without ligand stimulation of EGFR EGFR is activated. This line IGFR combined inhibition of EGFR may be additive verst Strengths the antineoplastic effect of the respective monotherapies in gastrointestinal cancers. Double-molecule inhibitors specifically promising the use of two small-molecule inhibitors targeting, less related kinases simultaneously blocking VEGFR and EGFR tyrosine kinases such as may, for the future treatment of BTC.