Nogova Lucia, Sequist Lecia V, Perez Garcia Jose Manuel, Andre Fabrice, Delord Jean-Pierre, Hidalgo Manuel, Schellens Jan H M, Cassier Philippe A, Camidge D Ross, Schuler Martin, Vaishampayan Ulka, Burris Howard, Tian G Gary, Campone Mario, Wainberg Zev A, Lim Wan-Teck, LoRusso Patricia, Shapiro Geoffrey I, Parker Katie, Chen Xueying, Choudhury Somesh, Ringeisen Francois, Graus-Porta Diana, Porter Dale, Isaacs Randi, Buettner Reinhard, Wolf Jürgen
Lucia Nogova, Reinhard Buettner, and Jürgen Wolf, University Hospital Cologne, Cologne; Martin Schuler, University Hospital Essen, and German Cancer Consortium (DKTK), Essen, Germany; Lecia V. Sequist, Massachusetts General Hospital; Geoffrey I. Shapiro, Dana-Farber Cancer Institute, Boston, MA; Jose Manuel Perez Garcia, Vall d'Hebron Institut d'Oncologia, Barcelona; Manuel Hidalgo, Spanish National Cancer Research Centre, Madrid, Spain; Fabrice Andre, Gustave Roussy, Villejuif; Jean-Pierre Delord, Institute Universitaire du Cancer de Toulouse, Toulouse; Philippe A. Cassier, Centre Regional Leon-Berard, Lyon; Mario Campone, Institute de Cancerologie de l'Ouest-René Gauducheau, Nantes, France; Jan H.M. Schellens, Netherlands Cancer Institute, Amsterdam, and Utrecht University, Utrecht, the Netherlands; D. Ross Camidge, University of Colorado, Aurora, CO; Ulka Vaishampayan, Barbara Ann Karmanos Cancer Institute, Detroit, MI; Howard Burris, Sarah Cannon Research Institute, Nashville; G. Gary Tian, The West Clinic, Memphis, TN; Zev A. Wainberg, UCLA School of Medicine, Los Angeles, CA; Wan-Teck Lim, National Cancer Centre, Singapore; Patricia LoRusso, Yale Cancer Center, New Haven, CT; Katie Parker, Xueying Chen, Somesh Choudhury, and Randi Isaacs, Novartis Pharmaceuticals Corporation, East Hanover, NJ; Dale Porter, Novartis Institutes for Biomedical Research, Cambridge, MA; Francois Ringeisen, Novartis Pharma AG; and Diana Graus-Porta, Novartis Institutes for Biomedical Research, Basel, Switzerland.
J Clin Oncol. 2017 Jan 10;35(2):157-165. doi: 10.1200/JCO.2016.67.2048. Epub 2016 Nov 21.
Purpose This two-part, first-in-human study was initiated in patients with advanced solid tumors harboring genetic alterations in fibroblast growth factor receptors (FGFRs) to determine the maximum tolerated dose (MTD), the recommended phase II dose (RP2D), and the schedule, safety, pharmacokinetics, pharmacodynamics, and antitumor activity of oral BGJ398, a selective FGFR1-3 tyrosine kinase inhibitor. Patients and Methods Adult patients were treated with escalating dosages of BGJ398 5 to 150 mg once daily or 50 mg twice daily continuously in 28-day cycles. During expansion at the MTD, patients with FGFR1-amplified squamous cell non-small-cell lung cancer (sqNSCLC; arm 1) or other solid tumors with FGFR genetic alterations (mutations/amplifications/fusions) received BGJ398 daily on a continuous schedule (arm 2), or on a 3-weeks-on/1-week-off schedule (arm 3). Results Data in 132 patients from the escalation and expansion arms are reported (May 15, 2015, cutoff). The MTD, 125 mg daily, was determined on the basis of dose-limiting toxicities in four patients (100 mg, grade 3 aminotransferase elevations [n = 1]; 125 mg, hyperphosphatemia [n = 1]; 150 mg, grade 1 corneal toxicity [n = 1] and grade 3 aminotransferase elevations [n = 1]). Common adverse events in patients treated at the MTD (n = 57) included hyperphosphatemia (82.5%), constipation (50.9%), decreased appetite (45.6%), and stomatitis (45.6%). A similar safety profile was observed using the 3-weeks-on/1-week-off schedule (RP2D). However, adverse event-related dose adjustments/interruptions were less frequent with the 3-weeks-on/1-week-off (50.0%) versus the continuous (73.7%) schedule. Antitumor activity (seven partial responses [six confirmed]) was demonstrated with BGJ398 doses ≥ 100 mg in patients with FGFR1-amplified sqNSCLC and FGFR3-mutant bladder/urothelial cancer. Conclusion BGJ398 at the MTD/RP2D had a tolerable and manageable safety profile and showed antitumor activity in several tumor types, including FGFR1-amplified sqNSCLC and FGFR3-mutant bladder/urothelial cancers.
目的 这项分两部分进行的首次人体研究纳入了成纤维细胞生长因子受体(FGFR)存在基因改变的晚期实体瘤患者,以确定口服BGJ398(一种选择性FGFR1 - 3酪氨酸激酶抑制剂)的最大耐受剂量(MTD)、推荐的II期剂量(RP2D)以及给药方案、安全性、药代动力学、药效学和抗肿瘤活性。
患者与方法 成年患者接受剂量递增的BGJ398治疗,剂量为每日5至150 mg,或每日两次、每次50 mg,持续28天为一个周期。在MTD剂量下的扩展阶段,FGFR1扩增的鳞状细胞非小细胞肺癌(sqNSCLC;第1组)或其他存在FGFR基因改变(突变/扩增/融合)的实体瘤患者接受BGJ398持续给药方案(第2组),或3周给药/1周停药方案(第3组)。
结果 报告了来自剂量递增组和扩展组的132例患者的数据(截止至2015年5月15日)。根据4例患者的剂量限制性毒性确定MTD为每日125 mg(100 mg时,3级转氨酶升高[n = 1];125 mg时,高磷血症[n = 1];150 mg时,1级角膜毒性[n = 1]和3级转氨酶升高[n = 1])。接受MTD治疗的患者(n = 57)常见的不良事件包括高磷血症(82.5%)、便秘(50.9%)、食欲减退(45.6%)和口腔炎(45.6%)。采用3周给药/1周停药方案(RP2D)时观察到了相似的安全性概况。然而,3周给药/1周停药方案(50.0%)与持续给药方案(73.7%)相比,与不良事件相关的剂量调整/中断频率更低。在FGFR1扩增的sqNSCLC和FGFR3突变的膀胱/尿路上皮癌患者中,BGJ398剂量≥100 mg时显示出抗肿瘤活性(7例部分缓解[6例确诊])。
结论 MTD/RP2D剂量的BGJ398具有可耐受且可控的安全性概况,并在包括FGFR1扩增的sqNSCLC和FGFR3突变的膀胱/尿路上皮癌在内的多种肿瘤类型中显示出抗肿瘤活性。