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更新于：2025-05-07

ADAM9

更新于：2025-05-07

基本信息

别名

a disintegrin and metalloproteinase domain 9 (meltrin gamma)、ADAM 9、ADAM metallopeptidase domain 9

+ [13]

简介

Metalloprotease that cleaves and releases a number of molecules with important roles in tumorigenesis and angiogenesis, such as TEK, KDR, EPHB4, CD40, VCAM1 and CDH5. May mediate cell-cell, cell-matrix interactions and regulate the motility of cells via interactions with integrins. May act as alpha-secretase for amyloid precursor protein (APP).

关联

项与 ADAM9 相关的药物

IMGC-936

靶点

ADAM9 x Tubulin

作用机制

ADAM9抑制剂 [+1]

在研机构

MacroGenics, Inc. [+1]

原研机构

ImmunoGen, Inc.

在研适应症

晚期恶性实体瘤

非在研适应症

胃癌

最高研发阶段临床1/2期

首次获批国家/地区-

首次获批日期1800-01-20

MGC-028

靶点

ADAM9 x Top I

作用机制

ADAM9抑制剂 [+1]

在研机构

MacroGenics, Inc.

原研机构

MacroGenics, Inc.

在研适应症

晚期恶性实体瘤 [+3]

非在研适应症-

最高研发阶段临床1期

首次获批国家/地区-

首次获批日期1800-01-20

Izeltabart

靶点

ADAM9

作用机制

ADAM9抑制剂

在研机构-

原研机构-

在研适应症-

非在研适应症-

最高研发阶段临床阶段不明

首次获批国家/地区-

首次获批日期1800-01-20

项与 ADAM9 相关的临床试验

NCT06723236

/ Recruiting临床1期

A Phase 1, First-in-Human, Open Label, Dose Escalation and Cohort Expansion Study of MGC028 in Participants With Advanced Solid Tumors

The goal of this clinical trial is to characterize the safety, tolerability, dose-limiting toxicities (DLT), and maximum tolerated dose (MTD) or maximum administered dose of MGC028 (if no MTD is defined). The study will enroll adult participants with relapsed or refractory, unresectable, locally advanced of metastatic solid tumors known to express ADAM9.
The main question the study aims to answer is:
* What types of side effects will participants experience when receiving MGC028?
* Can MGC028 cause cancer to shrink, remain stable, or able to control disease progression of participants with advanced solid tumors?
Participants will
* Undergo screening procedures to determine eligibility
* Receive study treatments initially every 3 weeks. Treatment intervals may be extended based on data.
* Have blood samples taken for routine and research tests
* Have other examinations to check heart and lung function, and general health status
* Be asked about any side effects that may be happening or other medications you are taking. The study doctor will provide treatment for side effects, if necessary.
* Have the study doctor assess your tumor status at regular intervals to determine how you are responding to treatment.

开始日期2025-02-13

申办/合作机构

MacroGenics, Inc.

NCT04622774

/ Completed临床1/2期

A Phase 1/2, First-in-Human, Open-Label, Dose-Escalation and Expansion Study of IMGC936 (Anti-ADAM9 Antibody Drug Conjugate) in Patients With Advanced Solid Tumors

This study is a Phase 1/2, first-in-human, open-label, dose-escalation, and expansion study designed to characterize the safety, tolerability, pharmacokinetics, immunogenicity, and preliminary antitumor activity of IMGC936 administered by intravenous (IV) infusion.

开始日期2020-10-29

申办/合作机构

ImmunoGen, Inc.

