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

NCT06769126

/ Not yet recruiting临床2期IIT

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2025-03-08

申办/合作机构

SWOG

[+1]

NCT06754761

/ Not yet recruiting临床1期

A Phase I, Open-label Study to Assess the Absolute Bioavailability of Ceralasertib (AZD6738) and Absorption, Distribution, Metabolism, and Excretion (ADME) of [14C]-Ceralasertib in Patients With Non-small Cell Lung Cancer, Ovarian Cancer, or Endometrial Cancer

This is an open-label, two-part study in participants with NSCLC, ovarian cancer, or endometrial cancer and will be conducted at multiple study sites.
Participants will be assessed for study eligibility prior to admission to the study site.
Part A will assess the absolute bioavailability, determine the excretory routes of [14C]-Ceralasertib, and evaluate the PK parameters of a Ceralasertib oral dose and a radiolabelled IV microdose of [14C]-Ceralasertib.
Participants will be admitted to the study site pre-dose Part A and will remain at the study site for excreta (urine and faeces) collections, PK sampling and safety assessments. A washout period days will be observed between dosing in Part A and Part B. Part B will assess the ADME of [14C]-Ceralasertib.
Participants will be readmitted to the study site for Part B and will remain at the study site for excreta (urine, faeces, and any vomitus) collections, PK sampling, and safety assessments.
Participants will return to the study site for a Follow-up Visit after the last dose of Ceralasertib which will include routine safety assessments.
After the completion of Parts A and B, and following the Follow-up Visit, participants may be allowed further access to Ceralasertib if in the opinion of the investigator and medical monitor they may derive clinical benefit.

开始日期2025-01-17

申办/合作机构

AstraZeneca PLC

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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263

