Phase I Clinical Trial of CA-4948 (Emavusertib) in Combination With FOLFOX Plus Bevacizumab as Frontline Treatment in Patients With Metastatic Colorectal Cancer

This phase I trial studies the side effects and best dose of CA-4948 when given together with fluorouracil, leucovorin, oxaliplatin (FOLFOX) plus bevacizumab in treating patients with colorectal cancer that has spread from where it first started (primary site) to other places in the body (metastatic). CA-4948 may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. The chemotherapy drugs used in FOLOX, fluorouracil and oxaliplatin, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Leucovorin is used with fluorouracil to treat colorectal cancer. Bevacizumab is in a class of medications called anti-angiogenic agents. It works by stopping the formation of blood vessels that bring oxygen and nutrients to the tumor. This may slow the growth and spread of the tumor. Giving CA-4948 with FOLFOX plus bevacizumab may be safe, tolerable and/or effective in treating patients with metastatic colorectal cancer.

开始日期2026-01-23

申办/合作机构

National Cancer Institute

NCT05296005

/ Withdrawn临床1期IIT

Total Neoadjuvant Therapy for the Treatment of Gastroesophageal Junction (GEJ) and Gastric Cancers: A Pilot Trial

This phase I trial tests the safety, side effects studies chemotherapy followed by chemotherapy at the same time as radiation therapy (chemoradiation) before surgery (neoadjuvant) in treating patients with stage gastric (stomach) or gastroesophageal junction cancer . Chemotherapy drugs, such as docetaxel, oxaliplatin , leucovorin, fluorouracil, and capecitabine, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Radiation therapy uses high energy x-rays to kill tumor cells and shrink tumors. Giving chemotherapy and chemoradiation before surgery may make the tumor smaller and may reduce the amount of normal tissue that needs to be removed.

开始日期2025-12-31

申办/合作机构

Ohio State University Comprehensive Cancer Center

NCT06780111

/ Not yet recruiting临床1/2期

A Phase 1/2 Open-Label, Umbrella Platform Design Study of Investigational Agents in Combination With Pembrolizumab (MK-3475) With or Without Chemotherapy in Participants With 1L Locally Advanced Unresectable/Metastatic Esophageal Cancer: KEYMAKER-U06 Substudy 06E

Researchers are looking for new ways to treat esophageal squamous cell carcinoma (ESCC). ESCC is a type of cancer that starts in certain cells that line the esophagus. The esophagus is the tube that connects the throat to the stomach. This study will look at ESCC that is either locally advanced unresectable, which means it has spread into tissue near where it started and cannot be completely removed by surgery, or metastatic, which means it has spread to other body parts.
Available treatments for these types of ESCC include pembrolizumab and chemotherapy. Pembrolizumab is an immunotherapy, which is a treatment that helps the immune system fight cancer. Chemotherapy is medicine that destroys cancer cells or stops them from growing.
Researchers want to learn about giving pembrolizumab and ifinatamab deruxtecan (I-DXd), a study medicine, with or without chemotherapy to treat ESCC. I-DXd is an antibody-drug conjugate (ADC). An ADC attaches to a protein on cancer cells and delivers treatment to destroy those cells.
The main goal of this study is to learn about the safety of I-DXd and pembrolizumab with or without chemotherapy and if people tolerate them. Researchers also want to learn how cancer responds (gets smaller or goes away) to the study treatments.

开始日期2025-08-07

申办/合作机构

Merck Sharp & Dohme LLC

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100 项与奥沙利铂相关的临床结果

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100 项与奥沙利铂相关的转化医学

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100 项与奥沙利铂相关的专利（医药）

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22,093

项与奥沙利铂相关的文献（医药）

2025-12-31·JOURNAL OF MEDICAL ECONOMICS

Budget impact of introducing glofitamab for treatment of relapsed or refractory diffuse large B-cell lymphoma after two or more lines of systemic therapy in the United States

Article

作者: Li, Jia ; Mahmoudjafari, Zahra ; Masaquel, Anthony ; Parisé, Hélène ; Bercaw, Eric ; Bognar, Katalin ; Wang, Si-Tien

BACKGROUND:

Glofitamab is a T-cell engaging bispecific monoclonal antibody that was granted accelerated approval from the United States Food and Drug Administration for adult patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL), not otherwise specified or large B-cell lymphoma arising from follicular lymphoma, after ≥2 lines of systemic therapy (3L+).

METHODS:

A budget impact model was developed for a hypothetical blended commercial/Medicare health plan with 1,000,000 members. Comparators were axicabtagene ciloleucel (Axi-cel), lisocabtagene maraleucel (Liso-cel), tisagenlecleucel (Tisa-cel), loncastuximab tesirine, polatuzumab vedotin + bendamustine + rituximab, rituximab + gemcitabine + oxaliplatin, tafasitamab + lenalidomide, and epcoritamab (Epcor). Total costs included those for drugs, wastage, administration, grade ≥3 adverse reactions, and all-grade cytokine release syndrome) and routine care. Market shares were based on internal projections and expert opinions. Total and per-member per-month (PMPM) net budget impacts over 3 years were calculated.

RESULTS:

Approximately nine patients were projected to be eligible for 3L + DLBCL treatment in a health plan of 1,000,000 members. The introduction of glofitamab as a treatment option resulted in estimated total and PMPM cost savings of $728,697 and -$0.0202, respectively, over 3 years. Costs were reduced across all cost categories but particularly in drug costs. Among the newer therapies, total 3-year cost per treated patient was lowest for glofitamab: $226,658 versus Tisa-cel = $564,113; Axi-cel = $540,002; Liso-cel = $516,272; and Epcor = $335,293. Across all sensitivity analyses, the inclusion of glofitamab had minimal PMPM budget impact, ranging from -$0.0256 to -$0.0108.

