PRISM: PRecIsion in SCLC Via a Multicohort Study: Randomized Phase II Studies Evaluating Maintenance Durvalumab With or Without Biomarker-Directed Therapy for Extensive Stage Small Cell Lung Cancer (ES-SCLC)

This phase II trial tests how well biomarker tests on patients tumor tissue works in selecting personalized treatments for patients with extensive stage small cell lung cancer (ES-SCLC). Biomarker tests look for certain features in cancer cells that may give doctors more information about what is driving cancer and how to treat it. Based on the biomarker test results, study doctors can determine the subtype of ES-SCLC that study treatments can target. This study also tests different types of maintenance treatment for ES-SCLC with drugs durvalumab, saruparib, ceralasertib or monalizumab. Maintenance treatment is given after initial treatment and is given to help keep the cancer under control and prevent it from getting worse. Immunotherapy with monoclonal antibodies, such as durvalumab and monalizumab, may help the body's immune system attack the cancer, and may interfere with the ability of tumor cells to grow and spread. Saruparib is a PARP inhibitor. PARP is a protein that helps repair damaged deoxyribonucleic acid (DNA). Blocking PARP may prevent cancer cells from repairing their damaged DNA, causing them to die. PARP inhibitors are a type of targeted therapy. Ceralasertib may stop the growth of tumor cells and may kill them by blocking some of the enzymes needed for tumor cell growth. Giving biomarker selected personalized maintenance treatment with durvalumab, saruparib, ceralasertib or monalizumab may work better in treating patients with ES-SCLC.

开始日期2025-09-08

申办/合作机构

SWOG

[+1]

NCT06732401

/ Not yet recruiting临床3期IIT

A Randomized Phase III Trial of Checkpoint Blockade in Lung Cancer Patients in the Adjuvant Setting Based on Pathologic Response Following Neoadjuvant Therapy (CLEAR)

This phase III trial compares the effect of adding AZD6738 to durvalumab versus durvalumab alone to increase time without cancer in patients with non-small cell lung cancer, following treatment with chemotherapy and surgery. AZD6738 may stop the growth of tumor cells and may kill them 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. A monoclonal antibody is a type of protein that can bind to certain targets in the body, such as molecules that cause the body to make an immune response (antigens). Adding AZD6738 to durvalumab may increase time without cancer in patients with non-small cell lung cancer, following treatment with chemotherapy and surgery.

开始日期2025-06-13

申办/合作机构

National Cancer Institute

NCT06929260

/ Not yet recruiting临床1期

A Phase I, Open-label, Fixed-sequence Study to Evaluate the Effect of Ceralasertib on Pharmacokinetics of Drug X, Drug Y and Drug Z in Participants With Advanced Solid Tumours

The study aims to assess the effect of ceralasertib on the pharmacokinetics (PK) of Drug X, Drug Y and Drug Z in participants with advanced solid tumours.

开始日期2025-04-22

申办/合作机构

AstraZeneca PLC

[+1]

100 项与 Ceralasertib 相关的临床结果

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100 项与 Ceralasertib 相关的转化医学

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100 项与 Ceralasertib 相关的专利（医药）

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260

项与 Ceralasertib 相关的文献（医药）

2025-04-01·JOURNAL OF THEORETICAL BIOLOGY

Simulations probe the role of space in the interplay between drug-sensitive and drug-resistant cancer cells

Article

作者: Pugh, Kira ; Powathil, Gibin ; Jones, Rhys D O ; Hamis, Sara

The interplay between drug-sensitive and drug-resistant cancer cells has been observed to impact cell-to-cell interactions in experimental settings. However, the role that space plays in these interactions remains unclear. In this study, we develop mathematical models to investigate how spatial factors affect cell-to-cell competition between drug-sensitive and drug-resistant cancer cells in silico. We develop two baseline models to study cells from the epithelial FaDu cell line subjected to two drugs, specifically the ATR inhibitor ceralasertib and the PARP inhibitor olaparib, that target DNA damage response pathways. Our baseline models are: (1) a temporally resolved ordinary differential equation (ODE) model, and (2) a spatio-temporally resolved agent-based model (ABM). The models simulate cells in well-mixed and spatially structured cell systems, respectively. The ODE model is calibrated against in vitro data and is thereafter mapped onto the baseline ABM which, in turn, is extended to enable a simulation-based investigation on how spatial factors impact cell-to-cell competition. Simulation results from the extended ABMs demonstrate that the in silico treatment responses are simultaneously affected by: (i) the initial spatial cell configurations, (ii) the initial fraction of drug-resistant cells, (iii) the drugs to which cells express resistance, (iv) drug combinations, (v) drug doses, and (vi) the doubling time of drug-resistant cells compared to the doubling time of drug-sensitive cells. These results reveal that spatial structures of the simulated cancer cells affect both cell-to-cell interactions, and the impact that these interactions have on the ensuing population dynamics. This leads us to suggest that the role that space plays in cell-to-cell interactions should be further investigated and quantified in experimental settings.

2025-03-13·JOURNAL OF MEDICINAL CHEMISTRY

Discovery of the Clinical Candidate YY2201 as a Highly Potent and Selective ATR Inhibitor

Article

作者: Chen, Xiaofang ; Liu, Wenjin ; Yang, Jingxin ; Ye, Xin ; Fan, Tianyun ; Li, Chang ; Hou, Huimin ; Wang, Haoran ; Wu, Meng ; Weng, Yali ; Zheng, Xiao

ATR is one of the key DNA damage response (DDR) regulatory factors to maintain genome stability. ATR inhibition induces DNA damage accumulation and apoptosis in DDR kinase mutation or deficiency cancer cells through synthetic lethality, making it a promising target for treatment of cancers with DDR defects. Herein, we describe the discovery and preclinical evaluation of YY2201, a highly potent and selective novel ATR inhibitor, with favorable ADME, safety pharmacology, and pharmacokinetics profiles. YY2201 efficiently inhibits tumor progression in broad-spectrum cancer types, both in vitro and in vivo. YY2201 shows superior in vivo anticancer efficacy and a better therapeutic index compared to AZD6738 in a lung cancer xenograft model. YY2201 also exhibits potent cancer suppression effects in combination with chemotherapy in vivo. Currently, the investigational new drug application of YY2201 has been approved by the FDA for further clinical investigation.