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）

2025-03-12

·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

2025-02-07

·E药经理人

阿斯利康2025开新局：全球及中国区收入均创新高，五大业务板块强势增长

2025年2月6日，阿斯利康用一份“漂亮”的年报，为其至少未来5年的发展，传递出了更多确定性。 2024年，阿斯利康全年营收同比增长21%达到540.73亿美元，高速增长直接让其在全球制药企业营收TOP10排名中，直接跃升至第5位，这是阿斯利康近几年来的最好成绩。更为重要的是，阿斯利康全球CEO苏博科在2024年年报中透露，阿斯利康的增长曲线在2025年仍然会持续，且是“高个位数增长”。不止如此，在阿斯利康“2030愿景”的指引下，其目标是到2030年阿斯利康全球收入达到800亿美元。业绩增长背后的推动因素是阿斯利康在研管线的丰富度和其后带来的市场潜力。据悉，2025年阿斯利康有7款新药的首个III期临床试验数据有望首次披露。苏博科认为阿斯利康2025年是一个新的开始，他用“史无前例”来形容阿斯利康开新局时在研产品的丰富程度。当然，阿斯利康全球好业绩也离不开中国市场的助力。2024年阿斯利康中国区实现营收64.13亿美元，同比增长11%。凭借这一成绩，阿斯利康中国再次成为跨国药企中国区营收TOP1。 01 阿斯利康中国区重回第一阿斯利康中国区业绩以64.13亿美元，创下历史新高，且凭借11%的强劲增长再次回到跨国药企中国区销售的头把交椅，中国区业绩也占到了其全球总营收的12%。一直以来，中国市场都是阿斯利康的重要战略布局的市场之一。随着中国居民对健康医药产品需求的增加，以及政府对生物医药产业的支持，跨国药企在中国市场的竞争将进一步加剧。在经历过药审改革、集采国谈等政策影响后，提升产品创新力已经成为众多跨国药企在中国市场布局时的关键共识。资料显示，阿斯利康深耕中国市场逾30年时间里，在肿瘤、心血管、代谢、肾脏、呼吸、消化及罕见病等疾病领域推出了40余款创新药物。自2024年以来，阿斯利康中国已达成11个新药/新适应症的获批，为中国患者未满足的医疗需求带来了更多治疗选择。在业务最庞大的肿瘤板块，截至2024年底，阿斯利康已累计成功引入11款全球领先的肿瘤创新药物至中国市场，这些药物覆盖了肺癌、乳腺癌、泌尿系肿瘤、妇科肿瘤、消化道肿瘤及血液肿瘤等六大高发肿瘤领域，全面响应了中国患者的治疗需求。未来三年，阿斯利康中国在肿瘤领域获批产品管线会进一步丰富，将带来4款新产品及37个适应症；到2030年，预计将带来10款新产品和80多个新适应症。近年来，阿斯利康持续加大在中国的研发投入，不断拥抱中国科创机遇。中国患者群体基数庞大、临床研究资源丰富，以及近年来中国基础科研能力、创新能力的厚积薄发，都为全球医药行业加深对疾病的认知与了解、推动相关领域医药研发进程带来积极影响。 2024年2月，阿斯利康全球研发中国中心升级为阿斯利康全球五大战略研发中心之一，这也是继2019年来的第二次升级，体现了该研发中心在加速全球医药研发、逐步引领中国高发疾病领域的全球临床研发、加速融合中国创新、赋能全球研发等方面做出的努力。阿斯利康在持续提升自身研发实力的同时，也不断促进外部合作，与多元合作伙伴进一步共建中国医药研发创新生态。自2023年以来，阿斯利康已与10家中国创新药企达成全球合作协议，累计总金额超85亿美元。通过融合中国创新，阿斯利康致力于加速全球新药研发，改善患者治疗结局并造福中国与全球患者。深耕中国市场是阿斯利康一项长远的战略布局。作为在中国运营已经超过30年的跨国药企，其在中国已累计投资近30亿美元。近年来，阿斯利康也在持续加大研发与生产供应，2023年3月起投资的位于青岛的吸入气雾剂生产基地项目总投资已达7.5亿美元，项目仍在稳步推进中；去年3月，阿斯利康又宣布在无锡增资4.75亿美元新建小分子药物工厂，其预计未来在国内上市的阿斯利康小分子创新药物将在无锡新工厂实现从制剂到包装的生产。 02 五大业务板块强势增长阿斯利康主要聚焦在肿瘤，心血管、肾脏及代谢，呼吸与免疫，疫苗和免疫疗法，罕见病等五大板块。2024年，这五大板块全部实现正增长，其中肿瘤板块毫无疑问是阿斯利康增长的核心驱动力之一，其收入占产品总收入的41%。具体来看，肿瘤业务贡献223.53亿美元，同比增长24%。