Fraisinib: a calix[4]pyrrole derivative effective in reducing NSCLC tumor in-vivo, is found to act as ligand of the Glycine-tRNA Synthase (GARS1), a new molecular target in oncology.

Adopting a multi-proteomic approach, we evaluated the possible involvement of GARS1 in the regulation of phenotypic alterations that reduced in vivo tumorigenicity of A549 cells exposed to Fraisinib over time. For this purpose, we performed a differential proteomic analysis followed by the generation of functional networks and enrichment analysis, and then we compared the obtained results after including the known GARS1 interactors identified in A549 cell line.