THE MOST THREATENING EGFR MUTATION MAY BE THE ONE YOU DON’T SEE

Exon 20 insertion mutations in EGFR+ mNSCLC are more elusive and life‑threatening than common EGFR mutations.^1-9

These mutations differ from common mutations, such as L858R and exon 19 deletions, in how they are detected and treated, leaving patients at risk of rapid disease progression on current targeted therapies.^1-9

Learn what makes EGFR exon 20 insertion mutations different

EGFR EXON 20 INSERTION MUTATIONS ARE THE 3^RD MOST PREVALENT PRIMARY EGFR MUTATION, YET THEY ARE OFTEN UNDERDETECTED^3,5,11

Current biomarker testing practices can make it difficult to identify these patients^3,4,6,10

PCR-based tests, which are mutation‑specific, have technical limitations and can only detect a limited number of exon 20 insertion mutations^3,6,10,11

Exon 20 insertion mutations cannot be treated effectively with most targeted therapies.^2,5-8

Through the use of testing techniques that detect a broader range of mutations—either liquid or tissue-based NGS—and careful examination of biomarker test results, you can better understand the full picture of treatment options for your patients with EGFR‑positive mNSCLC.^3,10,12

The NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines^®) strongly advise broader molecular profiling for eligible patients with advanced or metastatic NSCLC, with the goal of identifying rare driver mutations.¹³*

It is recommended at this time that, when feasible, molecular testing be performed via a broad, panel-based approach, most typically performed by next-generation sequencing (NGS).¹³*

*The NCCN Guidelines^® for NSCLC provide recommendations for certain individual biomarkers that should be tested and recommend testing techniques but do not endorse any specific commercially available biomarker assays or commercial laboratories.¹³

BUT ACCURATE DETECTION IS ONLY THE FIRST STEP IN FIGHTING THIS MUTATION

Disease driven by EGFR exon 20 insertion mutations does not respond well to most EGFR TKIs – Joshua Sabari, MD

MOST TKI THERAPIES INDICATED FOR COMMON EGFR MUTATIONS ARE NOT EFFECTIVE AT TREATING PATIENTS WITH EXON 20 INSERTION MUTATIONS, MAKING THEM MORE DIFFICULT TO TREAT THAN COMMON EGFR MUTATIONS^2,5-8

Compared with common mutations, EGFR exon 20 insertion mutations reduce the size of the drug‑binding pocket and affinity for most TKIs indicated for common EGFR mutations^2†

^†A763_Y764FQEA does not cause steric hindrance in the drug‑binding pocket and has been shown to be sensitive to currently approved TKIs.¹⁴

Response to most TKIs in treatment‑naïve patients:

EGFR exon 20 insertion mutations^15,16

EGFR TKIs indicated for classical EGFR mutations⁹

Classical EGFR exon 19 deletion or L858R mutation¹⁷

^‡Results from a real-world analysis of treatment patterns.⁹

^§The median overall survival was 38.6 months (95% CI, 34.5 to 41.8) in the osimertinib group and 31.8 months (95% CI, 26.6 to 36.0) in the comparator group (hazard ratio for death, 0.80; 95.05% CI, 0.64 to 1.00; P=0.046).¹⁷

The NCCN Guidelines recommend treating patients with mNSCLC with most EGFR exon 20 insertion mutations using first‑line systemic therapy, like platinum‑based chemotherapy.^13||

^||Exceptions include p.A763_Y764insFQEA and p.A763_Y764insLQEA. See the NCCN Guidelines for detailed recommendations for platinum‑based chemotherapy regimens for mNSCLC.¹³

Progression-free survival in treatment‑naïve patients with exon 20 insertion mutations:

Platinum‑based chemotherapy^9,18-20

TKIs^2¶

^¶TKIs in these trials included erlotinib, gefitinib, and afatinib.²

DON’T LET THIS MUTATION GET BY YOU. TEST FOR, FIND, AND APPROPRIATELY MANAGE EXON 20 INSERTION MUTATIONS.

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