Atezolizumab versus docetaxel in patients with previously treated non-small-cell lung cancer (OAK): a phase 3, open-label, multicentre randomised controlled trial

Achim Rittmeyer, Fabrice Barlesi, Daniel Waterkamp, Keunchil Park, Fortunato Ciardiello, Joachim von Pawel, Shirish M Gadgeel, Toyoaki Hida, Dariusz M Kowalski, Manuel Cobo Dols, Diego L Cortinovis, Joseph Leach, Jonathan Polikoff, Carlos Barrios, Fairooz Kabbinavar, Osvaldo Arén Frontera, Filippo De Marinis, Hande Turna, Jong-Seok Lee, Marcus Ballinger, Marcin Kowanetz, Pei He, Daniel S Chen, Alan Sandler, David R Gandara, OAK Study Group, Achim Rittmeyer, Fabrice Barlesi, Daniel Waterkamp, Keunchil Park, Fortunato Ciardiello, Joachim von Pawel, Shirish M Gadgeel, Toyoaki Hida, Dariusz M Kowalski, Manuel Cobo Dols, Diego L Cortinovis, Joseph Leach, Jonathan Polikoff, Carlos Barrios, Fairooz Kabbinavar, Osvaldo Arén Frontera, Filippo De Marinis, Hande Turna, Jong-Seok Lee, Marcus Ballinger, Marcin Kowanetz, Pei He, Daniel S Chen, Alan Sandler, David R Gandara, OAK Study Group

Abstract

Background: Atezolizumab is a humanised antiprogrammed death-ligand 1 (PD-L1) monoclonal antibody that inhibits PD-L1 and programmed death-1 (PD-1) and PD-L1 and B7-1 interactions, reinvigorating anticancer immunity. We assessed its efficacy and safety versus docetaxel in previously treated patients with non-small-cell lung cancer.

Methods: We did a randomised, open-label, phase 3 trial (OAK) in 194 academic or community oncology centres in 31 countries. We enrolled patients who had squamous or non-squamous non-small-cell lung cancer, were 18 years or older, had measurable disease per Response Evaluation Criteria in Solid Tumors, and had an Eastern Cooperative Oncology Group performance status of 0 or 1. Patients had received one to two previous cytotoxic chemotherapy regimens (one or more platinum based combination therapies) for stage IIIB or IV non-small-cell lung cancer. Patients with a history of autoimmune disease and those who had received previous treatments with docetaxel, CD137 agonists, anti-CTLA4, or therapies targeting the PD-L1 and PD-1 pathway were excluded. Patients were randomly assigned (1:1) to intravenously receive either atezolizumab 1200 mg or docetaxel 75 mg/m2 every 3 weeks by permuted block randomisation (block size of eight) via an interactive voice or web response system. Coprimary endpoints were overall survival in the intention-to-treat (ITT) and PD-L1-expression population TC1/2/3 or IC1/2/3 (≥1% PD-L1 on tumour cells or tumour-infiltrating immune cells). The primary efficacy analysis was done in the first 850 of 1225 enrolled patients. This study is registered with ClinicalTrials.gov, number NCT02008227.

Findings: Between March 11, 2014, and April 29, 2015, 1225 patients were recruited. In the primary population, 425 patients were randomly assigned to receive atezolizumab and 425 patients were assigned to receive docetaxel. Overall survival was significantly longer with atezolizumab in the ITT and PD-L1-expression populations. In the ITT population, overall survival was improved with atezolizumab compared with docetaxel (median overall survival was 13·8 months [95% CI 11·8-15·7] vs 9·6 months [8·6-11·2]; hazard ratio [HR] 0·73 [95% CI 0·62-0·87], p=0·0003). Overall survival in the TC1/2/3 or IC1/2/3 population was improved with atezolizumab (n=241) compared with docetaxel (n=222; median overall survival was 15·7 months [95% CI 12·6-18·0] with atezolizumab vs 10·3 months [8·8-12·0] with docetaxel; HR 0·74 [95% CI 0·58-0·93]; p=0·0102). Patients in the PD-L1 low or undetectable subgroup (TC0 and IC0) also had improved survival with atezolizumab (median overall survival 12·6 months vs 8·9 months; HR 0·75 [95% CI 0·59-0·96]). Overall survival improvement was similar in patients with squamous (HR 0·73 [95% CI 0·54-0·98]; n=112 in the atezolizumab group and n=110 in the docetaxel group) or non-squamous (0·73 [0·60-0·89]; n=313 and n=315) histology. Fewer patients had treatment-related grade 3 or 4 adverse events with atezolizumab (90 [15%] of 609 patients) versus docetaxel (247 [43%] of 578 patients). One treatment-related death from a respiratory tract infection was reported in the docetaxel group.

Interpretation: To our knowledge, OAK is the first randomised phase 3 study to report results of a PD-L1-targeted therapy, with atezolizumab treatment resulting in a clinically relevant improvement of overall survival versus docetaxel in previously treated non-small-cell lung cancer, regardless of PD-L1 expression or histology, with a favourable safety profile.

Funding: F. Hoffmann-La Roche Ltd, Genentech, Inc.