[+1]

100 项与 ADAM9 相关的临床结果

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100 项与 ADAM9 相关的转化医学

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0 项与 ADAM9 相关的专利（医药）

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459

项与 ADAM9 相关的文献（医药）

2025-08-01·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Differential roles of the ADAM9/NF-κB and the ADAM9/STAT3 feedback loops in HIV-1 Tat-induced microglial inflammatory response and subsequent neuronal apoptosis

Article

作者: Cao, Duo ; Sun, Weixi ; Wei, Hongke ; Ruan, Cailian ; Qiao, Xiaoting

ADAM has been implicated in causing several neurodegenerative diseases to progress. However, the precise function they play in HIV-associated neurocognitive disorders (HAND) remains incompletely elucidated. The HIV-1 transcriptional activator (Tat) has the capacity to evoke an inflammatory reaction within the microglia of the central nervous system. This, subsequently, initiates the apoptosis of neuronal cells. In the present research, our attention was centered on the part that ADAM9 plays in the microglia's response to Tat. We discovered that the stimulation with soluble Tat remarkably enhanced the manifestation of ADAM9 by means of the NF-κB and STAT3 pathway. In contrast, inhibition of ADAM9 significantly reduced Tat-triggered NF-κB and STAT3 signaling. Moreover, both ADAM9/NF-κB and ADAM9/STAT3 feedback loops exacerbated Tat-induced microglia inflammatory responses. However, further studies showed that the ADAM9/NF-κB feedback loop more significantly promoted neuronal apoptosis mediated by conditioned medium secreted by microglia after Tat stimulation. This study offers a novel perspective on the function of diverse feedback circuits in the etiopathogenesis of HAND. It can be posited that, when considered as a collective entity, ADAM9 may represent a viable candidate for therapeutic intervention in the context of preventing neuronal injury associated with HAND by modulating the inflammatory response of microglia and influencing neuronal injury.

2025-04-01·Ecotoxicology and Environmental Safety

Bioinformatics analysis to identify environmental endocrine chemicals that target endometriosis genes

Article

作者: Du, Kaile ; Zhang, Xiangcheng ; Luo, Ruihang ; Zhou, Boxuan ; Xiong, Haiwei

Endometriosis (EMS) significantly impacts women's health and is influenced by genetic factors and environmental endocrine-disrupting chemicals (EDCs), which interfere with hormonal balance. Using the Gene Expression Omnibus database, we identified differentially expressed genes and applied analytical methods, including WGCNA, GO, KEGG, and LASSO regression, to predict six key genes associated with EMS: ADAM9, IRAK3, NTRK3, PIK3CG, STK38, and TLR4. By integrating the Comparative Toxicogenomics Database and Endocrine Disruption Exchange Database, we identified 35 EDCs potentially linked to these genes. This study highlights the relationship between EMS and EDCs, offering insights into its pathogenesis and potential therapeutic targets for improved treatment.

2025-02-01·iScience

Perturbation of EPHA2 and EFNA1 trans binding amplifies inflammatory response in airway epithelial cells

Article

作者: Kamada, Yuka ; Okiyoneda, Tsukasa ; Fukuda, Ryosuke ; Hinata, Daichi ; Beppu, Shiori

The interactions between EPH receptors and ephrin (EFN) ligands play a crucial role in maintaining epithelial integrity and aiding in defense against infections. However, it remains unclear how the EPH-EFN trans-binding changes during infections and how this alteration affects inflammatory response. Here we report that pathogen-associated molecular patterns (PAMPs) disrupt the EPHA2-EFNA1 trans-binding in airway epithelial cells (AECs). Mechanistically, flagellin induces the TLR5-dependent EFNA1 cleavage through the metalloproteinase ADAM9 concomitant with the activation of ligand-independent EPHA2 signaling. We found that the ablation of EPHA2 reduced the responsiveness of respiratory inflammation induced by flagellin and Pseudomonas aeruginosa both in vitro and in vivo. Notably, even in the absence of PAMPs, the inflammatory response in AECs was stimulated by forcibly induced EFNA1 shedding. These findings illustrate that the perturbation of the EPHA2-EFNA1 trans-binding acts as a sensing mechanism for infections and amplifies the inflammatory response, providing a defense mechanism for respiratory epithelia.

