Open-label Phase 2 Study of Avutometinib (RAF/MEK Clamp) in Combination With Defactinib (FAK Inhibitor) and Cetuximab in Patients With Unresectable, Anti-EGFR-Refractory Advanced Colorectal Cancer

To learn if avutometinib in combination with defactinib and cetuximab can help to control unresectable, anti-EGFR-refractory, advanced colorectal cancer.

开始日期2024-10-31

申办/合作机构

The University of Texas MD Anderson Cancer Center

NCT06487221 / Recruiting临床2期IIT

A Phase II Trial of Avutometinib in Combination With Defactinib in Metastatic Diffuse Gastric Cancer

The purpose of this study is to determine if the combination study treatment with avutometinib and defactinib will prolong life in participants, is effective in decreasing the size of the tumor(s), and if it is safe in subjects with diffuse-type stomach cancer.

开始日期2024-10-15

申办/合作机构

Verastem, Inc.

NCT06495125 / Recruiting临床2期IIT

A Phase 2 Study of Defactinib and Avutometinib, in Combination With Nivolumab for Patients With Anti-PD1 Refractory LKB1-Mutant Advanced Lung Adenocarcinoma

This phase II trial tests how well defactinib and avutometinib in combination with nivolumab works in treating patients with LKB1-mutant non-small cell lung cancer that has not responded (refractory) to an anti-PD1 treatment and may have spread from where it first started to nearby tissue, lymph nodes, or distant parts of the body (advanced). Defactinib and avutometinib belong to a class of drugs called kinase inhibitors. These drugs target kinase proteins found in tumor cells. Tumor cells need these proteins to survive and grow. By blocking these proteins, defactinib and avutometinib may cause tumors to stop growing or grow more slowly. Immunotherapy with monoclonal antibodies, such as nivolumab, may help the body's immune system attack the tumor and may interfere with the ability of tumor cells to grow and spread. Giving defactinib and avutometinib in combination with nivolumab may kill more tumor cells in patients with anti-PD1 refractory LKB1-mutant advanced non-small cell lung cancer.

开始日期2024-07-31

申办/合作机构

Emory University

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100 项与 FAK 相关的临床结果

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100 项与 FAK 相关的转化医学

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0 项与 FAK 相关的专利（医药）

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14,383

项与 FAK 相关的文献（医药）

2024-12-01·Molecular biology reports

Adhesion, metastasis, and inhibition of cancer cells: a comprehensive review

Review

作者: Yayan, Josef ; Windisch, Wolfram ; Berger, Melanie ; Rasche, Kurt ; Franke, Karl-Josef

Abstract:

This comprehensive review delves into cancer’s complexity, focusing on adhesion, metastasis, and inhibition. It explores the pivotal role of these factors in disease progression and therapeutic strategies. This review covers cancer cell migration, invasion, and colonization of distant organs, emphasizing the significance of cell adhesion and the intricate metastasis process. Inhibition approaches targeting adhesion molecules, such as integrins and cadherins, are discussed. Overall, this review contributes significantly to advancing cancer research and developing targeted therapies, holding promise for improving patient outcomes worldwide. Exploring different inhibition strategies revealed promising therapeutic targets to alleviate adhesion and metastasis of cancer cells. The effectiveness of integrin-blocking antibodies, small molecule inhibitors targeting Focal adhesion kinase (FAK) and the Transforming Growth Factor β (TGF-β) pathway, and combination therapies underscores their potential to disrupt focal adhesions and control epithelial-mesenchymal transition processes. The identification of as FAK, Src, β-catenin and SMAD4 offers valuable starting points for further research and the development of targeted therapies. The complex interrelationships between adhesion and metastatic signaling networks will be relevant to the development of new treatment approaches.

2024-12-01·MOLECULAR BIOLOGY REPORTS

Nischarin inhibits the epithelial-mesenchymal transition process and angiogenesis in breast cancer cells by inactivating FAK/ERK signaling pathway via EGF like repeats and discoidin domains 3

Article

作者: Zheng, Ruzhen ; Wang, Rui ; Chen, Yidan ; Yang, Lingrong ; He, Yibo ; Xie, Shangnao

BACKGROUND:

Our previous study has demonstrated that Nischarin (NISCH) exerts its antitumor effects in breast cancer (BC) by suppressing cell migration and invasion. This study aims to explore the underlying mechanism through which NISCH functions in BC.