CONCLUSIONS:

With the lowest 3-year total cost per treated patient among the newer therapies, glofitamab being an available option in the 3L + DLBCL market is estimated to save a hypothetical 1,000,000-member health plan $728,697 in cumulative total costs and $0.0202 in PMPM costs over 3 years.

2025-12-31·RENAL FAILURE

Knowledge mapping and visualized analysis of research progress in onconephrology: a bibliometric analysis

Article

作者: Wang, Wei ; Wang, Yiwei ; Fan, Shuling

OBJECTIVES:

Onconephrology is an expanding subspecialty focused on the management of cancer patients with renal injury. This study used a comprehensive bibliometric analysis to emphasize the need for cooperation between oncologists and nephrologists, exploring current trends and future research areas in onconephrology.

METHODS:

Relevant literature on onconephrology published between 1 January 2000 and 27 April 2024 was retrieved from the Science Citation Index Expanded of the Web of Science Core Collection, followed by manual screening. Bibliometric analyses were performed using CiteSpace, VOSviewer, and Bibliometrix software.

RESULTS:

A total of 1,853 publications, including 1,647 articles and 206 reviews, by 11,606 authors from 2,757 institutions in 73 countries, were analyzed. Annual publications generally follow a steadily increasing trend, ranging from 25 to 161 documents. The United States (n = 464), The University of Texas MD Anderson Cancer Center (n = 39), Meletios A. Dimopoulos (n = 21), and Nephrology Dialysis Transplantation (n = 35) were the most productive country, institution, author, and journal, respectively. Immune checkpoint inhibitors, glomerular filtration rate, and cisplatin were clusters of highly cited references after 2015. Oxaliplatin, calcium, open-label, and thrombotic microangiopathy were trending topics after 2020. Outcome, acute kidney injury, immunotherapy, and chronic kidney disease were keyword bursts that persisted through 2024.

CONCLUSION:

Current research of onconephrology is focusing on chemotherapeutic nephrotoxicity, kidney function assessment, dosing of chemotherapeutic agents in chronic kidney disease, glomerular disease in cancer, immunotherapy, and electrolyte disturbances. Future directions in this field include clinical trials and thrombotic microangiopathy.

2025-12-01·MOLECULAR BIOLOGY REPORTS

Comparative effects of arsenic trioxide and chemotherapy on Chk1 and CDC25 gene expression in gastric cancer cells AGS and MKN45: a potential therapeutic strategy

Article

作者: Majd, Ahmad ; Nikbakht, Mohsen ; Mousavi, Seyed Asadoullah ; Babaei, Shadi

BACKGROUND:

Gastric cancer (GC) remains a significant global health burden, particularly in East Asia, where it is a leading cause of cancer-related morbidity and mortality. Despite advancements in chemotherapy, the development of chemoresistance continues to undermine the efficacy of standard treatments such as Docetaxel and Oxaliplatin. Arsenic trioxide (ATO) has emerged as a potential therapeutic agent capable of overcoming resistance by targeting DNA repair mechanisms, particularly through the downregulation of Checkpoint Kinase 1 (Chk1). This study investigates the cytotoxic effects of ATO and its capacity to enhance chemotherapy efficacy in GC cells.

METHODS:

AGS and MKN-45 gastric cancer cell lines were exposed to ATO, Docetaxel, Oxaliplatin, and their combinations. Cell viability was assessed via the MTT assay, while Chk1 and CDC25 expressions at the mRNA and protein levels was analyzed using real-time PCR and Western blotting. Statistical analyses were performed using ANOVA and Tukey's post hoc test.

RESULTS:

The MTT assay revealed significant dose- and time-dependent reductions in cell viability, with combination treatments achieving the most pronounced effects. The greatest cytotoxicity was observed with 4 µM ATO combined with 2500 µM Docetaxel or 100 µM Oxaliplatin, showing a high level of statistical significance (p < 0.0001). Additionally, ATO monotherapy significantly downregulated Chk1 and CDC25 expressions (p < 0.05), while its combination with chemotherapeutic agents further enhanced Chk1 and CDC25 suppressions, with ATO-Docetaxel demonstrating the most pronounced effect (p < 0.01).

CONCLUSIONS:

These findings highlight ATO's potential to sensitize GC cells to chemotherapy by impairing DNA repair mechanisms and inducing synergistic cytotoxicity. ATO holds promise as an adjuvant therapeutic agent for overcoming chemoresistance in gastric cancer.

