FUTURE Platform Trial - A Phase II Platform Trial of Futibatinib in Combination With (Chemo)Immunotherapy in Colorectal Cancer and Other Solid Tumor Entities

The FUTURE trial is a prospective, multicentre, exploratory, open-label phase II platform trial. Its goal is to evaluate the efficacy, feasibility and safety of futibatinib combined with immunotherapeutic, targeted or chemotherapeutic agents in colorectal and other solid tumors and to additionally identify biomarkers that correlate with clinical outcome.

开始日期2025-03-01

申办/合作机构

Institut fr Klinische Krebsforschung IKF GmbH

NCT06263153

/ Recruiting临床2期IIT

A Phase II Trial of Futibatinib in Combination with Durvalumab (MEDI4736) Administered to Cisplatin-Ineligible Patients with Muscle-Invasive Bladder Cancer Before Cystectomy

This phase II trial tests how well the combination of futibatinib and durvalumab given before cystectomy works in treating patients with muscle-invasive bladder cancer (MIBC) who are ineligible for cisplatin-based therapy. Cisplatin-based therapy is the standard of care for patients with MIBC. However, many patients cannot receive standard therapy due to poor renal function, peripheral neuropathy, poor functional status, or clinically significant heart failure. Futibatinib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Durvalumab is a monoclonal antibody that may interfere with the ability of tumor cells to grow and spread. Radical cystectomy is a surgery to remove all of the bladder as well as nearby tissues and organs. Giving futibatinib in combination with durvalumab before surgery may be an effective treatment option for patients with MIBC who are ineligible for cisplatin-based therapy.

开始日期2024-12-30

申办/合作机构

Ohio State University Comprehensive Cancer Center

[+1]

CTIS2024-512217-40-00

/ Recruiting临床2/3期

An Open-label, Rollover Study of Futibatinib in Patients Previously Enrolled in an Antecedent Futibatinib Study - TAS-120-404

开始日期2024-10-21

申办/合作机构

Taiho Oncology, Inc.

100 项与福巴替尼相关的临床结果

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100 项与福巴替尼相关的转化医学

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100 项与福巴替尼相关的专利（医药）

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139

项与福巴替尼相关的文献（医药）

2025-01-14·Future Oncology

Plain language summary: an analysis of the safety of futibatinib treatment in people with different types of cancer

Article

作者: Oh, Do-Youn ; Hangai, Nanae ; Bridgewater, John A. ; Furuse, Junji ; Goyal, Lipika ; Anderson, Bailey ; Hollebecque, Antoine ; Wacheck, Volker ; Meric-Bernstam, Funda

WHAT IS THIS SUMMARY ABOUT?:

Researchers combined information from three separate phase 1 and 2 clinical trials, including over 400 people who had one of 33 different cancer types and who all received futibatinib in their clinical trial. This type of study is called a pooled analysis. Futibatinib is taken orally (by mouth) as a tablet and works by reducing the activity of a group of proteins called fibroblast growth factor receptors (FGFRs). FGFRs drive the growth of some cancers, especially cancer cells with changes in FGFR genes that make the proteins more active. Researchers wanted to look at how common some side effects were in people treated with futibatinib, how soon the side effects happened after taking futibatinib, and how they could be managed. Researchers also wanted to provide recommendations to other health care professionals on how to manage these side effects in people with cancer.

WHAT WERE THE RESULTS?:

In this analysis, the researchers focused on side effects that they had seen in previously completed trials of futibatinib. Overall, futibatinib was safe and tolerable. Most people (82%) had a high phosphate level in their blood (hyperphosphatemia), 27% had nail disorders, 27% had liver side effects (changes in liver-related laboratory tests), 19% had a sore mouth (stomatitis), 13% had hand-foot syndrome (palmar-plantar erythrodysesthesia syndrome), 9% had a rash, 8% developed changes in the back of the eye (retinal disorders), and 4% of people developed cataracts. Most side effects were mild/moderate and reversible. The median time it took from starting treatment to experiencing a severe side effect ranged from 9 days (hyperphosphatemia) to 125 days (cataracts). Some side effects tended to occur early, while others developed later. Only 2% of people stopped taking futibatinib due to treatment-related side effects, and futibatinib caused no deaths.

WHAT DO THE RESULTS MEAN?:

The side effects from taking futibatinib were manageable and similar in people with different types of cancer. To fully understand the safety of futibatinib, researchers will need to look at what side effects are reported in people taking futibatinib over a longer time in the real-world setting (outside of clinical trials).

2024-12-01·ANNALS OF ONCOLOGY

Genomic correlates of response and resistance to the irreversible FGFR1-4 inhibitor futibatinib based on biopsy and circulating tumor DNA profiling

Article

作者: Bridgewater, J A ; Meric-Bernstam, F ; Okamura, S ; Silhavy, J L ; Hollebecque, A ; Kano, A ; Halim, A ; DiToro, D ; Shimura, M ; Goyal, L ; Wacheck, V

BACKGROUND:

Futibatinib is the only covalent inhibitor of FGFR1-4 to gain regulatory approval in oncology. In this article, we present genomic analyses of tissue biopsies and circulating tumor DNA (ctDNA) from patients with 1 of nearly 20 tumor types treated with futibatinib in the phase I/II FOENIX study.

PATIENTS AND METHODS:

Eligible patients included those with ctDNA samples collected per protocol at baseline and/or progression on futibatinib in the phase Ib portion of the study for FGF/FGFR-altered advanced solid tumors or the phase II portion of the study for FGFR2 fusion/rearrangement-positive cholangiocarcinoma. Assessments included analytical concordance between tumor and ctDNA analyses for detection of FGFR alterations, association of ctDNA-detected co-occurring genomic alterations with response to futibatinib, and determination of patterns of acquired resistance following progression on futibatinib.

RESULTS:

Among 300 patients treated with futibatinib, 226 were eligible for this analysis, including 139 (62%) with cholangiocarcinoma. Among patients with known FGFR2 fusions/rearrangements, FGFR1 fusions, FGFR3 fusions, or FGFR2 amplifications per tissue analysis, detection rates in ctDNA for these aberrations were 84%, 0%, 11%, and 59%, respectively. Objective response rates on futibatinib were not significantly different between patients with TP53-altered versus -unaltered solid tumors; progression-free survival was reduced in patients with CDKN2B-altered versus -unaltered cholangiocarcinoma (median 4.8 versus 11.0 months; P = 0.03). Acquired resistance to futibatinib was frequently polyclonal and driven by an array of mutations within the relevant FGFR kinase domain, predominantly V565L, V565F, and N550K variants.