METHODS AND RESULTS:

The relevance between EGF Like Repeats and Discoidin Domains 3 (EDIL3) mRNA expression and the overall survival of tumor patients was depicted by the Kaplan-Meier curve. The findings revealed that overexpressed NISCH attenuated cell motility and colony-forming capacities of Hs578T cells, yet silenced NISCH in MDA-MB-231 cells led to contrasting results. Western blot (WB) analysis indicated that overexpression of NISCH significantly down-regulated the Vimentin and Slug expression, and inactivated the FAK/ERK signaling pathway. RNA sequencing (RNA-seq) was performed in NISCH-overexpressed Hs578T cells and the control cells to analyze differentially expressed genes (DeGs), and the results showed a significant down-regulation of EDIL3 mRNA level upon overexpression of NISCH. Subsequent functional analyses demonstrated that overexpression of EDIL3 attenuated the inhibitory effect of NISCH on cell migration, invasion, colony formation, and tube formation.

CONCLUSION:

In summary, our finding preliminarily revealed that NISCH inhibits the epithelial-mesenchymal transition (EMT) process and angiogenesis in BC cells by down-regulating EDIL3 to inactivate the FAK/ERK signaling pathway, thereby suppressing the progression of BC. Our results hold promise for contributing to the deep understanding of BC pathogenesis and identifying new therapeutic strategies for clinical application.

2024-12-01·MOLECULAR BIOLOGY REPORTS

Capsaicin combined with stem cells improved mitochondrial dysfunction in PIG3V cells, an immortalized human vitiligo melanocyte cell line, by inhibiting the HSP70/TLR4/mTOR/FAK signaling axis

Article

作者: Bi, Xin ; Zhang, Jiayu ; Zhang, Wenhe ; Wang, Xiaochuan ; Du, Sha ; Xiang, Jie ; Wu, Yifei ; Li, Renfu ; Liu, Jing ; Wang, Zhiqiong ; Li, Jinrong

BACKGROUND:

Vitiligo is a common autoimmune skin disease. Capsaicin has been found to exert a positive effect on vitiligo treatment, and mesenchymal stem cells (MSCs) are also confirmed to be an ideal cell type. This study aimed to explore the influence of capsaicin combined with stem cells on the treatment of vitiligo and to confirm the molecular mechanism of capsaicin combined with stem cells in treating vitiligo.

METHODS AND RESULTS:

PIG3V cell proliferation and apoptosis were detected using CCK-8 and TUNEL assays, MitoSOX Red fluorescence staining was used to measure the mitochondrial ROS level, and JC-1 staining was used to detect the mitochondrial membrane potential. The expression of related genes and proteins was detected using RT‒qPCR and Western blotting. Coimmunoprecipitation was used to analyze the protein interactions between HSP70 and TLR4 or between TLR4 and mTOR. The results showed higher expression of HSP70 in PIG3V cells than in PIG1 cells. The overexpression of HSP70 reduced the proliferation of PIG3V cells, promoted apoptosis, and aggravated mitochondrial dysfunction and autophagy abnormalities. The expression of HSP70 could be inhibited by capsaicin combined with MSCs, which increased the levels of Tyr, Tyrp1 and DCT, promoted the proliferation of PIG3V cells, inhibited apoptosis, activated autophagy, and improved mitochondrial dysfunction. In addition, capsaicin combined with MSCs regulated the expression of TLR4 through HSP70 and subsequently affected the mTOR/FAK signaling pathway CONCLUSIONS: Capsaicin combined with MSCs inhibits TLR4 through HSP70, and the mTOR/FAK signaling pathway is inhibited to alleviate mitochondrial dysfunction and autophagy abnormalities in PIG3V cells.

