The purpose of this study is to see if using Patient Derived Organoids (PDO) to choose a drug for the treatment of pancreatic cancer individually for each patient is useful. The study will look at the number of participants who have a response to their assigned drug.

开始日期2025-02-17

申办/合作机构

University Health Network

NCT06522360

/ Withdrawn临床2期IIT

Brigatinib Plus Chemotherapy or Local Consolidation Therapy in ALK Positive Advanced Non-small Cell Lung Cancer (BrightStar-2)

The goal of this clinical research study is to learn if the combination of brigatinib and either local consolidation therapy (such as radiotherapy or surgery) or chemotherapy (pemetrexed and carboplatin) can help to control the disease compared with brigatinib alone. The safety of these combinations will also be studied.

开始日期2024-12-11

申办/合作机构

The University of Texas MD Anderson Cancer Center

NCT06532149

/ RecruitingN/AIIT

ERectile Dysfunctions, gOnadotoxicity and Sexual Health Assessment in Men With Lung Cancer (EROS)

Although many phase III clinical trials evaluate the quality of life as a secondary endpoint, male sexuality remains a neglected topic in oncology research. In light of the long-term efficacy of new-generation anticancer treatments for ANSCLC (i.e. targeted therapies and immunotherapy), there is a paucity of data about any detrimental effect on fertility and sexuality that could complicate the therapy proposal, especially in young patients.
The aim of this trial is to assess incidence of endocrine toxicity and sexual dysfuction in male patients receiving active treatment for ANSCLC

开始日期2024-08-05

申办/合作机构-

100 项与布格替尼相关的临床结果

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100 项与布格替尼相关的转化医学

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100 项与布格替尼相关的专利（医药）

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776

项与布格替尼相关的文献（医药）

2025-12-31·Hospital practice (1995)

Unraveling the unforeseen: anuric acute kidney injury induced by alectinib

Article

作者: Taha, Amro ; Ali, Shehzad ; Nguyen, Chau Doan ; Qadeer, Tahira ; Tran, Viet Nghi ; Kebato, Yusuf Hussein

INTRODUCTION:

Alectinib, a second-generation anaplastic lymphoma kinase (ALK) inhibitor, is pivotal in managing ALK-positive non-small cell lung cancer (NSCLC) due to its efficacy and favorable safety profile. However, severe renal toxicity, including acute kidney injury (AKI), remains a rare but significant adverse effect.

CASE REPORT:

We present the case of a 71-year-old female with a history of diabetes and recently diagnosed ALK-positive NSCLC. She had been on alectinib therapy (600 mg twice daily) for two months. The patient was admitted with symptoms of shortness of breath and anuria. Initial laboratory results revealed a significant rise in serum creatinine from a baseline of 1.0 mg/dL to 3.64 mg/dL, indicating AKI. Alectinib was discontinued, and the patient underwent a single session of hemodialysis. The patient exhibited rapid clinical improvement with significant recovery of renal function, and she was discharged without the need for further dialysis. A subsequent switch to brigatinib was well-tolerated, with stable renal function observed at the 4-month follow-up.

CONCLUSION:

This case underscores the potential for severe AKI associated with alectinib therapy, highlighting the importance of vigilant renal function monitoring in patients undergoing treatment, especially those with predisposing conditions. Early recognition and prompt intervention are crucial to mitigate renal complications and optimize patient outcomes. Brigatinib may serve as a suitable alternative for patients intolerant to alectinib.

2025-09-01·Journal of Computational Biophysics and Chemistry

Deciphering the Selective Targeting of Noncovalent, Wild Type-sparing, and ATP-competitive Tyrosine Kinase Inhibitors to EGFR T790M Gatekeeper Mutant