2025-02-01·BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

Molecular mechanisms restoring olaparib efficacy through ATR/CHK1 pathway inhibition in olaparib-resistant BRCA1/2MUT ovarian cancer models

Article

作者: Mikula, Michał ; Statkiewicz, Małgorzata ; Gajek, Arkadiusz ; Rusetska, Natalia ; Szymczak-Pajor, Izabela ; Biegała, Łukasz ; Rogalska, Aneta ; Marczak, Agnieszka ; Śliwińska, Agnieszka

Resistance to olaparib inevitably develops in ovarian cancer (OC) patients, highlighting the necessity for effective strategies to improve its efficacy. Here, we established a novel olaparib-resistant patient-derived xenograft model of high-grade serous OC with BRCA1/2 mutations and examined the molecular characteristics of acquired resistance and resensitization to olaparib in treatment-naïve tumors in vivo. Olaparib-resistant xenografts were treated with olaparib, ATR inhibitor (ATRi, ceralasertib), CHK1 inhibitor (CHK1i, MK-8776) or their combinations. Proliferation, apoptosis, ATR/CHK1 activity, PARP signaling, DNA damage response (DDR), epithelial-to-mesenchymal transition (EMT), and MDR1 expression, were examined via RT-qPCR, western blot, and immunohistochemistry. Resistant tumors exhibited defects in PARP and ATR/CHK1 signaling, accompanied by altered expression of proteins involved in DDR and EMT. Olaparib rechallenge combined with ATR/CHK1 inhibitors showed promising synergistic effects on tumor growth inhibition. Mechanistically, combined treatments suppressed tumor proliferation without increasing apoptosis or necrosis, while inducing tumor cell vacuolization indicative of cell death. ATRi combined with olaparib induced or augmented downregulation of ATR, CHK1, PARP1, PARG, BRCA1, γH2AX, and PARylated protein expression, while reversing olaparib-induced upregulation of vimentin, BRCA2, and 53BP1. Our collective findings indicate that ATR/CHK1 pathway inhibition restores the olaparib efficacy in resistant BRCA1/2^MUT high-grade serous OC, highlighting promising approach for olaparib rechallenge of non-responsive patients. Uncovered mechanisms might improve our understanding of acquisition and overcoming resistance to olaparib in ovarian cancer.

项与 Ceralasertib 相关的新闻（医药）

2025-04-14

·学术经纬

双管齐下，击杀“癌王”！新研究找到了攻击胰腺癌的关键弱点

▎药明康德内容团队编辑编者按：胰腺癌，因其发展迅速和治疗难度极大被称为"癌症之王"。据相关研究数据统计，胰腺癌患者的5年生存率不足10%，是预后最差的恶性肿瘤之一。预计到2030年，胰腺癌将成为仅次于肺癌的第二大癌症死亡原因。目前，化疗仍是胰腺癌的主要治疗手段，但其效果较为有限。因此，开发新的治疗策略对于改善胰腺癌患者的预后至关重要。近期，一项发表在Cell & Bioscience期刊的论文发现，通过靶向TOPBP1相关信号通路，可以显著增强胰腺癌细胞对抗癌药物PARP抑制剂——奥拉帕尼（olaparib）的敏感性，诱导癌细胞的凋亡。同时，TOPBP1有望成为一种生物标志物，用于判断和筛选受益于PARP抑制剂治疗的患者群体，实现更精准的胰腺癌治疗。药明康德为研究团队提供了模拟肿瘤在体内生长的模型，赋能后续的分析验证，从而助力科学家开发胰腺癌的创新疗法。DNA损伤修复（DDR）途径在胰腺癌的发生和发展中起着关键作用。正常细胞在受到DNA损伤时，会启动一系列修复机制，以维持基因组的稳定。然而，胰腺癌细胞的DDR途径常常发生异常并促进肿瘤的发生。TOPBP1是DDR途径中的一个重要蛋白，它参与了DNA复制、DNA损伤修复和细胞周期检查点等多个细胞过程。来自上海交通大学医学院附属瑞金医院、南通大学附属肿瘤医院、南京医科大学附属泰州人民医院的联合研究团队通过对179例胰腺癌患者的临床数据分析，发现了一个令人意外的现象：TOPBP1在胰腺癌组织中的表达水平显著高于正常组织，而且表达量越高，患者的预后越差。同时，TOPBP1的高表达与肿瘤的恶性程度呈正相关。他们发现，TOPBP1表达不同的胰腺癌细胞系对奥拉帕尼的敏感度具有差异，TOPBP1表达高的细胞系对药物的敏感度更低。当研究人员用基因编辑技术降低TOPBP1表达后，癌细胞对奥拉帕尼的敏感性几乎翻倍。分析结果显示，TOPBP1高表达的癌细胞更依赖DNA损伤修复相关的ATR通路来恢复。当TOPBP1被抑制时，ATR通路会发生"瘫痪"，迫使癌细胞转而依赖另一条修复路径——ATM通路。而奥拉帕尼的作用就是制造DNA损伤，当ATM通路不堪重负时，癌细胞就会因无法修复DNA损伤而走向死亡。▲研究指出，TOPBP1是预测奥拉帕尼和AZD6738联合疗法治疗胰腺导管腺癌疗效的潜在生物标志物（图片来源：参考资料[1]）这一发现不仅解释了TOPBP1的作用机制，更提供了一个绝佳的治疗思路：如果能同时抑制ATR通路和PARP，就能对TOPBP1高表达的癌细胞造成致命打击！随后，研究团队获取了胰腺导管腺癌患者的肿瘤组织，药明康德为团队建立了用于后续分析验证的模型，用于模拟肿瘤在体内的生长和反应。研究团队测试了奥拉帕尼与ATR抑制剂AZD6738联用的效果，结果发现原代细胞0037细胞系对奥拉帕尼和AZD6738联合治疗的敏感性较高。这类细胞TOPBP1的表达水平较高，因此提升了其对联合治疗的敏感性。这种超协同效应的产生源于癌细胞DNA修复系统的"双路封锁"：AZD6738抑制ATR通路，使癌细胞丧失主要的DNA损伤修复能力；奥拉帕尼持续制造DNA损伤，迫使癌细胞依赖已受损的ATM通路，最终引起细胞凋亡。这些结果表明， TOPBP1有望成为一种新的生物标志物，帮助医生更精准地筛选可能受益于PARP抑制剂治疗的患者群体。此外，研究也提出了一种创新的联合治疗方案，有望让更多胰腺癌患者从PARP抑制剂治疗中获益。参考资料：[1] Tang, Xiao-Mei, et al. "TOPBP1 as a Potential Predictive Biomarker for Enhanced Combinatorial Efficacy of Olaparib and AZD6738 in PDAC." Cell & Bioscience, vol. 15, no. 17, 2025, doi:10.1186/s13578-025-01350-9本文来自药明康德内容微信团队，欢迎转发到朋友圈，谢绝转载到其他平台。如有开设白名单需求，请在“学术经纬”公众号主页回复“转载”获取转载须知。其他合作需求，请联系wuxi_media@wuxiapptec.com。免责声明：药明康德内容团队专注介绍全球生物医药健康研究进展。本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。更多推荐点个“在看”再走吧~