项与 ADAM9 相关的新闻（医药）

2025-03-24

·抗体圈

研发决策风云：放弃一款，力推多款

MacroGenics 在仔细瞅了瞅最近两期的数据后，一咬牙，决定挥泪告别对自家一款超厉害的抗体 - 药物偶联物的研究啦。这可真是研发路上的一个大转折哟！暂停到放弃，vobra duo 的坎坷路早在 2023 年 11 月，这家生物技术公司就给 vobramitamab duocarmazine（vobra duo）的研究踩了刹车。当时他们还解释说，正眼巴巴地盼着 2 期单药前列腺癌试验的无进展生存期（PFS）数据呢。你瞧，vobra duo 这设计可牛了，弄了个能切割的肽连接子，就想着把 DNA - 烷基化 duocarmycin 药物 “小包裹” 精准地送到表达 B7 - H3 的实体瘤那儿。公司首席执行官斯科特・科尼格医学博士、哲学博士，当时跟投资者解释得那叫一个详细，说公司得综合看看最终的 PFS 数据、这疗法安不安全，再瞅瞅在其他研发项目的大背景下竞争情况咋样，才能决定要不要再给 vobra duo 投钱。尽管 MacroGenics 放弃了 vobramitamab duocarmazine（vobra duo），但公司首席执行官斯科特·科尼格医学博士、哲学博士表示，公司仍然认为 B7 - H3 作为靶点具有“潜力”。结果呢，如今数据出来咯，2mg/kg 和 2.7mg/kg 剂量组的中位放射学无进展生存期，一个是 9.5 个月，另一个是 10 个月。3 月 20 日，MacroGenics 在全年财报里还说，安全性数据 “跟之前透露的没啥两样”。然后，公司大手一挥，在声明里表示：“综合评估 vobra duo 的安全性和有效性，再看看内部资源和研发管线，我们决定不自己继续开发 vobra duo 啦，不过呢，打算找找把这个项目合作出去的机会。” 放弃一款，还有多款 “潜力股” 虽说 vobra duo 被放弃了，可科尼格还是很坚定地说，公司依旧觉得 B7 - H3这个靶点 “潜力无限” 呢。他还透露，公司对另一种抗 B7 - H3 抗体 - 药物偶联物 MGC026 的进展那是相当 “满意”。这 MGC026 可是基于 topoisomerase I inhibitor（拓扑异构酶 I 抑制剂）的抗体 - 药物偶联物，眼下正在对晚期实体瘤患者进行 1 期剂量递增研究呢。另外，公司还有个叫 MGC028 的抗体 - 药物偶联物也处在临床阶段，它也是基于 topoisomerase Iinhibitor，专门靶向 ADAM9，最近才刚开始在实体瘤里进行 1 期研究。期待新数据，研发不停步 MacroGenics 现在满心期待着今年晚些时候 lorigerlimab 的数据。这 lorigerlimab 可是个 PD - 1xCTLA - 4 双特异性抗体，公司正把它和多西他赛联合起来，用在 2 期前列腺癌试验里呢。科尼格在昨天盘后发布的声明里兴奋地说：“2024 年我们完成了好多临床开发的大目标，像 LORIKEET 2 期研究的入组工作都完成啦，这研究可是评估 lorigerlimab 和多西他赛联合用在 mCRPC 患者身上效果的哟。” 他还补充道：“2025 年，我们可得接着这股劲儿，努力推进我们那些创新的临床候选产品管线，像 lorigerlimab、MGC026 和 MGC028，都得加把劲啦！” 值得一提的是，2025 年初，MacroGenics 兜里还有 2.017 亿美元的现金储备呢，公司估计这些钱能撑到 2026 年下半年，看来研发资金暂时有着落咯，就看这些研发项目能不能一路 “开挂” 啦！参考资料： https://www.fiercebiotech.com/biotech/macrogenics-pulls-plug-vobra-duo-adc-after-seeing-phase-2-prostate-cancer-data 识别微信二维码，添加抗体圈小编，符合条件者即可加入抗体圈微信群！请注明：姓名+研究方向！本公众号所有转载文章系出于传递更多信息之目的，且明确注明来源和作者，不希望被转载的媒体或个人可与我们联系(cbplib@163.com)，我们将立即进行删除处理。所有文章仅代表作者观点，不代表本站立场。

