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更新于：2025-05-07

TrkB

更新于：2025-05-07

基本信息

别名

BDNF/NT-3 growth factors receptor、GP145-TrkB、neurotrophic receptor tyrosine kinase 2

+ [8]

简介

Receptor tyrosine kinase involved in the development and the maturation of the central and the peripheral nervous systems through regulation of neuron survival, proliferation, migration, differentiation, and synapse formation and plasticity (By similarity). Receptor for BDNF/brain-derived neurotrophic factor and NTF4/neurotrophin-4. Alternatively can also bind NTF3/neurotrophin-3 which is less efficient in activating the receptor but regulates neuron survival through NTRK2 (PubMed:15494731, PubMed:7574684). Upon ligand-binding, undergoes homodimerization, autophosphorylation and activation (PubMed:15494731). Recruits, phosphorylates and/or activates several downstream effectors including SHC1, FRS2, SH2B1, SH2B2 and PLCG1 that regulate distinct overlapping signaling cascades. Through SHC1, FRS2, SH2B1, SH2B2 activates the GRB2-Ras-MAPK cascade that regulates for instance neuronal differentiation including neurite outgrowth. Through the same effectors controls the Ras-PI3 kinase-AKT1 signaling cascade that mainly regulates growth and survival. Through PLCG1 and the downstream protein kinase C-regulated pathways controls synaptic plasticity. Thereby, plays a role in learning and memory by regulating both short term synaptic function and long-term potentiation. PLCG1 also leads to NF-Kappa-B activation and the transcription of genes involved in cell survival. Hence, it is able to suppress anoikis, the apoptosis resulting from loss of cell-matrix interactions. May also play a role in neutrophin-dependent calcium signaling in glial cells and mediate communication between neurons and glia.

关联

项与 TrkB 相关的药物

Repotrectinib

瑞普替尼

靶点

ROS1 x TrkA x TrkB x TrkC

作用机制

ROS1抑制剂 [+3]

在研机构

Bristol-Myers Squibb Pharma EEIG [+5]

原研机构

Turning Point Therapeutics, Inc.

在研适应症

NTRK融合阳性实体瘤 [+10]

非在研适应症

KRAS G12D突变实体瘤 [+2]

最高研发阶段批准上市

首次获批国家/地区

美国

首次获批日期2023-11-15

Entrectinib

恩曲替尼

靶点

ALK x ROS1 x TrkA x TrkB x TrkC

作用机制

ALK抑制剂 [+4]

在研机构

罗氏（中国）投资有限公司 [+9]

原研机构

Nerviano Medical Sciences S.r.l

在研适应症

非小细胞肺癌 [+31]

非在研适应症

晚期乳腺癌 [+10]

最高研发阶段批准上市

首次获批国家/地区

日本

首次获批日期2019-06-18

Larotrectinib Sulfate

硫酸拉罗替尼

靶点

TrkA x TrkB x TrkC

作用机制

TrkA 拮抗剂 [+2]

在研机构

Bayer AG [+6]

原研机构

Array BioPharma, Inc. [+2]

在研适应症

局部晚期恶性实体瘤 [+15]

非在研适应症-

最高研发阶段批准上市

首次获批国家/地区

美国

首次获批日期2018-11-26

387

项与 TrkB 相关的临床试验

NCT06502171

/ Not yet recruiting临床1期IIT

A Phase 1/1b/2 Study of Cabozantinib in Combination With Selumetinib for Plexiform Neurofibroma in Adults and Adolescents With Neurofibromatosis Type 1

Based on the clinical activity of both selumetinib and cabozantinib as monotherapies in clinical trials, the demonstrated activity of these agents in reduced doses in preclinical studies, and the non-overlapping toxicity profiles, the study will assess the tolerability and efficacy of selumetinib and cabozantinib in combination in participants with NF1 ≥16 years old with progressive and/or symptomatic PN in a phase 1/1b/2 clinical trial.
Trial Design Phase 1 This will be an open label, dose escalation phase. Dose level escalation will be determined by a rolling six design. In this design, up to 6 participants can be enrolled at a given dose level and then evaluated for dose limiting toxicity (DLT) within the DLT window. The DLT window is defined as 16 weeks in this study based on the long half-life of cabozantinib and the desire to have maximum confidence about long-term tolerability of the combination prior to proceeding to the next dose level.
Phase 1b Once the recommended phase 2 dose has been determined in phase 1, an expanded cohort of 12 participants will be enrolled in phase 1b portion of the study.
Phase 2 This will be an open label, single-arm phase using the recommended phase 2 dose.

