EGFR and neoplasm: Having shown that this new K1-K2 prototype could be hydrolyzed into the majorbioactive species in vivo and to strongly block EGFR (Kin-1)and c-Src (Kin-2) phosphorylation in vitro, we sought todetermine whether it could modulate its two targets in a tumour model invivo. This was performed in comparison with the administration ofthe two free clinical inhibitors (gefitinib and dasatinib) targeting Kin-1(EGFR) and Kin-2 (c-Src) using the mouse 4T1 cells in which we have shown thetwo targets to be modulated in vitro (Fig. 7B).