Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster display session

1986 - Survival and Safety of Atezolizumab by Best Overall Response (BOR) in the Ph III NSCLC OAK Study

Date

09 Sep 2017

Session

Poster display session

Presenters

Filippo de Marinis

Citation

Annals of Oncology (2017) 28 (suppl_5): v460-v496. 10.1093/annonc/mdx380

Authors

F. de Marinis1, F. Barlesi2, A. Rittmeyer3, J. von Pawel4, J. Han5, M. Kozloff6, A. Spira7, L. Fehrenbacher8, D.R. Gandara9, W. Yu10, P. He11, C. Yun12, M. Ballinger13, M. Gandhi12, S. Gadgeel14

Author affiliations

  • 1 Thoracic Oncology, European Institute of Oncology, 20141 - Milan/IT
  • 2 Multidisciplinary Oncology & Therapeutic Innovations, Aix Marseille University, Marseille/FR
  • 3 Thoracic Oncology, Lungenfachklinik Immenhausen, Immenhausen/DE
  • 4 Thoracic Oncology, Asklepios-Fachkliniken München-Gauting, Gauting/DE
  • 5 Center For Lung Cancer, National Cancer Center, Goyang/KR
  • 6 Medicine, Ingalls Memorial Hospital, Harvey/US
  • 7 Oncology, Virginia Cancer Specialists Research Institute, Fairfax/US
  • 8 Oncology, Kaiser Permanente Medical Center, Vallejo/US
  • 9 Thoracic Oncology, UC Davis Comprehensive Cancer Center, Sacramento/US
  • 10 Usma Biometrics, Genentech, South San Francisco/US
  • 11 Pd Biostatistics, Genentech, Inc., South San Francisco/US
  • 12 Usma, Genentech, South San Francisco/US
  • 13 Product Development Oncology, Genentech, South San Francisco/US
  • 14 Medical Oncology, University of Michigan, Ann Arbor/US
More

Resources

Abstract 1986

Background

Atezolizumab (atezo; anti–PD-L1) inhibits binding of PD-L1 to PD-1 and B7.1, thereby restoring tumor-specific T-cell immunity. OAK, the first randomized Ph III study of atezo vs docetaxel (doc) in 2L/3L NSCLC demonstrated a superior OS benefit of atezo (HR 0.73; 95% CI: 0.62, 0.87; P = 0 .0003) in patients (pts) regardless of PD-L1 expression levels on tumor cells (TC) or tumor-infiltrating immune cells (IC). Here we present efficacy and safety analyses in the OAK primary population (n = 850) by BOR subgroups.

Methods

Previously treated pts were randomized 1:1 to atezo (1200 mg) or doc (75 mg/m2) IV q3w. Co-primary endpoints were OS in ITT and PD-L1 expression subgroup (≥ 1% PD-L1 on TC or IC). Secondary endpoints included ORR and safety. BOR subgroups were defined based on RECIST v1.1 response determined by investigators. Time to response (TTR) was based on tumor assessment every 6 weeks. Data cutoff, July 7, 2016.

Results

Baseline demographics were generally similar across BOR subgroups except for PD-L1 expression status. TC1/2/3 or IC1/2/3 prevalence was 74% in CR/PR, 53% in SD and 55% in PD subgroups, respectively. The survival benefit of atezo vs doc was observed across BOR subgroups with greatest benefit occurring in the CR/PR subgroup (HR, 0.32; 95% CI 0.16, 0.63; see Table). Among pts in the CR/PR subgroup, the median TTR was comparable between atezo and doc arms (2.8 mo each). The median duration of response was longer in the atezo arm pts (16.3 mo, 95% CI: 10.0, NE) vs doc arm pts (6.2 mo, 95% CI: 4.9, 7.6). OS benefit with atezo was also observed in patients with SD and PD as BOR (see Table). No new safety findings were observed among BOR subgroups.

Conclusions

Atezo responses were durable. Atezo responders had more than two-thirds reduction in the risk of death compared with doc responders. In addition, the improved OS with atezo vs doc seen in pts with SD and PD suggests that clinical benefit also extended to patients who did not have a radiographic response.Table:

1310P Efficacy of atezolizumab vs docetaxel by BOR subgroups

Patient PopulationAtezolizumabDocetaxelHR (95% CI)a
nmOS (95% CI), monmOS, (95% CI) mo
ITT (N = 850)42513.8 (11.8, 15.7)4259.6 (8.6, 11.2)0.73 (0.62, 0.87)
BOR subgroups
CR/PR58NE (NE, NE)5720.0 (15.9, NE)0.32 (0.16, 0.63)
SD15017.6 (15.7, 20.2)17713.0 (11.5, 14.7)0.70 (0.53, 0.92)
PD1877.3 (6.7, 9.4)1176.4 (5.6, 7.3)0.72 (0.56, 0.93)
a

Stratified HR for ITT and unstratified HR for subgroups. 95% CI for HR were estimated using Cox regression.

NE, not estimable.

Clinical trial identification

NCT02008227

Legal entity responsible for the study

F. Hoffmann - La Roche Ltd.

Funding

F. Hoffmann - La Roche Ltd.

Disclosure

F. de Marinis: Consultation fees received from Roche/BMS/Boehringer/Novartis/Pfizer/MSD/Astrazeneca. F. Barlesi: Honarium from Roche. A. Rittmeyer: Grants as an advisor or speaker by: Astra Zeneca, BMS, Boehringer Ingelheim, Eli Lilly, Pfizer and Roche Genentech. J. von Pawel: Adboard: AbbVie, Pfizer, Bristol Myers Squibb, Novartis money paid to the institution. A. Spira: Research sponsored by Roche/Genentech (payable to institution), Speakers bureau. D.R. Gandara: Consultant: Genentech Clinical trial grant: Genentech. W. Yu: Genentech Employee. P. He: Employee of Roche/Genentech, and have stocks for Roche, Amgen. Husband has stocks for Allergan and Gilead. C. Yun: Employee of Genentech, Roche stock, Research funding from Genentech M. Ballinger: Employee of Genentech, Roche stock. M. Gandhi: Employee of Genentech. S. Gadgeel: Speaker\'s bureau: Astra‐Zeneca, Genentech/Roche Advisory Boards‐ Astra‐Zeneca, Ariad, Pfizer, Bristol Myers‐ Squibb and Genentech/Roche. All other authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.