开始日期2025-07-01

申办/合作机构

The University of Alabama at Birmingham

[+2]

NCT06900595

/ Not yet recruiting临床2期IIT

A Phase II Study of Cabozantinib in Combination With Cemiplimab (Cabo-Cemiplimab) Versus Cabozantinib Alone in Adolescents and Adults With Advanced Adrenocortical Cancer

This phase II trial compares the effect of giving cabozantinib with or without cemiplimab in patients with adrenocortical cancer that has spread to nearby tissue or lymph nodes (locally advanced), and that cannot be removed by surgery (unresectable) or that has come back after a period of improvement (recurrent) or that has spread from where it first started (primary site) to other places in the body (metastatic). Cabozantinib is in a class of medications called tyrosine kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply, which may help keep cancer cells from growing. Immunotherapy with monoclonal antibodies, such as cemiplimab, may help the body's immune system attack the cancer, and may interfere with the ability of tumor cells to grow and spread. Giving cabozantinib with cemiplimab may kill more tumor cells in patients with locally advanced unresectable or recurrent/metastatic adrenocortical cancer.

开始日期2025-06-13

申办/合作机构

National Cancer Institute

NCT06811116

/ Not yet recruiting临床1/2期IIT

A Phase I/II Trial of Sapanisertib in Combination With Cabozantinib in β-Catenin-Mutated Hepatocellular Carcinoma

This phase I/II trial studies the side effects and best dose of sapanisertib when given together with cabozantinib, and to see how well they work in treating patients with liver cancer that has spread from where it first started to other places in the body (metastatic) and contains a mutation (change) in the β-catenin gene. Sapanisertib and cabozantinib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Giving sapanisertib and cabozantinib together may work better than giving cabozantinib alone in treating β-catenin-mutated metastatic hepatocellular carcinoma.

开始日期2025-05-16

申办/合作机构

National Cancer Institute

100 项与 TrkB 相关的临床结果

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100 项与 TrkB 相关的转化医学

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0 项与 TrkB 相关的专利（医药）

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6,775

项与 TrkB 相关的文献（医药）

2025-08-01·Brain, Behavior, and Immunity

Inhibition of TrkB-BDNF positive feedback loop attenuates intervertebral disc degeneration and low back pain in a composite mouse model

Article

作者: Wei, Zhengnong ; Chen, Yujie ; Li, Kun ; Huang, Minjun ; Lai, Weiyi ; Lian, Zhengnan ; Ao, Xiang ; Zhang, Zhongmin ; Wang, Liang

Intervertebral disc degeneration (IVDD) is a significant contributor to low back pain (LBP); however, the specific mechanisms involved remain unclear. Herein, a novel LBP mouse model was developed by integrating a bipedal standing model with a lumbar spine instability model (BS + LSI). This model effectively reproduced the behavioral characteristics of LBP and the pathological features of IVDD. Notably, a higher degree of degeneration and innervation in the endplates were observed in the BS + LSI mice. Transcriptome analysis revealed a significant upregulation of Ntrk2, the gene encoding TrkB, in the intervertebral discs of BS + LSI mice. Immunohistochemical staining further confirmed elevated expression of TrkB and its ligand BDNF in the endplates of these mice. Moreover, cyclic tensile strain (CTS) (20 %, 0.1 Hz, 24 h) upregulated TrkB expression and activated NF-κB signaling pathway to promote inflammatory responses in endplate chondrocytes. siBDNF transfection or treatment with the TrkB inhibitor ANA-12 effectively inhibited these pathological changes. Mechanistically, TrkB promoted BDNF expression by enhancing CREB phosphorylation, thereby establishing a TrkB-CREB-BDNF positive feedback loop. In vivo injection of ANA-12 significantly alleviated endplate inflammation and LBP-related behaviors in BS + LSI mice. Thus, an effective and replicable mouse model of LBP was established to identify TrkB as both the receptor for and an upstream regulator of BDNF, making it a crucial target for interventions to alleviate CEP inflammation and LBP.