作者: Wang, Jing ; Wu, Hongyan ; Cheng, Jin ; Meng, Shu

Various tyrosine kinase inhibitors (TKIs) have been developed to target human epidermal growth factor receptor (EGFR) for cancer therapy. However, many patients treated with first-line TKIs are clinically observed to eventually establish a gatekeeper T790M mutation in the ATP-binding site of the EGFR kinase domain, which is primarily responsible for acquired drug resistance to cancers. Over the past decades, a number of noncovalent, wild-type-sparing and ATP-competitive inhibitors (NWAIs) were reported to selectively target the T790M mutant over wild-type kinase, which are independent of the traditional inhibitor classification system that categorizes EGFR TKIs into four generations. Here, we systematically investigated the intermolecular interaction of wild-type EGFR (EGFRWT) and its T790M mutant (EGFRT790M) with 15 existing NWAI inhibitors, paying attention to the structural and energetic responses of inhibitor ligands to the gatekeeper mutation. It was revealed that the NWAIs can be typed into three classes I, II and III, which can form S[Formula: see text] interactions, hydrophobic (van der Waals) contacts and weak hydrogen (halogen) bonding with the side-chain thioether moiety of the mutant Met790 residue, respectively, thus conferring additional affinity and specificity to inhibitor ligands upon the T790M mutation. In addition, we further performed 2D-chemical similarity search to identify new class I NWAIs, from which two Staurosporine analogs (i.e. UCN01 and ZHD0501) were identified to have a good selectivity for EGFRT790M over EGFRWT. They can be exploited as promising leading chemical scaffolds to further develop potent, selective, wild-type-sparing NWAI inhibitors of EGFRT790M gatekeeper mutant.

2025-09-01·EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY

Progression and expansion of ALK inhibitors against NSCLC: A dual target approach

Article

作者: Gupta, Ghanshyam Das ; Kumari, Shreya ; Akhter, Mymoona ; Sharma, Kalicharan

ALK gene is a member of the tyrosine kinase receptor family found on chromosome 2 (2p23) that plays an important role in the progression of the non-small cell lung cancer (NSCLC). Since the ALK inhibitors such as Crizotinib, Ceritinib, Brigatinib, Alectinib and Lorlatinib, was endorsed for the treatment of advanced NSCLC linked to ALK gene rearrangement. But eventually, patients become resistant to the medication, which will result in treatment failure. However, treatment for NSCLC could be greatly advanced by the development of dual inhibitors that target ALK in addition to other oncogenic pathways like ROS1, c-MET, EGFR, etc. These strategies seek to improve therapy efficacy, address resistance mechanisms, and provide treatment alternatives for patients with intricate molecular profiles. The aim of this review is to summarize the introduction to ALK and the synergy between ALK and other anti-tumor targets, recent developments in the synthesis of various dual inhibitors of the ALK. We also thoroughly discussed their design concepts, structure-activity relationships (SARs), preclinical and clinical data as well as in silico studies to provide ideas for further development of novel ALK based dual inhibitors.

