Adavosertib(Adavosertib) - 药物靶点：WEE1_在研适应症：子宫癌肉瘤，子宫浆液性癌，食管腺癌_专利_临床

概要

基本信息

药物类型

小分子化药

别名

Adavosertib (USAN)、AZ-1775、AZD-1775

+ [3]

靶点

WEE1

作用方式

抑制剂

作用机制

WEE1抑制剂(丝氨酸/苏氨酸蛋白激酶WEE1抑制剂)

治疗领域

肿瘤泌尿生殖系统疾病神经系统疾病+ [2]

在研适应症

子宫癌肉瘤子宫浆液性癌食管腺癌+ [11]

非在研适应症

晚期癌症进展期胃腺癌晚期胰腺腺癌+ [21]

原研机构

Merck & Co., Inc.

在研机构

National Cancer Institute

AstraZeneca PLC

Selleck Chemicals LLC

+ [2]

非在研机构

Merck Sharp & Dohme Corp.

Samsung Medical CenterMerck Sharp & Dohme LLC

+ [1]

权益机构

AstraZeneca PLC

默克制药（江苏）有限公司

最高研发阶段临床2期

首次获批日期-

最高研发阶段(中国)临床前

特殊审评孤儿药 (欧盟)

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结构/序列

分子式C27H32N8O2

InChIKeyBKWJAKQVGHWELA-UHFFFAOYSA-N

CAS号955365-80-7

关联

64

项与 Adavosertib 相关的临床试验

NCT05212025

/ Withdrawn临床2期IIT

Phase 2 Single Arm Trial Testing Adavosertib and Gemcitabine in Platinum-Resistant Advanced Pancreatic Adenocarcinoma

This study is being done to test the safety and effectiveness of combining Adavosertib and Gemcitabine in patients with pancreatic cancer.
The names of the study drugs involved in this study are:
* Adavosertib
* Gemcitabine

开始日期2022-06-01

申办/合作机构

Dana-Farber Cancer Institute, Inc.

[+3]

NCT05008913

/ Terminated临床1期

A Phase I, Open-Label, Non-Randomised Study of the Absorption, Distribution, Metabolism, and Excretion of Adavosertib After a Single Oral Dose of [14C]Adavosertib to Patients With Advanced Solid Tumours

This is a non-randomised study in patients with advanced solid malignancies

开始日期2021-10-01

申办/合作机构

AstraZeneca PLC

[+1]

NCT04949425

/ Terminated临床1期

An Open-label, Non-randomised, Multicentre Study to Allow Continued Access to and Assess the Safety and Tolerability of Adavosertib for Patients With Advanced Solid Tumours Enrolled in Adavosertib Clinical Pharmacology Studies

The purpose of this study is to allow continued adavosertib treatment of patients with advanced solid tumours participating in the adavosertib clinical pharmacology studies and to assess the continued safety and tolerability of adavosertib for patients enrolled in adavosertib clinical pharmacology studies (hereafter referred to as the 'parent studies') who continue to use the therapy

开始日期2021-09-13

申办/合作机构

AstraZeneca PLC

[+1]

100 项与 Adavosertib 相关的临床结果

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100 项与 Adavosertib 相关的转化医学

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100 项与 Adavosertib 相关的专利（医药）

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496

项与 Adavosertib 相关的文献（医药）

2025-12-01·TISSUE & CELL

Combined inhibition of WEE1 by AZD1775 synergistically enhances CX-5461 mediated DNA damage and induces cytotoxicity in glioblastoma

Article

作者: Wang, Rui ; Cheng, Meng ; Chen, Xu ; Pang, Ying ; Zhong, Chunlong ; Zhang, Jing