CONCLUSIONS:

In this largest and most systematic analysis of acquired resistance to an FGFR inhibitor from prospective clinical trials, emergence of secondary FGFR2 kinase domain mutations was observed in most patients receiving clinical benefit to futibatinib. ctDNA analysis shows clinically relevant potential as a noninvasive method for assessing genomic profiles, identifying patients who may benefit from FGFR inhibitor treatment, and exploring acquired resistance mechanisms.

2024-12-01·EXPERT OPINION ON INVESTIGATIONAL DRUGS

Fibroblast growth factor therapies in biliary tract cancers: current and future state

Review

作者: Siripoon, Teerada ; Mahipal, Amit ; Jin, Zhaohui ; O’Donnell, Conor

INTRODUCTION:

Cholangiocarcinoma is the rare and aggressive tumor with poor prognosis and limited therapeutic options. Recently, there have been promising developments in molecular targeted therapies for patients following the progression of first-line chemotherapy and immunotherapy combinations. Dysregulation of fibroblast Growth Factor Receptor (FGFR) signaling is significantly associated with tumorigenesis of intrahepatic cholangiocarcinoma and has been identified as a targetable alteration. This was possible through the discovery of crucial insights into the biochemical mechanisms and pathophysiology of the FGFR pathway.

AREAS COVERED:

This review summarizes the current state of FGFR targeted therapies, mechanisms of resistance, and future directions for FGFR-targeted therapies in patients with cholangiocarcinoma.

EXPERT OPINION:

Currently, pemigatinib and futibatinib are FDA approved FGFR-targeted therapies that have demonstrated remarkable responses. However, there is still a significant proportion of patients whose disease remains intrinsically resistant to treatment and most patients eventually develop secondary resistance after an initial response. Additionally, unique side effects of FGFR inhibitors may limit their efficacy in clinical practice and can have detrimental effects on quality of life. Several novel FGFR inhibitors are currently being investigated to overcome resistance mechanisms and reduce toxicities.