2025-08-01·Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology

Adolescent marginal zinc deficiency upregulated BDNF and TrkB expression, impaired hippocampal and cortical development, and induced abnormal behaviors in male mice

Article

作者: Wang, Yuxiang ; Zhao, Tianyang ; Li, Rou ; Yu, Tian ; Li, Yanxia ; Gao, Xia ; Xu, Hongbin ; Liu, Xiaozhi ; Dai, Qiwei ; Wang, Liang ; Sun, Yajing

Zinc deficiency during adolescence poses a significant yet understudied risk to brain development. The study aimed to investigate the effects of marginal zinc deficiency during adolescence on emotion and cognition, morphological changes and neuronal arrangement of hippocampus and cortical, and proBDNF, mBDNF and TrkB expression levels. The emotion was assessed using the open-field test and three-chamber test. Additionally, cognition was evaluated using the Morris water maze test and novel object recognition test. Morphological changes were evaluated using H&E staining, while Nissl staining was employed to analyze neuronal arrangement. Additionally, proBDNF, mBDNF and TrkB expression levels were quantified by western blot. The results showed that adolescent marginal zinc deficiency induced risk-taking behavior, impaired spatial learning and memory, and caused new object recognition deficits without affecting sociability. Moreover, marginal zinc deficiency critically disrupted hippocampal and cortical development, and aberrant neuronal arrangement. The expression levels of BDNF for both form states were not statistically significant upregulation in marginal zinc deficiency mice compared to controls, along with significantly increased TrkB expression. These findings suggested that adolescent marginal zinc deficiency increased the expression of BDNF and TrkB, as well as abnormal hippocampal and cortical development. These alterations may explain the observed abnormal behavior, including risk-taking behavior, impaired spatial learning and memory, and new object recognition decay.

2025-07-01·Brain, Behavior, and Immunity

Chronic stress leads to earlier cognitive decline in an Alzheimer’s mouse model: The role of neuroinflammation and TrkB

Article

作者: Rivkin-Natan, Maria ; David, Dekel ; Frenkel, Dan ; Bentulila, Ziv ; Doron, Ravid ; Shlomi-Loubaton, Shir ; Franko, Motty ; Nitzan, Keren ; Sabbah, Salomé ; Toledano, Roni

While most Alzheimer's disease (AD) studies focus on the cognitive aspects of the disease, less focus is given to affective symptoms. In this study, we investigated the long-term consequences of exposure to chronic stress. 5xFAD AD model mice were exposed to unpredictable chronic mild stress, and cognitive and emotional aspects were examined at 3-time points (up to 4 months after exposure to stress). We found that exposure to chronic stress accelerates neuropathology outcomes in the 5xFAD mouse model in adulthood, accompanied by changes in the neurotrophic system. Specifically, we found that chronic stress accelerated the appearance of short-term spatial memory deficits in the 5xFAD mice and decreased tyrosine kinase B full receptor (TrkB.FL) expression levels. In vitro, we showed that corticosterone impairs the ability of microglia to uptake Aβ and reduces microglial activation. To conclude, our study may shed light on the mechanisms through which mild chronic stress might contribute to the onset and progression of Alzheimer's disease symptoms.