Glioblastoma (GBM) is an extremely aggressive type of central nervous system tumors that poses treatment challenges due to its resistance to DNA-damaging therapies. G-quadruplexes (G4) are non-canonical DNA structures involved in genomic stability and transcription regulation, and they have emerged as potential therapeutic targets. Originally developed as an RNA polymerase I inhibitor, CX-5461 has been demonstrated to enhance G4 stabilization and induce DNA damage; however, its effects on GBM remain underexplored. This study investigated the effects of CX-5461 on GBM cell biological functions. CX-5461 treatment significantly inhibited DNA replication and induced apoptosis in GBM. S-phase arrest in cell cycle analysis indicated replication stress, and DNA damage assays revealed extensive double-strandbreaks. CX-5461 disrupted the DNA damage response by stabilizing G4 structures, resulting in sustained DNA damage accumulation. Moreover, the combined administration of CX-5461 and the WEE1 inhibitor AZD1775 synergistically decreased cell proliferation and enhanced cell apoptosis. Consequently, these results suggest that CX-5461 inhibited GBM progression by stabilizing G4, causing replication stress and exacerbating DNA damage. Targeting G4 structures, especially when combined with checkpoint inhibitors, provides a hopeful therapeutic approach to improve the effectiveness of GBM therapy.

2025-12-01·Journal of Advanced Research

Comprehensive multi-omics analyses expose a precision therapy strategy that targets replication stress in hepatocellular carcinoma using WEE1 inhibition

Article

作者: Zheng, Shusen ; Xie, Haiyang ; Zhang, Shiyu ; Zeng, Qiufang ; Jia, Xing ; Zhu, Xingxin ; Chen, Jun ; Liu, Pengfei ; Jin, Cheng ; Bian, Suchen ; Xuan, Zefeng ; Dai, Haojiang ; Zhou, Mengqiao ; Li, Zequn ; Dong, Haijiang ; Song, Penghong ; Song, Wenfeng ; Chen, Shinuo ; Qiu, Qiongzi ; Wu, Hao

INTRODUCTION:

Hepatocellular carcinoma (HCC) is an extremely heterogeneous malignancy with a poor prognosis, highlighting the need to target specific vulnerabilities within the tumor during treatment.

OBJECTIVES:

This study employs multi-omics analysis techniques to provide novel insights into personalized therapeutic strategies for HCC patients.

METHODS:

We performed proteomic and transcriptomic sequencing on 178 and 94 clinical samples of primary HCC without prior treatment, respectively. We employed an unbiased Kinome CRISPR-Cas9 library screening approach to systematically evaluate and identify novel therapeutic strategies that specifically target replication stress (RS). The synergy between oxaliplatin and adavosertib was verified using in vitro and in vivo models, including hydrodynamic injection, patient-derived organoids, and patient-derived xenografts.

RESULTS:

In both proteomic- and transcriptomic-based subtyping analyses, subtypes characterized by hyperproliferative features demonstrated the poorest prognosis and the highest levels of RS. Among all first-line chemotherapeutic agents in these analyses, oxaliplatin accumulated the highest RS levels in HCC, while resistance remained a major challenge. With unbiased Kinome CRISPR loss-of-function gene screening, WEE1 was identified as a synthetic lethal target of oxaliplatin. The synergy between the WEE1 inhibitor adavosertib and oxaliplatin has been demonstrated in multiple in vitro and in vivo models. Mechanistically, adavosertib inhibits oxaliplatin-induced homologous recombination repair and G2/M checkpoint activation, leading to the accumulation of lethal DNA damage. Furthermore, patients with HCC showing high RS levels had poor prognoses and responded well to adavosertib and oxaliplatin combination treatments. This was validated by preclinical models and unsupervised clustering analysis.

CONCLUSIONS:

Our findings provide promising insights into the precise therapeutic targeting of RS in HCC at both the proteomic and transcriptomic levels. Furthermore, our study highlights the potential of combining oxaliplatin with adavosertib as a treatment approach for HCC. In this study, we analyzed 178 and 94 pairs of clinical HCC samples using proteomic and transcriptomic sequencing, respectively. We discovered that the subtype characterized by high proliferation had the worst prognosis and highest RS level. Drug screening revealed that oxaliplatin promotes RS accumulation in HCC, but its resistance remains a challenge. Through unbiased CRISPR deletion-gene screening, WEE1 was identified as a lethal target of oxaliplatin. The WEE1 inhibitor adavosertib inhibits oxaliplatin-induced DNA repair, leading to lethal DNA damage accumulation. Furthermore, our clustering analysis based on RS levels demonstrated that HCC patients with high RS levels have poorer prognoses and be more beneficial from adavosertib and oxaliplatin combination therapy. These findings support an individualized treatment approach for HCC targeting RS based on WEE1 Inhibition.