1,444

项与奥沙利铂相关的新闻（医药）

2025-06-08

·ioncology

CGCC 2025丨求同存异，合作共赢——日本知名学者畅谈东亚胃癌诊疗合作前景

CGCC 2025微专辑扫描二维码可查看更多内容编者按2025年5月23~25日，由中国抗癌协会胃癌专业委员会(CGCA) 主办，四川大学华西医院承办的“中国抗癌协会胃癌专业委员会第19届学术会议（CGCC 2025）”在美丽的天府之国成都隆重召开。大会特设胃癌国际巅峰对话专家，邀请国际知名学者发表主题报告。会后，我们特邀日本临床肿瘤研究组（JCOG）胃癌研究小组主席、日本静冈癌症中心Masanori Terashima教授分享胃癌领域的热点话题。肿瘤瞭望消化时讯：日本指南与NCCN/ESMO标准差异最大的领域是？Terashima医生：我认为最大的不同在于围手术期治疗。在西方国家，NCCN/ESMO 推荐新辅助化疗，然后是手术和辅助化疗。在日本的指南中，我们仍然不推荐新辅助化疗。我们的指南建议对 II/III 期胃癌进行辅助化疗。我们不认可新辅助化疗的推荐级别，因为我们没有足够的新辅助化疗的证据。即使在韩国和中国的前瞻性试验之后，新辅助化疗的疗效意义也不是很明确。因此，日本指南不推荐对局部晚期胃癌进行新辅助化疗。另外，略有不同的是，因为早期胃癌占比很少，所以 NCCN/ESMO 没有关于早期胃癌的推荐。然而我们有很多早期胃癌患者，所以对早期胃癌有很多推荐，包块内镜治疗和功能保留手术以及淋巴结手术。Dr Terashima: I think the most different thing is the perioperative treatment. In Western countries, NCCN/ESMO recommends neoadjuvant chemotherapy followed by surgery and adjuvant chemotherapy. In the Japanese Guideline, we still do not recommend neoadjuvant chemotherapy. Our Guideline recommendation is for adjuvant chemotherapy for Stage 2/3 gastric cancer. We do not recognize a recommendation level for neoadjuvant chemotherapy because we do not have sufficient evidence for neoadjuvant chemotherapy. Even after prospective trials in Korea and China, the significance of the efficacy of neoadjuvant chemotherapy is not so clear. So, the Japanese Guideline does not recommend neoadjuvant chemotherapy for locally advanced gastric cancer. Otherwise, the other thing that is a little different is that because they see little early gastric cancer, the NCCN/ESMO have no recommendations for early-stage gastric cancer. But we have so many early gastric cancer patients that we have many recommendations for early gastric cancer from endoscopic treatment to function-preserving surgery and lymph node surgery as well.肿瘤瞭望消化时讯：除HER2外，Claudin 18.2、MSI等新兴标志物如何影响治疗选择？Terashima医生：目前日本胃癌协会 (JGCA) 发布了生物标志物指南，并建议同时检测 HER2、Claudin 18.2、MSI 状态和 CPS 评分这四种生物标志物，并据此决定治疗方案。现在，我们超过 70% 的机构都遵循这些指南。Dr Terashima: Now, in Japan, the Japanese Gastric Cancer Association (JGCA) have published guidelines for biomarkers, and recommend measurement of HER2, Claudin 18.2, MSI status and CPS score. It is recommended to simultaneously measure these four biomarkers and decide treatment accordingly. Nowadays, more than 70% of our institutions follow these guidelines.肿瘤瞭望消化时讯：中日韩三国在胃癌临床试验方面有哪些潜在合作方向？Terashima医生：我认为对于转移性疾病，如果有新药研发出来的话，日本、韩国和中国之间应该可以开展试验合作。中国早期胃癌较少，晚期或 IV 期胃癌更多，是可以开展寡转移治疗方法相关临床试验的潜在合作对象，且转化手术也是这些国家之间开展合作试验的重要方向。Dr Terashima: I think for metastatic disease, if somebody has a new drug, it should be possible to conduct a collaborative trial between Japan, Korea and China. In China, they don’t see so many early gastric cancers, but having more advanced or Stage 4 gastric cancers makes that a good candidate for a collaborative clinical trial looking at treatment for oligometastasis, and also conversion surgery is a good candidate for a collaborative trial between these countries.肿瘤瞭望消化时讯：为何日本坚持对II期胃癌患者使用辅助化疗，而其他国家不推荐？Terashima医生：我认为大多数西方国家不推荐辅助化疗，而推荐围手术期化疗。西方国家和日本之间最重要的区别是诊断能力。术前诊断对于进行新辅助化疗非常重要，但是在日本以外，术前影像学诊断并不那么准确。他们用新辅助化疗然后手术来治疗相对晚期的病例。因为分期不够完善，许多患者在治疗前已经处于 IV 期。在日本，正如我提到的，有针对 II 期和 III 期患者的辅助化疗建议。因为 II 期胃癌患者的生存率很高，但还不够，所以即使在 II 期添加 S-1 单药治疗也可以实现 10% 的生存率提高，这就是我们对 II 期患者使用辅助化疗的原因。 III 期则不同，对于 III 期患者，我们推荐双药治疗，奥沙利铂和S-1或多西他赛和S-1联合。但是对于 II 期，仅 S-1 单药治疗就足以提高生存率。Dr Terashima: I think most Western countries don’t recommend adjuvant chemotherapy. They recommend perioperative chemotherapy. The most important difference between Western countries and Japan is diagnostic ability. Preoperative diagnosis is very important to perform neoadjuvant chemotherapy, but outside Japan, preoperative diagnostic imaging is not so accurate. They treat relatively advanced cases with neoadjuvant chemotherapy and then surgery. Many patients are already at Stage 4 before treatment because of insufficient staging. In Japan, as I have mentioned, we have recommendations for adjuvant chemotherapy for Stages 2 and 3. Because survival in patients with Stage 2 gastric cancer is high, but not high enough, adding S-1 monotherapy can achieve a 10% increase in survival, even at Stage 2. That is why we use adjuvant chemotherapy for Stage 2. It is different for Stage 3. For Stage 3, we recommend doublet treatment, such as Oxaliplatin plus S-1 or docetaxel plus S-1. But for Stage 2, just S-1 monotherapy is sufficient to improve survival. That is the reason why we recommend adjuvant chemotherapy even for Stage 2.（来源：肿瘤瞭望消化时讯）声明凡署名原创的文章版权属《肿瘤瞭望》所有，欢迎分享、转载。本文仅供医疗卫生专业人士了解最新医药资讯参考使用，不代表本平台观点。该等信息不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议，如果该信息被用于资讯以外的目的，本站及作者不承担相关责任。