临床结果临床1期临床2期

2025-03-12

·今日头条

免疫疗法无果后，TIL细胞逆风翻盘，助患者肿瘤大幅消退

据外媒报道，一位42岁女性患者在接受肿瘤浸润淋巴细胞（TIL）治疗后，取得显著效果。该患者患有4期结膜黑色素瘤，多年来一直饱受疾病折磨。此前还遭受过严重的毒性作用。能够采用TIL疗法并看到她状况良好，实在令人欣慰。肿瘤内科医生Lucy Kennedy医学博士表示：“患者恢复得非常好，PET扫描清晰显示，治疗后患者的肿瘤正显著缩小。随着TIL持续发挥作用，不断搜寻并消灭癌细胞，预计治疗效果还会随时间推移而进一步提升”！一、免疫疗法失败后，一位黑色素瘤患者在TIL疗法助力下的重生 2014年，这位患者被诊断出患有结膜黑色素瘤，由于复发风险较高，最初的治疗方案是切除眼部结缔组织中的肿块。2020年，病情复发，随后两年她接受了免疫治疗药物伊匹单抗和纳武单抗的治疗。然而，病情不仅没有得到有效控制，反而持续恶化，患者还出现了严重的不良反应，包括严重的结肠炎，需要服用四种药物才能控制。她多次住院，其中一次还出现了类似贝尔氏麻痹症的神经系统变化，被认为与免疫疗法有关。与此同时，黑色素瘤还转移到了她腹部的淋巴结。好在天无绝人之路，2024年2月16日，恰逢全球首款上市的TIL疗法——Lifileucel（LN-144，Amtagvi®）获美国食品和药物管理局（FDA）批准，用于对免疫疗法（如PD-1抗体）无反应的不可切除或转移性黑色素瘤成人患者。该患者的临床团队将其病例提交至黑色素瘤委员会。虽然TIL疗法对黑色素瘤负担重或体力差的患者颇具挑战。但该患者较为年轻，无其他合并症，体能状态良好，且肿瘤相对较小，种种因素使其成为TIL疗法的理想人选。最终经评估，所有成员一致判定患者适合TIL疗法。随后，病例又被提交给骨髓移植委员会，确认患者符合接受这一新疗法的全部临床标准。该患者遂入组接受TIL细胞治疗，并最终在2024年8月完成了TIL输注，主要治疗过程如下： 1）首先，外科医生切除肿瘤，并将1-4厘米的肿瘤切片送到实验室； 2）接着，来自肿瘤的TIL细胞在实验室中进行扩增，并悬浮在静脉注射袋中，以便重新输入患者体内； 3）与此同时，患者入院接受3天的淋巴细胞清除化疗（氟达拉滨和环磷酰胺），以清除其免疫系统，使其能够接受TIL细胞治疗； 4）最后，患者接受一次性输注自身的TIL细胞，同时还接受IL-2输注，以激活TIL并刺激其增殖。一旦TIL细胞注入患者体内，它们就会主动寻找并摧毁患者的癌细胞（详见下图）。 ▼TIL细胞疗法的治疗过程示例图 ▲图源“ASCO daily news”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除结果显示：患者治疗反应良好，未出现严重副作用，两周后便出院回家，出院时她感觉良好，并期待着不久后重返工作岗位。自那时起，两组PET扫描清晰地显示：治疗后肿瘤正在显著缩小（详见下图）。 ▼该患者治疗前后的PET扫描 ▲图源“Cleveland Clinic”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除医学博士James Isaacs表示：“T细胞疗法是一种令人兴奋的新选择，为我们持续探索创新疗法带来了巨大希望。尽管免疫疗法对某些类型的黑色素瘤效果显著且具有长期持久性，但近半数患者对其并无反应，而其他传统疗法又存在严重副作用。在这样的情况下，TIL疗法正逐渐成为这部分患者的重要选择之一”。二、GT316 TIL首次人体试验成绩亮眼，一例患者完全缓解持续8个月 GT316是一种CRISPR/Cas9-dualKO抗衰竭TIL产品，近期已启动首次人体试验（NCT06145802），旨在评估其在晚期实体瘤中的初步安全性与有效性。这项开创性研究主要招募晚期难治性实体瘤患者，特别是妇科肿瘤患者。截至2024年1月22日，剂量递增研究共招募了4名女性患者，中位年龄58岁，她们此前均接受过1~9线的全身治疗。输注的TIL细胞数中位数为1.0E+10。入选患者先接受非清髓性（NMA）淋巴细胞清除方案预处理，再输注GT316 TIL产品进行治疗，随后接受IL-2给药。研究结果颇为亮眼：一名历经9项全身疗法的卵巢癌患者，在治疗4周后确认达到部分缓解（PR），截至目前，缓解持续时间已达22周（依据RECIST 1.1标准）。另一位卵巢癌患者病情稳定（SD）（详见下图）。 ▲图源“ASCO”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除尤其值得关注的是，一位患有难治性宫颈癌的患者，在GT316 TIL细胞治疗4周后, 出现确认的完全缓解（CR）。该患者阴道内残留的转移性病灶，基线（治疗前）测量为24mm ，在第38周时经放射影像显示，病灶已100%缩小（详见下图）。更为惊喜的是，截至目前，该患者缓解持续时间已有32周（即8个月，RECIST 1.1）。 ▲图源“ASCO”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除综上所述，首次人体研究表明，GT316作为晚期实体癌患者的单一疗法，耐受性良好，初步抗肿瘤效果令人振奋。三、TIL疗法+检查点抑制剂强强联合痛击卵巢癌，患者肿瘤皆消退，靶病灶缩减8%-35% 全球肿瘤学期刊《Oncotarget》曾报道一项关于“应用体外扩增的T细胞（REP-TIL），联合检查点抑制剂治疗卵巢癌”的研究，其数据十分惊艳。在本次研究中，共纳入7例晚期铂类耐药性高级别浆液性卵巢癌患者。所有患者在进行肿瘤切除手术前，均接受了伊匹单抗治疗，且肿瘤采集和TIL体外扩增均获成功。具体情况为：1名患者（#6）因无法接受手术，进行了双肝活检（2mm）；4名患者通过腹腔镜手术切除腹膜内转移瘤；1名患者切除了肺转移瘤。在快速扩增方案（REP）实施前，中位扩增时间为25天（范围：18-42天）。研究结果显示：T细胞输注后不久，所有患者的肿瘤均出现消退，靶病灶大小减小8%-35%，中位无进展生存期（PFS）为86天。