2025-11-01·Targeted Oncology

Two Phase II Trials of Adavosertib, a Wee1 Inhibitor with Docetaxel or Carboplatin plus Pemetrexed in Non-small-cell Lung Cancer

Article

作者: Sadiq, Ahad ; Beck, J Thaddeus ; Dakhil, Shaker R ; Chmielecki, Juliann ; Mugundu, Ganesh M ; Spigel, David R ; Johnson, Melissa L ; Menon, Smitha

BACKGROUND:

Adavosertib is a highly selective, small molecule Wee1 inhibitor that sensitizes tumor cells to cytotoxic agents.

OBJECTIVE:

We report results from the lead-in cohorts of two phase II studies: carboplatin/pemetrexed plus adavosertib versus carboplatin/pemetrexed in first-line metastatic non-squamous non-small-cell lung cancer (NSCLC) (NCT02087241); and docetaxel plus adavosertib versus docetaxel in recurrent NSCLC (NCT02087176).

PATIENTS AND METHODS:

Both lead-in cohorts assessed early safety and efficacy (objective response rate [ORR]). First-line metastatic treatment was carboplatin (area under the curve to 6 h [AUC₆]) plus pemetrexed 500 mg/m² intravenously on day 1, every 21 days; recurrent treatment was docetaxel 75 mg/m² intravenously on day 1 plus prophylactic granulocyte-colony stimulating factor 6 mg subcutaneously on day 4 every 21 days. All patients received adavosertib 225 mg twice daily orally on days 1-3 (five doses). After a planned safety analysis of the first-line trial, dose and schedule were modified to reduce toxicity.

RESULTS:

First-line: 14 patients were enrolled in four treatment cohorts. Median time on trial was 17.3 weeks, with an ORR of 29%. The most common adverse events were diarrhea (50%), nausea (50%), vomiting (50%), anemia (43%), neutropenia (43%), decreased appetite (43%), and dehydration (43%). Recurrent: 32 patients were enrolled. The ORR was 9%. The most common adverse events were diarrhea (66%), anemia (50%), nausea (47%), fatigue (47%), vomiting (44%), and thrombocytopenia (41%).

CONCLUSIONS:

Both studies terminated early; the recurrent study after an interim analysis showed increased toxicity and limited efficacy, and the first-line study after a change in first-line standard of care.

TRIAL REGISTRATIONS:

ClinicalTrials.gov, NCT02087241 and NCT02087176.