奥希替尼作为治疗非小细胞肺癌（NSCLC）的重要药物，全球销售额达到65.80亿美元，同比增长16%。同时，奥希替尼在辅助治疗（ADAURA研究）和一线治疗（FLAURA、FLAURA-2研究）方面也持续展现出强劲的全球市场需求。心血管、肾脏及代谢（CVRM）业务贡献125.17亿美元，同比增长20%，达格列净作为SGLT2类药物的代表，全年销售额达到77.17亿美元，同比增长31%，在心力衰竭和慢性肾脏病（CKD）治疗领域持续扩大着其市场份额。呼吸与免疫（R&I）业务贡献78.76亿美元，同比增长25%。值得注意的是，治疗哮喘药物特泽利尤单抗在过去一年有着87%的增长，凭借全年12.19亿美元（合并安进报告的收入）的整体销售，成为新晋的重磅炸弹药物。疫苗和免疫疗法（V&I）业务贡献14.62亿美元，同比增长8%。此外，罕见病业务贡献87.68亿美元，同比增长16%。其中，雷夫利珠单抗全球销售额达39.24亿美元, 同比增长34%。多款新晋重磅炸弹出现的同时，过去一年的销售三甲也随之出炉。达格列净以77.17亿美元，成为当之无愧的销冠，在降糖、肾病和心衰三个适应症领域撑起了阿斯利康CVRM业务的“半边天”。第二名则是贡献65.8亿美元的奥希替尼，虽然面临众多EGFR-TKI的竞争，但仍表现出强劲的增长势头。抗肿瘤药物占据三甲两席，度伐利尤单抗以21%的增速实现全年47.17亿美元的销售。度伐利尤单抗在肝细胞癌（HCC）、胆管癌（BTC）等适应症领域的增长也推动了肿瘤板块的整体表现。同比21%的整体业绩增长，除了明星产品保持强势增速、几乎大部分产品都实现两位数增长之外，还有包括HER2 ADC德曲妥珠单抗、AKT抑制剂Truqap、TSLP单抗Tezspire、同类首创红斑狼疮药物Saphnelo等产品，实现超过50%的增速的强力加持。 03 丰富的管线驱动未来业绩过去一年，阿斯利康所取得的亮眼业绩也为其向着2030年实现800亿美元总营收的目标打下了坚实的基础。在其2024财报中，也预计2025年总营收将实现高个位数百分比增长。持续保持高增长并非纸上谈兵，又该如何实现？阿斯利康在年报中透露，这一增长预期基于公司在全球主要市场的持续扩张以及新药的陆续上市。研发创新永远是核心竞争力，阿斯利康在研发方面的持续投入为其未来的增长奠定了坚实基础。2024年，阿斯利康的研发支出达到135.83亿美元，同比增长25%，主要用于支持其丰富的产品管线，包括多个处于关键临床阶段的药物。 2024年5月，阿斯利康宣布计划到2030年在全球带来20款突破性创新药，并实现800亿美元的总收入，目前有8款新药已上市。同时，阿斯利康还为其后续增长布局了强大的在研产品管线。截至2024 年，该公司有191个研发管线项目，19个后期研发管线项目。聚焦在2025年，阿斯利康表示将有多款新分子实体关键数据读出，其中7款NMEs 将迎来首次 III 期数据读出，包括 camizestrant（治疗 HR+/HER2 - 乳腺癌）、ceralasertib（治疗非小细胞肺癌）、baxdrostat（治疗高血压）等。同时，在体重管理和健康风险、ADC和放射性偶联药物、下一代 IO 双特异性抗体、细胞治疗和 T 细胞接合剂、基因治疗和基因编辑五大领域，阿斯利康已取得了重要进展，这些项目将驱动阿斯利康在2030年以后持续增长。声明：本材料由阿斯利康支持，涉及在中国尚未获批的产品/适应症，在任何情况下均不应作为治疗或使用建议。一审| 黄佳二审| 李芳晨三审| 李静芝精彩推荐 CM10 | 集采 | 国谈 | 医保动态 | 药审 | 人才 | 薪资 | 榜单 | CAR-T | PD-1 | mRNA | 单抗 | 商业化 | 国际化｜猎药人系列专题 | 出海启思会 | 声音·责任 | 创百汇 | E药经理人理事会 | 微解药直播 | 大国新药 | 营销硬观点 | 投资人去哪儿 | 分析师看赛道 | 药事每周谈 | 医药界·E药经理人 | 中国医药手册创新100强榜单 | 恒瑞 | 中国生物制药 | 百济 | 石药 | 信达 | 君实 | 复宏汉霖｜翰森 | 康方生物 | 上海医药 | 和黄医药 | 东阳光药 | 荣昌 | 亚盛医药 | 齐鲁制药 | 康宁杰瑞 | 贝达药业 | 微芯生物 | 复星医药｜再鼎医药｜亚虹医药跨国药企50强榜单 | 辉瑞 | 艾伯维 | 诺华 | 强生 | 罗氏 | BMS | 默克 | 赛诺菲 | AZ | GSK | 武田 | 吉利德科学 | 礼来 | 安进 | 诺和诺德 | 拜耳 | 莫德纳 | BI | 晖致 | 再生元