最佳总体肿瘤反应（BOR）方面，患者#1出现1例部分反应（PR），其余5例达到病情稳定（SD）。尤其值得注意的是，患者#2在治疗后近一年内，一直维持长期病情稳定（SD）状态。 ▲图源“Oncotarget”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除综上，体外扩增的T细胞（REP-TIL）治疗耐受性良好。与T细胞疗法（含预处理化疗）相关的毒性处于可控范围，符合预期。四、TIL疗法横扫卵巢癌、肠癌、胰腺癌，以62.5%疾病控制率力挽狂澜，1例患者生存期超4年全美排名第一的美国 MD 安德森癌症中心公布了一项关于 “TIL 疗法用于经各类治疗均无效的转移性癌症患者” 的临床试验数据，涉及8 例转移性结直肠癌（CRC）、5 例胰腺癌（PDAC）、3 例卵巢癌（OVCA），其结果十分振奋人心！研究结果显示：所有入组患者的疾病控制率（DCR）达到了62.5% （95%CI 35.4%-84.8%）。在TIL细胞治疗12周时，有 31.3%（5例）的患者病情处于稳定（SD）状态。 ▲图源“J Immunother Cancer”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除此外，各队列患者的中位总生存期（OS）长达18.86个月,中位无进展生存期（PFS）为2.53个月。 ▲图源“J Immunother Cancer”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除尤其值得关注的是，一位晚期胰腺癌患者接受 TIL 细胞治疗后，病情稳定长达17个月。随后，该患者又陆续接受了单药派姆单抗治疗+两种 1 期临床试验疗法（一种是 RAD51 抑制剂，另一种是针对体细胞 ARID1A 突变的药物 ——AZD6738）。令人惊喜的是，从接受 TIL 治疗起算，4 年后这位患者仍存活。 ▼该患者TIL细胞治疗前后的连续CT图像对比 ▲图源“J Immunother Cancer”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除注：连续CT图像显示：该患者靶肝病变尺寸减小。五、国研TILs疗法上市在即！ 2024年2月，全球首款TIL疗法产品Lifileuce1获批上市，定价高达51.5万美元。相比之下，我国TIL疗法的自主研发和临床试验取得了显著进展，为国内患者提供了更具可及性的治疗选择，国研TILs疗法和美国TIL疗法的区别如下： ▼国研TILs疗法和美国TIL疗法的区别六、小编寄语肿瘤浸润淋巴细胞（TIL）疗法自1988年首次应用于临床以来，已走过30余载的发展历程。相较于其他免疫细胞疗法，TIL疗法独具将患者自身肿瘤组织“变废为宝”的神奇功效，堪称实体瘤治疗领域当之无愧的抗癌黑科技。它既适用于早期癌症患者，可有效预防肿瘤的复发与转移；又能作为晚期患者的挽救性治疗手段，为癌症患者带来一线生机。然而，令人遗憾的是，以往许多患者在手术切除肿瘤组织后，通常仅会提取一小部分用于制作病理蜡块以进行病理诊断，而其余大部分肿瘤组织则会被当作医疗垃圾丢弃，这无疑致使患者体内潜藏的抗癌能力极强的肿瘤浸润淋巴细胞（TIL）被白白浪费。此外，值得关注的是，TILs 细胞数量会随着肿瘤的进展而逐渐减少，并且在术后接受辅助性治疗（如放疗、化疗）时，不仅癌细胞会受到杀伤，体内的免疫细胞也可能受到影响。因此，建议患者务必珍惜这或许仅有一次的宝贵抗癌机会。在术前应积极与主治医师进行沟通，尽可能地保留新鲜的肿瘤标本组织，并联系专业机构对 TIL 细胞进行分离和冻存，做到未雨绸缪。七、参考资料 [1]Guo J,et al.A first-in-human study of CRISPR/Cas9-engineered tumor infiltrating lymphocytes (TILs) product GT316 as monotherapy in advanced solid tumors[J]. 2024. https://meetings.asco.org/abstracts-presentations/233956/poster [2]Kverneland AH,et al.Adoptive cell therapy in combination with checkpoint inhibitors in ovarian cancer. Oncotarget. 2020 Jun 2;11(22):2092-2105. https://pmc-ncbi-nlm-nih-gov.libproxy1.nus.edu.sg/articles/PMC7275789/ [3]Amaria R,et al.Efficacy and safety of autologous tumor-infiltrating lymphocytes in recurrent or refractory ovarian cancer, colorectal cancer, and pancreatic ductal adenocarcinoma. J Immunother Cancer. 2024 Feb 2;12(2):e006822. https://pmc-ncbi-nlm-nih-gov.libproxy1.nus.edu.sg/articles/PMC10840042/ [4]https://consultqd.clevelandclinic.org/case-study-first-patient-at-cleveland-clinic-treated-with-tumor-infiltrating-lymphocyte-therapy [5]https://dailynews-ascopubs-org.libproxy1.nus.edu.sg/do/there-role-autologous-tumor-infiltrating-lymphocyte-therapy-gastrointestinal-cancers 本文为全球肿瘤医生网原创，未经授权禁止转载。