143

项与 TrkB 相关的新闻（医药）

2025-04-24

·肿瘤界

JCO | 周彩存教授团队证实他雷替尼在ROS1阳性非小细胞肺癌中的疗效与安全性

点击蓝字关注我们2025年4月3日，同济大学医学院、附属东方医院、肺科医院周彩存教授团队在Journal of Clinical Oncology上发表题为“Taletrectinib in ROS1+ Non–Small Cell Lung Cancer: TRUST”的研究。该研究报告了他雷替尼（taletrectinib）在ROS1融合阳性非小细胞肺癌（NSCLC）注册研究中的整合疗效与安全性数据。结果显示，他雷替尼在ROS1阳性NSCLC患者中展现出令人鼓舞的疗效和良好的安全性，且在克服现有ROS1酪氨酸激酶抑制剂（TKI）的耐药性和神经系统毒性方面表现突出。此次分析证实，TRUST-I试验中观察到的他雷替尼的疗效与安全性可推广至全球ROS1阳性NSCLC人群。c-ros原癌基因1酪氨酸激酶（ROS1）基因融合于2007年首次报道，属于致癌分子改变，可导致ROS1激酶结构域持续激活，驱动下游信号传导异常及细胞分化、增殖和存活失调。ROS1融合是罕见遗传事件，在包括NSCLC在内的多种实体瘤中均有报道，其在NSCLC中的发生率约为0.9%-2.6%。ROS1融合阳性（ROS1+）NSCLC患者通常具有独特的临床特征，多为女性、较无驱动基因突变患者更年轻、确诊时多为晚期（III-IV期），组织学以腺癌为主，且多数无吸烟史。约1/3的ROS1+ NSCLC患者在确诊时已存在脑转移，经治患者的脑转移率可高达50%。ROS1酪氨酸激酶抑制剂（TKI）的出现显著改善了ROS1+ NSCLC患者的临床结局，然而接受第一代TKIs治疗的患者仍会因脱靶旁路激活导致疾病进展，进而发展为难治性肿瘤、出现靶点依赖性-获得性耐药突变（如G2032R）或脑转移。目前FDA批准了3种用于ROS1+ NSCLC的TKI：克唑替尼（crizotinib）、恩曲替尼（entrectinib）和瑞普替尼（repotrectinib）。尽管一线克唑替尼的客观缓解率（ORR）和中位无进展生存期（PFS）较化疗（CT）更优，但近50%的ROS1+ NSCLC患者会发生中枢神经系统（CNS）转移。恩曲替尼虽可通过血脑屏障，但对既往CNS进展患者的整体缓解有限（颅内[IC]ORR=11%），且对克唑替尼治疗后最常见的获得性耐药突变G2032R（发生率为30%-40%）无效。瑞普替尼虽对G2032R和脑转移有效，但多数患者会出现高发且广泛的神经系统不良事件（AE）。目前另一种新一代ROS1-TKI zidesamtinib正在ROS1+实体瘤（包括NSCLC）中开展评估。因此，ROS1+ NSCLC患者仍亟需兼具强效全身与颅内缓解、延长疾病控制、克服靶点依赖性-获得性耐药且神经系统毒性可控的治疗方案。他雷替尼（taletrectinib）是一种口服、具有CNS活性的新一代ROS1-TKI。他雷替尼对ROS1的选择性是对TrKB的11-20倍，这种高选择抑制性表明他雷替尼可能降低神经系统AE的发生率、严重程度及类型。基于美国和日本的I期试验及TRUST-I研究的安全性导入期数据，确定其推荐II期剂量为600 mg每日一次。群体药代动力学（PK）分析集显示，他雷替尼在美日人群中的PK特征相似。为增加样本量以更可靠的评估疗效，并验证TRUST-I中观察到的疗效和安全性结果是否适用于全球ROS1+ NSCLC患者群体，本研究对关键II期区域性TRUST-I试验（NCT04395677）和全球性TRUST-II试验（NCT04919811）的注册队列进行整合分析。分析集本研究的疗效分析集来自TRUST-I和TRUST-II试验关键研究队列的疗效可评估ROS1+ NSCLC患者（n=273）。安全性分析集则纳入了所有接受口服他雷替尼（600 mg/日）治疗的352例患者。研究的主要终点是经独立评审委员会确认的客观缓解率（cORR），次要终点包括颅内客观缓解率（IC-ORR）、无进展生存期（PFS）、缓解持续时间（DOR）和安全性。研究结果（数据截至2024年6月7日）：疗效分析集（n=273）：TKI初治组（n=160）：cORR=88.8%，IC-cORR=76.5%；中位DOR为44.2个月，中位PFS为45.6个月。TKI经治组（n=113）：cORR=55.8%，IC-cORR=65.6%；中位DOR为16.6个月，中位PFS为9.7个月。G2032R突变亚组：cORR=61.5%（8/13）。安全性分析集（n=352）：最常见治疗相关不良事件（TEAE）为胃肠道事件（88%）、天冬氨酸转氨酶（AST）升高（72%）和丙氨酸转氨酶（ALT）升高（68%），多为1级。神经系统TEAE发生率低（头晕21%，味觉异常15%），且多为1级。TEAE致停药率仅6.5%。研究结论：在TRUST-I和TRUST-II的整合分析中，他雷替尼在TKI初治和TKI经治患者中均展现出高且持久的整体及颅内缓解率、延长PFS，并对G2032R获得性耐药突变有效。该整合分析进一步验证了TRUST-I试验中他雷替尼的疗效和安全性特征，并确认其结果可推广至全球ROS1+ NSCLC患者群体。长期生存的额外随访仍在进行中。此外，在另一项针对局部晚期或转移性ROS1+ NSCLC初治患者的III期随机试验（NCT06564324）中，他雷替尼的安全性和疗效将与克唑替尼进行直接对比。声明：本文由“肿瘤界”整理与汇编，欢迎分享转载，如需使用本文内容，请务必注明出处。编辑：lagertha审核：南星