289

项与 FAK 相关的新闻（医药）

2024-09-19

·PRNewswire

FDA FAST TRACK DESIGNATION FOR NARMAFOTINIB IN ADVANCED PANCREATIC CANCER

HIGHLIGHTS The US FDA has granted Fast Track Designation to Amplia's lead drug narmafotinib in advanced pancreatic cancer Fast Track Designation facilitates the development of investigational drugs and allows for expedited review MELBOURNE, Australia, Sept. 19, 2024 /PRNewswire/ -- Amplia Therapeutics Limited (ASX: ATX), ("Amplia" or the "Company"), is pleased to announce that the United States Food and Drug Administration (FDA) has granted Fast Track Designation to Amplia's Focal Adhesion Kinase inhibitor, narmafotinib, for the treatment of advanced pancreatic cancer. Continue Reading Fast Track Designation is available to drugs that may provide an advantage over current therapies in the treatment of serious conditions. It is designed to speed the development of these drugs to enable patients to receive them sooner. This Designation will grant the Company access to more frequent meetings, and written communication, with the FDA. In future, narmafotinib may be eligible for Accelerated Approval and Priority Review. The Company has previously received Orphan Drug Designation from the FDA for narmafotinib in pancreatic cancer. The Company's CEO and Managing Director, Dr Chris Burns, commented, "Fast Track Designation for narmafotinib is a significant milestone for the Company. With this designation, we can work more closely with the FDA to accelerate our clinical program and gather the most compelling evidence for regulatory approval in this devastating disease." Amplia's clinical trial in advanced pancreatic cancer, the ACCENT trial, is ongoing in Australia and South Korea. Earlier this year, the Company announced that the US FDA had cleared its IND[1] application for a trial of narmafotinib in pancreatic cancer in the US. This trial is in advanced planning stages. This ASX announcement was approved and authorised for release by the Board of Amplia Therapeutics. About Narmafotinib Narmafotinib (AMP945) is the company's best-in-class inhibitor of the protein FAK, a protein over-expressed in pancreatic and other cancers, and a drug target gaining increasing attention for its role in solid tumours. The drug, which is a highly potent and selective inhibitor of FAK, has shown promising data in a range of preclinical cancer studies. The drug has successfully completed a healthy volunteer study and is currently in an open-label Phase 2a trial in pancreatic cancer where a combination of narmafotinib and the chemotherapies gemcitabine and Abraxane® is being assessed for safety, tolerability and efficacy. About Amplia Therapeutics Limited Amplia Therapeutics Limited is an Australian pharmaceutical company advancing a pipeline of Focal Adhesion Kinase (FAK) inhibitors for cancer and fibrosis. FAK is an increasingly important target in the field of cancer and Amplia has a particular development focus in fibrotic cancers such as pancreatic and ovarian cancer. FAK also plays a significant role in a number of chronic diseases, such as idiopathic pulmonary fibrosis (IPF). For more information visit and follow Amplia on Twitter (@ampliatx), Threads (@ampliatx) and LinkedIn. SOURCE Amplia Therapeutics Ltd WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

