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C. Matheny



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    PL04a - Plenary Session: Immune Checkpoint Inhibitors in Advanced NSCLC (ID 430)

    • Event: WCLC 2016
    • Type: Plenary
    • Track: Chemotherapy/Targeted Therapy/Immunotherapy
    • Presentations: 1
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      PL04a.02 - OAK, a Randomized Ph III Study of Atezolizumab vs Docetaxel in Patients with Advanced NSCLC: Results from Subgroup Analyses (Abstract under Embargo until December 7, 7:00 CET) (ID 5822)

      08:45 - 09:40  |  Author(s): C. Matheny

      • Abstract
      • Presentation
      • Slides

      Background:
      Atezolizumab inhibits PD-L1 binding to its receptors PD-1 and B7.1, thereby restoring tumor-specific T-cell immunity. Primary analysis of the Phase III OAK study in previously-treated NSCLC revealed superior survival for atezolizumab vs docetaxel in the ITT population (mOS, 13.8 vs 9.6 months; HR, 0.73) and in patients expressing ≥1% PD-L1 on TC or IC (TC1/2/3 or IC1/2/3; mOS, 15.7 vs 10.3; HR, 0.74). Here we present further subgroup analyses.

      Methods:
      OAK evaluated atezolizumab vs docetaxel in an unselected NSCLC population who had failed prior platinum-containing chemotherapy. Patients were stratified by PD-L1 expression, prior chemotherapy regimens and histology, and randomized 1:1 to atezolizumab (1200 mg) or docetaxel (75 mg/m[2]) IV q3w. PD-L1 expression by IHC and mRNA was centrally evaluated by VENTANA SP142 IHC assay and Fluidigm, respectively. Data cutoff, July 7, 2016.

      Results:
      For the first 850 of 1225 randomized patients (primary study population), OS was improved with atezolizumab vs docetaxel regardless of histology and this benefit was observed across PD-L1 subgroups within each histology (Table). PD-L1 gene expression showed a similar association with OS as PD-L1 IHC. In nonsquamous patients ORR was 14.4% vs 15.2%; in squamous patients ORR was 11.6% vs 8.2% (atezolizumab vs docetaxel). OS benefit vs docetaxel was seen across subgroups including patients with treated baseline brain metastases (n=85; mOS 20.1 vs 11.9 mo; HR 0.54, 95% CI 0.63-0.89) and never smokers (n=156; mOS 16.3 vs 12.6 mo, HR 0.71, 95% CI 0.47-1.08). Further secondary endpoints and exploratory biomarker analyses for these subgroups and by age and EGFR/KRAS status will be presented.

      Conclusion:
      OAK demonstrated clinically relevant improvements with atezolizumab in the ITT population, including in both histology subgroups regardless of PD-L1 expression (measured by IHC or tumor gene expression), and among other subgroups including never smokers and in patients with baseline brain metastases.

      OS
      Atezolizumab Docetaxel HR[a]95% CI
      n Median, mo n Median, mo
      Nonsquamous
      TC3 or IC3 49 22.5 47 8.7 0.35(0.21-0.61)
      TC2/3 or IC2/3 89 18.7 99 11.3 0.61(0.42-0.88)
      TC1/2/3 or IC1/2/3 171 17.6 162 11.3 0.72(0.55-0.95)
      TC0 and IC0 140 14.0 150 11.2 0.75(0.57-1.00)
      All 313 15.6 315 11.2 0.73(0.60-0.89)
      Squamous
      TC3 or IC3 23 17.5 18 11.6 0.57(0.27-1.20)
      TC2/3 or IC2/3 40 10.4 37 9.7 0.76(0.45-1.29)
      TC1/2/3 or IC1/2/3 70 9.9 60 8.7 0.71(0.48-1.06)
      TC0 and IC0 40 7.6 49 7.1 0.82(0.51-1.32)
      All 112 8.9 110 7.7 0.73(0.54-0.98)
      [a]Unstratified HRs. TC=tumor cell, IC=tumor-infiltrating immune cell


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