临床研究

2025-06-07

·ioncology

ASCO热评丨周辉教授：靶向CD79b ADC破局复发/难治性DLBCL，点亮治疗新曙光

编者按：2025年美国临床肿瘤学会（ASCO）年会于当地时间5月30日至6月3日在美国芝加哥盛大举行。作为全球临床肿瘤学领域规模最大、学术水平最高且最具权威性的盛会，ASCO年会吸引了全球肿瘤学界的医生、专业人士、患者倡导者、工业界代表以及主流媒体等各方目光，共同聚焦国际前沿的研究发现与临床试验成果。在本次大会上，我国学者的一项多中心研究成果成功入选大会快速口头报告（摘要号：7013），为不适合移植的复发或难治性弥漫大B细胞淋巴瘤（r/r DLBCL）患者带来了新的希望。《肿瘤瞭望-血液时讯》特邀湖南省肿瘤医院周辉教授进行权威点评，深入剖析该研究成果的重要价值与临床意义。研究简介摘要号：7013标题：CD79b-targeted antibody-drug conjugate (ADC) SHR-A1912 in combination with rituximab, gemcitabine, and oxaliplatin (R-GemOx) in relapsed or refractory (r/r) diffuse large B-cell lymphoma (DLBCL): Data from a phase 1b/2 study中文标题：靶向CD79b抗体-药物偶联物（ADC）SHR-A1912联合利妥昔单抗、吉西他滨和奥沙利铂（R-GemOx）治疗复发或难治性（r/r）弥漫大B细胞淋巴瘤（DLBCL）：来自1b/2期研究的数据第一作者：李亚军背景对于不适合移植的r/r DLBCL患者，存在未被满足的治疗需求，其客观缓解率（ORR）约为40%。CD79b是B细胞受体的关键组成部分，并在大多数B细胞来源的成熟恶性肿瘤中表达，是DLBCL治疗的一个有吸引力的靶点。我们启动了一项1b/2期研究，以评估新型靶向CD79b ADC SHR-A1912联合化疗在r/r或初治DLBCL患者中的安全性和有效性。本次报告SHR-A1912联合R-GemOx方案在r/r DLBCL队列中的研究结果。方法该研究包括1b期的剂量递增（D-ESC）和剂量扩展（D-EXP）部分，以及2期的疗效扩展部分。在r/r DLBCL队列中，纳入既往接受≥1线抗癌治疗无效或疾病进展的患者，接受 SHR-A1912联合R-GemOx（每3周1次，静脉注射）治疗，最多8个周期，随后接受SHR-A1912 维持治疗，直至疾病进展、不可耐受的毒性或研究者决定。1b期部分的主要终点是安全性和推荐2期剂量（RP2D），2期部分的主要终点是ORR。结果截至2024年11月19日的截止日期，共纳入41例患者（D-ESC部分7例，D-EXP部分8例，2期部分26例）。在D-ESC阶段，4例接受 SHR-A1912（2.7 mg/kg）联合R-GemOx治疗的患者中观察到2例剂量限制性毒性（DLT）（1例为4级血小板计数下降，1例出现3级乏力和 3 级食欲减退）；随后，3例患者接受SHR-A1912（1.8 mg/kg）联合 R-GemOx 治疗，未发生DLT。确定SHR-A1912联合R-GemOx的RP2D为1.8 mg/kg。在研究中，共有37例r/r DLBCL患者接受了SHR-A1912（1.8 mg/kg）联合R-GemOx治疗。37 例患者中有21例（56.8%）发生≥3级治疗相关不良事件，最常见的为血液学毒性[血小板计数下降（32.4%）、白细胞计数下降（21.6%）、中性粒细胞计数下降（27.0%）、贫血（16.2%）、淋巴细胞计数下降（10.8%）]。在37例患者中，19例获得完全缓解（CR），8例获得部分缓解。ORR为73.0%（95%CI：55.9-86.2），CR率为 54.1%（95%CI：36.9-70.5）。在27例有反应的患者中，23例（85.2%）在首次抗肿瘤评估时显示出客观缓解，中位反应时间为 1.4个月（95%CI：1.2-3.5）。截至截止日期，所有反应仍在持续。结论在r/r DLBCL患者中，SHR-A1912（1.8 mg/kg）联合R-GemOx治疗具有耐受性，且安全性与各单一药物成分一致。该联合方案显示出强大的抗肿瘤活性，以及快速且持久的反应。专家点评DLBCL是最常见的淋巴瘤亚型，约有30%~40%的患者发展为复发/难治，R/R DLBCL的患者预后较差，治疗首选挽救性化疗序贯自体造血干细胞移植（ASCT）或CAR-T细胞治疗，然而真实世界中接受ASCT或CAR-T治疗的患者比例较低，而不适合移植的R/R DLBCL患者客观缓解率（ORR）仅约40%，疗效有限且生存预后差。CD79b作为B细胞受体的关键组成部分，已成为DLBCL治疗领域极为重要的靶点。作为国内自主研发的新型CD79b ADC，SHR-A1912是一种靶向CD79b的新型ADC，由靶向CD79b的人源化IgG1单克隆抗体、可裂解连接子及DNA拓扑异构酶I抑制剂构成。本次ASCO会议上公布的这项研究显示SHR-A1912联合R-GemOx治疗R/R DLBCL的疗效令人鼓舞，ORR高达73%，CR率达54.1%。这一数据远超传统二线方案的疗效水平，而且缓解快速且持久：85.2%的应答者在首次评估即观察到客观缓解（中位反应时间仅1.4个月），截至数据截止时所有缓解仍在持续，提示该方案能快速控制疾病并带来深度、持久的缓解。同时SHR-A1912的安全性良好：导致SHR-A1912剂量减少的治疗期间不良事件（TEAE）发生率较低，没有患者因任何TEAE而停用SHR-A1912，该方案在R/R DLBCL中的长期疗效和安全性值得进一步关注。该研究入组患者均为至少一线治疗失败者，代表真实世界难治群体。联合方案展现的高缓解率和快速起效特性，为这部分预后极差、治疗选择匮乏的患者提供了全新的、极具潜力的治疗选择。未来亟需开展更大规模的III期随机对照研究以确证其疗效优势，并进一步探索其延长PFS和OS的潜力。该方案有望成为不适合移植的R/R DLBCL患者新的标准治疗选择。专家简介周辉教授湖南省肿瘤医院肿瘤学博士、教授、主任医师、硕士生导师湖南省肿瘤医院党委委员、副院长国家肿瘤质控中心淋巴瘤质控专家委员会委员中国抗癌协会淋巴瘤整合康复专业委员会副主任委员中国老年保健协会肿瘤免疫治疗专委会候任主任委员中国临床肿瘤学（CSCO）理事湖南省淋巴瘤诊疗中心主任淋巴瘤精准诊疗湖南省工程研究中心主任中华医学会肿瘤学分会淋巴瘤学组委员中华医学会肿瘤学分会肿瘤转化医学组委员CSCO淋巴瘤专家委员会常委中国抗癌协会淋巴瘤专业委员会常委湖南省医学会肿瘤内科学专业委员会候任主任委员（来源：《肿瘤瞭望–血液时讯》编辑部）声明凡署名原创的文章版权属《肿瘤瞭望》所有，欢迎分享、转载。本文仅供医疗卫生专业人士了解最新医药资讯参考使用，不代表本平台观点。该等信息不能以任何方式取代专业的医疗指导，也不应被视为诊疗建议，如果该信息被用于资讯以外的目的，本站及作者不承担相关责任。