快速通道孤儿药临床2期

2024-09-19

·药渡Daily

亚盛医药的成功上岸早在意料之中

亚盛医药的成功上岸早在意料之中。 2024年上半年，亚盛医药实现营业收入8.24亿元，同比增长477%；首次实现扭亏为盈，净利润达1.63亿元。抛开奥雷巴替尼出海带来的巨额收入不说，单就在国内的商业化成绩就已开始放量。2024年上半年，奥雷巴替尼的销售收入较2023年下半年及上半年分別增加120%及5%；进入国家医保定点医院数量较2023年底增加79%。7月又在澳门获批，适应症为治疗任何酪氨酸激酶抑制剂（TKI）耐药、并伴有T315I突变的慢性髓细胞白血病（CML）慢性期（-CP）和加速期（-AP）的成年患者，以及治疗对一代和二代TKI耐药及/或不耐受的CML-CP成年患者。奥雷巴替尼的最新进展还包括被纳入2024美国国家综合癌症网络（NCCN）慢性髓细胞白血病（CML）治疗指南、被纳入2024版《CSCO恶性血液病诊疗指南》，作为涉及慢性髓系白血病(CML)、费城染色体阳性急性淋巴细胞白血病（Ph+ ALL）领域的治疗的指南。临床研究也取得诸多进展，2024年5月，获国家药监局临床试验许可开展奥雷巴替尼针对系统性全身治疗失败的琥珀酸脱氢酶（SDH）缺陷型胃肠间质瘤（GIST）患者的注册III期临床研究POLARIS-3；2024年2月，获得美国FDA的许可开阵奥雷巴替尼针对过往接受过治疗的慢性髓细胞白血病慢性期（CML-CP，伴有及并无伴有T315I突变）患者的注册III期临床试验POLARIS-2。另外在EHA 2024、第60届ASCO年会、美国癌症研究协会（AACR）年会公布的最新临床数据都显示了奥雷巴替尼依旧强悍。奥雷巴替尼的商业化前景从来不是需要担忧的选项，但出海的预期却大大出人意料。 2024年6月，亚盛医药与武田订立独家选择权协议，授予武田制药独家选择权以就奥雷巴替尼订立独家许可协议。根据协议，武田拥有全球范围内（除中国、香港特别行政区、澳门特别行政区及台湾等地区以外）开发以及商业化奥雷巴替尼的独家权利。亚盛医药可收取1亿美元的选择权付款，并将有资格获得最高约12亿美元的选择权行使费和额外的潜在里程碑付款，以及年销售额两位数百分比的销售分成。此外，亚盛医药还向武田制药成功发行及配发合共2430.73万股股份，总额为7500万美元，武田由此成为亚盛医药的二股东。 MNC巨头的站台，无疑为亚盛医药巩固血液瘤龙头地位提供了有力支持，以至于其股价在三个月时间内就实现了翻倍。那么武田为何不惜下血本也要夺得奥雷巴替尼的海外权益？事实上，武田很早就拥有全球首款第三代BCR-ABL抑制剂，或许这个化学名对大部分中国人来说比较陌生，但如果换成“格列卫”，就耳熟能详了。电影《我不是药神》把治疗慢性粒细胞白血病（慢粒）的格列卫（一种BCR-ABL抑制剂）带入大众认知范围，伊马替尼为一代格列卫。伊马替尼疗效显著，但获得性耐药一直是慢粒白血病治疗的主要挑战。BCR-ABL激酶区突变是获得性耐药的重要机制之一，其中T315I突变是常见的耐药突变类型之一，在耐药慢粒白血病中的发生率为25%左右。因此二代达沙替尼、尼洛替尼和博舒替尼登场，但很快也耐药了，直到2012年12月，武田的三代格列卫普纳替尼在美国上市才缓解了耐药的局面。不过令人惋惜的是，一年以后，因“危及生命的血栓和血管重度狭窄”风险，美国FDA要求武田暂停这款药的销售和推广，普纳替尼也成了首个被要求撤市的小分子激酶抑制剂类抗肿瘤药。不过，由于临床需求太大，FDA最终没有让这款药物彻底退市，而是要求企业在说明书上以黑粗框警告风险。更让武田焦虑的是，2021年美国FDA批准诺华的阿思尼布用于慢性髓系白血病（Ph+CML-CP）的三线治疗，阿思尼布也是一款三代格列卫。阿思尼布在2023年销售额达4亿美元，入选2023年20大畅销新药，并且，今年6月1日，一项关于阿思尼布用于慢性髓系白血病一线治疗的三期临床达到主要终点，销售额可能还会再翻一番。武田的普纳替尼存在心脑血管不良事件等安全短板，而且专利在2026-2027年到期，选择和竞争对手亚盛医药合作，成了武田的最优选择。