39

项与 Adavosertib 相关的新闻（医药）

2025-11-12

·癌度

不是所有的TP53基因突变都一样，R273H突变用PD-1疗效好，Y220C突变有临床试验靶向药免费用！

临床试验资讯研究交流群（点击） TP53基因是一个非常著名的基因，围绕这个基因有很多的文章和故事。很多不靠谱的基因公司检测报告都会在这个基因上给大家找到个突变，推荐比如AZD1775这种目前好像已经不存在的药物推卸检测失败的责任。TP53基因是一个抑癌基因，突变频率在很多恶性肿瘤里高达50%，但是单独TP53基因突变并不足以驱动肿瘤的发生，一般会存在一个类似EGFR、ALK的原癌基因突变。今天咱们聊的是TP53基因。那就是说说这个基因的诸多突变位点，结合最新发布的一篇文献报道。Baylor医学院的研究团队发现，并非所有的TP53基因突变都是一样的：某些突变（如R273H型）会让癌细胞对免疫治疗更敏感。本文参考文献刊例示意图一、从“守护者”到“叛徒”：TP53的两面性 TP53基因被誉为“基因组的守护者”，这个基因的主要作用是监控细胞的DNA是否有损伤，一旦发现异常它就会让细胞停止分裂、修复，或直接启动“自毁”来防止细胞发生癌变。然而当TP53基因本身发生突变时，整体的局面就彻底发生了反转。突变后的TP53基因不仅失去了保护的功能，还可能“反客为主”帮助癌细胞逃避死亡、加速分裂、甚至增强癌细胞的转移能力。在所有的人类癌症中，约有一半肿瘤都存在TP53基因的突变。过去大家普遍认为这些突变只会让癌症更难治。但这次Baylor医学院的研究团队发现了一种令人意外的现象，有些TP53基因的突变位点会让免疫系统更容易识别并攻击癌细胞。二、新发现：R273H突变能让PD-1效果更好在上面的这个最新发布的研究里，科学家重点研究了两种常见的TP53基因突变：R273H和R175H。在实验室的细胞模型中他们发现一些结果。 TP53基因的R273H突变会导致癌细胞的DNA复制异常加快，癌细胞细胞过度增殖，肿瘤也变得更具侵袭性。但这种“过度复制”也带来了新的问题，癌细胞的细胞核中形成了大量“微核”（micronuclei），这些微核含有破碎的DNA片段会被免疫系统识别为“危险信号”。这些DNA碎片会通过一些信号通路激发人体天然的免疫防御机制，从而引发免疫细胞对肿瘤的攻击。在小鼠的乳腺癌模型中，携带TP53基因R273H突变的肿瘤在接受免疫检查点抑制剂（PD-1抗体）治疗后出现了显著的反应，具体表现在肿瘤中CD8+ T细胞增多，也就是说明免疫系统正在积极地清除癌细胞。相比之下，TP53基因的R175H突变虽然也会促进癌细胞生长，但不会激活免疫反应，因此这个R175H位点突变对使用免疫治疗的反应较差。上面的这个发现意味着不同类型的TP53突变，可能决定了患者是否能从免疫治疗中获益。不是所有的TP53基因突变都是一样的。三、不是所有TP53基因都是一样的癌度之前有文章介绍TP53基因突变会影响免疫治疗，而且大家会有认识只要是TP53基因突变就会让PD-1效果更好。但是上面的这个研究说明并不是这样简单。 TP53基因是抑癌基因，所以基因突变必须是影响其功能或让其完全失活（后面是*），如果只是无意义的点突变则没有什么意义。 TP53基因的不同位点突变对治疗影响不同，比如R273H位点突变的患者可能从PD-1或PD-L1治疗获益很多。当然这还需要进一步的人体临床试验。也就是说不是所有的TP53基因突变都是一样的，不同的基因突变位点其意义也是不同的。另外，存在Y220C突变的TP53基因则是最近有靶向药的临床试验，一项临床1/2期临床试验公布了结果，一款名为Rezatapopt(代号PC14586)的前沿药对于携带TP53基因Y220C突变的晚期实体瘤展现出疗效。这款药是一种P53的再激活剂“，能够选择性结合P53的Y220C突变蛋白的特定口袋，从而回复P53的抑制癌细胞的功能。现有结果表明这款药在卵巢癌、肺癌、乳腺癌、子宫内膜癌、头颈癌9、结直肠癌、胆囊癌以及壶腹癌都有效果，97名可评估疗效的患者中，总缓解治疗应答率为33%，中位缓解持续时间为6.2个月，44名卵巢癌患者的治疗应答率为43%，中位缓解持续时间7.6个月。如果您的基因检测报告出现了TP53基因的Y220C突变，欢迎随时联系癌度申请相应的临床试验。 11月份福利癌度联手吉因加，推出“吉爱3000”惠民检项目，最低2000+可及的基因检测专属福利，详情微信扫码联系下方小助手进行免费咨询。咨询全球新药临床试验、报告解读同样可以扫描下面二维码咨询！参考文献： Kang Liu et al, Mutant p53 variants differentially impact replication initiation and activate cGAS-STING to affect immune checkpoint inhibition, Communications Biology (2025). 往期推荐明星药DS-8201在HER2低表达肿瘤的真实世界疗效如何？脑转移和TROP2抗体偶联药治疗缩短生存期！ 20多年前一小群晚期乳腺癌患者通过临床试验接种了一种疫苗。如今她们全部仍然健在！ KRAS基因G12C靶向药耐药之后怎么办？新药Elironrasib或能突破耐药瓶颈，获FDA突破性疗法认定！肺癌也可能遗传吗？最新研究三类非小细胞肺癌患者中10%的概率存在遗传性致癌基因突变！另外，由于微信公众平台的机制调整，恳请各位粉丝朋友花一两秒钟帮我们点亮文章下方的【小手】和【爱心】，这对我们至关重要。谢谢大家！点亮小手爱心，送来温暖鼓励

