Hsp90 client proteins Raf 1 and Akt would be the principal client proteins that undergo degradation in these cell lines. Lung Cancer: Hsp90 term is up-regulated in non small cell lung cancer cells, specifically: A549, H226B and ChaGo K1, As is seen in most cancer cells. With the high purchase IPA-3 quantities of Hsp90, several Hsp90 customer proteins have been identified as crucial proteins for promoting development in NSCLC cells. These up regulated and activated customer proteins add a mutated EGF receptor, a receptor kinase that activates and promotes cell proliferation and survival, Akt, and a mutated p53, whose normal function would be to regulate the cell cycle and reduce tumor growth. These three consumer proteins are found to play a key role within the NSCLS cell survival. The EGF receptor is a tyrosine kinase receptor that is frequently mutated in non-small cell lung cancer and it’s over expressed in 40-80 of NSCLC areas. The activation of Akt is seen in 51% of NSCLC cell lines, p53 and Papillary thyroid cancer is mutated in 5000-10,000 of NSCLC areas. 17 AAG inhibited cell growth with IC50 values 124nM, 61nM, and 110nM for A549, H226B, and ChaGo K1 cell lines, respectively. Much like other cell lines, it was observed that addition of 17 AAG generated decrease and destruction in p53 and Akt, thus describing the effective IC50s observed against this cell line. These data suggest that 17 AAG is a possible therapeutic option for treating NSCLC. Gastrointestinal Cancers Colon Cancer: 17 AAG disappears Hsp90 client protein Raf 1 in four human colon adenocarcinoma cell lines HCT116, HT29, KM12 and HCT15. Of the four cell lines, HT29, a cell line that responds well to the drug treatment of preference was the most sensitive HDAC Inhibitors to 17 AAG. KM12 and hct116, that are established as drugresistant cancer cell lines, were moderately sensitive and painful to 17 AAG. HCT15 cells, also drug-resistant, were the least sensitive to 17 AAG therapy. To be able to determine if the cytotoxic effects of 17 AAG were associated with a procedure involving Hsp90, Raf 1 levels were monitored in these four cell lines. In HT29, Raf 1 levels were not restored, even after 48-hours of 17 AAG treatment. But, a moderate recovery of Raf 1 was seen in HCT116 and KM12 cells. Finally, HCT15 cells showed full restoration to manage degrees of Raf 1. These data link the efficiency of 17 AAG in colon cancer cell lines towards the restoration of the Hsp90 consumer protein, Raf 1. Recently it had been noticed that treatment of HCT116 cells with 17 AAG caused a G2 checkpoint arrest. In the G2 phase of the cell cycle, the cell continues to grow in preparation for mitosis, which does occur in the final stage of the cell cycle, the M phase. Before entering the M phase, the cell must go though a G2 checkpoint to assure the cell is prepared to divide. Wee1 and cdk1 are two proteins that are needed to drive the cell from G2 to M phase.