奥雷巴替尼目前已成为三代格列卫中事实上的Best-in-class，因其对普纳替尼、阿思尼布耐药或者无效的慢粒白血病患者有效。临床数据显示，奥雷巴替尼对比普纳替尼用于慢粒白血病慢性期的MMR率（主要分子学缓解率，是评估慢粒白血病患者治疗反应的重要指标）分别为53%和40%，对比用于慢粒白血病加速期的MMR率分别为40%和22%。从全球临床进展来看，奥雷巴替尼2024年2月获得FDA批准开展针对慢粒白血病慢性期的全球III期注册性临床，预计2026年完成注册临床并在美国申报上市，刚好与专利到期的普纳替尼实现无缝衔接。这是一个双赢的局面，武田获得续血的大秘宝，亚盛医药则成功获得巨额资金并将借此机会在美国申请高价发行股票上市。在现金流充裕之后，亚盛医药的脚步可能要更快了。根据半年报显示，截至上半年结束，亚盛医药的现金及银行结余为11亿元，7月，收到武田支付的独家选择权协议项下知识产权收入及选择权付款相关的1亿美元，后续很快还会有大额里程碑付款进账，如今的亚盛医药可谓兵强马壮，粮草充足。后续的研发进度可能将加快脚步。 Lisaftoclax（APG-2575）是一款由亚盛医药自主研发的、全球领先的Bcl-2选择性抑制剂，它通过阻断Bcl-2来恢复癌细胞的正常凋亡过程，已在中国、美国、澳洲及欧洲开展21项针对多种血液恶性肿瘤和实体瘤的Ib/II期临床研究，并获得了FDA授予的五项孤儿药资格认定。作为全球第二个进入全球注册临床试验的Bcl-2选择性抑制剂，Lisaftoclax相较于维奈克拉具备更优的有效性和安全性，展现出Best-in-class潜力。据临床验证，Lisaftoclax在治疗维奈克拉（唯一上市药物）无效的BTK耐药患者中显示出有效性，并且与BTKi联合使用时，对于TN CLL/SLL患者达到100%的ORR，对于r/r CLL/SLL患者也实现了98%的ORR。在安全性方面，Lisaftoclax中性粒细胞减少症和血小板减少症的发生率分别为30.3 %和13%，相较于维奈克拉显著降低（45%和21%），同时临床肿瘤溶解综合征的风险也较低。此外， Lisaftoclax与BTKi的联用中未观察到药物相互作用，且无剂量限制毒性，目前尚未达到最大耐受剂量。 2024年6月，在2024年欧洲血液学协会年会（EHA 2024）上，以壁报形式公布了Lisaftoclax联合新型治疗方案用于复发/难治性（R/R）多发性骨髓瘤（MM）或免疫球蛋白轻链（AL）淀粉样变性患者的最新数据。在A组（Lisaftoclax联合泊马度胺及地塞米松）中，ORR为70.4%，3级及以上治疗相关的中性粒细胞减少症发生率为14.3%。 2024年6月，在第60届美国临床肿瘤学会（ASCO）年会上以壁报展示形式公布了Lisaftoclax单药或联合治疗华氏巨球蛋白血症（WM）患者的全球多中心Ib/II期研究，以及Lisaftoclax联合阿扎胞苷（AZA）治疗新诊断AML或复发/难治性（R/R）急性髓性白血病（AML）患者的Ib/II期临床研究的最新成果。在39例新诊断为AML的老年/不耐受标准化疗的患者中，ORR及复合缓解率（CRc）分別为64.1%及51.3%。亚盛医药计划于2024年向国家药监局递交Lisaftoclax用于复发/难治性慢淋白血病/小淋巴细胞淋巴瘤的上市申请。除Lisaftoclax外，Pelcitoclax（APG-1252）、APG-2449（全球首个ALK/FAK/ROS1-TKI）、APG-5918（国内首个进入临床的EED抑制剂）都获得不错的进展。作为立志做BIC新药的企业，多年来亚盛医药十分执着且低调，以至于在某些时期非常不受投资者待见，股价长期被严重低估。但经过与武田合作一事，更进一步证明，坚持长期主义，坚持创新至上才是Biotech最好的出路。首度扭亏为盈值得纪念，今后很快将能摘B。在中国大地上，事实上还有很多这样坚持创新情怀的Biotech，正是这些药企在泥泞中的坚持，才让我们看到了中国创新药的未来。后续发展如何，药渡还将持续关注。