项与福巴替尼相关的新闻（医药）

2025-01-21

·ioncology

年度盘点丨曹彦硕教授：2024年晚期食管癌内科治疗重磅研究进展

点击蓝字关注我们年度盘点微专辑扫描二维码可查看更多内容编者按中国是食管癌食管鳞状细胞癌（ESCC）的高发区，虽然近年来食管癌的早期诊断、筛查与治疗均取得了长足进步，但仍有相当数量的患者初诊时已经出现远处转移，或治疗后出现复发转移。内科治疗作为食管癌的重要治疗手段，贯穿于食管癌诊治的全程。近年来，免疫治疗的飞速发展，为食管癌患者带来了切实的获益。值此岁末年初之际，《肿瘤瞭望消化时讯》特邀北京大学肿瘤医院曹彦硕教授为我们回顾盘点2024晚期食管癌内科治疗领域的重磅研究进展，以期为食管癌的诊治研究提供更多的视角和思路！曹彦硕医生北京大学肿瘤医院北京大学肿瘤学博士消化肿瘤内科副主任医师 2016-2018年于加拿大玛格丽特公主癌症中心（Princess Margarete Cancer Centre）完成专科临床培训（clinical fellowship）中国临床肿瘤学会（CSCO）青年专家委员会常务委员中国临床肿瘤学会（CSCO）翻译小组组长中国抗癌协会（CACA）食管肿瘤整合康复专委会委员北京癌症防治学会食管癌专委会秘书长中国女医师协会临床肿瘤专委会委员、秘书北京肿瘤防治研究会消化肿瘤分委会秘书全文内容概览一、免疫治疗联合化疗一线治疗晚期ESCC探索舒格利单抗联合化疗一线治疗晚期ESCC 既往已开展多项免疫检查点抑制剂（ICI）联合化疗治疗ESCC的相关临床研究，多款ICI在国内获批联合化疗作为晚期ESCC标准的一线治疗方案（图1）。2024年又新增了一项免疫联合化疗的研究：GEMSTONE-304研究[1~3]，其结果于2024年发表于Nature Medicine。图1. 免疫联合化疗一线治疗研究汇总 GEMSTONE-304研究是一项随机、双盲、多中心、安慰剂对照的Ⅲ期临床试验，旨在评估舒格利单抗联合FP化疗方案（氟尿嘧啶+顺铂）一线治疗不可切除的局部晚期、复发或转移性ESCC的疗效和安全性。舒格利单抗联合化疗组最终共纳入358例患者，安慰剂联合化疗组182例。试验组在近期疗效和长期生存中均获得了更好的结果，基于BICR评估的中位PFS为6.2 vs. 5.4 个月，中位OS为15.3 vs. 11.5 个月，ORR（60.1% vs. 45.2%）和DoR（6.0 vs. 4.5 个月）。对人群进行亚组分析，在各个亚组中舒格利单抗联合化疗组在PFS和OS上都显示出了明显的获益趋势。本研究再一次证明了免疫联合化疗一线治疗晚期ESCC的疗效。除上述研究外，KEYNOTE-590（中位OS：12.6 vs. 9.8个月）、CheckMate 648（4年OS率：14% vs. 10%）、ESCORT-1st（3年OS率：25.6% vs. 12.8%）、RATIONALE-306（3年OS率：22.1% vs. 14.1）也更新了其长期随访数据，这些扎实的数据也进一步夯实了免疫+化疗在食管癌一线治疗中的地位。免疫治疗联合化疗待解决的问题尽管数据很扎实，但不可否认的是这其中仍有不少问题值得思考：第一，不同的化疗骨架（TP/FP）是否会影响联合治疗疗效？事实上，对于化疗骨架的选择，由于当前还没有大型、随机对照的头对头研究，所以无法明确FP与TP间的差异，但从几项Ⅲ期随机对照研究的结果来看，似乎TP方案对比FP存在一定的优势，但目前在指南当中，推荐首位的仍然是FP方案。第二，不同的免疫治疗药物（PD-1/PD-L1单抗）是否有不同的疗效差异？对此，当前还很难给出证据充分的结论。讲者认为不同的药物间的疗效和不良反应的差异并不显著。在不同研究中得出的OS不同HR值，可能与入组人群差异、选择化疗的差异、包括后线治疗的选择都相关。第三，PD-L1表达是否影响一线免疫治疗疗效？针对有效的生物标志物的选择，虽然研究者们做了大量的探索，但目前针对食管癌，特别是ESCC，最为常用的筛选指标就是PD-L1 CPS或PD-L1 TPS评分。2022年发表于JAMA Oncology的一项汇总17项Ⅲ期随机对照研究的荟萃分析[4]探索了PD-L1表达和其他变量与晚期食管癌免疫治疗获益的关系，结果显示，PD-L1 CPS是除微卫星不稳定性之外，免疫治疗是否获益的最强预测因素，在PD-L1表达缺失或较低的患者中，免疫治疗获益通常较小。此外，2024年FDA一项汇总分析显示，在晚期ESCC人群中，PD-L1 CPS＜1人群占比8%~10%，当PD-L1 CPS＜1时，OS的HR为1.1，免疫+化疗组的中位OS为11.6个月，单独化疗组为12.8个月，这表示，免疫治疗的加入并没有降低患者的死亡风险，反而缩短了1.2个月的OS。但当PD-L1 CPS≥1时，OS HR为0.68，免疫+化疗组的中位OS为14.6个月，单独化疗组为9.8个月，免疫治疗的生存期改善是明确的（图2），因此在2024年9月26日下午，FDA ODAC以11:1的比例反对PD-1抑制剂一线治疗PD-L1阴性（CPS<1）、不可切除性或转移性ESCC[5]。图2. FDA汇总分析但需要指出的是，FDA ODAC仅纳入了KEYNOTE-590、CHECKMATE-648以及RATIONALE-306三项纳入了美国患者的食管癌一线临床研究。而在食管癌一线治疗中有8项随机对照临床研究进行了PD-1或PD-L1单抗联合化疗对比化疗的探索。在JUPITER-06研究的事后分析和荟萃分析中[6]，无论是在PD-L1高表达还是低表达的患者中，PD-1单抗联合化疗均带来显著的临床获益。对5项Ⅲ期随机对照试验的进一步荟萃分析发现，对于PD-L1表达低（TPS<1%或CPS<10）的晚期ESCC患者，作为一线治疗，PD-1单抗联合化疗比单独化疗具有显著的总生存率、无进展生存率和客观反应率改善。总之，当前PD-L1表达低的ESCC患者是否真正能从PD-1单抗联合化疗中获益仍是一个备受争议的问题，希望后续能有更多的数据作为支撑。二、晚期ESCC治疗新靶点药物探索一线治疗：TIGIT靶点 2024年ASCO GI发布了两项研究——SKYSCRAPER-08研究[7] vs. MOPHEUS-EC研究[8]，均旨在评估tiragolumab（抗TIGIT）+阿替利珠单抗（抗PD-L1）+化疗 vs. 安慰剂+化疗一线治疗不可切除局部晚期、不可切除复发或转移性ESCC亚洲人群的疗效和安全性。 SKYSCRAPER-08研究是一项双盲、多中心、随机对照Ⅲ期研究，而MOPHEUS-EC研究是一项Ⅰb/Ⅱ期开放标签随机研究，两项研究的主要研究终点都是PFS和OS。结果显示，SKYSCRAPER-08研究的中位OS为15.7 vs. 11.1个月，中位PFS为6.2 vs. 5.4个月，MOPHEUS-EC研究的中位OS为16.0 vs. 13.1个月，中位PFS为6.9 vs. 6.8个月。将两项研究进行对比分析发现（图3），两项研究中的tiragolumab+阿替利珠单抗+化疗组的ORR相较于化疗组，均提高了14%，中位PFS和OS的HR也几乎相同。这表明两项研究中双免+化疗组合的疗效基本吻合，与安慰剂+化疗相比，Tiragolumab+阿替利珠单抗+化疗的PFS和OS均有统计学意义和临床意义上的改善。图3. SKYSCRAPER-08研究 vs. MOPHEUS-EC研究 TIGIT是一种具有抑制功能的新型免疫检查点受体，在T细胞和自然杀伤（NK）细胞上表达。因其可与抗PD-L1疗法联用，能同时防止或逆转T细胞与NK细胞耗竭，成为了备受关注的明星靶点，一度被视为免疫疗法的未来，甚至有人将其称作“下一个PD-1”。但如果把SKYCRPAPER-08的结果与其他8项食管癌一线免疫联合化疗的结果对比，并未看到TIGIT抑制剂加入带来的更优的生存或疗效结果。就目前的临床探索进展以及其在临床的经济-效益价值而言，TIGIT能否走向成功还是一个未知数。二线治疗：EGFR × HER3双靶点 BL-B01D1是一种基于双特异性拓扑异构酶抑制剂的ADC，由通过基于四肽的可切割接头与新型拓扑异构酶Ⅰ抑制剂有效载荷（Ed-04）连接的EGFR x HER3双特异性抗体组成。