135

项与布格替尼相关的新闻（医药）

2025-05-21

·ioncology

例例在望丨“钻石恒久远，一颗永流传”——ALK阳性晚期NSCLC治疗的今生今世

点击蓝字关注我们▌马锐，王雪莹丨辽宁省肿瘤医院胸内二科ALK阳性非小细胞肺癌（NSCLC）发生率约为5%-7%，主要分为融合、点突变、扩增突变三种形式，其中ALK融合是ALK+的NSCLC致癌的主要驱动因素，在NSCLC中，以EML4-ALK融合突变为主。EML4-ALK融合有不同的融合亚型，其中以V1和V3a/3b亚型最为常见；ALK的点突变和扩增突变相对少见，通常导致ALK-TKI耐药。ALK基因融合通常出现在较为年轻且非吸烟（或轻度吸烟者）的肺腺癌患者中，ALK-TKI治疗有效率高，生存时间较长，常被称为“钻石突变”。目前ALK-TKI“三代同堂”用于晚期ALK阳性NSCLC的一线治疗，如克唑替尼、塞瑞替尼、阿来替尼、恩沙替尼、布格替尼、洛拉替尼、伊鲁阿克和依奉阿克等。这些ALK-TKI通过抑制ALK融合蛋白磷酸化发挥抗肿瘤作用，约60%-80%的ALK基因融合的NSCLC患者对靶向药敏感，肿瘤显著缩小，同时让很多患者轻松跨越了五年生存大关。ALEX研究表明初治晚期ALK阳性NSCLC患者应用阿来替尼治疗后，中位无进展生存（PFS）长达34.8个月，对比克唑替尼的10.9个月具有显著优势。eXalt 3研究表明恩沙替尼的晚期一线治疗中位PFS达到31.3个月，相较于克唑替尼组的12.7个月有显著延长。CROWN研究结果更为惊艳，一线应用洛拉替尼治疗患者，中位 PFS突破60个月，且5年PFS率高达60%。这彻底改写了ALK基因融合NSCLC的生存预后，让这类患者的“长生存”目标从理想走向现实，让ALK阳性晚期NSCLC的治疗逐步迈入了慢病化时代。现分享2例ALK阳性晚期肺腺癌患者分别在一线及多线应用ALK-TKI治疗病例。马锐教授辽宁省肿瘤医院胸内二科主任，肿瘤学博士中国医科大学、大连医科大学硕士研究生导师学术兼职：中国临床肿瘤学会理事会理事，中国老年学学会老年肿瘤专业委员执行委员，中国老年学学会老年肿瘤专业委员肺癌分委会常务委员，中国医药教育协会肺部肿瘤专委会常务委员，辽宁省生命科学学会常务理事，中国抗癌协会肺癌专业委员会委员，辽宁省抗癌协会理事会理事，辽宁省生命科学学会肺癌专业委员会主任委员，辽宁省抗癌协会肿瘤转移专业委员会主任委员，辽宁省抗癌协会肿瘤标志物专业委员会副主任委员，辽宁省医学会内科学分会委员会常务委员，辽宁省生命科学学会老年肿瘤专业委员会常务委员，沈阳市医学会肺部肿瘤学分会副主委，中国肿瘤生物治疗杂志、中国实用内科、医学与哲学，沈阳医学院学报等多家杂志编委及审稿专家。沈阳市领军人才。主持省部级、市级课题9项，获辽宁省科技进步三等奖2项、沈阳市科技进步二等奖1项，第一及通讯作者发表论文50余篇。王雪莹教授辽宁省肿瘤医院主治医师毕业于中国医科大学附属第一医院硕士研究生学历任职：中国抗癌协会指南专家学术成果：曾在Stem Cells and Regenerative Medicine发表文章病例134岁，女性，无吸烟史饮酒史，既往体健。2015年11月无明显诱因出现咳嗽咳痰，痰为黄色粘液状，就诊于铁西华康医院，胸部CT示右肺上叶尖段可见结节影，邻近胸膜局限牵拉。2015年12月于胸科医院行肺肿物穿刺活检病理回报为肺腺癌。2015年12月16日全麻下行右肺上叶肺癌根治术及纵隔淋巴结清扫术，术后病理：肺组织中部分脉管内见腺癌组织，断端支气管旁淋巴结内见癌组织，淋巴结中见到转移癌（2/6），未行基因检测。2016年1月复查CT提示支气管截断可见新发小结节，一线治疗采用培美曲塞+DDP方案化疗4周期（培美曲塞 3.36,DDP 480mg）。化疗后复查胸部CT：右肺见不规则结节样影，最大层面大小约19mm * 8mm，较前比较明显增大，疗效评估PD。2017.3-2017.4予单药多西他赛化疗3周期，疗效评估SD。2018年5月末复查CT提示结节较前增大，评效为PD，2018年6-10月予多西他赛+CBP化疗4周期，疗效评估SD。2022年5月患者出现活动后气短，复查胸部CT示右肺膨胀不良；右侧胸腔积液增多。胸腔积液包埋病理示符合肺腺癌细胞。行NGS基因检测：EML4：exon13-ALK:exon20融合。PD-L1（克隆号22C3） TPS<1%。临床诊断：右肺上叶恶性肿瘤rT0N0M1a IVA期（第9版分期）；恶性胸腔积液。诊疗经过：2022年5月始口服克唑替尼3个月，出现肝功能异常（DILI 2级伴临床症状），改用恩沙替尼靶向治疗至今，目前评效为维持PR。恩沙替尼应用期间出现轻度肝功能异常（DILI 1级），对症处理后好转。截止目前PFS 33个月。2018.072022.052022.082023.052024.12病例256岁，女性，无吸烟史饮酒史，既往体健。2023年02月患者体检发现肺占位性病变，胸部增强CT：右肺下叶后基底段结节；右侧锁骨上及纵隔内多发淋巴结肿大。PET-CT：右肺下叶周围型肺癌可能性大；1R、2L、3P、4R、4L及7组淋巴结转移可能性大。2023年02月就诊于本院胸外科行超声胃镜下纵隔肿物穿刺活检术，病理：结合免疫组化，符合肺腺癌。行NGS基因检测：EML4：exon20-ALK:exon20融合。PD-L1（克隆号22C3）TPS=55%。临床诊断：右肺下叶恶性肿瘤cT1bN3M0，IIIB（第9版分期），纵隔淋巴结继发恶性肿瘤，锁骨上淋巴肿继发恶性肿瘤治疗经过：2023年3月27日始行恩沙替尼靶向治疗至今，最佳疗效为PR，末次评效为维持PR。期间出现轻度肝功能异常（DILI 1级），对症处理后好转。截止目前PFS为26个月。2023年2月20日基线检查2024年6月复查PR（最佳疗效）2024年12月复查维持PR2025年3月复查维持PR小结上述2例病例NGS基因检测结果均提示EML4-ALK融合突变，但是应用ALK-TKI治疗时间点却截然不同。第1例病例由于当时检测和治疗费用昂贵的受限，并没有及时进行基因检测。在精准治疗时代，分子诊断已经是必须，各大指南均有推荐。目前基因检测的应用不仅适用于晚期患者治疗前或疾病进展、复发后决策，更已经趋向于术前和术后辅助治疗前决策。