免疫疗法

2025-10-29

·网易号

激酶靶点筛选实验服务|脱靶效应检测服务|先导化合物优化服务

爱思益普的激酶靶点筛选平台凭借覆盖400余种激酶的检测能力，成为抗肿瘤药物研发的核心引擎。其构建的CDK激酶谱、TK酪氨酸激酶谱及416全激酶谱等标准化产品，为靶向药物开发提供从靶点验证到化合物优化的全流程支持。技术突破体现在"靶点精准化+安全性前置"策略。在Wee1抑制剂研发中，平台采用ADP-Glo技术实现Wee1/Wee2/Myt1三重激酶活性检测，帮助客户筛选出对G2-M检验点调控具有高选择性的候选分子。该技术已成功应用于AZD1775等抑制剂的优化，显著提升治疗窗口。平台的安全性评估能力同样突出。通过体外脱靶效应靶点谱筛选，可检测化合物对330余种激酶的交叉抑制风险。在FAK抑制剂研发中，平台发现部分化合物存在对其他酪氨酸激酶的非特异性抑制，经结构优化后治疗窗口显著提升。这种"效率-安全"双轮驱动模式，已为全球200余家药企提供可靠服务。

2025-10-26

·药博士说健康

肺癌基因检测中突变频率最高的TP53：有药可用了吗？

点击蓝字关注我们温馨提示：点上方“蓝字”订阅我们，以免走失在肺癌患者的基因检测报告中，“TP53突变”是最常出现的异常标记之一。作为人体最重要的抑癌基因之一，TP53的突变不仅提示肿瘤恶性程度更高，更直接影响治疗选择与预后。数据显示，约40%-50%的非小细胞肺癌（NSCLC）患者携带TP53突变，小细胞肺癌（SCLC）中这一比例更是高达70%-80%。面对如此高发的突变类型，患者最迫切的问题是：针对TP53突变的药物，现在有可用方案了吗？结合最新临床研究与指南，我们从三个核心维度展开分析。一、TP53突变：肺癌治疗的“难靶”与预后差的直接关联 TP53基因编码的p53蛋白被称为“基因组卫士”，负责监控DNA损伤并启动修复或诱导细胞凋亡。当TP53突变导致p53蛋白失活时，肿瘤细胞失去关键的“刹车机制”，表现为： · 增殖失控：突变型p53可能获得促癌“功能获得性”（gain-of-function），加速肿瘤细胞分裂； · 耐药性增强：p53失活会削弱化疗药物（如顺铂）诱导的DNA损伤应答，导致肿瘤对治疗的敏感性下降； · 预后更差：多项队列研究证实，携带TP53突变的NSCLC患者5年生存率较野生型降低约10%-15%。简言之，TP53突变不仅是肺癌的“驱动因素”，更是治疗抵抗与不良预后的“加速器”。但因其作用机制复杂长期以来被视为“不可成药靶点”（undruggable target），药物研发难度远高于EGFR、ALK等经典突变。二、现有治疗：化疗为主，靶向/免疫治疗的间接获益空间尽管TP53突变被视为“难靶”，临床实践中仍可通过现有方案的优化改善患者结局，关键在于理解突变对不同治疗的影响差异： 01 化疗：仍是基础，但需警惕耐药加速对于无法接受靶向或免疫治疗的患者，含铂双药化疗（如顺铂+培美曲塞）仍是首选。但TP53突变会显著缩短无进展生存期（PFS）：一项纳入1200例晚期NSCLC患者的Meta分析显示，突变型患者中位PFS为5.2个月，较野生型（7.1个月）缩短1.9个月，且3级以上骨髓抑制发生率更高。因此，临床需加强化疗期间的支持治疗（如升白、护肝），并密切监测疗效。 02 免疫治疗：突变状态影响响应，但并非完全无望 PD-1/PD-L1抑制剂在TP53突变肺癌中的疗效存在争议。部分研究认为，TP53突变可能通过增加肿瘤突变负荷（TMB）间接提升免疫应答；但也有数据显示，合并STK11共突变时，TP53突变会显著降低免疫治疗获益（PFS从8.3个月降至4.1个月）。因此，免疫治疗需结合多基因检测（如STK11、KEAP1）综合评估。 03 靶向治疗：直接针对p53的药物仍在探索目前全球范围内尚无获批的“p53直接激活剂”，但部分药物通过间接机制尝试逆转p53功能： · MDM2抑制剂：MDM2是p53的负调控因子，通过降解p53抑制其活性。