临床2期财报临床终止临床1期

2025-03-21

·FierceBiotech

MacroGenics pulls plug on vobra duo ADC after seeing phase 2 prostate cancer data

Despite giving up on vobra duo, MacroGenics CEO Scott Koenig, M.D., Ph.D., said that the company still believes B7-H3 has “potential” as a target.\n MacroGenics has made the final decision to abandon work on one of its more advanced antibody-drug conjugates after taking a look at the latest phase 2 data.The biotech had already paused work on vobramitamab duocarmazine (vobra duo) back in November, explaining that it was awaiting progression-free survival (PFS) data from a phase 2 monotherapy prostate cancer trial. Vobra duo has a cleavable peptide linker designed to deliver a DNA-alkylating duocarmycin payload to solid tumors that express B7-H3.CEO Scott Koenig, M.D., Ph.D., explained to investors at the time that the company would make a call on whether to invest further in vobra duo after considering the final PFS data, the therapy’s safety profile and the competitive landscape in the context of the rest of its pipeline.The results are now in, and they show a median radiographic PFS of 9.5 months and 10 months for the 2-mg/kg and 2.7-mg/kg doses, respectively. Safety data “remained consistent with prior data disclosures,” MacroGenics said in its full-year earnings results March 20.“Based on its assessment of the vobra duo safety and efficacy profile and an internal resource and portfolio review, MacroGenics has decided not to pursue further internal development of vobra duo and will instead explore potential alternatives for partnering this program,” the company said in the release.Despite giving up on vobra duo, Koenig said the company still believes B7-H3 has “potential” as a target, adding that the biotech is “pleased with the progress being made with our alternate anti-B7-H3 ADC, MGC026.” MGC026, which is a TOP1i-based ADC, is undergoing a phase 1 dose-escalation study in patients with advanced solid tumors. The biotech also has another ADC in the clinic in the form of MGC028, a TOP1i-based ADC that targets ADAM9 and recently started a phase 1 study in solid tumors.MacroGenics is awaiting a readout later this year for lorigerlimab, a PD-1xCTLA-4 bispecific that the company is testing in a phase 2 prostate cancer trial in combination with docetaxel.“We concluded 2024 with the achievement of multiple clinical development milestones, including the completion of enrollment in the LORIKEET phase 2 study evaluating lorigerlimab in combination with docetaxel in patients with mCRPC,” Koenig said in yesterday\'s postmarket release.“We look forward to building upon this momentum in 2025 as we work to advance our novel pipeline of clinical product candidates, including lorigerlimab, MGC026 and MGC028,” the CEO added.MacroGenics entered the year with $201.7 million in the bank, which the company expects to last into the second half of 2026.