免疫疗法ASCO会议临床结果细胞疗法临床3期

2025-03-06

·PRNewswire

TEPMETKO Continues to Strengthens its Position as a Leading METex14 Skipping NSCLC Therapy | DelveInsight

With increasing biomarker-driven cancer treatments, TEPMETKO benefits from growing adoption in precision oncology. Competition from other MET inhibitors like TABRECTA (capmatinib) exists, but TEPMETKO's once-daily dosing and efficacy profile offer differentiation. LAS VEGAS, March 6, 2025 /PRNewswire/ -- DelveInsight's " TEPMETKO Market Size, Forecast, and Market Insight Report" highlights the details around TEPMETKO, a kinase inhibitor indicated for the treatment of adult patients with metastatic NSCLC harboring MET exon 14 skipping alterations. The report provides product descriptions, patent details, and competitor products (marketed and emerging therapies) of TEPMETKO. The report also highlights the historical and forecasted sales from 2020 to 2034 segmented into 7MM [the United States, the EU4 (Germany, France, Italy, and Spain), the United Kingdom, and Japan]. EMD Serono's TEPMETKO (tepotinib) Overview TEPMETKO is a kinase inhibitor prescribed for adult patients with metastatic non-small cell lung cancer (NSCLC) carrying MET exon 14 skipping alterations. The active component is Tepotinib (as hydrochloride monohydrate), administered orally. Patients should be cautioned about the heightened risk of severe or fatal interstitial lung disease/pneumonitis, liver toxicity, and potential embryo-fetal toxicity, necessitating effective contraception during and shortly after treatment. Tepotinib specifically targets MET, including variants with exon 14 skipping mutations. It blocks HGF-dependent and independent MET phosphorylation, disrupting MET-driven signaling pathways. Additionally, at clinically relevant concentrations, Tepotinib inhibits melatonin 2 and imidazoline 1 receptors. In vitro studies show that it suppresses tumor cell proliferation, anchorage-independent growth, and migration of MET-dependent cancer cells. In mouse models with MET-driven tumors, including those with MET exon 14 skipping alterations, Tepotinib reduced tumor growth, sustained MET phosphorylation inhibition, and, in one case, decreased metastasis formation. The recommended dose of TEPMETKO is 450 mg taken orally once daily until disease progression or intolerable toxicity occurs. Patients should take it at the same time each day, swallowing tablets whole without chewing, crushing, or splitting them. If a dose is missed and less than eight hours remain until the next scheduled dose, patients should skip it. In cases of vomiting after taking TEPMETKO, the next dose should be taken at the usual time. Learn more about TEPMETKO projected market size for NSCLC @ TEPMETKO Market Potential Non-small cell lung cancer (NSCLC) is the most common type of lung cancer, accounting for 81% of all diagnosed cases. Early detection greatly improves outcomes, but diagnosing NSCLC and other lung cancers is challenging because their symptoms are often mistaken for common illnesses or the long-term effects of smoking. Consequently, 80% of NSCLC cases are already at advanced stages by the time they are identified, making treatment more difficult. Around 80% of EGFR mutations in NSCLC involve either exon 19 deletions or the exon 21 L858R substitution, both of which are classified as sensitizing mutations. Until the last decade, chemotherapy was the primary treatment for advanced and metastatic lung cancer. However, this changed in 2015 with the approval of the first immune checkpoint inhibitor (ICI), KEYTRUDA (pembrolizumab), as a second-line therapy for advanced cases. This was followed by TECENTRIQ (atezolizumab) in 2016. Both therapies were later approved for first-line treatment, broadening their use to a larger patient population. In 2020, the combination of OPDIVO (nivolumab) and ipilimumab also received approval as a first-line treatment for metastatic NSCLC. According to DelveInsight, the NSCLC market size across the 7MM is projected to grow from USD 30 billion in 2024, with a substantial CAGR through 2034. This growth is largely driven by the introduction of emerging therapies during the forecast period (2025–2034). Discover more about the NSCLC market in detail @ Non-small Cell Lung Cancer Market Report Emerging Competitors of TEPMETKO The NSCLC pipeline is very robust with the promising therapies such as Telisotuzumab vedotin (AbbVie), Patritumab deruxtecan (Daiichi Sankyo/AstraZeneca), Datopotamab deruxtecan (Daiichi Sankyo/AstraZeneca), Eftilagimod alpha (Immutep), BNT311/GEN1046 (acasunlimab) (Genmab), V940 (mRNA-4157) + Pembrolizumab (Moderna Therapeutics/Merck), Plinabulin + Docetaxel (BeyondSpring), Olomorasib (LY3537982) (Eli Lilly and Company), Zipalertinib (Cullinan Oncology/Taiho Pharma), Ceralasertib (AZD6738) (AstraZeneca), TEDOPI (EP-2101; IDM 2101; OSE-2101) (OSE Immuno-therapeutics), Sigvotatug vedotin (PF08046047) (Pfizer), ANKTIVA (N-803) (ImmunityBio), Aumolertinib/Almonertinib/HS-10206 (Jiangsu Hansoh Pharmaceutical), Niraparib (GSK), Savolitinib (AstraZeneca/Hutchison MediPharma), TRODELVY (Gilead Sciences), Pyrotinib (Jiangsu HengRui Medicine), Ociperlimab (BGB-A1217) (BieGene), Volrustomig (AstraZeneca), Gotistobart (BNT316/ONC-392) (OncoC4/BioNTech), Ivonescimab (AK112/SMT112) (Akeso Biopharma/Summit Therapeutics), ZYNYZ (retifanlimab/INCMGA00012) (Incyte/Macrogenics), Divarasib (GDC-6036) (Roche/Genentech), Tiragolumab (RG6058) (Roche), Sacituzumab Tirumotecan (Merck and Kelun-Biotech), JEMPERLI (dostarlimab/TSR-042) (GSK and AnaptysBio), Zongertinib (BI-1810631) (Boehringer Ingelheim), BAY 2927088 (Bayer), Serplulimab (HLX10) (Shanghai Henlius Biotech), Rilvegostomig (AZD2936) (AstraZeneca), MK-1084 (Merck, Taiho Pharmaceutical, and Astex), Domvanalimab (Arcus Biosciences and Gilead Sciences), OPDUALAG (nivolumab and relatlimab) (Bristol-Myers Squibb), Belrestotug + JEMPERLI (iTeos Therapeutics and GSK), Firmonertinib (ArriVent BioPharma), Sunvozertinib (DZD9008) (Dizal Pharmaceutical), Cobolimab (GSK), Livmoniplimab (AbbVie), Fianlimab (REGN3767) (Regeneron Pharmaceuticals), BNT327/PM8002 (Biotheus/BioNTech), HS-20117 (Hansoh BioMedical), IO102-IO103 + Pembrolizumab (IO Biotech), Naptumomab estafenatox (NeoTX Therapeutics/Active Biotech), FF-10832 (FUJIFILM Corporation), BNT116 (BioNTechSE/Regeneron Pharmaceuticals), CAN-2409 (Candel Therapeutics), Mecbotamab Vedotin (BA3011/CAB-AXL-ADC) (BioAtla), Bemcentinib (BGB 324/BGB-3234/R-428) (BerGenBio/Rigel Pharmaceuticals), DOVBLERON (taletrectinib/AB-106/IBI-344) (Nuvation Bio/Innovent Biologics/Daiichi Sankyo/Nippon Kayaku), Lifileucel (Iovance Biotherapeutics), IBI363 (Innovent Biologics), Sotevtamab (AB-16B5) (Alethia Biotherapeutics), Avutometinib (VS6766) (Verastem Oncology), Vebreltinib (APL-101) (Apollomics), LP-300 (Lantern Pharma), JNJ-90301900 (Johnson & Johnson Innovative Medicine), AMG 193 (Amgen), Luveltamab tazevibulin (Sutro Biopharma), PRT3789 (Prelude Therapeutics), Disitamab vedotin (Seagen), PADCEV (enfortumab vedotin) (Astellas Pharma), RP1 (Replimune), TIVDAK (tisotumab vedotin) (Seagen), Zanidatamab (Jazz Pharmaceuticals), Utidelone injectable (UTD1) (Beijing Biostar Pharmaceuticals), REGN5093-M114 (Regeneron Pharmaceuticals), SLC-391 (SignalChem Lifesciences), fulzerasib (GenFleet), Davutamig (REGN5093) (Regeneron Pharmaceuticals), TAS3351 (Taiho Oncology), H002 (RedCloud Bio), JIN-A02 (J INTS BIO), FWD1509 (Forward Pharma), Sabestomig (AZD7789) (AstraZeneca), Sasanlimab (Pfizer), Selvigaltin (GB1211) (Galecto Biotech), Vepafestinib Helsinn (Healthcare/Taiho Pharmaceutical), EP0031 (A400/ KL590586) (Ellipses Pharma/Kelun-Biotech), Pamvatamig (MCLA-129) (Merus), Zidesamtinib (NVL-520) (Nuvalent), NVL-655 (Nuvalent), RMC-4630 (Revolution Medicines), REQORSA (quaratusugene ozeplasmid) (Genprex), PDC*lung01 (PDC*line Pharma), Evalstotug (BA3071) (BioAtla and BeiGene), PT-112 (Promontory Therapeutics), MRT-2359 (Monte Rosa Therapeutics), GAIA-102 (GAIA BioMedicine), Rigosertib (Traws Pharma), HMBD-001 (Hummingbird Bioscience), PLB1004 (Avistone Biotechnology), ANS03 (Avistone Biotechnology), MYTX-011 (Mythic Therapeutics), A166 (Sichuan Kelun-Biotech Bio-pharmaceutical), Atamparib (BN-2397) (Ribon Therapeutics), DELTACEL (KB-GDT-01) (Kiromic BioPharma), Carotuximab (ENV-105) (Kairos Pharma), YL202 (MediLink Therapeutics), and others. To know more about the number of competing drugs in development, visit @ TEPMETKO Market Positioning Compared to Other Drugs Key Milestones of TEPMETKO In February 2024, the FDA granted traditional approval to TEPMETKO for adult patients with metastatic NSCLC harboring MET exon 14 skipping alterations. In February 2022, the EC approved TEPMETKO as monotherapy for the treatment of adult patients with advanced NSCLC harboring alterations leading to METex14 skipping who require systemic therapy following prior treatment with immunotherapy and/or platinum-based chemotherapy. In February 2021, Merck announced that the US FDA has approved TEPMETKO following priority review for the treatment of adult patients with metastatic NSCLC harboring MET exon 14 skipping alterations. This indication was approved under accelerated approval based on ORR and DOR. In October 2020, TEPMETKO received ODD for treating NSCLC with MET genomic tumor aberrations In March 2020, EMD Serono (the biopharmaceutical business of Merck KGaA), announced that the MHLW approved TEPMETKO for the treatment of patients with unresectable, advanced, or recurrent NSCLC with METex14 skipping alterations. In September 2019, the US FDA granted BTD for tepotinib in patients with metastatic NSCLC harboring METex14 skipping alterations who progressed following platinum-based cancer therapy Discover how TEPMETKO is shaping the NSCLC treatment landscape @ TEPMETKO NSCLC TEPMETKO Market Dynamics TEPMETKO competes in a growing but highly specialized market where