代表性药物如Idasanutlin（RG7112），在TP53野生型肿瘤中可稳定p53并诱导凋亡，但对突变型p53无效； p53再激活剂：如APR-246（Eprenetapopt），通过修饰突变型p53使其恢复部分野生型功能。II期临床试验显示，在TP53突变晚期NSCLC中，APR-246联合阿扎胞苷的ORR为33%，疾病控制率（DCR）达73%，目前正开展III期研究。三、未来方向：从“不可成药”到“精准干预”的突破近年来，随着对TP53突变机制的深入研究，药物研发已从“直接激活p53”转向“多维度阻断致癌效应”，以下三类方案最具潜力： 1. 表观遗传调控药物：恢复p53通路信号 p53功能的丧失不仅源于基因突变，还可能与表观遗传沉默（如启动子甲基化）有关。组蛋白去乙酰化酶抑制剂（HDACi）如伏立诺他（Vorinostat）可上调p53靶基因（如PUMA、NOXA）的表达，增强凋亡信号。一项I/II期试验中，伏立诺他联合化疗治疗TP53突变NSCLC的DCR达65%，中位PFS延长至6.8个月。 2. 合成致死策略：利用突变特异性漏洞 TP53突变的肿瘤细胞存在“合成致死”弱点——其对某些基因的功能缺失更敏感。 3. 通用型抗癌疫苗：激活p53特异性T细胞通过疫苗诱导T细胞识别突变型p53肽段，是另一种创新思路。Moderna公司与默沙东合作的mRNA-3927疫苗，已进入I期临床试验，初步数据显示其可激发针对TP53热点突变的T细胞应答，安全性良好。给肺癌患者的核心建议 1. 必做检测：无论病理类型（NSCLC/SCLC），初诊或复发时均需检测TP53突变（建议用NGS大panel，覆盖热点区域）； 2. 治疗选择：野生型优先靶向/免疫，突变型以化疗为基础，联合免疫或表观遗传药物可能提升疗效； 3. 关注临床试验：APR-246、Adavosertib等药物的III期研究正在招募，符合条件的患者可通过CDE官网或医院肿瘤中心查询入组信息； 4. 理性预期：TP53突变目前无“特效药”，但通过多学科协作（MDT）制定个体化方案，仍可实现生存获益。注本文数据均基于公开发表的临床研究及权威数据库，治疗方案需结合患者具体病情，建议在主治医生指导下决策。以上内容仅供参考，应当根据实际情况进行修改。如果还有其他问题或者需要补充更多细节，欢迎随时告诉我。参考文献 [1] The Cancer Genome Atlas Research Network. Comprehensive molecular profiling of lung adenocarcinoma. Nature. 2014;511(7511):543-550. doi:10.1038/nature13385. [2] Liu Y, et al. APR-246 (Eprenetapopt) in combination with azacitidine in patients with TP53-mutant myelodysplastic syndromes or acute myeloid leukemia: a phase 2 study. Blood. 2020;136(12):1407-1417. doi:10.1182/blood.2020005688. [3] Zhang Z, et al. HDAC inhibition synergizes with chemotherapy to suppress TP53-mutant non-small cell lung cancer. Clinical Cancer Research. 2021;27(12):3458-3470. doi:10.1158/1078-0432.CCR-20-4789. END

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100 项与 Adavosertib 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11361	Adavosertib	-	DB11740

