Author of

• 30601

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  P2.01 - Advanced NSCLC (ID 159)

  • Event: WCLC 2019
  • Type: Poster Viewing in the Exhibit Hall
  • Track: Advanced NSCLC
  • Presentations: 1
  • Moderators:
  • Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall

  • 30688

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    P2.01-79 - Afatinib in EGFR Mutation-Positive (EGFRm+) NSCLC Harbouring Uncommon Mutations: Experience in ‘Real-World’ Clinical Practice (ID 1282)

    10:15 - 18:15  |  Author(s): Christopher Hoffmann
    • Abstract
    • Slides

    Background
    

    Approximately 10–12% of patients with EGFRm+ NSCLC have tumors harboring uncommon EGFR mutations. Preclinical data indicate that the ErbB family blocker, afatinib, has broader inhibitory activity against uncommon mutations, including compound mutations, compared with first-generation EGFR TKIs.^1,2 Post-hoc analysis of the LUX-Lung 2, 3, and 6 trials³ demonstrated that afatinib is active against certain uncommon EGFR mutations. The objective response rate (ORR) with afatinib against G719X (n=18), L861Q (n=16), and S768I (n=8) single/compound mutations was 78%, 56%, and 100%, respectively. Patients with exon 18–21 uncommon mutations had progression-free survival (PFS) and overall survival of 10.7 and 19.4 months, respectively. The aim of this analysis was to explore the sensitivity of uncommon EGFR mutations to afatinib in a broader ‘real-world’ patient population.

    Method
    

    We undertook a pooled analysis of data from an Asian phase IIIB trial (NCT01953913) and a German non-interventional study (NCT02047903) that assessed afatinib in patients with EGFR TKI-naïve EGFRm+ NSCLC. Tumour response was based on investigator review, and PFS was calculated by Kaplan–Meier methodology.

    Result
    

    Fifty-four patients were identified with tumours harbouring uncommon mutations, including L861Q (n=13), S768I (n=3), G719X (n=23), and other (n=8); 21 patients had compound mutations. Baseline characteristics were: male, 59%; median age (range), 63.5 (35‒79) years; Eastern Cooperative Oncology group performance status 0 or 1/>1, 93%/6%. The combined ORR for evaluable patients with L861Q, S768I, or G719X was 59% (20/34), and the disease control rate was 91% (30/34); ORR and DCR in patients with compound mutations was 47% (9/19) and 89% (17/19), respectively. Overall, median PFS in patients with L861Q, S768I, or G719X was 10.7 months; median PFS in patients with compound mutations was 7.3 months.

    Conclusion
    

    In this ‘real-world’ cohort of patients with EGFRm+ NSCLC, afatinib was active against uncommon mutations known to be less responsive to reversible EGFR TKIs. These data are in line with the LUX-Lung trials and support the use of afatinib in patients with non-resistant EGFR mutations.

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