抗体药物偶联物ASCO会议临床结果临床2期临床1期

2025-06-06

·靶点圈

下一代免疫之王登场：探索LAG-3靶点从机制突破到临床获批的十年征程

01LAG3的基本结构与功能 No.1LAG3的全称与别名淋巴细胞活化基因3 Lymphocyte activation gene3 (LAG3)，又称CD223，是一种新兴的免疫检查点分子，与PD-1、CTLA-4同属免疫抑制性受体(IRs)。 No.2LAG3的分子结构LAG3是一种Ⅰ型跨膜蛋白，属于免疫球蛋白超家族，与CD4结构相似，其结构包括4个Ig样胞外结构域(D1-D4)、跨膜区和胞内结构域(包含FxxL、KIEELE和EP等抑制性基序)，需同源二聚化发挥功能。图1 CD4和LAG3的结构比较和相似性图2 LAG3细胞质尾部的基序与介导抑制作用有关 No.3LAG3的同源二聚化D2结构域的疏水残基(如Trp180、Leu221)介导二聚化，是配体结合和信号传导的必要条件。靶向D2结构域的抗体(如C9B7W)可阻断二聚化，增强抗肿瘤免疫。 No.4LAG3的配体结合◆ FGL1(纤维蛋白原样蛋白1)：作为主要的免疫抑制配体，是肝脏分泌的可溶性蛋白，与LAG3高亲和力结合，干扰TCR-CD3复合体近端信号传导，降低T细胞增殖和细胞毒性(如IFN-γ、穿孔素分泌减少)。在多种癌症中高表达，与肝癌、胃癌的不良预后、免疫治疗耐药相关，阻断FGL1-LAG3轴可增强抗肿瘤免疫。◆ MHCII类分子(pMHCII)：作为经典配体，LAG3选择性结合稳定的pMHCII复合物，优先抑制识别该复合物的T细胞，阻断TCR信号传导并激活肿瘤细胞生存通路(如MAPK/Erk、PI3K/Akt)，增强肿瘤细胞抗凋亡能力并促进肿瘤免疫逃逸。◆ TCR-CD3复合体：作为顺式配体，在无MHCII时与LAG3结合，通过EP基序降低免疫突触pH值，干扰酪氨酸激酶Lck与共受体结合，抑制T细胞活化。◆ LSECtin(肝窦内皮细胞凝集素)：在黑色素瘤细胞表达，抑制效应T细胞增殖及IFN-γ分泌，促进肿瘤生长，但在其他肿瘤中作用有限。◆ Galectin-3(半乳凝素-3)：Galectin-3通过糖基化结合LAG3，抑制CD8+T细胞增殖和APC功能，在子宫内膜癌、多发性骨髓瘤等肿瘤中参与免疫抑制。◆ α-突触核蛋白(α-syn)：神经元中LAG3配体，促进α-syn纤维传递，与帕金森病发病相关。图3 LAG3的结构及其与配体的相互作用 No.5可溶性LAG3（sLAG3）胞外域被ADAM10/17蛋白酶剪切后产生可溶性sLAG3，其高水平与黑色素瘤、头颈部鳞癌等部分癌症预后不良相关，但其功能仍不明确。血清中sLAG3水平可能作为预测免疫治疗反应的生物标志物。RenyuBio仁域生物02LAG3的表达调控与功能机制 No.1LAG3的细胞分布与组织定位◆ 免疫细胞：广泛表达于T细胞、B细胞、NK细胞、树突状细胞(DCs)以及非免疫细胞(如神经元)表面。在肿瘤浸润T细胞(TILs)中也高表达，是T细胞耗竭的标志性分子之一。◆ 肿瘤细胞：在多种实体瘤以及血液瘤的肿瘤细胞中异常表达，其水平与肿瘤分期、转移能力、生存期和预后正相关。 No.2LAG3的调控机制◆ 转录调控：IL-6通过激活STAT3通路直接诱导LAG3在CD8+T细胞中表达。此外，FSTL1(卵泡抑素样蛋白1)也参与LAG3的调控，诱导产生CD11b+DIP2A+LAG3+细胞，促进结直肠癌的免疫逃逸，形成“FSTL1-LAG3轴”。◆ 表观遗传：LAG3甲基化状态与结直肠癌肿瘤风险呈负相关，但其甲基化状态在不同瘤种中稳定性不足，需更大样本验证。此外，LAG3的表观修饰还调控免疫检查点共表达，如PD-L1与LAG3的共甲基化影响免疫治疗响应。图4 LAG3在肿瘤细胞中的表达调控 No.3LAG3在免疫细胞中的功能◆ T细胞：LAG3通过结合配体抑制CD4+/CD8+T细胞的增殖、细胞因子分泌(如IL-2、IFN-γ、TNF-α)及细胞毒性，导致T细胞耗竭。◆ 调节性T细胞(Tregs)：Tregs表面LAG3表达上调可增强其免疫抑制能力，通过抑制效应T细胞和促进APC功能失活维持免疫耐受。LAG3缺陷会削弱Tregs的抑制功能，加剧自身免疫反应。◆ NK细胞：LAG3可抑制NK细胞的细胞毒性和细胞因子生成，但单独阻断对NK细胞毒性影响有限，联合IL-12可恢复其抗转移活性。◆ 树突状细胞(DCs)：膜结合LAG3与树突状细胞(DCs)表面MHCII结合，促进DCs成熟，分泌IL-12和TNF-α；但可溶性LAG3抑制单核细胞向DCs分化，削弱免疫应答。此外，在浆细胞样树突状细胞(pDCs)中，LAG3抑制pDCs产生I型干扰素，影响抗病毒和抗肿瘤免疫。图5 LAG3的功能机制 No.4LAG3在肿瘤中的作用机制◆ 肿瘤微环境(TME)调控：LAG3通过结合pMHCII或FGL1，诱导CD8+T细胞耗竭，促进Tregs和M2型巨噬细胞浸润，构建免疫抑制性微环境，促进肿瘤免疫逃逸。