Tepotinib plus gefitinib in patients with EGFR-mutant non-small-cell lung cancer with MET overexpression or MET amplification and acquired resistance to previous EGFR inhibitor (INSIGHT study): an open-label, phase 1b/2, multicentre, randomised trial

医学 吉非替尼 T790米 内科学 肺癌 临床终点 表皮生长因子受体 肿瘤科 临床研究阶段 实体瘤疗效评价标准 代理终结点 临床试验 癌症
作者
Yi‐Long Wu,Ying Cheng,Jianying Zhou,Shun Lü,Yiping Zhang,Jun Zhao,Dong‐Wan Kim,Ross A. Soo,Sang‐We Kim,Hongming Pan,Yuh‐Min Chen,Chih‐Feng Chian,Xiaoqing Liu,Daniel S.W. Tan,Rolf Bruns,Josef Straub,Andreas Johne,J. Scheele,Keunchil Park,James Chih‐Hsin Yang
出处
期刊:The Lancet Respiratory Medicine [Elsevier]
卷期号:8 (11): 1132-1143 被引量:248
标识
DOI:10.1016/s2213-2600(20)30154-5
摘要

Background We evaluated the efficacy and safety of tepotinib, a potent and highly selective oral MET inhibitor, plus gefitinib in patients with epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) with MET overexpression (immunohistochemistry [IHC]2+ or IHC3+) or MET amplification having acquired resistance to EGFR inhibition. Methods In this open-label, phase 1b/2, multicentre, randomised trial (the INSIGHT study), we enrolled adult patients (≥18 years) with advanced or metastatic NSCLC, and Eastern Cooperative Oncology Group performance status of 0 or 1, from academic medical centres and community clinics in six Asian countries. In phase 1b, patients received oral tepotinib 300 mg or 500 mg plus gefitinib 250 mg once daily. In phase 2, patients with EGFR-mutant, T790M-negative NSCLC MET overexpression or MET amplification were randomly assigned (initially in a 1:1 ratio and then 2:1 following a protocol amendment) to tepotinib plus gefitinib at the recommended phase 2 dose or to standard platinum doublet chemotherapy. Randomisation was done centrally via an interactive voice-response system. The primary endpoint was investigator-assessed progression-free survival (PFS). Secondary endpoints included overall survival (OS) and safety. Subgroup analyses were preplanned in patients with high MET overexpression (IHC3+) or MET amplification (mean gene copy number ≥5 or MET to centromere of chromosome 7 ratio ≥2). Efficacy and patient characteristics were assessed on an intention-to-treat basis and safety was assessed for all patients who received at least one dose of study medication. Low recruitment led to early termination of phase 2, so all analyses are considered to be exploratory. This study is registered with ClinicalTrials.gov, NCT01982955, and the European Union Drug Regulating Authorities Clinical Trials Database, Eudra-CT 2016-001604-28. Findings From Dec 23, 2013, to May 25, 2017, 18 patients were enrolled in phase 1b (n=6 in the 300 mg tepotinib group; n=12 in the 500 mg tepotinib group) and 55 patients in phase 2 (n=31 in the tepotinib plus gefitinib group; n=24 in the chemotherapy group). No dose-limiting toxicities were observed in phase 1b, so tepotinib 