由于当时经济因素的局限，上述两例患者应用ALK-TKI治疗的时线上虽有差异，但两者PFS还是令人惊喜的。基于在CROWN研究中展现出的疗效与安全性以及三代TKI进入医保，对于ALK+的晚期NSCLC患者，“3+X”的治疗排兵布阵模式正逐渐更多应用。随着ALK-TKI用药选择逐渐增多，患者的疾病管理模式也正逐步转向“慢病化”管理，在维持高质量生活的基础上，通过规范的诊治，实现与疾病长期共存。“慢病化”全程管理模式确保每一位患者都能在“健康中国2030”的宏伟蓝图中，享受高质量生活带来的无限美好。分子诊断指导晚期肺癌后续治疗，事半功倍。ALK-TKI让“钻石”更加闪耀。参考文献（上下滑动可查看）1. Tony Mok, et al. Patterns of Progression with Lorlatinib and Insights into Subsequent Anticancer Therapy Ef ficacy in Advanced ALK+ NSCLC. 2024 WCLC, MA06.07.2. Bearz A, Bertoli E, et al. EML4-ALK: Update on ALK Inhibitors. Int J Mol Sci. 2025 Jan 1;26(1):308. doi: 10.3390/ijms26010308.3. Hong S,Fang W, Hu Z, et al. A large-scale cross-sectional study of ALK rearrangements and EGFR mutations in non-small-cell lung cancer in Chinese Han population [J]. Sci Rep, 2014,4: 7268.4. Mok T, et al. Updated overall survival and final progression-free survival data for patients with treatment-naive advanced ALK-positive non-small-cell lung cancer in the ALEX study[J]. Annals of oncology, 2020, 31(8): 1056-1064.5. Zhou Q. eXalt 3 study: First release of Asian population’s efficacy in ALK-positive non-small cell lung cancer (NSCLC). 2022. Available online: https://www.liangyihui. net/class/102928?6. Solomon BJ, et al. Lorlatinib Versus Crizotinib in Patients with Advanced ALK-Positive Non–Small Cell Lung Cancer: 5-Year Outcomes from the Phase III CROWN Study. JCO. 2024: JCO. 24.00581.7. WatanabeS,al.Phase II Trial of the Combination of Alectinib with Bevacizumab in Alectinib Refractory ALK-Positive Nonsquamous Non-Small-Cell Lung Cancer (NLCTG1501). Cancers (Basel). 2022;15(1):204. Published 2022 Dec 29.8. Li Y, et al. Alectinib continuation beyond progression in ALK-positive non-small cell lung cancer with alectinib-refractory. Transl Lung Cancer Res. 2024;13(1):152-1629. Benjamin J Solomon, Tony Mok, Dong-Wan Kim, et al. First-line crizotinib versus chemotherapy in ALK-positive lung cancer.[J] . 2014 Dec 4;371(23):2167-77.10. Zheng J, et al. Updated overall survival and circulating tumor DNA analysis of ensartinib for crizotinib-refractory ALK-positive NSCLC from a phase II study. Cancer Commun (Lond). 2024 Apr;44(4):455-468.11. WatanabeS,al.Phase II Trial of the Combination of Alectinib with Bevacizumab in Alectinib Refractory ALK-Positive Nonsquamous Non-Small-Cell Lung Cancer (NLCTG1501). Cancers (Basel). 2022;15(1):204. Published 2022 Dec 29.12. Xing P, Hao X, Zhang X, Li J. Efficacy and safety of brigatinib in ALK-positive non-small cell lung cancer treatment: A systematic review and meta-analysis. Front Oncol. 2022;12:920709. Published 2022 Nov 3. doi:10.3389/fonc.2022.920709（来源：《肿瘤瞭望》编辑部）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会议临床结果高管变更