此外，LAG3还可通过抑制CD8+T细胞功能，间接促进肿瘤细胞上皮-间质转化(EMT)相关信号通路(如TGF-β)活化。图6 LAG3在肿瘤中的作用机制◆ 免疫逃逸协同作用：FGL1/LAG3轴与PD-1/PD-L1轴存在协同抑制效应，共表达于多种肿瘤的耗竭T细胞，双重阻断可显著增强T细胞活化。在PD-1耐药肿瘤中，FGL1/LAG3轴成为主要免疫逃逸途径，单独阻断即可恢复抗肿瘤免疫。图7 LAG3与PD-1的联系 No.5LAG3在自身免疫性疾病中的作用机制LAG3作为负调控因子，限制T细胞的增殖和免疫功能，防止其攻击正常组织。LAG3缺陷导致T细胞增殖失控，加速自身免疫病(如1型糖尿病、心肌炎)进展。Tregs中LAG3表达受IL-27调控，通过结合MHCII抑制DCs成熟，维持免疫耐受。类风湿关节炎、多发性硬化等患者血清sLAG3水平与疾病活动度正相关，可作为预后标志物。激动剂抗体(如IMP-761)通过激活LAG3抑制T细胞功能，缓解炎症模型症状。图8 LAG3在自身免疫性疾病中的功能和机制 No.6LAG3作为预后生物标志物的双重性◆ 阳性预后关联：在三阴性乳腺癌(TNBC)、胃癌(GC)、结直肠癌(CRC)中，高LAG3+TILs与更长的无转移生存期(MFS)和总生存期(OS)相关，可能反映活化T细胞的持续抗肿瘤效应。◆ 阴性预后关联：在肝细胞癌(HCC)、卵巢癌、黑色素瘤中，高LAG3表达与肿瘤进展、耐药及不良预后相关，可能与T细胞过度耗竭有关。图9 靶向LAG3的潜在治疗策略RenyuBio仁域生物03LAG3靶向治疗的临床进展图10 LAG3靶向治疗癌症的临床进展 No.1靶向LAG3的单克隆抗体表1 用于治疗癌症的临床试验中靶向LAG3的单克隆抗体 No.2靶向LAG3的特异性单抗联合疗法◆ Relatlimab(抗LAG3单抗)+Nivolumab(抗PD-1单抗)：已获批用于晚期黑色素瘤，且在结直肠癌、膀胱癌的III期试验中均显示生存获益，在CLL、FL、HL中也在开展I/II期临床试验。相比Nivolumab单药，联合治疗显著延长中位无进展生存期(PFS)，且安全性良好。◆ Fianlimab(抗LAG3单抗) +Cemiplimab(抗PD-1单抗)：I期试验中客观缓解率(ORR)达61.2%，但3级以上不良事件(AE)发生率为44%，主要为肾上腺功能不全。目前III期试验正在评估其在黑色素瘤和NSCLC中的疗效。◆ Favezelimab(抗LAG3单抗)+Pembrolizumab(抗PD-1单抗)：用于复发/难治性霍奇金淋巴瘤(R/RcHL)的II期试验显示，ORR达31%，12个月PFS率39%，对PD-1治疗失败患者仍有效。III期试验中，正在探索用于结直肠癌和霍奇金淋巴瘤的治疗。◆ 其他组合：LAG3 mAbs与CTLA4、TIM3、VEGF等靶点联合疗法正在临床试验中，但其中部分因疗效不足终止。表2 涉及LAG3与其他分子的III期临床试验 No.3靶向LAG3的双特异性抗体◆ 靶向免疫细胞表面多重IRs：①Tebotelimab(MGD013)：靶向LAG3/PD1的四价BsAb，I期试验显示单药ORR为19.4%，但免疫相关不良事件(irAEs)发生率较高(68.4%)，用于弥漫大B细胞淋巴瘤(DLBCL)的I期试验以及联合Margetuximab(抗HER2单抗)用于胃癌的II/III期试验正在进行。②Tobemstomig(RO7247669)：优先结合PD1的LAG3/PD1-BsAb，单药ORR为17.1%，联合化疗或TIGIT抑制剂的试验正在开展。③Pavunalimab(XmAb22841)：靶向LAG3/CTLA4的BsAb，与XmAb23104(PD-1/ICOS BsAb)联用的I期试验显示AE发生率低(20–24%)，安全性优于传统联合疗法。◆ 促进细胞间相互作用：①FS118、ABL501、IBI323：靶向LAG3/PDL1的BsAb，通过桥接T细胞与肿瘤细胞或抗原呈递细胞(APCs)增强T细胞活化和抗肿瘤免疫。FS118的I期试验显示疾病控制率为54.8%，且毒性较低。②GB266T：三特异性抗体(PDL1/TIGIT/LAG3)，保留Fc功能以增强APCs与T细胞的相互作用，临床前模型中显示强效抗肿瘤活性。表3 用于治疗癌症的临床试验中靶向LAG3的双特异性抗体 No.4其他新型疗法◆ 融合蛋白：如Eftilagimod alpha(IMP321)，sLAG3的Ig融合蛋白，通过结合DCs表面MHCII，促进DC成熟及CD8+T细胞活化，III期试验评估其与紫杉醇联用在转移性乳腺癌中的疗效。与Pembrolizumab联用在黑色素瘤中ORR达50%，并可增强化疗疗效。◆ 纳米药物：利用纳米载体共递送siLAG3和siPD-L1可下调肿瘤微环境中免疫检查点表达，增强T细胞浸润。