临床1期抗体药物偶联物临床2期

2025-02-03

·精准药物

靶向NRG1融合肿瘤

NRG1基因编码神经调节蛋白 1（Neu Re Gulin 1，NRG1），是一种能够结合 HER3 和 HER4 并激活 ErbB 信号通路的神经调节生长因子。NRG1是表皮生长因子（EGF）配体家族的一员，NRG1基因框内融合可激活并保留NRG1蛋白的EFG样结构域，它可与 ERBB3 结合。ERBB3本身缺乏激酶域，但是它可以与ERBB2结合形成异二聚体，进而激活下游信号通路（MAPK和PI3K通路），导致细胞增殖或分化，并最终导致癌症的发生。 NRG1篇概要临床病理特征 1. 属于罕见靶点：很罕见、频率低（肺0.3%）、驱动基因、有药可用 2. NRG1融合常见因素：女性、不吸烟者、腺癌（黏液亚型） 3. 检测方法：RNA-seq NGS（优选）靶向治疗 4. Zenocutuzumab-zbco：后线，ORR为33%，DOR为7.4个月 5. 阿法替尼、吡咯替尼、Seribantumab等正在进行晚期泛癌种的NRG1融合试验 6. 目前临床个例报道疗效较多的药物有阿法替尼临床病理特点融合类型（泛瘤种） 2019年4月，《Clin Cancer Res》杂志上发表实体瘤中NRG1融合的数据0.19%（41/21858）[1]，非小细胞肺癌中25例中融合伙伴为CD74（15例），SLC3A2（1例），TNC（1例），MDK（1例），ATP1B1（1例），DIP2B（1例），RBPMS（1例），MRPL13（1例），ROCK1（1例），DPYSL2（1例），PARP8（1例）；卵巢癌3例中SETD4（1例），TSHZ2（1例），ZMYM2（1例）；胰腺导管癌3例中ATP1B1（1例），CDH1（1例），VTCN1（1例）；乳腺癌2例中ADAM9（1例），COX10-AS1（1例）；胆囊癌3例中ATP1B1（2例），NOTCH2（1例）；结直肠癌中POMK（1例）；肾细胞癌中RBPMS（1例）；尿路上皮癌中GDF14（1例）；肉瘤中WHC1L1（1例）；鼻咽神经内分泌肿瘤中HMOX1（1例）。 NRG1融合实体瘤非小细胞肺癌有研究纳入了117名携带NRG1融合的NSCLC患者[2]，并对他们的临床特征进行总结，最终观察到NRG1融合常见因素，包括：女性和从不吸烟者；发生NRG1融合最常见的肿瘤类型主要为腺癌和粘液亚型。 NSCLC基因融合谱检测方法目前，有多种方法可用于检测基因融合，比如RNA-seq NGS（优先），DNA-seq NGS，RT-PCR，FISH。NRG1融合一般与EGFR、ALK和ROS1等驱动基因不共存，TP53突变是其最常见的共存基因突变，见上右图。 RNA-seq NGS优势[3]：在对17,485例实体瘤的大规模分析中，所有肿瘤样本使用NGS（MSK-IMPACT）进行检测，对某些肿瘤采用靶向RNA测序（MSK-Fusion Solid Assay，Archer Fusion Plex）进行检测。测序发现在多个KRAS野生型IMA和一例胰腺腺癌中检测到NRG1融合，而之前仅靠NGS DNA测序是漏检的。这些发现表明，由于融合结构的复杂性和多样性以及NRG1具有较大的内含子区域，单NGS DNA测序可能会漏检一些NRG1融合，也就是说RNA测序可能比DNA NGS更可靠。可用于检测NRG1和其他基因融合的不同方法的优缺点靶向治疗根据NRG1融合致癌的原理，可发现抑制NRG1融合的潜在方法，主要有两大类：一类是针对 EGFR/HER2 的小分子TKIs（Tyrosine Kinase Inhibitors，酪氨酸激酶抑制剂）：比如阿法替尼，吡咯替尼，拉帕替尼，来那替尼，Tarloxitinib 等。一类是针对HER2或HER3的大分子mAb（monoclonal Antibody，单克隆抗体）/ADCs：比如针对HER2的曲妥珠单抗，Margetuximab等；针对HER3的 Patritumab，Seribantumab，Zenocutuzumab (MCLA-128)，Lumretuzumab，GSK2849330，U3-1402等。 