These findings conclusively confirm the in silico predictions, highlighting the superior potential of compounds in CRE, particularly C2, in suppressing SRC, STAT3, PIK3CA, MAPK1, EGFR, and JAK1 as proteins involved in the pathways of EGFR tyrosine kinase inhibitors’ resistance in NSCLC. This evidence concerns the gene EGFR and non-small cell lung carcinoma.