MET-targeted therapies are gaining traction due to their efficacy in addressing MET-altered tumors. The market for MET inhibitors is expanding as precision oncology advances and molecular diagnostics become more widely available, enabling better identification of patients who would benefit from targeted treatments like TEPMETKO. A key factor shaping TEPMETKO's market dynamics is competition. It directly competes with Novartis' TABRECTA (capmatinib), another MET inhibitor approved for the same indication. While TEPMETKO offers the advantage of once-daily dosing compared to TABRECTA's twice-daily regimen, both drugs have similar efficacy profiles, making physician and patient preference an important differentiator. Additionally, broader competition from next-generation MET inhibitors and combination therapies in clinical trials could impact TEPMETKO's long-term market position. Regulatory approvals and market access play a crucial role in TEPMETKO's adoption. The drug has been approved in multiple regions, including the U.S., Europe, and Japan, but reimbursement and pricing strategies vary by market. Payer policies, along with the cost-benefit analysis of MET inhibitors compared to other targeted therapies, influence prescription trends. Furthermore, real-world evidence and post-marketing studies will be critical in demonstrating TEPMETKO's sustained effectiveness and safety, which could support expanded indications and increased market penetration. Looking ahead, the MET inhibitor market is expected to grow with advances in biomarker-driven therapy, further refining patient selection. TEPMETKO's success will depend on continued clinical development, potential label expansions, and strategic partnerships to strengthen its competitive edge. As new entrants emerge, Merck KGaA's ability to differentiate TEPMETKO through combination strategies or enhanced formulations may determine its long-term sustainability in this evolving landscape. Dive deeper to get more insight into TEPMETKO's strengths & weaknesses relative to competitors @ TEPMETKO Market Drug Report Table of Contents Related Reports Non-small Cell Lung Cancer Market Non-small Cell Lung Cancer Market Insights, Epidemiology, and Market Forecast – 2034 report deliver an in-depth understanding of the disease, historical and forecasted epidemiology, as well as the market trends, market drivers, market barriers, and key NSCLC companies including Daiichi Sankyo, AstraZeneca, Gilead Sciences, BieGene, AbbVie, Roche, Merck, Novartis, Pfizer, Takeda Pharmaceuticals, Eli Lilly, BerGenBio, GlaxoSmithKline, Duality biologics, among others. Non-small Cell Lung Cancer Pipeline Non-small Cell Lung Cancer Pipeline Insight – 2025 report provides comprehensive insights about the pipeline landscape, pipeline drug profiles, including clinical and non-clinical stage products, and the key non-small cell lung cancer companies, including BridgeBio Pharma, Daiichi Sankyo, EMD Serono, Merck, BridgeBio Pharma, Abbvie, Pfizer, Eli Lilly and Company BioNTech SE, Shenzhen TargetRx, Taiho Pharmaceutical, Chong Kun Dang, Bristol Myers Squibb, Innovent Biologics, Xuanzhu Biopharmaceutical, Bayer, GeneScience Pharmaceuticals, InventisBio, Apollomics, Imugene, Ono Pharmaceutical, Pierre Fabre, Jiangsu Hengrui Medicine Co., Bristol-Myers Squibb, Surface Oncology, Inhibrx, Sinocelltech, Mirati Therapeutics, REVOLUTION Medicines, Yong Shun Technology Development, Iovance Biotherapeutics, Galecto Biotech, among others. C-MET Metastatic Non-small Cell Lung Cancer Market C-MET Metastatic Non-small Cell Lung Cancer Market Insights, Epidemiology, and Market Forecast – 2034 report deliver an in-depth understanding of the disease, historical and forecasted epidemiology, as well as the market trends, market drivers, market barriers, and key C-MET mNSCLC companies, including Novartis, Merck, EMD Serono, AbbVie, Regeneron Pharmaceuticals, Mythic Therapeutics, Apollomics, Johnson & Johnson Innovation, Haihe Biopharma, among others. C-MET Non-small Cell Lung Cancer Pipeline C-MET Non-small Cell Lung Cancer Pipeline Insight – 2025 report provides comprehensive insights about the pipeline landscape, pipeline drug profiles, including clinical and non-clinical stage products, and the key C-MET non-small cell lung cancer companies, including AbbVie, Janssen Research & Development, Beijing Pearl Biotechnology Limited Liability Company, Novartis, among others. About DelveInsight DelveInsight is a leading Business Consultant and Market Research firm focused exclusively on life sciences. It supports pharma companies by providing comprehensive end-to-end solutions to improve their performance. Get hassle-free access to all the healthcare and pharma market research reports through our subscription-based platform PharmDelve . Contact Us Shruti Thakur [email protected] +14699457679 Logo: SOURCE DelveInsight Business Research, LLP WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