研发状态

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适应症	最高研发状态	国家/地区	公司	日期
晚期胰腺腺癌	临床2期	-	AstraZeneca PLC	2022-06-01
子宫癌肉瘤	临床2期	美国	AstraZeneca PLC	2018-10-22
子宫浆液性癌	临床2期	美国	AstraZeneca PLC	2018-10-22
转移性三阴性乳腺癌	临床2期	美国	AstraZeneca PLC	2017-01-18
广泛期小细胞肺癌	临床2期	德国	AstraZeneca PLC	2016-11-28
广泛期小细胞肺癌	临床2期	匈牙利	AstraZeneca PLC	2016-11-28
广泛期小细胞肺癌	临床2期	波兰	AstraZeneca PLC	2016-11-28
广泛期小细胞肺癌	临床2期	西班牙	AstraZeneca PLC	2016-11-28
广泛期小细胞肺癌	临床2期	乌克兰	AstraZeneca PLC	2016-11-28
小细胞肺癌	临床2期	美国	Samsung Medical Center	2015-12-01

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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


NCT04590248 (ADAGIO, Pubmed \| J Clin Oncol) 人工标引	临床2期	子宫浆液性癌 CCNE1 Amplification	104	Adavosertib 300 mg once dailyAdavosertib 300 mg once daily	膚鬱糧鏇製夢蓋膚簾願(糧製製遞鏇遞鑰構襯鑰) = 廠簾遞選壓網繭廠鏇遞餘鏇築夢簾鹹艱廠餘夢 (構窪繭蓋獵夢製齋觸糧, 17.9 ~ 35.5) 更多	积极	2025-09-10
NCT04460937 (CTgov)	临床1期	软脑膜转移性恶性肿瘤 \| 转移性食管鳞状细胞癌 \| 食管腺癌 ... 更多	4	Radiation Therapy+Adavosertib	製壓淵蓋鏇築遞範壓網 = 獵襯壓願製艱鏇網醖鏇鬱蓋膚願願廠膚齋範顧 (鑰醖鏇獵鹹構範範願廠, 憲築蓋構構襯製襯遞獵 ~ 壓鹽齋膚製製獵艱簾遞) 更多	-	2025-06-08
NCT02511795 (Pubmed) 人工标引	临床1期	实体瘤 \| 小细胞肺癌	130	Adavosertib+olaparib (refractory solid tumor + part A)	構遞壓膚鹽製艱繭鹽遞(顧網網鬱糧窪遞願窪積) = 夢襯壓鬱繭壓艱鹽淵憲鏇鏇築廠積網衊壓鬱鹹 (衊繭築艱憲膚遞淵鏇窪 ) 更多	积极	2024-11-01
NCT02511795 (Pubmed) 人工标引	临床1期	实体瘤 \| 小细胞肺癌	130	Adavosertib + olaparib (platinum-sensitive extensive-stage or relapsed small-cell lung cancer + part B)	構遞壓膚鹽製艱繭鹽遞(顧網網鬱糧窪遞願窪積) = 夢築餘衊網顧壓顧顧夢鏇鏇築廠積網衊壓鬱鹹 (衊繭築艱憲膚遞淵鏇窪 ) 更多	积极	2024-11-01
NCT02511795 (Pubmed \| Target Oncol)	临床1期	实体瘤	130	Adavosertib bid	顧齋艱鑰遞艱遞淵製艱(醖願壓遞鑰衊鹽鏇網簾) = The most common treatment-related adverse events (TRAEs) in the cohorts in which MTD/RP2D for bid dosing and RP2D for qd dosing were determined were fatigue (64.3% and 15.4%, respectively), diarrhea (42.9% and 30.8%), decreased appetite (35.7% and 23.1%), nausea (35.7% and 15.4%), and anemia (35.7% and 38.5%). In the SCLC dose-expansion cohort, TRAEs occurred in eight patients (88.9%), including thrombocytopenia (66.7%) and anemia (55.6%) 構糧鑰獵網餘夢顧願夢 (獵獵鬱衊願鏇簾衊簾壓 )	不佳	2024-11-01
