Thus, the objectives of this study were threefold: (i) to determine whether hypoxia upregulates GRPR expression in SCLC cells; (ii) to define whether a newly synthesised BU peptide antagonises GRP–GRPR signalling through the PI3K/AKT and MAPK/ERK pathways; and (iii) to evaluate the cytotoxic and pro-apoptotic effects of BU peptide under normoxic and hypoxic conditions. Here, AKT1 is linked to small cell lung carcinoma.