2024 ESMO大会报告了BL-B01D1在治疗ESCC的Ⅰ期研究中的安全性和有效性数据[9]。该Ⅰ期研究纳入了局部晚期或转移性胃肠道肿瘤患者。在剂量扩展阶段，入组的ESCC患者主要接受每3周一疗程、第1天和第8天给药，剂量分别为2.0、2.5和3.0 mg/kg的治疗。截至2024年1月31日，共有83例既往接受过治疗的ESCC患者按每3周一疗程的方案入组，其中22例患者接受2.0 mg/kg剂量治疗，60例患者接受2.5 mg/kg剂量治疗，1例患者接受3.0 mg/kg剂量治疗。本次报告了2.0 mg/kg和2.5 mg/kg D1D8 Q3W的数据。在入组的ESCC患者中，94.0%曾接受过抗PD-1/L1抗体与含铂化疗药物的联合或序贯治疗。既往接受过全身治疗的平均线数为2，中位随访时间为6.3个月。在入组患者中，有74例患者可评估疗效。ORR为33.8%，cORR为29.7%，疾病控制率为70.3%，中位DOR未达到，中位PFS为4.1个月，中位OS为6.6个月，6个月生存率为57.5%。对于接受2.5 mg/kg剂量（推荐Ⅱ期剂量RP2D）的患者，ORR为42.3%，cORR为36.5%，DCR为80.8%，mDOR未达到，mPFS为5.0个月，mOS未达到，6个月生存率为64.5%。在2.5 mg/kg剂量组，≥3级治疗相关不良事件（TRAEs）的发生率为53%，未观察到新的安全性信号。总之，在既往接受过多线治疗的ESCC患者中，BL-B01D1显示出可控的安全性，并具有鼓舞人心的抗肿瘤活性。目前研究正继续在该患者群体中进一步评估BL-B01D1。 ≥2线治疗：Nectin-4靶点 Nectin-4是一种细胞粘附分子，在尿路上皮癌和其他实体恶性肿瘤（包括胃食管癌）中高度表达。Enfortumab Vedotin（EV）是一种针对Nectin-4的ADC，在局部晚期或转移性尿路上皮癌中显示出临床益处，目前已被批准单药或者与帕博利珠单抗联合治疗局部晚期或转移性尿路上皮癌的成年患者。目前正在进行中的一项多中心、多队列、开放标签的Ⅱ期研究EV-202（NCT04225117）评估了EV治疗局部晚期或转移性实体瘤患者。2024年ASCO大会公布了研究中胃食管癌队列（胃食管腺癌[GEA]和ESCC）的结果[10]。结果显示，EV在经治ESCC患者队列中的ORR为18.2%，mPFS和mOS分别为2.10个月和7.39个月；而在经治胃食管腺癌患者队列中的ORR仅为9.5%，mPFS和mOS分别为3.06个月和8.31个月。EV在ESCC达到了具有潜在的抗肿瘤活性的阈值，而GEA未达到。此外，在经治ESCC患者队列中，与既往治疗≥3线患者相比，EV在既往治疗<3线患者中的疗效通常更好。三、寡转移患者在化免基础上联合放疗的探索免疫治疗+同步放化疗+巩固免疫治疗 2024年ASCO大会公布了一项前瞻性、Ⅱ期研究（NCT04821765）[11]，旨在探讨同步放化疗和免疫治疗对根治性术后寡转移复发的ESCC患者的疗效和安全性。研究设计如图4所示图4. NCT04821765研究设计结果显示，中位随访19个月，替雷利珠单抗联合放化疗治疗ESCC根治术后寡转移性复发患者1年OS率高达83.2%，1年PFS率为73.8%，ORR为84.1%，中位OS和PFS均未达到，毒性可控。免疫治疗+化疗+巩固放疗 2024 ESMO大会公布了一项单臂、开放标签、Ⅱ期临床试验，旨在评估卡瑞利珠单抗+化疗联合巩固性放疗作为寡转移性ESCC一线治疗的疗效和安全性（ESCORT-1ST-RT）[12]。结果显示，卡瑞利珠单抗联合化疗后巩固放疗治疗晚期寡转移性ESCC的ORR为79.3%，mPFS为13.7个月，mOS未达到。最常见的3~4级TEAE为淋巴细胞计数减少(65.5%)、中性粒细胞计数减少(27.6%)和白细胞计数减少(20.7%)，1例患者因放射性食管炎停止卡瑞利珠单抗治疗。未发生4~5级TEAE。总之，卡瑞利珠单抗联合化疗后巩固放疗对晚期寡转移性ESCC患者具有潜在的疗效和可控的耐受性。四、晚期ESCC免疫治疗耐药后治疗策略 Futibatinib是一种口服、高选择性、强效、不可逆的FGFR1-4抑制剂，基于FOENIX-CCA2关键Ⅱ期研究结果，已获批用于治疗FGFR2融合或重排的晚期肝内胆管癌患者。 2024年ASCO大会发布了公布了Futibatinib在食管癌中的数据，这是一项开放标签、多中心、非随机、多队列的Ⅰb期研究，包括可行性阶段和扩展阶段[13]。研究根据患者免疫治疗状态分为3个队列：队列A，ICI初治；队列B，ICI难治；队列D，化疗和ICI初治，本次报道了这3个队列扩展阶段结果。研究队列B探索了Futibatinib联合帕博利珠单抗针对免疫治疗难治的FGF/FGFR突变阳性的食管癌患者的抗肿瘤活性及耐受性，队列B以三线治疗为主，占62%，Futibatinib+帕博利珠单抗ORR为6.1%，DCR为53.1%；队列A的ORR为42.4%，DCR为75.8%；队列D的ORR为76.9%，DCR为92.3%。总之，Futibatinib联合帕博利珠单抗/化疗在一线及后线晚期或转移性食管癌中显示出抗肿瘤活性，特别是其一线治疗的数据超过了一线帕博利珠单抗/化疗的历史疗效数据（ORR：70% vs. 45%[KEYNOTE-590研究]），并且在一线治疗中没有观察到新的安全信号。对于既往没有接受过免疫治疗的经治患者，futibatinib联合帕博利珠单抗也展示出较高的ORR和DCR，但对于免疫经治患者的疗效仍欠满意。事实上，在晚期食管癌免疫耐药后继续免疫治疗的多项Ⅰ/Ⅱ期研究中，均显示出初步的有效性和可管理的安全性（图5）。同时，多项临床研究探索免疫耐药后治疗策略，正在如火如荼的开展。图5. 免疫耐药后继续免疫治疗的研究综上所述，多项Ⅲ期研究显示，免疫治疗+化疗较化疗一线治疗ESCC，显著提高了患者的ORR、延长了OS和PFS，当前免疫治疗+化疗已成为ESCC一线治疗标准方案。此外，与化疗相比，PD-L1单抗联合TIGIT抑制剂+化疗一线治疗ESCC，也可提高患者的ORR、延长OS和PFS，但与单免+化疗相比，PFS和OS的绝对获益未见明显突破，同时联合放疗或其他局部治疗手段也需进一步探索。最后，在ESCC一线免疫治疗进展的患者中，ADC、免疫治疗+靶向治疗、靶向治疗+化疗均显示出令人鼓舞的抗肿瘤活性，未来或可作为ESCC一线免疫治疗进展后的新的治疗选择。并且，对于转移较为局限的患者，放疗的适时加入也是目前探索的热点之一。参考文献（上下滑动可查看） [1]Li J, et al. 2023 WCGIC. Abstract O-4. [2]Date on file. [3]Li J, et al. Nat Med. 2024 Mar;30(3):740-748. [4]Harry H Yoon et al, JAMA Oncol 2022; Wu HX, ... Wang F. J Clin Oncol. 2023 [5]https://www.fda.gov/media/182143/download [6]JCO 41, 1735-1746(2023). [7]Chih-Hung Hsu,et al. 2024 ASCO GI. Oral 24 [8]Jong-Mu Sun, et al. ASCO-GI 2024. Poster 324. [9]Chang Liu, et al. 2024 ESMO #1426P [10]Kei Muro, et al. Presented at 2024 ASCO. Poster number:4046 [11]2024 ASCO 4057P; NCT04821765 [12]Jing Xu, et al. 2024 ESMO #1452P [13]Akira Ooki, et al. 2024 ASCO 4047 （来源：肿瘤瞭望消化时讯）声明凡署名原创的文章版权属《肿瘤瞭望》所有，欢迎分享、转载。本文仅供医疗卫生专业人士了解最新医药资讯参考使用，不代表本平台观点。该等信息不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议，如果该信息被用于资讯以外的目的，本站及作者不承担相关责任。

