Milind Javle and Rachna T. Shroff, The University of Texas MD Anderson Cancer Center, Houston, TX; Maeve Lowery and Ghassan K. Abou-Alfa, Memorial Sloan Kettering Cancer Center, and Weill Cornell Medical College, New York, NY; Karl Heinz Weiss and Christoph Springfeld, Universitäts Klinikum Heidelberg, Heidelberg, Germany; Mitesh J. Borad, Ramesh K. Ramanathan, and Tanios Bekaii-Saab, Mayo Clinic, Phoenix, AZ; Lipika Goyal and Andrew X. Zhu, Massachusetts General Hospital Cancer Center, Boston, MA; Saeed Sadeghi and Richard S. Finn, David Geffen School of Medicine at UCLA; Anthony El-Khoueiry, USC Norris Comprehensive Cancer Center, Keck School of Medicine, Los Angeles; Robin Kate Kelley, UCSF Helen Diller Family Comprehensive Cancer Center, San Francisco, CA; Teresa Macarulla, Vall d'Hebron University Hospital and Vall d'Hebron Institute of Oncology, Barcelona, Spain; Ivan Borbath, Cliniques Universitaires Saint-Luc, Brussels; Eric Van Cutsem, University Hospitals Gasthuisberg and KU Leuven, Leuven, Belgium; Su Pin Choo, National Cancer Centre of Singapore, Singapore; Do-Youn Oh, Seoul National University, Seoul, South Korea; Philip A. Philip, Karmanos Cancer Institute, Detroit, MI; Li-Tzong Chen, National Institute of Cancer Research and National Cheng Kung University Hospital, Tainan; Kun-Huei Yeh, National Taiwan University Hospital Cancer Center, and Cancer Research Center, National Taiwan University College of Medicine, Taipei, Taiwan; Thanyanan Reungwetwattana, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; Kristen Ciombor, The Ohio State University Wexner Medical Center, Columbus, OH; and Anuradha Patel, Suman Sen, Dale Porter, and Randi Isaacs, Novartis Pharmaceuticals Corporation, East Hanover, NJ.
J Clin Oncol. 2018 Jan 20;36(3):276-282. doi: 10.1200/JCO.2017.75.5009. Epub 2017 Nov 28.
Purpose No standard treatment exists for patients with cholangiocarcinoma for whom first-line gemcitabine-based therapy fails. Fibroblast growth factor receptor 2 ( FGFR2) fusions/translocations are present in 13% to 17% of intrahepatic cholangiocarcinomas. BGJ398, an orally bioavailable, selective pan-FGFR kinase inhibitor, has shown preliminary clinical activity against tumors with FGFR alterations. Methods A multicenter, open-label, phase II study ( ClinicalTrials.gov identifier: NCT02150967) evaluated BGJ398 antitumor activity in patients age ≥ 18 years with advanced or metastatic cholangiocarcinoma containing FGFR2 fusions or other FGFR alterations whose disease had progressed while receiving prior therapy. Patients received BGJ398 125 mg once daily for 21 days, then 7 days off (28-day cycles). The primary end point was investigator-assessed overall response rate. Results Sixty-one patients (35 women; median age, 57 years) with FGFR2 fusion (n = 48), mutation (n = 8), or amplification (n = 3) participated. At the prespecified data cutoff (June 30, 2016), 50 patients had discontinued treatment. All responsive tumors contained FGFR2 fusions. The overall response rate was 14.8% (18.8% FGFR2 fusions only), disease control rate was 75.4% (83.3% FGFR2 fusions only), and estimated median progression-free survival was 5.8 months (95% CI, 4.3 to 7.6 months). Adverse events included hyperphosphatemia (72.1% all grade), fatigue (36.1%), stomatitis (29.5%), and alopecia (26.2%). Grade 3 or 4 treatment-related adverse events occurred in 25 patients (41%) and included hyperphosphatemia (16.4%), stomatitis (6.6%), and palmar-plantar erythrodysesthesia (4.9%). Conclusion BGJ398 is a first-in-class FGFR kinase inhibitor with manageable toxicities that shows meaningful clinical activity against chemotherapy-refractory cholangiocarcinoma containing FGFR2 fusions. This promising antitumor activity supports continued development of BGJ398 in this highly selected patient population.
对于一线吉西他滨为基础的治疗失败的胆管癌患者,目前尚无标准治疗方法。成纤维细胞生长因子受体 2(FGFR2)融合/易位存在于 13%至 17%的肝内胆管癌中。BGJ398 是一种口服生物可利用的、选择性的泛 FGFR 激酶抑制剂,对具有 FGFR 改变的肿瘤显示出初步的临床活性。
一项多中心、开放标签、II 期研究(ClinicalTrials.gov 标识符:NCT02150967)评估了 BGJ398 对年龄≥18 岁的晚期或转移性胆管癌患者的抗肿瘤活性,这些患者的疾病含有 FGFR2 融合或其他 FGFR 改变,且在接受先前治疗时疾病进展。患者接受 BGJ398 125mg 每日一次,连用 21 天,然后停药 7 天(28 天为一个周期)。主要终点为研究者评估的总缓解率。
61 名患者(35 名女性;中位年龄 57 岁)参加了 FGFR2 融合(n=48)、突变(n=8)或扩增(n=3)的研究。在预定的数据截止日期(2016 年 6 月 30 日),50 名患者已停止治疗。所有有反应的肿瘤均含有 FGFR2 融合。总缓解率为 14.8%(仅 FGFR2 融合为 18.8%),疾病控制率为 75.4%(仅 FGFR2 融合为 83.3%),估计中位无进展生存期为 5.8 个月(95%CI,4.3 至 7.6 个月)。不良反应包括高磷血症(72.1%所有级别)、疲劳(36.1%)、黏膜炎(29.5%)和脱发(26.2%)。25 名患者(41%)发生 3 级或 4 级与治疗相关的不良事件,包括高磷血症(16.4%)、黏膜炎(6.6%)和手掌-足底红斑感觉异常(4.9%)。
BGJ398 是一种首创的 FGFR 激酶抑制剂,具有可管理的毒性,对含有 FGFR2 融合的化疗耐药性胆管癌具有显著的临床活性。这种有希望的抗肿瘤活性支持在这一高度选择的患者群体中继续开发 BGJ398。