500 mg was used as the recommended phase 2 dose. In phase 2, survival outcomes were similar between groups: median PFS was 4·9 months in the tepotinib plus gefitinib group (90% CI 3·9–6·9) versus 4·4 months in the chemotherapy group (90% CI 4·2–6·8; hazard ratio [HR] 0·67, 90% CI 0·35–1·28). Median OS was 17·3 months in the tepotinib plus gefitinib group (12·1–37·3) versus 18·7 months in the chemotherapy group (15·9–20·7; HR 0·69, 0·34–1·41). PFS and OS were longer with tepotinib plus gefitinib than with chemotherapy in patients with high (IHC3+) MET overexpression (n=34; median PFS 8·3 months [4·1–16·6] vs 4·4 months [4·1–6·8]; HR 0·35, 0·17–0·74; median OS 37·3 months [90% CI 24·2–37·3] vs 17·9 months [12·0–20·7]; HR 0·33, 0·14–0·76) or MET amplification (n=19; median PFS 16·6 months [8·3–not estimable] vs 4·2 months [1·4–7·0]; HR 0·13, 0·04–0·43; median OS 37·3 months [90% CI not estimable] vs 13·1 months [3·25–not estimable]; HR 0·08, 0·01–0·51). The most frequent treatment-related grade 3 or worse adverse events were increased amylase (5 [16%] of 31 patients) and lipase (4 [13%]) concentrations in the tepotinib plus gefitinib group and anaemia (7 [30%] of 23 patients) and decreased neutrophil count (3 [13%]) in the chemotherapy group. Interpretation Despite early study termination, in a preplanned subgroup analysis, our findings suggest improved anti activity for tepotinib plus gefitinib compared with standard chemotherapy in patients with EGFR-mutant NSCLC and MET amplification, warranting further exploration. Funding Merck KGaA.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
量子星尘发布了新的文献求助10
刚刚
彭于晏应助WHITE采纳,获得10
刚刚
JamesPei应助陈泽宇采纳,获得10
1秒前
1秒前
luermei完成签到,获得积分10
1秒前
大模型应助友好的灯泡采纳,获得10
2秒前
3秒前
3秒前
深情安青应助自然的南露采纳,获得10
4秒前
FashionBoy应助kxm采纳,获得10
4秒前
小马完成签到,获得积分10
5秒前
右二森发布了新的文献求助10
5秒前
Planta完成签到,获得积分10
6秒前
小星完成签到,获得积分10
6秒前
6秒前
Daybreak完成签到,获得积分10
7秒前
8秒前
simon应助一条鱼采纳,获得10
8秒前
小杜在此完成签到,获得积分20
8秒前
内向的冰棍完成签到,获得积分10
8秒前
小马发布了新的文献求助10
8秒前
苦茶子发布了新的文献求助10
8秒前
璐璐完成签到 ,获得积分10
9秒前
9秒前
bkagyin应助高高的咖啡豆采纳,获得10
9秒前
酆百川发布了新的文献求助10
9秒前
10秒前
yaohuici发布了新的文献求助10
11秒前
11秒前
斯文败类应助辛勤雨柏采纳,获得10
11秒前
hoaye完成签到,获得积分10
11秒前
11秒前
111完成签到,获得积分10
11秒前
陈泽宇发布了新的文献求助10
12秒前
小星发布了新的文献求助10
12秒前
jing发布了新的文献求助10
13秒前
mike_007发布了新的文献求助10
13秒前
量子星尘发布了新的文献求助10
13秒前
metare完成签到,获得积分10
13秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Binary Alloy Phase Diagrams, 2nd Edition 8000
Comprehensive Methanol Science Production, Applications, and Emerging Technologies 2000
Building Quantum Computers 800
Translanguaging in Action in English-Medium Classrooms: A Resource Book for Teachers 700
二氧化碳加氢催化剂——结构设计与反应机制研究 660
碳中和关键技术丛书--二氧化碳加氢 600
热门求助领域 (近24小时)
化学 材料科学 生物 医学 工程类 计算机科学 有机化学 物理 生物化学 纳米技术 复合材料 内科学 化学工程 人工智能 催化作用 遗传学 数学 基因 量子力学 物理化学
热门帖子
关注 科研通微信公众号,转发送积分 5660573
求助须知:如何正确求助?哪些是违规求助? 4834676
关于积分的说明 15091117
捐赠科研通 4819141
什么是DOI,文献DOI怎么找? 2579102
邀请新用户注册赠送积分活动 1533630
关于科研通互助平台的介绍 1492396