CSCO会议临床结果临床3期

2025-01-02

·GlobeNewswire-Health Care

Bionano Announces Publication from Johns Hopkins School of Medicine Showing that OGM Outperformed Multiple Cytogenetic Assays in a Study of Bone and Soft Tissue Tumor Analysis

In the largest study to date of bone and soft tissue tumors, OGM detected 100% of the variants found by multiple standard techniques, including karyotyping, fluorescent in-situ hybridization (FISH) & gene fusion assays OGM was also more sensitive, including detection of diagnostic or pathogenic variants missed by karyotype in 74% (14/19) of cases that failed or were negative by karyotyping When OGM results and next-generation sequencing (NGS) results were combined, diagnostic and pathogenic structural variants (SVs), copy number variants (CNVs), and/or single nucleotide variants (SNVs) were found in ~98% of cases, a substantially greater rate than when karyotyping, FISH and NGS are used Dec. 23, 2024 -- Bionano Genomics, Inc. (Nasdaq: BNGO) today announced a publication in Modern Pathology by a group of researchers at the Johns Hopkins University School of Medicine, showing that optical genome mapping (OGM) can outperform traditional techniques in analysis of bone and soft tissue tumors. Several prior publications have shown the utility of OGM compared to traditional cytogenetics in studies of hematologic malignancies, however, data on the application of OGM in solid tumors has been relatively sparse. This study provides compelling support for extending the utility of OGM in cancer beyond hematologic malignancies to solid tumors. OGM detected all variants revealed by conventional cytogenetics: OGM showed 100% concordance, identifying all pathogenic variants detected by standard of care cytogenetic methods. The specificity of OGM was assessed to be 100%, i.e. OGM correctly identified the same pathogenic SVs and CNVs detected by standard of care/routine cytogenetics (karyotyping and FISH). OGM detected pathogenic variants missed by karyotyping: In 74% of cases with normal or failed karyotype, OGM detected diagnostic or pathogenic SVs that were missed by karyotyping. Further, in 6 cases that failed to yield any karyotyping results due to culture failure, OGM detected pathogenic SVs in all of them. Variants found by OGM but missed by standard of care included the EWSR1::ETV1 fusion, which is a key molecular hallmark of clear cell sarcoma and helps to differentiate it from other soft tissue sarcomas and melanomas. OGM resolved complex cancer genomes: Study authors found that OGM data could re-characterized and better defined complex structural rearrangements including chromoanagenesis in 27% of cases and complex 3-6-way translocations in 15% of cases when compared to traditional cytogenetic methods. OGM combined with NGS found pathogenic variants in 98% of cases, a substantially greater rate than when karyotyping, FISH and NGS are used: The integrated approach of the combination of OGM and NGS resulted in the detection of pathogenic SVs and sequence variants in ~98% of cases. OGM was 100% concordant with NGS for aneuploidy detection. OGM findings have the potential to qualify subjects for targeted therapies that otherwise would not have been possible: The authors state that several of the OGM findings could result in the potential for these cases to qualify for either targeted treatments or clinical trials. For example, cases with potential to be treated by CDK4/6 inhibitors (palbociclib, ribociclib, abemaciclib), TRK inhibitors (larotrectinib, entrectinib), pan-FGFR inhibitors (erdafitinib or futibatinib) were highlighted. Erik Holmlin, president and chief executive officer of Bionano commented, “Approximately 50% of bone and soft tissue tumor samples fail to reveal actionable information for proper classification of disease, prognosis and therapeutic management because they either fail to culture or because traditional techniques in cytogenetics lack adequate sensitivity and specificity to reliably detect relevant variants. We have seen increasing evidence for OGM as a valuable alternative to cytogenetic methods in blood cancers, and we are thrilled to see researchers at Johns Hopkins publishing this compelling case for extending OGM’s utility to bone and soft tissue tumors.” The full research publication is available at: https://doi-org.libproxy1.nus.edu.sg/10.1016/j.modpat.2024.100684 Bionano is a provider of genome analysis solutions that can enable researchers and clinicians to reveal answers to challenging questions in biology and medicine. The Company’s mission is to transform the way the world sees the genome through optical genome mapping (OGM) solutions, diagnostic services and software. The Company offers OGM solutions for applications across basic, translational and clinical research. The Company also offers an industry-leading, platform-agnostic genome analysis software solution, and nucleic acid extraction and purification solutions using proprietary isotachophoresis (ITP) technology. Through its Lineagen, Inc. d/b/a Bionano Laboratories business, the Company also offers OGM-based diagnostic testing services. The content above comes from the network. if any infringement, please contact us to modify.