◆ 疫苗：双靶点疫苗(如FGL1/CAIX DNA疫苗)通过激活DCs，增强CD8+T细胞对肾癌的免疫应答。◆ 小分子抑制剂：靶向LAG3与MHC-II/FGL1结合的小分子药物进入临床前研究，具口服生物利用度和肿瘤穿透性优势，处于早期研发阶段。 No.5联合治疗策略◆ 与其他免疫检查点抑制剂联用：LAG3与TIM3、TIGIT等共阻断可克服PD-1耐药，如在肺癌模型中联合阻断LAG3和TIGIT显著抑制肿瘤生长，在AML模型中LAG3与TIM3双阻断可协同恢复T细胞功能。◆ 与靶向治疗联用：①EGFR抑制剂：LAG3抑制剂可逆转EGFR-TKI耐药，如在NSCLC中联合Gefitinib增强抗肿瘤效应。②PI3Kδ抑制剂：LAG3阻断可增强PI3Kδ抑制剂的抗肿瘤效应，机制与减少Treg抑制和促进CD8+T细胞活化相关。③GSK-3抑制剂：与LAG3单抗联用在B16黑色素瘤模型中诱导肿瘤消退，与CD8+T细胞增殖和细胞因子分泌增加相关。◆ 与放化疗联用：①化疗增敏：部分肿瘤对单一的LAG3阻断响应有限，需结合化疗(如阿扎胞苷)或表观调控药物(如HDAC抑制剂)逆转免疫抑制微环境。Tebotelimab与化疗(如卡培他滨+奥沙利铂)联用在HER2+胃癌的II/III期试验中显示初步疗效。②放疗协同：微波消融或纳米粒子放疗联合LAG3阻断可增强CD8+T细胞浸润，在MC38结直肠癌模型中显著抑制肿瘤生长。◆ 与中药疗法联用：氧化苦参碱通过下调IL-6/STAT3通路降低FGL1表达，增强LAG3免疫治疗效果。◆ 与细胞疗法联用：①CAR-T细胞疗法：LAG3抗体增强CD4+T细胞和双阴性T细胞(CD4-CD8-TC)的细胞毒性，在乳腺癌模型中上调T-bet和穿孔素表达。临床前研究显示，LAG3抗体可增强CAR-T细胞对CLL的杀伤作用，相关临床试验待开展。②肿瘤浸润淋巴细胞(TILs)：LAG-3阻断联合TILs疗法在黑色素瘤中显示增强的持久应答。图11 涉及靶向LAG3的新治疗策略RenyuBio仁域生物04LAG3在不同疾病中的病理机制 No.1实体瘤应用◆ 黑色素瘤：LAG3表达水平与黑色素瘤的进展、耐药相关。LAG3在TILs表面高表达，可诱导T细胞耗竭，同时增强Tregs的免疫抑制功能，促进肿瘤免疫逃逸。此外还能协同PD-1通路促进免疫耐受。双重阻断可逆转T细胞功能失调，增强抗肿瘤免疫应答，显著延长PFS和OS，且毒性低于CTLA-4/PD-1联合方案。◆ 肾细胞癌(RCC)：LAG3与PD-1在肿瘤微环境中协同表达，抑制CD8+T细胞和NK细胞功能，且LAG3表达水平与RCC患者预后呈负相关。单药LAG3抑制剂疗效有限，联合PD-1抑制剂在初治患者中客观缓解率(ORR)达30%，但对PD-(L)1经治患者响应不足(ORR 7%)。◆ 非小细胞肺癌(NSCLC)：NSCLC患者对PD-1抑制剂耐药后常上调LAG3，通过抑制T细胞代谢(如糖酵解)和DC成熟维持免疫抑制。Relatlimab+Nivolumab可诱导病理缓解(MPR30%)，安全性与单药相当。◆ 结直肠癌(CRC)：①微卫星不稳定型(MSI-H/dMMR)：LAG3抑制剂联合PD-1抑制剂治疗显示高病理缓解率(92%)，可能与肿瘤免疫原性高相关。②微卫星稳定型(MSS)：LAG3靶向治疗单药疗效有限，需结合其他通路(如Wnt/β-catenin)异常筛选患者。◆ 胃癌/胃食管交界癌(GC/GEJC)：LAG3+Tregs在肿瘤微环境中富集，抑制效应T细胞浸润，联合化疗未能显著提升ORR(48%vs.61%)，提示需更精准的生物标志物指导治疗。◆ 肝癌(HCC)：LAG3与PD-L1在肝细胞癌中共表达，通过抑制CD8+T细胞和NK细胞功能促进肿瘤生长。Relatlimab+Nivolumab在TKI经治患者中疾病控制率(DCR)达60%，双特异性抗体Tebotelimab单药ORR17.1%，显示初步活性但需更大样本验证。◆ 三阴性乳腺癌(TNBC)：LAG3抑制CD8+T细胞浸润和细胞毒性，与Gal-3协同促进肿瘤进展。Leramilimab+Spartalizumab在初治患者中ORR26.3%，但经治患者仅5.3%，提示早期干预可能更有效。◆ 其他肿瘤：LAG3的表达还与膀胱癌、子宫内膜癌等的免疫细胞浸润密度和预后相关，如肌层浸润性膀胱癌中LAG3+T细胞浸润与化疗耐药和不良生存独立相关。表4 靶向LAG3治疗实体瘤的临床试验 No.2血液肿瘤应用◆ 慢性淋巴细胞白血病(CLL)：CLL患者的白血病细胞及血清中sLAG3水平显著升高，与疾病进展和不良预后相关。在CLL的临床前模型中，阻断LAG3可恢复T细胞对白血病细胞的杀伤能力，联合PD-1抑制剂进一步增强疗效。◆ 霍奇金淋巴瘤(HL)：HL患者的TILs中LAG3高表达，与PD-1共表达于耗竭CD8+T细胞，抑制抗原特异性免疫应答。