NRG1融合阳性肿瘤患者使用ErbB靶向治疗的报道病例备注：Lung adenocarcinoma,肺腺癌；IMA，浸润性黏液腺癌；NSCLC，非小细胞肺癌；PDAC，胰腺导管腺癌 Zenocutuzumab[4-5]FDA加速批准首个NRG1基因融合靶向疗法，你了解多少？ Zenocutuzumab 是一种双特异性抗体，可与 HER2 和 HER3 的细胞外结构域结合。该药可通过阻断 NRG1/HER3 结合和 HER2/HER3 二聚化，从而通过 PI3KAKT-mTOR 致癌信号通路，抑制肿瘤细胞增殖和存活。生理→病理 eNRGy研究（NCT02912949）是一项多中心、开放标签、多队列的临床试验，共招募了64例NRG1融合阳性晚期或转移性NSCLC成人患者，以及30例NRG1融合阳性晚期或转移性胰腺癌成人患者，这些患者在接受标准治疗后出现疾病进展。NRG1融合阳性状态的确认由下一代测序（NGS）检测方法前瞻性确定。研究的主要终点包括经独立盲法中央审查依据RECIST v1.1标准评估的确认总体缓解率（ORR）和缓解持续时间（DOR）。结果显示，在NSCLC患者中，ORR为33%（95% CI：22%-46%），中位DOR为7.4个月（95% CI：4.0-16.6）。在胰腺癌患者中，ORR为40%（95% CI：23%-59%），DOR范围为3.7个月至16.6个月。安全性分析显示，在汇总的安全性人群中，最常见的不良反应（≥10%）包括腹泻、肌肉骨骼疼痛、疲劳、恶心、输液相关反应、呼吸困难、皮疹、便秘、呕吐、腹痛和水肿。最常见的3级或4级实验室异常（≥10%）包括γ-谷氨酰转移酶升高、血红蛋白降低、钠降低和血小板减少。经典报道(阿法替尼) 2014-01 CD74⁃NRG1融合基因首次由Fernandez⁃Cuesta等在《Cancer Discov》报道，通过对25例从未吸烟的KRAS和EGFR基因阴性的肺腺癌患者进行转录组测序，发现了CD74⁃NRG1融合基因占4%（1/25），随后作者运用逆转录聚合酶链式反应（RT⁃PCR）在15例浸润性黏液肺腺癌患者中，发现CD74⁃NRG1融合基因占27%（4/15），提示了CD74⁃NRG1融合基因与浸润性黏液肺腺癌有着密切的关系。 2014-06 Nakaoku等在《Clin Cancer Res》上首次报道了SLC3A2⁃NRG1融合基因，他们在从未吸烟的浸润性黏液肺腺癌患者中，发现6例患者拥有SLC3A2⁃NRG1融合基因，频率为17.6%（6/34）。 2014-07 Gow等在《Med Oncol》上也报道了台湾的一个小组在13 例浸润性黏液肺腺癌中发现了1例CD74⁃NRG1融合基因的病例（8%）。 2014-12 2014年12月，Dhanasekaran等在《Nat Commun》上报道了NRG1新的融合伙伴：RBPMS和SDC4。 2015-07 Jung等在《J Thorac Oncol》上首次报道了1例拥有VAMP2⁃NRG1融合基因的非小细胞肺癌，作者运用RNA测序技术分析了100多例非小细胞肺癌患者，发现了1例CD74⁃NRG1融合基因患者和1例VAMP2⁃NRG1融合基因患者，其中VAMP2⁃NRG1融合基因患者是1名67 岁从未吸烟的女性，基因测序没有发现EGFR、KRAS和BRAF基因突变和ALK、ROS1、RET等融合基因。 2016-09 Shin等也在《Oncotarget》上报道，通过二代测序检测59例浸润性黏液肺腺癌患者，NRG1融合为16例，融合伙伴SLC3A2占13例（81.25%），融合伙伴CD74⁃NRG1占3例（18.75%）。其中10例NRG1融合并发KRAS基因突变（62.5%），2 例NRG1 融合并发NRAS Q61L突变和EML4⁃ALK融合。 2017-05 Gay等在《J Thorac Oncol》上发表文章，报道了2个有趣的案例：2位NRG1融合的肺癌患者通过二代EGFR⁃TKI阿法替尼治疗，无进展生存时间分别为12个月和10个月。 2017-05 案例1 患者是一位42岁从不吸烟的男性白种人，肺腺癌伴随肝转移和颞骨转移，二代基因测序没有发现EGFR、ALK、ROS1、KRAS等突变，只有TP53突变。