Conflict of interest statement

Declaration of interests

AR received grants and personal fees from Roche, Eli Lilly, Bristol-Myers Squibb, AstraZeneca, MSD, Boehringer Ingelheim, and Pfizer. FB received personal fees from Roche. DW, MB, and AS are Genentech employees and holders of Roche stock. KP received personal fees and research funding from AstraZeneca, and personal fees from Astellas, AVEO, Boehringer Ingelheim, Clovis, Eli Lilly, Hanmi, KHK Novartis, Ono, and Roche. FC received personal fees from Merck Serono, AstraZeneca, Eli Lilly, Roche, and Bayer. JvP received advisory board fees paid to institution from Daiichi Sankyo, Clovis, Roche, Vertex, and Novartis. SMG received personal fees from Roche/Genentech, Pfizer, Bristol-Myers Squibb, Ariad, Boehringer Ingelheim, and AstraZeneca. TH received grants and personal fees from Chugai, Eli Lilly, Ono, Novartis, Taiho Pharmaceutical, Nippon Boehringer Ingelheim, Pfizer, Bristol-Myers Squibb, Clovis, and AstraZeneca, and grants from Eisai, Takeda, Dainippon Sumitomo Pharma, Abbvie, Merck, Kyowa Hakko Kirin, Daiichi Sankyo, and Astellas. DMK, MCD, DLC, JL, JP, FK, OAF, FDM, HT, J-SL declare no competing interests. CB received clinical research fees from Pfizer, Novartis, Amgen, AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Roche/Genentech, Eli Lilly, Sanofi, Taiho Pharmaceutical, Mylan, Merrimack, Merck, Abbvie, Astellas, BioMarin, Bristol-Myers Squibb, Daiichi Sankyo, Abraxis BioScience, AB Science, Asana Biosciences, Medivation, Exelixis, ImClone Systems, LEO Pharma, Millennium, and personal fees from Boehringer Ingelheim, GlaxoSmithKline, Novartis, Pfizer, Roche (Genentech), Eisai, and Bioepis. MK and DSC are Genentech employees, holders of Roche stock, and have a Genentech patent pending for biomarkers and methods treating PD-1-related and PD-L1-related conditions. PH is a Genentech employee, holder of Roche and Amgen stock, and reports that a family member holds Gilead and Allergan stock. DRG received grants for serving as a consultant to Bristol-Myers Squibb, Genentech, and Merck.

Copyright © 2017 Elsevier Ltd. All rights reserved.

Figures

Figure 1:. Trial profile
Figure 1:. Trial profile
*One patient randomly assigned to docetaxel received atezolizumab. †The deaths of one patient in the atezolizumab group and of one patient in the docetaxel group were collected via public records. This is why the number of deaths for the overall survival analysis is 271 in the atezolizumab group and 298 in the docetaxel group and not 270 vs 297 as shown. These two patients are shown as patient withdrawal.
Figure 2:. Overall survival in the ITT…
Figure 2:. Overall survival in the ITT population and PD-L1 subgroups
(A) Kaplan-Meier estimates in the ITT primary population, stratified according to PD-L1 expression on tumour-infiltrating immune cells (IC0 vs IC1 vs IC2 vs IC3), the number of previous chemotherapy regimens (one vs two), and histology (non-squamous vs squamous). (B) Kaplan-Meier estimates in theTC1/2/3 or IC1/2/3 group with the same strata. (C) Kaplan-Meier estimates in the TC2/3 or IC2/3 group (unstratified). (D) Kaplan-Meier estimates in the TC3 or IC3 group (unstratified). (E) Kaplan-Meier estimates in the TC0 and IC0 group (unstratified). (F) HRs for overall survival in PD-L1 subgroups. Median overall survival was estimated by Kaplan-Meier analysis. HR=hazard ratio. IC=tumour-infiltrating immune cells. ITT=intention-to-treat. NE=not evaluable. PD-L1=programmed death-ligand 1. TC=tumour cells.
Figure 2:. Overall survival in the ITT…
Figure 2:. Overall survival in the ITT population and PD-L1 subgroups
(A) Kaplan-Meier estimates in the ITT primary population, stratified according to PD-L1 expression on tumour-infiltrating immune cells (IC0 vs IC1 vs IC2 vs IC3), the number of previous chemotherapy regimens (one vs two), and histology (non-squamous vs squamous). (B) Kaplan-Meier estimates in theTC1/2/3 or IC1/2/3 group with the same strata. (C) Kaplan-Meier estimates in the TC2/3 or IC2/3 group (unstratified). (D) Kaplan-Meier estimates in the TC3 or IC3 group (unstratified). (E) Kaplan-Meier estimates in the TC0 and IC0 group (unstratified). (F) HRs for overall survival in PD-L1 subgroups. Median overall survival was estimated by Kaplan-Meier analysis. HR=hazard ratio. IC=tumour-infiltrating immune cells. ITT=intention-to-treat. NE=not evaluable. PD-L1=programmed death-ligand 1. TC=tumour cells.
Figure 3:. Overall survival in prespecified subgroups
Figure 3:. Overall survival in prespecified subgroups
(A) Median overall survival was estimated by Kaplan-Meier analysis. Stratified for ITT and unstratified for subgroups. (B) Kaplan-Meier estimates in the non-squamous histology subgroup (unstratified). (C) Kaplan-Meier estimates in the squamous histology subgroup (unstratified). ECOG PS=Eastern Cooperative Oncology Group performance status. HR=hazard ratio. ITT=intention-to-treat.
Figure 4:. All-cause and treatment-related adverse events…
Figure 4:. All-cause and treatment-related adverse events in the safety population
(A) Adverse events that occurred within 30 days from the last study treatment were included in the analysis. Proportions of patients having treatment-related adverse events, by grade. (B) All-cause adverse events that differed by 5% or more between study groups. Additional adverse events with 5% or higher frequency in the docetaxel arm were not shown, and were neutrophil count decreased (10% vs

Source: PubMed

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