财报临床3期

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

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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	鬱衊窪願觸選壓艱淵鏇(願鏇積艱壓壓觸鏇蓋衊) = n=1, grade 3 or higher AEs with 7on/7off dosing 鬱獵繭鹽淵淵鏇淵遞築 (廠遞壓獵積衊膚鑰淵糧 ) 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))	憲製窪膚糧淵鏇憲襯鬱 = 觸積顧鏇遞衊夢憲築鬱鹽築構夢網顧獵網艱鏇 (齋淵繭窪餘膚艱艱顧蓋, 獵膚鑰鹽範鹽築糧鑰鬱 ~ 糧願獵膚淵餘鹹製醖範) 更多	-	2024-08-12
				Olaparib+AZD6738 (Cohort 2 (DRDef))	願淵繭鬱積鬱鑰餘積鏇(淵築夢餘鬱繭醖願鹹齋) = 獵壓築膚糧膚衊夢鏇繭膚夢窪築遞選窪蓋簾艱 (鏇構醖積蓋鏇鏇襯醖齋, 鏇鹹憲築鏇構鬱獵積鏇 ~ 鑰製夢艱襯鹹窪觸餘艱) 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)	積齋積衊鑰壓醖壓衊窪 = 憲醖鏇蓋餘鏇蓋鑰鬱襯餘鬱鬱膚構窪糧簾襯廠 (顧築廠窪憲選觸醖憲鏇, 憲製窪願願構顧襯憲鑰 ~ 顧鹽衊齋糧淵繭簾簾鹹) 更多	-	2024-06-25
				Ceralasertib (Cohort B (mCRPC): 160 mg of Ceralasertib)	繭顧蓋簾憲襯鹹艱鹽繭 = 鹹網餘構構齋膚淵齋淵鑰衊壓觸築願製夢壓夢 (鹹遞築簾艱簾蓋艱簾醖, 鹹繭獵夢鏇憲襯憲簾壓 ~ 齋鏇淵窪廠選壓獵糧淵) 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	餘網繭鏇範範夢夢艱艱(鹽淵顧鬱鬱餘廠鬱網壓) = 顧鑰願蓋製壓獵製蓋膚廠積鏇簾鹽衊膚觸範鑰 (醖餘繭壓觸衊繭蓋糧壓 ) 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	遞製顧艱範築積廠衊夢(顧醖廠齋糧願餘壓鬱餘) = 蓋餘餘鬱簾餘淵選糧餘鹽夢蓋鏇鬱鑰鏇衊獵夢 (製積膚觸衊顧範繭範窪, 1.9 ~ 17.9) 更多	不佳	2024-04-05
				Ceralasertib (mCRPC)	遞製顧艱範築積廠衊夢(顧醖廠齋糧願餘壓鬱餘) = 顧築齋壓壓願築衊齋鑰鹽夢蓋鏇鬱鑰鏇衊獵夢 (製積膚觸衊顧範繭範窪, 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	襯獵製餘願範選觸範願(簾糧膚網艱窪夢繭淵齋) = 齋憲築襯積蓋構簾糧醖窪壓蓋遞鏇築遞蓋窪觸 (積製鏇壓夢襯繭獵齋壓 ) 更多	积极	2024-03-01
				Durvalumab-olaparibdanvatirsenoleclumab	襯獵製餘願範選觸範願(簾糧膚網艱窪夢繭淵齋) = 選膚構選網廠艱蓋醖築窪壓蓋遞鏇築遞蓋窪觸 (積製鏇壓夢襯繭獵齋壓 ) 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	糧廠鏇網觸獵簾獵衊鏇(襯憲遞鬱夢蓋蓋積淵夢) = 窪衊遞觸齋鬱顧鑰醖願繭鹽範遞糧築願鹹餘醖 (顧獵繭製遞簾製齋襯鬱 ) 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)	廠範夢遞衊築簾構醖網(構製願獵鬱窪餘醖蓋鬱) = 鬱淵鑰憲艱襯選顧蓋壓憲範獵膚蓋蓋鹽窪壓膚 (鹽遞範鬱獵獵積糧齋糧 ) 更多	积极	2023-09-10
				Ceralasertib+Durvalumab (ICB exposed KRAS wild-type patients)	廠範夢遞衊築簾構醖網(構製願獵鬱窪餘醖蓋鬱) = 構範蓋淵製鬱夢鬱築構憲範獵膚蓋蓋鹽窪壓膚 (鹽遞範鬱獵獵積糧齋糧 ) 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	鏇鑰淵鏇願糧鏇範糧構(顧網選窪夢築願製餘鬱) = 蓋選夢繭顧築窪鹹醖鬱襯顧願廠構繭獵壓顧遞 (壓憲積簾選獵願鹹遞壓, 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	願選顧鬱遞鏇選鏇網壓(鏇糧選餘製顧願繭網顧) = The net result of TCR changes after ceralasertib followed by durvalumab treatment was an overall increase in clonality in most patients 觸憲網壓衊淵醖築廠憲 (淵窪窪願鏇壓醖齋糧鑰 )	积极	2023-04-14