gefitinib treatment had no impact on cholesterol content of the cells, and didn’t change the ability of lovastatin to cut back total cellular cholesterol. The degrees of cholesterol reduction produced by the statins are comparable order Gemcitabine with published results. Mobile counting assays were used to measure growth, to find out if lovastatin has got the capability to sensitize breast cancer cells to gefitinib. Cells were counted on days 1, 4, and 8 and treated every other day with the drugs. As explained previously, the four EGFR TKI resistant cell lines continued to proliferate in the presence of gefitinib. When comparing to gefitinib or lovastatin therapy alone apparently, lovastatin was able to dramatically reduce proliferation in the presence of gefitinib. Taken together, these data suggested that treatment with lovastatin sensitizes EGFR TKI resistant Pyrimidine cell lines to gefitinib. In order to determine if the results of lovastatin and gefitinib were complete in EGFR TKI resistant breast cancer cells, mobile viability assays were performed. Briefly, cells were treated for 72 h with the combination of gefitinib and lovastatin just before doing tetrazoliumbased cell viability assays. It can be noted the IC50 values for cell viability studies were higher than doses found to be effective in cellular proliferation assays. While growth assays enable the description of the number of cells with time, cell viability assays reveal the metabolic activity of the cell population. The IC50 of gefitinib was determined at different doses of lovastatin, and then isobolograms were developed. An interaction in HCC1954 and SUM149 cells was calculated from these assays. On the other hand, synergistic effects were observed in all four EGFR TKI resistant cell lines. Mix index values were calculated in line with the IC50 values. These values were significantly below one in most of the EGFR TKI resistant cell lines. Bosutinib 380843-75-4 These results suggested that the inhibition of lipid raft construction and EGFR kinase activity resulted in a decrease in cell viability when EGFR is localized to lipid rafts. For that reason, using lovastatin and gefitinib in combination might efficiently reduce viability and growth of breast cancers that have EGFR within lipid rafts. Statin medications work by inhibiting HMG-COA reductase. In addition to cholesterol biosynthesis, isoprenoid synthesis is also regulated by this enzyme. For that reason, as a way to determine if the synergistic effect between lovastatin and gefitinib is mediated by the cholesterol wearing ramifications of the clinically appropriate statin drug, the experimental drug NB 598 was used. NB 598 is really a squalene monooxygenase inhibitor, and consequently inhibits cholesterol biosynthesis although not isoprenoid synthesis.