Lung cancer is the most common cause of cancer death worldwide and it has one of the lowest survival rates among tumours, thus the need to develop new drugs to treat the disease is clear. Among the different kinases involved in cancer pathologies in general, and in lung cancer, we focused our efforts on the validation of RSK4 as a tumour promoter in the lungs. Preliminary unpublished results suggested the antibiotics trovafloxacin and moxifloxacin inhibit RSK4 activation and as consequence increase chemosensitisation to cisplatin, decreasing cell survival and preventing cell invasion and migration. To validate these findings and try to establish the necessary features for compound activity, trovafloxacin was successfully synthesised in gram scale, along with 47 analogues to allow for structure-activity relationship studies. To do so, a biochemical assay was envisioned to study the ability of our compounds to inhibit RSK activation by its upstream kinase ERK. To this end, both kinases were recombinantly expressed and purified, and we have ongoing efforts to achieve the necessary conditions for compound assessment. Additionally, we were able to develop a HEK-293 cell line stably overexpressing RSK4 for a cell-based assay aimed at the measurement of RSK4 phosphorylation levels, and preliminary results show that some of our analogues were able to decrease RSK4 activation in comparison to the controls used. This assay was supported by analyses by tandem mass spectrometry. Finally, in vivo studies using trovafloxacin in a xenograft mouse model highlighted the ability of the antibiotic to prevent cell survival, invasion and migration, and to enhance cisplatin effects.