2025-05-14

·Business Wire

Kesmalea Therapeutics Appoints Industry Veteran Tim Clackson to Board of Directors

LONDON--(BUSINESS WIRE)--Kesmalea Therapeutics, a biopharmaceutical company developing a pipeline of novel therapeutics founded on the ability to transform large heterobifunctional protein degraders into small molecules, today announced the appointment of senior life sciences executive Dr. Tim Clackson to its Board of Directors. Dr. Clackson brings to Kesmalea more than three decades of experience building oncology companies, including leading the R&D behind three approved drugs. He most recently served as Chief Executive Officer of Boston-based IDRx, Inc., a precision oncology therapy developer which was acquired by GSK in 2025 for up to $1.15 billion. “Kesmalea’s science represents a highly innovative, modular and scalable solution to unlock the full potential of targeted protein degradation,” said Dr. Clackson. “Kesmalea’s science represents a highly innovative, modular and scalable solution to unlock the full potential of targeted protein degradation,” said Dr. Clackson. “I look forward to working with their impressive team and the Board to help bring SELFTAC technology to the clinic and maximize its value.” “Targeted protein degradation holds enormous promise for medicine, but its most prominent drug class, PROTACs, faces innate issues caused by molecular size and structure. As we work to solve these challenges with our unique approach, we're assembling a world-class team to bring our mission to life," said Clive Dix, Chairman of the Kesmalea Board. "We're delighted to welcome Tim to the Board - his impressive track record of discovering and developing high impact targeted therapies for a range of cancer types will be invaluable as we translate our drug discovery research into revolutionary new medicines.” As IDRx CEO, Dr. Clackson led a team developing a best-in-class targeted therapy for gastrointestinal stroma tumor (GIST), through clinical proof-of-concept, a Series B financing and the acquisition by GSK. Prior to IDRx, Dr. Clackson was President and CEO of Theseus Pharmaceuticals, a clinical stage biotechnology company focused on development of targeted oncology therapies, where he led the Company through its initial public offering and early clinical development for its lead product candidate for GIST and other targeted therapies in its pipeline. Prior to Theseus, he served as President at Xilio Therapeutics, a privately held oncology company developing tumor-selective immunotherapies, where he led the development of the company’s technology and product strategy. From 1994 to 2018, Dr. Clackson was with ARIAD Pharmaceuticals, serving as President of R&D and Chief Scientific Officer from 2010. He played a key role in the company’s evolution from early research to a global commercial oncology company, and its subsequent acquisition by Takeda for $5.2 billion. Dr. Clackson led the multi-disciplinary R&D team that internally discovered and developed five clinical-stage product candidates, including ICLUSIG® (ponatinib), approved for patients with treatment-resistant Ph+ leukemias; ALUNBRIG® (brigatinib), approved for ALK+ non-small cell lung cancer (NSCLC); and EXKIVITY™, approved for Exon20 insertion+ NSCLC. Dr. Clackson received his B.A. in Biochemistry from the University of Oxford, his Ph.D. in Biology from the University of Cambridge, and completed a postdoctoral fellowship at Genentech. He serves as a Director on the Board of Elevation Oncology and previously served as a Director on the Boards of Forma Therapeutics (acquired by Novo Nordisk), Spring Bank Pharmaceuticals, and the Massachusetts Biotechnology Council (MassBio). About Kesmalea Therapeutics Kesmalea is developing a pipeline of novel therapeutics founded on the ability to transform large protein degraders into small molecules. This is achieved through SELFTAC®, a platform designed to combine the power of protein degradation with small molecule advantages such as oral bioavailability and central nervous system (CNS) penetration, among others. Kesmalea’s current research spans targets in oncology and diseases of the CNS, with broader applicability. The company is built on foundational scientific work by founder & CSO Harry Finch, Ph.D., a noted medicinal chemist and entrepreneur. Kesmalea has offices and labs in London, UK. Kesmalea's £25m Series A was led by Syncona Ltd alongside Oxford Science Enterprises. For more information, please visit: www.kesmalea.com.

