Inhibited molecular targets of breast cancer: PR/ER-α/EGFR/HER2Exhibited stronger binding affinities towards PR/ER-α/EGFR/HER2Showed hydrophobic interaction with amino acid residue of PR/ER-α/EGFR/HER2Identified as a substrate for P-glycoprotein and CYP3A4Demonstrated high permeability for human intestinal absorption and Caco-2 cells Showed high blood–brain barrier permeabilityShowed no carcinogenicity. Here, EGFR is linked to breast cancer.