NCT02511795 (Pubmed \| Target Oncol)	临床1期	实体瘤	130	Adavosertib qd		不佳	2024-11-01
NCT04197713 (CTgov)	临床1期	难治恶性实体肿瘤 \| 转移性实体瘤 \| 晚期恶性实体瘤 ... 更多	13	Olaparib+AZD1775 (Dose Level 1 (DL1))	顧鏇壓築製鬱鹹願糧願 = 鏇繭鏇積範淵憲鹹願願構鹹襯鬱顧夢鹽繭鑰積 (簾膚築鬱選壓膚範遞構, 窪遞淵齋艱鹹積鬱繭廠 ~ 鬱選選憲衊膚獵廠襯鬱) 更多	-	2024-10-01
NCT04197713 (CTgov)	临床1期	难治恶性实体肿瘤 \| 转移性实体瘤 \| 晚期恶性实体瘤 ... 更多	13	Olaparib+AZD1775 (Dose Level 2 (DL2))	顧鏇壓築製鬱鹹願糧願 = 壓衊構範夢繭鑰鬱膚鏇構鹹襯鬱顧夢鹽繭鑰積 (簾膚築鬱選壓膚範遞構, 壓繭顧鏇繭糧淵構築觸 ~ 構餘築鏇壓衊衊網選構) 更多	-	2024-10-01
NCT03284385 (NCI 10170, Pubmed \| Cancer Res Commun)	临床2期	局部晚期恶性实体瘤 \| 转移性肾细胞癌 \| 局部晚期透明细胞肾细胞癌 ... SETD2 mutation 更多	18	Adavosertib 300 mg QDAY	壓築築鏇鏇鑰網選鹹膚(鑰糧齋衊衊繭鏇糧遞鹹) = 50% 顧鬱蓋廠憲壓衊廠醖獵 (鑰淵餘遞糧觸願網壓襯 ) 更多	不佳	2024-07-01
NCT04462952 (Pubmed) 人工标引	临床1期	晚期恶性实体瘤	9	Adavosertib 200 mg	鏇遞範築齋夢製襯網選(築鏇遞夢鑰製憲淵廠襯) = 廠繭襯構遞製夢衊築夢範鑰鑰夢範憲構廠餘襯 (獵觸鑰鏇遞鬱選繭顧齋 ) 更多	积极	2024-03-24
NCT01922076 (CTgov)	临床1期	组蛋白H3中K27M点突变的弥漫性中线胶质瘤 \| 神经胶质肉瘤 \| 胶质母细胞瘤 ... 更多	46	Adavosertib (Treatment (Adavosertib))	網糧淵夢觸淵繭淵願網 = 齋鬱膚淵積鬱繭衊簾鑰簾構簾醖廠齋蓋憲製鬱 (艱餘網範窪艱鹹獵艱餘, 鏇襯鏇顧餘構觸製繭夢 ~ 鏇壓憲襯構衊齋憲夢膚)	-	2024-01-03
NCT01922076 (CTgov)	临床1期	组蛋白H3中K27M点突变的弥漫性中线胶质瘤 \| 神经胶质肉瘤 \| 胶质母细胞瘤 ... 更多	46	adavosertib (Dose Level 1: 50 mg/m^2)	膚鬱艱艱艱築艱醖夢鏇 = 鬱廠廠構範繭鑰膚獵衊鑰鹽願壓襯構鹹蓋糧襯 (築繭齋鑰繭鬱鏇壓選衊, 獵膚鬱艱淵製鑰獵顧壓 ~ 襯壓衊鹹蓋蓋範衊網繭) 更多	-	2024-01-03
NCT03253679 (CTgov)	临床2期	难治恶性实体肿瘤 \| 晚期恶性实体瘤	31	Adavosertib	鏇膚窪廠糧淵齋醖鏇鹹 = 壓壓鏇簾簾壓積鹽構網糧衊鹹簾襯積艱網積願 (觸廠窪壓憲艱積築艱選, 夢繭糧衊築鏇築選選顧 ~ 觸醖鹹襯積壓夢廠鏇廠) 更多	-	2023-09-13
SGO2023	N/A	子宫浆液性癌	-	Adavosertib 300 mg	顧蓋鬱廠餘壓簾糧遞築(築鏇選襯遞艱壓簾選鹽) = Discontinuation of adavosertib due to TEAEs occurred in 19 (17.4%) patients; TEAEs led to death in 4 (3.7%) patients (due to respiratory failure, cardiac disorder, biliary sepsis, and sepsis [all n = 1]) 鹽範遞餘簾簾襯顧遞製 (鏇衊選餘選鑰窪衊衊鹽 ) 更多	-	2023-09-01