高管变更上市批准并购免疫疗法

2025-05-09

·GBIHealth

再鼎、武田发布财报

企业动态No.1 / 再鼎医药2025Q1：收入增长22%至1.065亿美元2025年5月9日，再鼎医药（NASDAQ：ZLAB；HKEX：9688）公布了2025年第一季度（2025Q1）的财务业绩。公司报告期内总收入为1.065亿美元，同比增长22%；经营亏损显著改善，同比缩窄20%至5630万美元，有望稳步实现2025年第四季度盈利的目标。期内研发开支6070万美元，期末现金及现金等价物、短期投资和流动受限制现金总计为8.573亿美元。再鼎医药2025Q1产品收入净额为1.057亿美元，同比增长21%。这一增长主要由卫伟迦、则乐和纽再乐销售额增长所驱动。得益于销售放量与重症肌无力新适应证纳入新版国家医保目录（NRDL），卫伟迦（艾加莫德α静脉输注）及卫力迦（艾加莫德α皮下注射）期内录得1810万美元，市场覆盖率和渗透率持续提升。则乐（尼拉帕利）Q1收入净额为4950万美元，继续保持中国内地卵巢癌领域PARP抑制剂院内销售领军者地位。纽再乐（奥玛环素）录得1510万美元。在研管线中，ZL-1310（靶向 DLL3 的抗体药物偶联物）正在快速推进，近期将公布用于广泛期小细胞肺癌（ES-SCLC）的相关数据，预计2025年下半年启动用于ES-SCLC的注册性临床研究。ZL-6201（LRRC15 ADC）和ZL-1222（PD-1/IL-12双靶点抑制剂）近期也报告了积极数据，有望进一步扩充再鼎抗肿瘤创新管线。用于中重度特应性皮炎的ZL-1503（IL-13/IL-31R双靶点抑制剂）也将推进至全球I期临床研究阶段。->点击文末阅读原文，解锁完整双语新闻No.2 / 武田FY2024财报：核心收入增长2.8%，产品收入147亿美元2025年5月8日，武田药品（TSE：4502；NYSE：TAK）公布了2024财年（2024年4月1日至2025年3月31日，FY2024）财务业绩。报告期内，公司收入45816亿日元（约合306亿美元），核心收入45798亿日元（约合306亿美元），同比增长2.8%（按固定汇率计算，下同）。公司增长与上市产品持续强劲的势头，抵消了专利到期的影响，推动了收入和核心营业利润的增长。公司6个领域产品销售收入达22019亿日元（约合147亿美元），同比增长14.7%。消化系统药物销售收入同比增长7%，包括Entyvio（维得利珠单抗）销售额9141亿日元（+8.5%），Eohilia（布地奈德口服混悬剂）销售额55亿日元（+2501%）；罕见病药物销售收入增长5%，包括Takhzyro（拉那利尤单抗）销售额2232亿日元（+18.9%），Livtencity（马立巴韦）销售额330亿日元（+64.5%），Adzynma（阿帕达酶α）销售额71亿日元（+1516%）；血浆衍生疗法（PDT）销售收入增长9%，包括免疫球蛋白销售额7578亿日元（+11.5%），人血白蛋白销售额1414亿日元（+1.1%）；肿瘤药收入增长17%，包括与和黄医药合作的呋喹替尼销售额480亿日元（+351%），Alunbrig（布格替尼）销售额364亿日元（+22.7%）；疫苗收入增长8%，其中Qdenga（四价登革热减毒活疫苗）销售额356亿日元（+259%）；神经系统药物收入下滑14%。针对最近的关税政策，武田公司认为可能面临来自美国和中国关税的潜在风险是有限的。武田公司总收入中约有50%来自美国，进口价值（主要来自欧洲/日本/新加坡）约占美国总收入的8%到10%。武田公司总收入中约有4%来自中国，进口价值（来自美国）约占中国总收入的12%到15%。->点击文末阅读原文，解锁完整双语新闻No.3 / 英矽智能拟赴港股上市2025年5月8日，英矽智能发布招股书，拟赴中国香港联交所上市，摩根士丹利、中金公司和广发融资担任联席保荐人。英矽智能成立于2014年，是全球领先的AI驱动生物科技公司。目前，公司临床阶段资产包括一项处于II期临床阶段的资产，即强效选择性TNIK小分子抑制剂ISM001-055（Rentosertib），该候选药物拟用于治疗特发性肺纤维化（IPF）。通过自主开发的生成式人工智能平台Pharma.AI，英矽智能已产生逾20项临床或IND阶段的资产，其中三项资产已授权给国际制药及医疗保健公司，合约总价值超过20亿美元。英矽智能从新型TNIK靶点发现到首次人体临床试验的快速推进仅耗时18个月，充分展现了Pharma.AI相比传统方法（约4.5年）能大幅缩短药物发现流程。->点击文末阅读原文，解锁完整双语新闻全球医疗情报领导者解锁隐藏在数据中的商业潜力关于 G B I”自从2002年成立以来，GBI始终以技术为驱动，为药企、器械及行业相关服务商提供贯穿生命周期的全球药品市场竞争数据、全球行业资讯、HCPs洞察、全国医疗器械数据等商业信息与洞察，助力企业在进行战略布局和决策时，脱颖而出。历经20余年的深耕细作GBI已成为95%以上跨国药企、国内头部药企、咨询与投资机构等医疗圈灯塔用户值得信赖的长期合作伙伴。联系我们投稿 | 发稿 | 媒体合作▶ xujingou@baidu.com数据库 | 咨询服务 | 资讯追踪▶ 点击左下“阅读原文”完成表单填写点击阅读原文，解锁完整双语新闻

