Different doses SGLT Pathway of erlotinib or HKI 272 for 72 h Lebensf Ability was determined colorimetrically by WST assay according to the manufacturer’s recommendations. The Lebensf Conductivity was calculated as a percentage of the untreated control after subtraction of background. Immunocompetent cells were either harvested in the presence or absence of various doses of drugs, and lysed, cultured as described. Whole cell lysates were analyzed for protein content rpern with antique, The EGFR, ErbB2, Akt, Erk, or the phosphorylation of these proteins By immunoblotting using standard methods. The blots were probed for actin or tubulin as controlled Them. of exon 19 that neratinib deletions.28 The starting dose of neratinib, 320 mg per day, which is above the one owned diarrhea, and therefore the dose to 240 mg per day, the Grade 3 Diarrh at 25% decline is limited. Although this rate has improved from the 320 mg is still high and is approx Hr observed four times, with the erlotinib.32 Although only four patients ceased treatment for diarrhea, perhaps because the symptoms were intermittent dose, cuts, and supportive treatment, and tended to decrease the force of gravity over time. Reduction of the dose in case of above the Owned diarrhea may reduce the bioavailability of drugs below the threshold of T ACTION for most EGFR mutations. The first Phase I trial was the hour HIGHEST average concentration of neratinib after t Dose adjusted by 240mgwas 73.5 ng / ml, which corresponds to 20 131 nmol / l, although not directly measured in our study, the equilibrium concentration of typical neratinib state at or below 60 nmol / l is required to E746A750 deletion of exon 19 or 90 to 800 nmol / L required to inhibit 240mgdailymayhave T790M.15 to inhibit 28 in contrast, was the inhibitory concentration for the G719S mutation probably reached easily . Pharmacokinetic data are not available to patients on this study, whether the exploratory analysis, no significant differences in PFS in patients treated with low dose showed. Other side effects were consistent with EGFR-TKI-class, including normal skin rash, fatigue, nausea and vomiting. There were no F ll Of interstitial lung disease, the most severe toxicity t of EGFR-TKI, has been observed in this study, when the phase I study a case of interstitial lung diseases include disease.20 Although neratinib also inhibits human factor receptor epidermal growth factor 2, an important class of associated cardiac toxicity were th not in this big saw s process in accordance with previous data. An important aspect of the design of the study was the mandate of the tumor tissue in all patients. Although we did not collect data on patients who are examined due to lack of available tissue, some patients have struggled dir For registration experience, was w During elective biopsy performed. Despite the challenges, clinical trials have increasingly NSCLC showed the feasibility of universal molecular testing, which is a step forward for the r 8.33 field.6 The crucial EGFR genotyping before therapy the first line by the first line Iressa was created as compared to carboplatin / paclitaxel in the study of Asia, in which patients with EGFR mutations, a gain of TKI therapy PFS achieved compared with chemotherapy first- line, w during TKI have been impressive at the expense of the wild-type patients.4 In the second row.