临床结果放射疗法临床研究CSCO会议申请上市

2025-04-11

·PMLiVE

Bayer’s Vitrakvi receives full FDA approval for NTRK gene fusion-positive tumours

Bayer’s Vitrakvi (larotrectinib) has been granted traditional approval by the US Food and Drug Administration (FDA) to treat neurotrophic receptor tyrosine kinase (NTRK) gene fusion-positive solid tumours. The TRK inhibitor is now fully authorised for use in adult and paediatric patients with solid tumours that do not have a known acquired resistance mutation, are metastatic or where surgical resection is likely to result in severe morbidity, and have no satisfactory alternative treatments or have progressed following treatment. The FDA first approved Vitrakvi in 2018 under its accelerated approval pathway, under which the US regulator may approve therapies for serious diseases like cancer earlier, on the condition that companies conduct studies to confirm the anticipated clinical benefit. Tumours with NTRK gene fusion produce an altered TRK protein, which causes the uncontrolled growth of cancer cells. Vitrakvi is designed to block the action of this protein to prevent the excessive growth of cancer cells and slow the worsening of the disease. TRK fusion cancer can occur in any part of the body, including the lungs, thyroid, colon, pancreas and salivary glands. Commenting on the authorisation, Andrea Ferris, president and chief executive officer of the non-profit lung cancer foundation LUNGevity, said: “The full approval of Vitrakvi by the FDA is a welcome step forward, solidifying its place as a treatment option for patients with NTRK gene fusion-positive cancers. “This milestone not only benefits patients today but also paves the way for further advancements in NTRK gene therapies in the future.” The FDA’s latest decision on Vitrakvi was supported by positive data from three open-label trials, which included adult and paediatric patients with unresectable or metastatic solid tumours with an NTRK gene fusion. Pooled efficacy results demonstrated an overall response rate of 60%, a complete response rate of 24% and a partial response rate of 36% for Vitrakvi-treated patients, as well as median duration of response of 43.3 months. Chandra Goda, executive director, US Vitrakvi brand lead, said: “This first full approval of an NTRK inhibitor by the FDA represents the culmination of research and dedication by the Bayer team.”