财报抗体药物偶联物专利到期

100 项与布格替尼相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D10866	布格替尼	L01XE43	DB12267

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
ALK阳性非小细胞肺癌	美国	Takeda Pharmaceuticals U.S.A., Inc.	2017-04-28

未上市

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
ALK阳性肺癌	临床3期	美国	ARIAD Pharmaceuticals, Inc.	2016-05-26
ALK阳性肺癌	临床3期	澳大利亚	ARIAD Pharmaceuticals, Inc.	2016-05-26
ALK阳性肺癌	临床3期	奥地利	ARIAD Pharmaceuticals, Inc.	2016-05-26
ALK阳性肺癌	临床3期	加拿大	ARIAD Pharmaceuticals, Inc.	2016-05-26
ALK阳性肺癌	临床3期	丹麦	ARIAD Pharmaceuticals, Inc.	2016-05-26
ALK阳性肺癌	临床3期	法国	ARIAD Pharmaceuticals, Inc.	2016-05-26
ALK阳性肺癌	临床3期	德国	ARIAD Pharmaceuticals, Inc.	2016-05-26
ALK阳性肺癌	临床3期	中国香港	ARIAD Pharmaceuticals, Inc.	2016-05-26
ALK阳性肺癌	临床3期	意大利	ARIAD Pharmaceuticals, Inc.	2016-05-26
ALK阳性肺癌	临床3期	卢森堡	ARIAD Pharmaceuticals, Inc.	2016-05-26

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临床结果

适应症

分期

评价

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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