上市批准免疫疗法优先审批

100 项与 Ceralasertib 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11787	-	-	DB14917

研发状态

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
非小细胞肺癌	临床3期	美国	阿斯利康全球研发（中国）有限公司	2023-05-18
非小细胞肺癌	临床3期	美国	阿斯利康制药有限公司	2023-05-18
非小细胞肺癌	临床3期	中国	阿斯利康全球研发（中国）有限公司	2023-05-18
非小细胞肺癌	临床3期	中国	阿斯利康制药有限公司	2023-05-18
非小细胞肺癌	临床3期	日本	阿斯利康全球研发（中国）有限公司	2023-05-18
非小细胞肺癌	临床3期	日本	阿斯利康制药有限公司	2023-05-18
非小细胞肺癌	临床3期	阿根廷	阿斯利康制药有限公司	2023-05-18
非小细胞肺癌	临床3期	阿根廷	阿斯利康全球研发（中国）有限公司	2023-05-18
非小细胞肺癌	临床3期	澳大利亚	阿斯利康全球研发（中国）有限公司	2023-05-18
非小细胞肺癌	临床3期	澳大利亚	阿斯利康制药有限公司	2023-05-18

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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


ASH2024	N/A	慢性粒单核细胞白血病 \| 骨髓增生异常综合征	-	Ceralasertib 160mg BID 7on/7off	顧鑰遞積淵觸積製顧製(觸艱壓醖鹽鏇淵鑰淵膚) = n=1, grade 3 or higher AEs with 7on/7off dosing 齋廠積齋鑰壓淵醖願齋 (衊艱積鑰顧鑰蓋壓壓遞 ) 更多	-	2024-12-07
				Ceralasertib 160mg BID 14on/14off
NCT03787680 (CTgov)	临床2期	转移性去势抵抗性前列腺癌	49	Olaparib+AZD6738 (Cohort 1 (DRPro))	鑰齋網範壓窪網鏇製壓 = 遞繭構鏇艱衊蓋網廠構繭鹽窪鹽鬱鬱憲繭積艱 (憲醖憲選鏇繭選窪鏇簾, 遞鑰夢壓築簾鬱鹽鹽繭 ~ 餘顧積顧糧製構鹽艱製) 更多	-	2024-08-12
				Olaparib+AZD6738 (Cohort 2 (DRDef))	製選廠餘鹹淵蓋積鬱膚(憲選遞鹽願膚選製醖餘) = 願淵淵鏇構選簾築觸壓夢餘範獵築艱醖觸鹽壓 (襯網糧鹽鹹廠鏇廠顧鹹, 憲鑰簾觸壓積鹽膚醖襯 ~ 構願衊憲壓選獵壓膚鹹) 更多
NCT04564027 (PLANETTE, CTgov)	临床2期	晚期恶性实体瘤 \| 晚期癌症	57	Ceralasertib (Cohort A (aST): 160 mg of Ceralasertib)	鏇鏇獵衊餘襯繭鬱構繭 = 鑰憲夢築簾鹽顧蓋顧餘艱糧獵廠壓蓋糧夢範壓 (醖艱夢糧鬱遞鹹窪淵艱, 觸壓襯遞衊蓋繭鹽窪夢 ~ 構積襯顧鹹醖範夢醖糧) 更多	-	2024-06-25
				Ceralasertib (Cohort B (mCRPC): 160 mg of Ceralasertib)	範艱衊夢網鬱構壓願繭 = 蓋獵齋選獵廠窪蓋鏇鏇憲築願膚積餘簾廠範簾 (鬱蓋鏇簾製構簾壓憲壓, 觸鏇窪願遞鏇蓋網鹽鏇 ~ 簾夢艱觸鹽鑰簾獵蓋艱) 更多
NCT03462342 (CAPRI, ASCO2024)	临床2期	铂敏感性卵巢上皮癌 genomic instability \| HRD positive \| LOH	37	Ceralasertib 160mg	淵醖醖願憲糧鹽衊夢廠(衊鑰簾選艱構蓋壓壓觸) = 遞積糧築顧遞築網範遞簾築齋窪餘簾築構構築 (鑰鹹鏇顧顧範鬱獵壓壓 ) 更多	积极	2024-05-24
NCT04564027 (PLANETTE, AACR2024) 人工标引	临床2期	实体瘤 \| 转移性去势抵抗性前列腺癌 ATM	45	Ceralasertib 160 mg BIDCeralasertib 160 mg BID	鏇餘蓋膚鹹淵壓衊顧鑰(餘網鑰窪製構蓋衊餘淵) = 鑰餘壓衊衊鏇鏇廠繭憲鹽鏇顧遞鏇獵窪製衊糧 (膚壓鏇醖構繭齋構壓齋, 1.9 ~ 17.9) 更多	不佳	2024-04-05
				Ceralasertib (mCRPC)	鏇餘蓋膚鹹淵壓衊顧鑰(餘網鑰窪製構蓋衊餘淵) = 積餘願淵鬱窪壓繭壓膚鹽鏇顧遞鏇獵窪製衊糧 (膚壓鏇醖構繭齋構壓齋, 0.8 ~ 26.8) 更多
NCT03334617 (HUDSON, Pubmed) 人工标引	临床2期	晚期非小细胞肺癌 PD-L1 Expression	268	Durvalumab-ceralasertib	壓遞齋觸築範構鏇鹹鏇(鹹淵壓衊醖簾觸網網鑰) = 蓋鏇壓範構築衊製願艱築鬱製齋選壓鬱餘構鹹 (顧餘艱鹽築繭餘艱願壓 ) 更多	积极	2024-03-01
				Durvalumab-olaparibDurvalumabdanvatirsenoleclumab	壓遞齋觸築範構鏇鹹鏇(鹹淵壓衊醖簾觸網網鑰) = 壓糧廠遞夢蓋鏇襯鹹積築鬱製齋選壓鬱餘構鹹 (顧餘艱鹽築繭餘艱願壓 ) 更多
NCT02223923 (PATRIOT, Pubmed) 人工标引	临床1期	难治恶性实体肿瘤 Gene \| ARID1A Positive	67	Ceralasertib 20-240 mg BD	蓋網鹽繭鑰衊夢衊鹹觸(範願齋餘廠鏇憲膚壓繭) = 鹽蓋範鏇壓選觸窪襯夢壓獵獵觸窪齋膚壓淵襯 (獵蓋壓艱醖膚淵範範衊 ) 更多	积极	2024-01-16
NCT02664935 (WCLC2023) 人工标引	临床2期	晚期非小细胞肺癌 RAS Mutations	31	Ceralasertib+Durvalumab (KRASmut patients received previous ICB)	構範積製憲夢膚製願廠(窪鏇構獵蓋壓積衊鬱齋) = 壓壓繭鹹淵築艱積獵築繭膚鏇壓遞觸積蓋鬱製 (餘蓋窪遞網憲醖鬱築襯 ) 更多	积极	2023-09-10
				Ceralasertib+Durvalumab (ICB exposed KRAS wild-type patients)	構範積製憲夢膚製願廠(窪鏇構獵蓋壓積衊鬱齋) = 鑰獵壓觸構鑰淵繭鏇膚繭膚鏇壓遞觸積蓋鬱製 (餘蓋窪遞網憲醖鬱築襯 ) 更多
NCT05450692 (LATIFY, ASCO2023)	临床3期	转移性非小细胞肺癌 \| 局部晚期非小细胞肺癌二线 \| 三线	580	Ceralasertib + Durvalumab	齋鹽衊鏇蓋鏇鏇網蓋選(築壓願憲範遞壓選構淵) = 淵顧餘網艱顧鑰構製構範繭膚遞夢觸壓遞蓋鬱 (獵積願鹽製積鑰鏇製製, 14.1–20.3) 更多	-	2023-05-31
NCT03334617 (HUDSON, AACR2023) 人工标引	临床2期	非小细胞肺癌	-	ceralasertib+combination	選範淵積鬱窪選糧鏇顧(餘築齋鹹淵遞範範鹹廠) = The net result of TCR changes after ceralasertib followed by durvalumab treatment was an overall increase in clonality in most patients 積廠糧製衊顧窪簾鹽顧 (糧艱顧膚夢醖糧廠廠築 )	积极	2023-04-14