上市批准加速审批

2025-04-02

·今日头条

疾病控制率高达100%！国研“泛癌种”新药ICP-723申报上市！

100%肿瘤患者接受“泛癌种”新药治疗后肿瘤不同程度缩小或控制稳定，超过 60% 患者肿瘤显著缩小30%以上，国研新一代“不限癌种”靶向药ICP-723成为NTRK阳性肿瘤患者抗癌新希望！肿瘤靶向药物的成功研发正在不断创造更多的生存奇迹，研究人员发现首个不区分癌种的可用药基因--NTRK，一种导致多种成人和儿童恶性癌症发生的致癌基因，成为全球最火的抗癌靶点之一。针对这一靶点已上市的两款靶向药物拉罗替尼和恩曲替尼因临床数据卓越，每年可以帮助成千上万的人，很多NTRK融合癌症患者接受治疗后重新回到了正常生活，这两款药物也在国内病友们的期待中在中国获批上市。相关阅读：治疗8周肿瘤完全消退！260万的天价抗癌药可治疗25类癌症，国内已有患者用药然而耐药问题是所有正在接受靶向治疗的患者无法避免的生存挑战。好消息是新一代靶向药物的出现已经让众多面临绝境的耐药患者成功续命！近期，国研第二代小分子泛 TRK 抑制剂 Zurletrectinib 2期注册试验已在中国成功完成，并已于2025年3月底提交NDA上市申请。旨在治疗 NTRK基因融合阳性的癌症患者，无论患者是否首次接受TRK抑制剂治疗或已对第一代TRK抑制剂产生耐药性，且不限制癌症类型。疾病控制率高达100%！国研新一代“泛癌种”新药ICP-723让多名肿瘤患者奇迹缓解 Zurletrectinib（ICP-723）是我国自主研发的新一代 “超级” 泛TRK抑制剂，与美国研发的两款第二代NTRK抑制剂相比，ICP-723不仅能够有效抑制 TRKA、TRKB、TRKC，而且能够有效抑制 TRKA的耐药性突变G595R和 G667C等，可以克服第一代 TRK抑制剂的获得性耐药。 ICP-723可以治疗携带NTRK融合基因的晚期或转移性实体瘤，包括乳腺癌、结直肠癌、肺癌、甲状腺癌等，以及对第一代NTRK抑制剂拉罗替尼和恩曲替尼耐药的患者。 2021年8 月 31 日InnoCare Pharma公司宣布其第二代泛 TRK 抑制剂 ICP-723 获得美国食品药品监督管理局（FDA）的研究性新药批准在美国开始 I 期临床试验。在2022年的ASCO大会上，我们首次看到了这款国研药物的初步临床数据，非常振奋人心！多名接受治疗的患者不仅病情得到了稳定，甚至出现了肿瘤明显缩小的喜人情况。在这项 I 期剂量递增研究中，截止到2022年2月11日，共有17 名患者接受 ICP-723 治疗，剂量为 1 mg QD 至 8 mg QD，其中6名为NTRK融合阳性的患者。结果显示： 6例NTRK融合患者中，总客观缓解率（ORR，靶病灶缩小30%以上）为66.7%（4例），疾病控制率（DCR）高达100%，这意味着6例NTRK融合阳性的患者在接受ICP-723治疗后，病情都得到了有效控制，病灶稳定或显著缩小。值得一提的是，1名脑转移的患者也达到了部分缓解，脑部靶病灶从 10 毫米缩小到 3 毫米。所有获得部分缓解的患者在 4 周治疗后的第一次肿瘤评估时均对 ICP-723 做出反应，并且所有达到部分缓解的患者在数据截止时仍持续响应。根据上述初步研究数据表明，ICP-723在晚期实体瘤患者中安全且耐受性良好。各种癌症类型的NTRK基因融合的患者出现了得到了令人鼓舞的临床疗效，包括入脑活性。目前，无论年龄大小（2-75周岁），无论肿瘤部位，无论什么类型的恶性癌症，只要存在特定的NTRK融合基因，就有机会参加ICP-723在国内开展的临床，接受新药治疗。