NCT05361564 (WILDERNESS, ASCO2025)	临床2期	ALK阳性肺癌新辅助	12	Brigatinib 180 mg	構遞憲齋夢遞網憲壓範(獵鹹簾鑰繭鹽糧廠壓願) = 50.0% 膚鑰鹹獵範構簾齋範顧 (鹽餘選願網艱顧廠遞鏇 ) 更多	积极	2025-05-30
P3-6.013 (AAN2025)	N/A	神经系统肿瘤 anaplastic lymphoma kinase fusion	1,016	Brigatinib	衊遞顧範鹽艱簾醖襯醖(糧窪蓋鑰餘夢蓋鹽顧鹹) = 醖襯鑰顧積鏇鹽淵齋鬱鹹網蓋壓觸窪願網願積 (憲壓積鬱窪壓糧觸鏇選, 48.03 ~ 65.67)	积极	2025-04-07
Adelphi NSCLC Disease Specific Programme™ (ESMO_ELCC2025)	N/A	ALK阳性非小细胞肺癌一线	331	Brigatinib 1L	鏇築淵範壓壓壓鑰醖衊(淵壓鹹鹹憲艱衊範夢鬱) = The most common events on the Patient-Reported Outcomes version of the Common Terminology Criteria for Adverse Events (PRO CTCAE) during 1L BRG treatment were gastrointestinal toxicities (64%, 34/53), including nausea (77%, 26/34), vomiting (56%, 19/34) and diarrhea (56%, 19/34) 鑰積繭鏇積窪蓋艱築鹽 (製衊餘夢構糧醖襯範襯 )	-	2025-03-26
NCT03596866 (ALTA-3, CTgov)	临床3期	ALK阳性非小细胞肺癌	248	Brigatinib (Brigatinib)	糧鏇網網夢選築淵鬱網(壓壓簾糧簾鹽淵鏇顧艱) = 鹹觸鏇壓觸膚顧餘淵艱範鹽鹹醖鬱製壓獵鑰夢 (觸鹽淵鹹鹹鹽構窪醖蓋, 鹹鏇鑰醖鹽築鏇鬱糧選 ~ 繭鏇遞網鬱齋製蓋遞鏇) 更多	-	2025-02-19
NCT03596866 (ALTA-3, CTgov)	临床3期	ALK阳性非小细胞肺癌	248	Alectinib (Alectinib)	糧鏇網網夢選築淵鬱網(壓壓簾糧簾鹽淵鏇顧艱) = 築壓鬱鹹憲窪築淵觸衊範鹽鹹醖鬱製壓獵鑰夢 (觸鹽淵鹹鹹鹽構窪醖蓋, 醖積衊窪艱鑰觸餘網壓 ~ 顧築醖鹽範醖齋鹽夢廠) 更多	-	2025-02-19
NCT02737501 (ALTA-1L, ESMO2024) 人工标引	临床3期	ALK阳性非小细胞肺癌一线 ALK+	136	Brigatinib	艱簾獵築鬱鹹築鹽製夢(憲齋築鑰餘淵願選網鬱) = 築鹹窪繭獵鏇選選憲製窪醖構壓糧鏇顧鑰繭繭 (顧鹹繭鹹選鹹鏇繭衊觸, 21.1 ~ 44.1) 更多	积极	2024-09-14
NCT02737501 (ALTA-1L, ESMO2024) 人工标引	临床3期	ALK阳性非小细胞肺癌一线 ALK+	136	Placebo	艱簾獵築鬱鹹築鹽製夢(憲齋築鑰餘淵願選網鬱) = 願製選範遞廠餘獵醖範窪醖構壓糧鏇顧鑰繭繭 (顧鹹繭鹹選鹹鏇繭衊觸, 23.9 ~ NR)	积极	2024-09-14
ESMO2024 人工标引	N/A	ALK阳性非小细胞肺癌一线 ALK Rearrangement	242	Alectinib	繭願醖網壓鏇衊繭觸衊(觸製壓網積選夢簾鑰憲) = 鏇範鹹觸願襯廠鑰簾繭廠範構艱醖獵衊壓網淵 (鬱鏇鑰顧鹹願窪窪觸衊 ) 更多	积极	2024-09-14
ESMO2024 人工标引	N/A	ALK阳性非小细胞肺癌一线 ALK Rearrangement	242	Alectinib	繭願醖網壓鏇衊繭觸衊(觸製壓網積選夢簾鑰憲) = 選膚醖範觸鹹齋廠鏇鹽廠範構艱醖獵衊壓網淵 (鬱鏇鑰顧鹹願窪窪觸衊 ) 更多	积极	2024-09-14
NCT04223596 (ESMO2024)	临床2期	非小细胞肺癌IIIB期 \| 转移性非小细胞肺癌一线 ALK fusion variants \| tumor mutational burden (TMB) \| ctDNA levels	30	Brigatinib	獵廠製鑰蓋窪齋窪醖鹹(窪鹽鑰夢觸糧窪廠構餘) = 淵餘醖壓範廠餘夢鹹蓋廠廠鹽簾獵鹽壓鬱鹽築 (遞齋築壓夢繭網膚廠獵, 75.1 ~ 98.4) 更多	-	2024-09-14
NCT02737501 (ALTA-1L, WCLC2024) 人工标引	临床3期	ALK阳性非小细胞肺癌一线 ALK Positive	48	ALK TKI brigatinib (post-1L brigatinib)	築繭窪顧獵夢膚顧製選(願廠簾壓淵醖糧糧蓋淵) = 廠壓糧蓋餘鬱遞憲築網簾衊餘鹹鑰繭選窪窪製 (鏇築糧構醖構憲築構鹹 ) 更多	积极	2024-09-08
NCT02737501 (ALTA-1L, WCLC2024) 人工标引	临床3期	ALK阳性非小细胞肺癌一线 ALK Positive	48	Lorlatinbrigatinib	築繭窪顧獵夢膚顧製選(願廠簾壓淵醖糧糧蓋淵) = 餘繭願築襯窪蓋網鹽鹽簾衊餘鹹鑰繭選窪窪製 (鏇築糧構醖構憲築構鹹 ) 更多	积极	2024-09-08
NCT04374305 (INTUITT-NF2, Pubmed)	临床2期	室管膜瘤 \| 脑膜瘤 \| 2型神经纤维瘤病	40	Brigatinib 180 mg	鹹築齋簾鏇顧積襯遞憲(觸淵鏇膚製鹽餘觸選簾) = 製壓壓糧選艱廠遞壓簾積窪選齋憲醖襯衊餘範 (壓網膚壓範齋衊構繭窪, 3 ~ 24) 更多	积极	2024-06-27