引进/卖出CSCO会议临床3期ASCO会议AACR会议

2024-09-18

·BiG生物创新社

百济提交两项IND：CEA ADC，EGFR/MET三抗

10.12日，深圳，BiG自免研讨会！以原创科学、临床需求和项目合作为出发点，讨论创新疗法（双抗/ADC/细胞疗法/PROTAC等）在自免和炎症方向的重大进展和发展前景，共寻下一个自免神药！近期，根据CDE官网显示，受理了百济神州递交的两款一类新药的临床试验申请，两款应该均为冻干制剂，其中BG-C477为靶向CEA的ADC药物，BG-T187可能为一款EGFR/MET三特异性抗体。 2024年5月30日，PCT中专利进行更新，其中百济神州公布了CEA ADC药物的专利，内部项目号为BG-C477，针对适应症为胃癌和肺癌。抗体部分，百济采用了杂交瘤技术筛选得到母本抗体BGA7592，可以选择性的只结合CEA，而不结合CEACAM6。随后，BGA7592进行了人源化和亲和力成熟，最终得到终抗体BAG5384，亲和力达到1.77nM。确定抗体后，进行了一系列payload-linker的筛选，采用DXd类似物作为paylaod，linker方面和B7H3 ADC一样（ADC抗体新药专利速递：映恩生物、百济神州、Angiex、EXELIXIS），在GGFG的基础上，通过如溶酶体糖苷酶、蛋白酶和自分解等不同裂解方式进行串联组合，亲水性为提升，更有利于payload的旁观者效应实现，DAR值为8左右，确定最终的ADC分子为BGA9962。体外活性方面，BGA9962无论是在CEA高表达细胞还是低表达细胞中均表现明显的肿瘤抑制活性。体内活性方面，采用自己制备的Sanofi同靶点ADC药物tusamitamab ravtansine作为对照物（BGA-7650）（410例：Seagen启动CEACAM5C ADC一期临床）,BGA9962同样无论是在CEA高表达细胞还是低表达细胞中均表现出更强的抗肿瘤活性。在胃癌的PDX模型中，BGA9962同样表现出更强的抗肿瘤活性。食蟹猴的单剂量PK考察中，BGA9962同样表现出显著的稳定性。 BG-T187并没有公布相关产品信息，2024年年中汇报中透漏其在肺癌领域将布局一款EGFR/MET的三抗，根据产品命名形式，BG-T187大概率就是该款三抗。值得注意的是，和大多数受体酪氨酸激酶一样，基于MET结构的特殊性，早期的双价MET抗体很容易造成MET受体二聚体形成，其位于胞内的酪氨酸蛋白激酶PTK结构域也会激活，激活的PTK使c-Met位于β链胞内激酶活性区内的Tyr1234和Tyr1235两个磷酸化位点发生磷酸化，并进一步导致位于C末端的Tyr1349和Tyr1356磷酸化，最终导致肿瘤的生长，转移等，这也是相关项目失败的主要原因。获批的强生EGFR/MET双抗Amivantamab一方面采用单价结构，另一方面也在抗体筛选中检测抗体对MET的磷酸化可以避免抗体对MET通路的激活，从而防止抗体药效的折损。5个MET抗体和8个EGFR抗体根据两两配对原则，组合成40个双特异抗体分子进行MET磷酸化检测，其中双价MET抗体5D5为阳性对照，单价MET 抗体5D5 x b12为阴性对照。根据磷酸化程度对不同双特异抗体进行打分并舍弃磷酸化分数大于等于3的双特异抗体。嘉和生物GB263T是全球首个EGFR/c-Met/c-Met三特异性抗体，针对EGFR和两个不同c-Met表位。且拥有两个Fab结合EGFR，Fc片段发生了突变，增强了Fc功能。因此，GB263T高度差异化的设计具有多种作用机制，可同时抑制原发性及继发性EGFR突变及c-Met信号通路。体外研究及体内动物模型已经证明了其抗肿瘤活性。临床前研究表明，与Amivantamab(JNJ-372) 类似物相比，GB263T有效地阻断了EGFR和c-Met的配体诱导磷酸化，并显示出对EGFR和c-Met信号通路更佳的双重抑制。同时，GB263T有效诱导了EGFR和c-Met的内吞，并显著降低EGFR与c-Met的蛋白表达水平。 2023年ESMO期间，嘉和公布了GB263T用于晚期EGFR突变(EGFRm)非小细胞肺癌(NSCLC)患者治疗的I/II期临床试验初步临床结果，共15例患者接受了至少一次GB263T治疗。所有患者既往均接受过3代EGFR-TKI和含铂化疗治疗，既往接受系统治疗的中位线数为3线。临床试验结果表明：GB263T在治疗剂量（1260-1680mg）显示出富有前景的疗效。EGFR敏感突变且接受3代TKI治疗耐药的患者在有效治疗剂量的客观缓解率（ORR）为28.6%；3例既往接受3代EGFR-TKI治疗失败后，且伴有cMET改变的患者可观察到明确的获益。同时显示了具有优势的安全性特征。输液相关反应发生率较低（33%），且程度较轻；甲沟炎、皮疹均为轻度（1/2级）、腹泻仅为1级；未发生MET靶点相关的外周水肿毒性。希望百济两款药物早日获批进入临床探索。共建Biomedical创新生态圈！如何加入BiG会员？ ▼

抗体药物偶联物蛋白降解靶向嵌合体临床1期细胞疗法临床申请