This 3D printed protein model of EGFR TK Mutant without Inhibitor visualizes the impact of T790M/L858R mutations on TK structure. The protein is in its active state, evident by the downward position of the active loop (orange), allowing for ATP to travel deep into its binding pocket. Bound to this binding pocket is TAK-285 (colored by atom type). This protein model is colored to visualize the atomic temperature and printed in full-color plastic.
Designed to be used with EGFR TK Mutant Small Molecule Inhibitor (3W2O)
Protein Description
Epidermal growth factor receptor (EGFR) gene mutations (G719X, exon 19 deletions/insertions, L858R, and L861Q) predict favorable responses to EGFR tyrosine kinase inhibitors (TKIs) in advanced non-small cell lung cancer (NSCLC). However, EGFR exon 20 insertion mutations (~10% of all EGFR mutations) are generally associated with insensitivity to available TKIs (gefitinib, erlotinib, and afatinib). The basis of this primary resistance is poorly understood. We studied a broad subset of exon 20 insertion mutations, comparing in vitro TKI sensitivity with responses to gefitinib and erlotinib in NSCLC patients, and found that most are resistant to EGFR TKIs
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Created from PDB ID: 3W2O.