国内已有多名患者入组成功接收治疗并得到奇迹缓解！以下病历来自中山大学肿瘤防治中心儿童肿瘤科公众号分享： 01 涎腺癌缩小50%以上 12岁的花季少年因为左耳垂下肿胀1年去医院进行检查，结果确诊为涎腺源性肿瘤，并且因为肿瘤巨大（52*41*62mm），差不多和橙子一样，累及左侧下颌骨，无法手术，于是在2022-10-24入组新一代NTRK抑制剂ICP-723在实体肿瘤患者中的安全性、耐受性、药代动力学的多中心、非随机、开放性Ⅰ/Ⅱ期临床试验。2022-10-25 开始接受ICP-723治疗后，奇迹出现，仅3天，肿瘤显著缩小，15天后的照片对比能看到肿瘤持续消退。截至2023年7月，肿瘤已经缩小一半以上（20*14*25mm），并且仍在持续治疗中。 02 恶性梭形细胞瘤11周缩小51.9% 15岁的恶性梭形细胞肿瘤患者在接受了左侧腹股沟肿物切除后复发，化疗后病情进展。幸运的是基因检测发现 TPM3-NTRK1融合阳性，在接受8mg ICP-723治疗后一个周期，经影像学评估，首次肿瘤疗效评估即达到部分缓解（PR），靶病灶缩小37%，接受第11周期的治疗时靶病灶已缩小51.9%, 疗效进一步维持。 03 1代NTRK抑制剂耐药，ICP-723治疗后肿瘤显著缩小一位软组织恶性梭形细胞肿瘤伴肺部转移的患者，基因检测显示ETV6-NTRK3融合，接受化疗和9个周期的第一代TRK抑制剂后出现疾病进展。在国内接受5个周期ICP-723的治疗后，肺部非靶病灶明显缩小、右大腿靶病灶达到手术条件，右大腿病灶手术切除后病理提示已未见肿瘤组织。 04 宫颈癌肺及多发骨转移花季少年病灶缩小一位确诊为宫颈透明细胞癌伴肺部及多发骨转移的花季女孩，接受了子宫及双附件切除手术和放化疗后出现进展，接受ICP-723治疗仅1周期部转移灶较基线缩小近20% 。喜讯！ICP-723临床研究启动，国内多家癌症中心招募成人及儿童患者！值得振奋的是，目前在中国，ICP-723的临床试验目前正在招募患者，已经有大量NTRK阳性的患者通过全球肿瘤医生网成功入组。药品名称： ICP-723（Zurletrectinib）作用靶点： NTRK 研发公司： InnoCare Pharma公司适应症： NTRK融合阳性实体瘤（成人及儿童）招募信息（部分）： 1.经组织病理学证实手术不可切除的局部晚期或者转移性实体瘤或原发性中枢神经系统肿瘤，已知的治疗方式无效或复发的；标准治疗下仍发生进展、不耐受标准治疗或不存在标准治疗的患者； 2.经指定的中心实验室检测到携带NTRK基因融合； 3.既往未接受过其他TRK抑制剂规范治疗总之，Zurletrectinib作为一款新型、高效的抗癌药物，为NTRK融合阳性肿瘤患者带来了新的治疗选择。在某些罕见的肿瘤类型（例如先天性婴儿纤维肉瘤等）中，NTRK基因融合发生率高达 90% 。NTRK基因融合与至少 19种成人和儿童的肿瘤类型相关，包括肺癌、结直肠癌、乳腺癌、胰腺癌和胃癌等。 Zurletrectinib的出现，不仅为这些患者带来了希望之光，也让我们看到了人类在抗癌道路上的不断进步和突破。Zurletrectinib正在中国推进注册临床试验，预计今年年底提交新药上市申请。8毫克及以上剂量组，不同实体瘤NTRK基因融合阳性患者中，总缓解率（ORR）高达 80-90% 。让我们共同期待ICP-723在未来能够带来更多的惊喜和突破，为更多肿瘤患者带来治愈的可能。本文为全球肿瘤医生网原创，未经授权严禁转载

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