患者在接受了4个周期的培美曲塞联合铂类化疗后，进行了RNA测序，发现其具有SLC3A2⁃NRG1基因融合，随后应用了阿法替尼（40 mg qd）治疗，在服药2-3天后，患者咳嗽和气短症状便有了很大的改善。CT和MRI显示原发肿瘤和颞骨转移灶都发生了明显缩小，疗效评估达到部分缓解并维持了12个月。 2017-05 案例2 患者是一位62岁从不吸烟的男性白种人，诊断为早期肺癌，行右下肺切除术+淋巴结清扫。手术后几个月，发现了左肾上腺转移，二代测序显示只有TP53和 MYC基因突变，RNA测序发现患者具有CD74⁃NRG1基因融合，于是也应用了阿法替尼（40mg qd）治疗，疗效评估部分缓解并维持了10个月。 2017-10 Muscarella 等在《J Thorac Oncol》上报道了1例 CD74⁃NRG1融合基因与ALK基因融合基因同时存在的晚期肺腺癌病例，患者为65岁从不吸烟的男性白种人，2012年5月病理诊断为印戒细胞肺腺癌伴随淋巴结、脾脏、骨转移，二代基因测序显示CD74⁃NRG1融合基因与ALK基因突变同时存在，患者随后接受了化疗和克唑替尼、色瑞替尼等多重治疗，生存至今已5年。 2017-12 Cheema等也在《J Thorac Oncol》上报道了1例拥有CD74⁃NRG1融合基因的肺腺癌病例，患者为62岁从不吸烟的亚洲女性，没有远处转移，肺部肿块穿刺证实病理类型为浸润性黏液腺癌，且没有检测到常见的EGFR和ALK等基因状态改变，由于肿瘤多发且不可切除，该患者接受了培美曲塞联合铂类化疗，病情得到一定的缓解。但随后患者的病情恶化，二代测序检测显示该患者具有CD74⁃NRG1融合，随后应用了阿法替尼（40 mg qd）治疗，治疗2周后患者的症状得到了明显改善，影像学资料也显示肿瘤明显缩小，疗效评估为部分缓解并维持了26周。参考资料 [1]Jonna S, Feldman RA, Swensen J, et al. Detection of NRG1 Gene Fusions in Solid Tumors. Clin Cancer Res. 2019 Aug 15;25(16):4966-4972. doi: 10.1158/1078-0432.CCR-19-0160. [2]Duruisseaux M, Liu SV, Han JY, et al. NRG1 fusion-positive lung cancers: clinicopathologic profile and treatment outcomes from a global multicenter registry. J Clin Oncol. 2019;37. Abstract 9081. [3]Laskin J, Liu SV, Tolba K, et al. NRG1 fusion-driven tumors: biology, detection, and the therapeutic role of afatinib and other ErbB-targeting agents. Ann Oncol. 2020 Dec;31(12):1693-1703. doi: 10.1016/j.annonc.2020.08.2335. [4]https://www.fda.gov/drugs/resources-information-approved-drugs/fda-grants-accelerated-approval-zenocutuzumab-zbco-non-small-cell-lung-cancer-and-pancreatic [5]https://www.accessdata.fda.gov/drugsatfda_docs/label/2024/761352s001lbl.pdf 声明：发表/转载本文仅仅是出于传播信息的需要，并不意味着代表本公众号观点或证实其内容的真实性。据此内容作出的任何判断，后果自负。若有侵权，告知必删！长按关注本公众号粉丝群/投稿/授权/广告等请联系公众号助手觉得本文好看，请点这里↓

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