寡核苷酸

2024-12-21

·ioncology

年度盘点丨Kohei Shitara教授盘点胃肠肿瘤热门靶点研究进展和方向

点击蓝字关注我们年度盘点微专辑扫描二维码可查看更多内容年度盘点 2024 编者按：近年来胃肠道肿瘤治疗领域新药新靶点不断涌现，为患者治疗带来了新的希望。在2024年欧洲肿瘤内科学会亚洲年会（ESMO ASIA 2024）上，日本国立癌症中心医院Kohei Shitara教授针对胃肠道肿瘤的新兴靶向药物进行了精彩的报告。《肿瘤瞭望消化时讯》在会议现场邀请Kohei Shitara教授对胃肠道肿瘤治疗新靶点的研发情况以及面临的问题进行了盘点。一致癌基因相关的热门治疗靶点 1 FGFR2[1~4] 在胃癌中，大约有3%~5%患者存在FGFR2高水平扩增，其与组织学扩散和不良预后相关。FGFR2抑制剂相关研究结果如下：在Shine研究中AZD4547与PTX对比，结果显示两组的PFS无统计学差异。Futibatinib治疗FGFR2扩增（拷贝数>10）的胃癌患者，ORR为18%。Infigratinib治疗FGFR阳性胃癌患者的ORR为25%。研究人员对FGFR靶向治疗耐药问题进行探索时发现脱靶效应或旁路机制会使缓解持续时间（DoR）缩短。 2 染色体外DNA（ecDNA）[5~7] 染色体外发现的环状DNA携带有原癌基因，其产生于染色体断裂或断裂-融合-桥接循环。可通过驱动遗传异质性、快速基因组改变（使用超级增强子）和抗性基因扩增产生肿瘤耐药。一项在HER2阳性肿瘤患者的研究显示，ecDNA的HER2拷贝数增加，化疗联合HER2治疗可延长PFS。靶向ecDNA的治疗研究方向包括：氟、奥沙利铂能否增加复制压力、DNA损伤、破坏ecDNA的灵活性；NCT05827614研究正验证检测点激酶1（CHK1）抑制剂靶向复制压力的有效性；PARP/DNA-PK抑制剂能否破坏其结构完整性。 3 FGFR2b[8~11] FGFR2的剪接变异体有FGFR2b（上皮型）、FGFR2c（间质型），大约30%的胃癌中有FGFR2b表达。一项抗FGFR2b单抗Bemarituzumab研究显示，单药治疗ORR为18%；相比TKI很少有电解质异常，但存在可逆的角膜毒性。 FIGHT试验在胃/胃食管交界处腺癌对比了FOLFOX6联合Bemarituzumab或安慰剂的疗效，中位PFS（ITT人群：9.5 vs. 7.4个月，HR 0.72）、中位OS（ITT人群：19.2 vs. 13.5个月，HR 0.77）均有延长。两项Ⅲ期研究（NCT05052801、NCT05111626）和一项篮子试验正在进行中。针对Bemarituzumab耐药的研究集中于FGFR2c和上皮间质转换（EMT）。FGFR2c增高与较差的OS相关。 4 EGFR[12~16] 在食管鳞癌（ESCC）中主要为EGFR1异常（胃癌为EGFR2），EGFR-TKI与抗PD-1联合研究已显示初步疗效。化疗联合EGFR抑制剂联在MET、EGFR、HER2、融合突变富集的结直肠癌患者中显示出一定疗效，但在胃癌、食管癌中却为阴性结果，在RAS/RAF突变较少的患者或在EGFR扩增或高表达的患者亚组中提示有获益。 Amivantamab是一种EGFR、MET双特异抗体，在抗-EGFR治疗后的CRC患者中显示出初步疗效。不良事件（AE）主要有输注反应、皮肤毒性、低白蛋白血症。在胃癌、食管鳞癌中，Amivantamab与化疗联合，在靶标高表达的患者中显示出高的治疗活性。 5 MET[12~16] ABBV-400（Telisotuzumab Adizutecan）是种靶向MET的ADC，在MET扩增的胃癌患者和CRC患者两项Ⅰ期研究中观察到了初步疗效。 6 胃癌全外显子（WES）的其他基因拷贝数改变[17~20] CCNE1扩增，在研药物有CDK2抑制剂INCB123667、Wee1抑制剂Adavosertib。MYC扩增，在研药物有MYC抑制剂OMO-103。KRAS扩增，在研药物有BI 3706674。 7 MTAP缺失[21~22] MTAP缺失可增加肿瘤对MAT2A/PRMT5轴的依赖。普遍存在染色体9p21的CDKN2A共缺失。肿瘤中MTAP缺失约占10~15%，在胰腺导管腺癌（PDAC）、胆道癌（BTC）、ESCC和胃癌中均有检出。MTAP缺失患者对PRMT5、MAT2A抑制剂敏感。 8 TP53[23~24] TP53 Y220C突变位点在DNA结合域，约3%的卵巢癌患者，0.5%~1.5%的胃肠癌（胰腺导管腺癌或胃癌）患者存在此突变。在研新药Rezatapopt（PC14586）可重激活TP53的转录活性。在PYNNACLE研究中，PC14586在野生型RAS肿瘤患者中取得了30%的ORR和7个月的DOR。不良事件有恶心、呕吐、腹泻和肌酐升高。二非致癌基因相关的热门治疗靶点 1 Claudian[25~33] Claudian家族是种紧密连接的膜蛋白，有防御和调节通透性的作用。正常情况下，Claudian18.1在肺组织中高表达，Claudian18.2在胃粘膜中高表达。Claudian在胃癌、胃食管交界处肿瘤持续表达，在胰腺等恶性肿瘤中呈异位表达。首个针对Claudian18.2靶点的单克隆抗体Zolbetuximab已成功上市，该药物是一种纯IgG1单克隆抗体，本身没有显示出任何细胞阻断活性。其疗效主要依赖于抗体依赖性细胞毒性（ADCC）和补体依赖性细胞毒性（CDC），而非Claudian18.2的直接作用。在SPOTLIGHT和GLOW研究的人群中，大于75%的患者免疫组化Claudian18.2呈2+或3+，Zolbetuximab联合化疗取得了PFS和OS的显著提高。研究者正筹备开展进一步的随机对照研究。目前有大于30个靶向Claudian18.2的制剂正在进行临床试验，这些产品有增强型单抗、ADC、双特异药物、CAR-T等。 Osemitamab（TST001或ASKB589）是一种高亲和性Claudian18.2单抗。在早期实体瘤研究中与CAPOX联合用药ORR达到67%，与CAPOX、抗PD-1联合用药ORR达到80%。Osemitamab联合纳武利尤单抗和CAPOX作为晚期胃或胃食管结合部腺癌一线治疗的Ⅰ/Ⅱa期研究在开展中。 CT041（satri-cel）是种靶向Claudian18.2的CAR-T细胞，在Ⅰ期Claudian18.2阳性晚期胃肠道肿瘤研究中，总ORR为39%，胃癌ORR为55%，胰腺导管腺癌ORR为20%。97%的患者发生1~2级细胞因子释放综合征（CRS），没有3级CRS。恶心发生率67%，呕吐发生率53%。 C-CAR031是一种磷脂酰肌醇蛋白聚糖-3（GPC3）特异的、TGFβRIIDN装备的CAR-T细胞。在22例肝细胞癌患者中，ORR为50.0%（GPC3 CAR-T为15%）。中位DOR为7.4月。92%患者出现CRS，4 %（1例）患者出现3级CRS。 IM96是种靶向鸟苷酸环化酶2C（GUCY2C）的CAR-T。在19例结直肠癌中ORR为26%，常见不良事件有腹泻（55%）、皮疹（70%）、黏膜炎（35%）。 CLDN/CD3双特异性T细胞Engager（BITE），同时结合表达在肿瘤细胞上的肿瘤相关抗原Claudian18.2和表达在 T 细胞上的CD3，将癌细胞与免疫系统的T细胞连接起来，促进T细胞识别并杀死癌细胞。IBI研究中，胃癌患者ORR为31%，PDCA患者ORR为11.1%。QLS31905患者的ORR为11.1%。主要不良事件为CRS，胃肠道毒性。 Givastomig是种Claudian18.2 / 41BB双特异抗体，Q1802是种CLDN18.2 / PD-L1双特异抗体，已开展首次人体试验。 Claudian18.2 ADC主要有：CMG901或AZD0901是Claudian18.2单抗与微管抑制剂MMAE的偶联物；SHR-A1904是Claudian18.2单抗与拓扑异构酶Ⅰ抑制剂（topo1）的偶联物；IBI343是Claudian18.2单抗与拓扑异构酶Ⅰ抑制剂exatecan的偶联物，已进入Ⅱ期或Ⅲ期临床试验。以上研究Claudian18.2表达使用了不同的cut-off水平，并使用多种分层标志物，如肿瘤相关标志物MMR、HER2、CLDN18.2、FGFR2b、CPS等；免疫相关生物标志物包括PD-1、CD3、CD4、CD8、CD163、FOXP3、CCR8、CTLA4、TIGIT等。 2 TROP-2[34-36] Trop-2是一种在多种肿瘤中异常表达的糖蛋白。目前针对这一靶标的ADC有sacituzumab tirumotecan (sac-TMT)，已完成Ⅰ期研究。在TROP-2 ADC治疗中，Trop2表达可作为生物标志物。在TROP-2 ADC药物Dato-DXd研究中，自动成像分析标准化膜比例[膜Trop2 /总Trop2（膜+细胞浆）]可反映其表达，比例降低（细胞浆染色更多）者预后较好。 3 CEA[37~39] CEACAM5是一种与细胞粘附分化相关的细胞表面糖蛋白。在结直肠癌、胃癌、非小细胞肺癌中高表达。针对这一靶标的ADC有Tusamitamab ravtansine (SAR408701)、M9140。 4 B7-H3[40~41] B7-H3是种I型跨膜糖蛋白，和免疫检测点抑制分子同属B7家族。针对这一靶标的ADC有DS7300 (I-DXd)、YL201。 5 组织因子（TF）[42] TF在宫颈癌中高表达，针对这一靶标的ADC药物Tisotumab已经上市。ADC产品的研发也产生了新的问题，如耐药性。目前的研究主要集中于联合用药，如与免疫检查点抑制剂或CD47抑制剂联合用药、与受体酪氨酸激酶（RTK）治疗联合用药、与Weel或EZH1/2抑制剂联合用药、制备双特异ADC、ADC与ADC联合。研究者说目前在胃癌、结直肠癌、胆管癌等消化道肿瘤领域有许多新兴靶点以及相对应的靶向药物，例如，HER2靶点，当前靶向其治疗的ADC药物德曲妥珠单抗（T-DXd），其在抗肿瘤活性已经明确。KRAS和组织因子（TF）也是令人惊喜的靶点，不仅针对结直肠癌有效，对其他类型的肿瘤也显示出潜力。当前TF和其他靶点的联合用药已经在结直肠癌等临床试验中得到了验证。对于p53突变型结直肠癌，KRAS和Trop靶点的检出推动了化疗与靶向治疗的联合用药研究。此外，在胰腺癌中，KRAS抑制剂也展现出显著的疗效。除了述药物外，还有许多针对新靶标的药物正处于研发阶段，这标志着该领域正在蓬勃发展。同时，上消化道肿瘤的其他靶点，如靶向Claudian18.2的药物——Zolbetuximab已上市，针对该靶点的CAR-T、高特异性药物、ADC药物等也正在各类患者中进行研究。对于HER2扩增，即使不是过表达，也可以作为靶标，目前已有多个相关试验正在进行。此外，肿瘤中MTAP缺失约占10%~15%，在PDAC、BTC、ESCC和胃癌中均有检出，这也是一个令人惊喜的靶标，其对PRMT5、MAT2A抑制剂表现出高度敏感。最后，TROP-2、CCR家族、B7-H3及组织因子等许多分子也被确认为新的治疗靶标。总之，我们期望针对上消化道靶标的创新疗法能够显著提升患者的治疗效果，为患者带来更佳的预后。参考文献（上下滑动可查看） [1]JOGO T ,et al.CCR 2020 [2]Calenacci DVT et al. ASCO 2021 [3]Gastric Cancer 2021; [4]an Clsem E, etal Arnab of0nel2017; DoiT, et al. Cancer Science 2022 [5]Huang Q, et al Heliyon 2024 [6]Tang J, et al. Nature 2024 [7]Tshai C, et al ASCO 2024 [8]Tumer N, et al Nat Rev Cancer, 2010 [9]Powers J, et al.AACR 2016 [10]Kaloh M, et al, Nature Revie Clinical Oncol 2024 [11]Wainberg ZA, et al Lancet Oncol 2022,ESMO-G1 2023 [12]Nakamura Y ,Shitara K JCO PO 2020 [13]Oberstein PE, et al ASC0-G1 2024 [14]Kotani D, et al. ASCO-G1 2024 [15]Shama MR, et al ASCO 2024 [16]Strickler JH, et al.ESMO 2024 [17]Garralda E, et al. EORTC-NCI-AACR 2022 [18]Wee S,et al. EORTC-NCI-AACR 2022 [19]Garralda E, et al. Nature Med 2024 [20]Simoneli M, et al. ESMO 2024 [21]Rodon J, et al. EORTC-NCI-AACR 2023 [22]Seguchi K et al. ESMO 2024 [23]Dumbrava EE, et al ASCO 2022 [24]Schram A, et aL AACR-NCLEORTC 2023 [25]Nakayama l, Shitara K et al Nature Revise Clinical Oncol. 2024 [26]Shitara K, et al. N EnglJ Med 202 [27]Nakayama l, Shitara K. et al. Nature Revise Clinical Oncol 2024 [28]Guo W et al.ASCO GI2023 [29]Zhang M et al.ASCO GI 2023; [30]chare Q et al.ASCO 2023 [31]Shen et al. ASCO 2023 [32]PengZ,et al. ASCO GI 2024 [33]zhang X, et al. ASCO 2024 [34]Bardia A, et al. Annals of Oncol 2021 [35]Kobitzsch B, et al. ESMO Gastroinestinal Oncol 2024 [36]Wainberg ZA, et al. AACR 2024 [37]Decary S, et al. CCR2020 [38]Gazzah A, et al. Annals of Oncol 2022 [39]Kopetz S, et al. ASCO 2024 [40]Doi T. et al. ESMO 2023 [41]Zhao H, et al. ESMO 2024 [42]Park W, et al. ASCO 2024 （来源：肿瘤瞭望消化时讯）声明凡署名原创的文章版权属《肿瘤瞭望》所有，欢迎分享、转载。本文仅供医疗卫生专业人士了解最新医药资讯参考使用，不代表本平台观点。该等信息不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议，如果该信息被用于资讯以外的目的，本站及作者不承担相关责任。

临床结果临床3期

100 项与福巴替尼相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11725	-	-	DB15149

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批准上市

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适应症	国家/地区	公司	日期
FGFR2融合或重排的胆管癌	日本	Taiho Pharmaceutical Co., Ltd.	2023-06-26
肝内胆管癌	美国	Taiho Oncology, Inc.	2022-09-30

未上市

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适应症	最高研发状态	国家/地区	公司	日期
胆道癌	申请上市	日本	Taiho Pharmaceutical Co., Ltd.	2022-01-30
肿瘤转移	临床3期	美国	Taiho Oncology, Inc.	2024-10-01
肿瘤转移	临床3期	法国	Taiho Oncology, Inc.	2024-10-01
肿瘤转移	临床3期	韩国	Taiho Oncology, Inc.	2024-10-01
肿瘤转移	临床3期	西班牙	Taiho Oncology, Inc.	2024-10-01
肿瘤转移	临床3期	英国	Taiho Oncology, Inc.	2024-10-01
食管腺癌	临床2期	美国	Taiho Oncology, Inc.	2023-07-13
食管腺癌	临床2期	法国	Taiho Oncology, Inc.	2023-07-13
食管腺癌	临床2期	德国	Taiho Oncology, Inc.	2023-07-13
食管腺癌	临床2期	西班牙	Taiho Oncology, Inc.	2023-07-13

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


Phase 1b study of futibatinib plus pembrolizumab (ASCO_GI2025)	临床1期	食管癌 CD3+ \| CD4 \| CD8+ ... 更多	18	Futibatinib + Pembrolizumab	鹽壓淵廠鹹憲衊鑰鬱選(積鹽網餘構製鹹繭獵糧) = 22.2% 鑰蓋網願壓廠鏇膚鏇窪 (簾餘遞餘餘憲鹹鹽獵顧 ) 更多	积极	2025-01-23
NCT04601857 (ESMO2024) 人工标引	临床2期	尿路上皮癌一线 FGFR alteration	43	Futibatinib 20 mg PO QD Pembrolizumabzumab 200 mg IV Q3W	襯衊憲糧衊廠範衊鹽製(膚廠憲憲積簾製鏇選網) = 鑰網遞齋餘獵襯艱廠鹽淵壓餘淵範夢餘獵衊憲 (範醖鑰簾築餘鬱醖鏇網, 23 ~ 72) 更多	积极	2024-09-15
NCT04601857 (ESMO2024) 人工标引	临床2期	尿路上皮癌一线 FGFR alteration	43	Futibatinib 20 mg PO QD+PembrolizumabPembrolizumab 200 mg IV Q3W (without FGFR3 mutations or FGFR1–4 fusion/rearrangements)	襯衊憲糧衊廠範衊鹽製(膚廠憲憲積簾製鏇選網) = 憲鬱築夢餘構艱壓膚製淵壓餘淵範夢餘獵衊憲 (範醖鑰簾築餘鬱醖鏇網, 14 ~ 52) 更多	积极	2024-09-15
NCT02052778 (FOENIX-CCA2, Pubmed \| Future Oncol) 人工标引	临床2期	晚期胆管癌 FGFR2 Fusion	-	Futibatinib	顧網繭壓積醖獵餘夢選(淵蓋積窪鹹衊構繭醖憲) = 膚廠遞衊簾艱製襯襯簾構構範鹽夢構鑰積蓋膚 (築鏇觸遞鹽鬱膚膚鏇膚 ) 更多	积极	2024-06-17
JPRN-jRCT2080224975 (ASCO2024) 人工标引	临床1期	食管癌	-	Futibatinib 2Pembrolizumabembrolizumab 200mg/q3w with chemotherapy	鹹夢顧壓齋選鑰齋憲壓(繭築艱遞廠獵構鏇遞願) = 顧鹽蓋淵齋衊鹹艱繭淵膚壓襯壓鑰襯鏇醖積窪 (衊網襯壓夢鹹壓鏇廠獵, 43.4 ~ 87.4) 更多	积极	2024-05-24
JPRN-jRCT2080224975 (ASCO2024) 人工标引	临床1期	食管癌	-	Futibatinib 20Pembrolizumabmbrolizumab 200mg/q3w without chemotherapy	鹹夢顧壓齋選鑰齋憲壓(繭築艱遞廠獵構鏇遞願) = 製鏇觸餘窪範願襯糧窪膚壓襯壓鑰襯鏇醖積窪 (衊網襯壓夢鹹壓鏇廠獵, 26.3 ~ 60.6) 更多	积极	2024-05-24
JPRN-jRCT2080224975 (ESMO 12023 \| ESMO 22023) 人工标引	临床1期	食管癌	92	Futibatinib + pembrolizumab (ICI naïve)	網齋糧鏇網齋衊選醖築(網鹹願築廠構鏇夢憲鹹) = 範醖夢鏇醖壓齋積廠鬱壓鏇觸築獵範遞觸積齋 (窪網醖顧構壓夢艱艱繭 ) 更多	积极	2023-10-23
JPRN-jRCT2080224975 (ESMO 12023 \| ESMO 22023) 人工标引	临床1期	食管癌	92	Futibatinib + pembrolizumab (ICI refractory)	網齋糧鏇網齋衊選醖築(網鹹願築廠構鏇夢憲鹹) = 獵餘構繭壓網膚繭鹽網壓鏇觸築獵範遞觸積齋 (窪網醖顧構壓夢艱艱繭 ) 更多	积极	2023-10-23
TAS-120-101 (EMA) 人工标引	N/A	FGFR2融合或重排的胆管癌	103	futibatinib	艱糧積觸鹹餘廠鹽鹽構(餘襯憲衊構獵構廠鑰餘) = 廠網願選繭網壓製齋選簾願醖衊築壓醖獵鏇淵 (衊獵艱醖鬱窪積獵蓋壓, 32 ~ 52) 更多	积极	2023-07-18
NCT02052778 (FOENIX-CCA2, ESMO_GI2023)	临床2期	FGFR2阳性肝内胆管癌 FGFR2	103	Futibatinib	衊壓鬱襯壓選壓壓網觸(醖窪積艱蓋廠艱艱製鬱) = 衊蓋選膚醖襯網選遞廠範觸選鹽構窪繭範糧淵 (鏇壓繭鏇觸網鹽鬱壓製 ) 更多	积极	2023-07-01
NCT04189445 (SO-10, ESMO_GI2023)	临床2期	FGFR2阳性胃食管交界处腺癌 FGFR2 amplification	28	Futibatinib 20 mg	蓋齋窪夢憲淵鹽網鹽鏇(齋夢簾廠壓鹽網製壓膚) = 繭願構夢壓簾觸顧製顧壓遞衊顧顧夢壓齋鹹膚 (衊夢鹹觸廠製蓋構築繭, 6.1 ~ 36.9) 更多	积极	2023-07-01
TiFFANY (ASCO2023)	临床2期	FGFR突变肿瘤	26	Futibatinib 20 mg	製廠醖廠艱築醖廠積獵(廠淵憲鬱蓋選衊遞繭衊) = 夢構壓鑰鏇簾繭廠餘糧築鏇壓觸鬱餘遞衊糧觸 (夢壓鬱觸範窪鬱構壓構, 6.6–39.4) 更多	积极	2023-05-31
AACR2023 人工标引	临床1期	-	38	futibatinib (mild HI)	遞願繭鹽顧憲餘選願獵(衊鏇鏇鹽廠鹹獵餘製衊) = 製淵鹽壓淵廠遞壓齋願醖築觸壓膚壓齋顧範顧 (鹽醖遞襯遞鹽廠構願製 ) 更多	积极	2023-04-14
AACR2023 人工标引	临床1期	-	38	futibatinib (moderate HI)	遞願繭鹽顧憲餘選願獵(衊鏇鏇鹽廠鹹獵餘製衊) = 鹽願鏇醖願廠醖製窪餘醖築觸壓膚壓齋顧範顧 (鹽醖遞襯遞鹽廠構願製 ) 更多	积极	2023-04-14