LAG3+CD4+T细胞的存在与HL患者的肿瘤进展相关，清除此类细胞可增强CD8+T细胞的抗肿瘤效应。◆ 急性髓系白血病(AML)：AML患者骨髓中LAG3+PD-1+CD8+T细胞比例显著高于健康人群，提示T细胞功能耗竭。◆ 滤泡淋巴瘤(FL)：LAG3表达于TILs，与PD-1共表达时预示患者预后不良，且与肿瘤微环境中免疫抑制性细胞因子(如IL-10)水平升高相关。表5 血液系统癌症中靶向LAG3的临床试验 No.3自身免疫疾病应用◆ 系统性红斑狼疮(SLE)：SLE患者中LAG3在Tregs和效应T细胞表面高表达，与疾病活动度(SLEDAI评分)正相关，其血清浓度可反映炎症程度。并且血清sLAG3水平降低与SLE患者病情进展相关，可能成为预测疾病恶化的指标。LAG3缺陷间接增强CD4+T细胞对B细胞的辅助功能，促进自身抗体(如抗dsDNA抗体)产生，加剧SLE模型中的肾小球炎症。◆ 1型糖尿病(T1D)：LAG3通过维持CD8+T细胞的“restrained”表型(类似耗竭状态)抑制其攻击胰岛β细胞。在LAG3缺陷小鼠中，CD8+T细胞的“restrained”表型消失，糖酵解代谢增强，加速T1D进展；而Tregs表面LAG3缺失则无法有效抑制自身免疫反应。传统认为CD4+T细胞主导T1D，但LAG-3缺陷模型显示CD8+T细胞也可独立驱动疾病，提示LAG-3对两类T细胞均有调控作用。◆ 类风湿关节炎(RA)：RA患者中LAG3+Tregs比例升高，但其分泌IL-10的能力下降，导致促炎因子(如TNF-α、IL-6)失衡。血清sLAG-3水平与疾病活动度(如关节肿胀程度)正相关，其主要来源于Tregs表面LAG3的蛋白酶切割。靶向LAG3可增强Tregs的抑制功能，减少关节炎症，如激动剂抗体IMP-761在动物模型中显示抗炎潜力。◆ 多发性硬化(MS)：MS患者外周血中LAG3+T细胞数量减少，与中枢神经系统炎症加重相关；血清sLAG3水平较高者预后较好，提示LAG3可能抑制自身反应性T细胞向脑内浸润。LAG-3可能通过抑制Th1/Th17细胞分化，减少其分泌IFN-γ和IL-17，从而减轻神经髓鞘损伤。◆ 炎症性肠病(IBD)：LAG-3+T细胞在肠道黏膜中富集，其数量与内镜下炎症程度正相关。阻断LAG-3可激活效应T细胞，加重结肠炎；而维持LAG-3功能可抑制过度免疫反应。LAG-3通过抑制CD4+T细胞的糖酵解代谢，减少促炎细胞因子(如IL-17)分泌，维持肠道免疫稳态。表6 靶向LAG3疗法在自身免疫疾病中的临床前和临床开发RenyuBio仁域生物05LAG-3靶向治疗的挑战与未来方向 No.1机制研究的局限性◆ 配体复杂性：MHCII作为主要配体的作用已明确，但FGL1、LSECtin等配体的贡献仍需验证，且不同物种间存在差异(如小鼠vs.人类MHCII稳定性)。◆ 信号通路未知：缺乏LAG3下游信号分子的明确研究，需通过蛋白质组学、CRISPR筛选等技术解析。 No.2未来发展方向◆ 生物标志物开发：缺乏统一的生物标志物检测标准，目前LAG3表达水平、FGL1的预测价值有限，sFGL1和sLAG3的临床意义尚不明确，需探索LAG3表达水平、T细胞耗竭状态(如PD-1共表达)及肿瘤微环境细胞组成(如Treg比例)的联合预测价值。◆ 毒性管理与联合优化：尽管LAG3抑制剂单药毒性较低，但与其他ICIs联用可能增加irAEs(如肾上腺功能不全)，需探索剂量优化和个体化治疗策略。◆ 新型药物设计：开发同时阻断LAG3与多种配体(如MHCII/FGL1)的双特异性抗体，或小分子抑制剂靶向胞内信号基序。◆ 联合治疗策略：探索LAG3抑制剂与放疗、表观药物或多靶点阻断(如TIM3、TIGIT)的协同效应，以克服耐药性。RenyuBio仁域生物抗体发现服务 & 产品01羊驼免疫&骆驼免疫—自建现代化养殖农场02万亿级天然抗体库产品—轻松DIY科研抗体03配套产品—助您轻松搭建基因工程抗体平台仁域生物成都仁域生物成立于2019年1月，是一家专注基因工程抗体技术和天然抗体库开发的公司，拥有优化的噬菌体展示抗体库技术和现代化的骆驼/羊驼养殖免疫基地。可为客户提供14天、100%成功率的先导抗体分子发现服务，彻底解决传统抗体定制的周期长、失败率高、成本高三大难题。目前已经成功完成300+靶点抗体筛选项目！protocol 获取 / 产品咨询邮箱｜find@renyubio.com电话｜19136178673地址｜成都市经开区科技产业孵化园关注我们，持续更新相关内容参考文献Hu K, Zhang G, Niu H, Sun L. Research advances in FGL1/LAG3 for cancer diagnosis and treatment: From basics to clinical practice. J Cancer Res Ther. 2025 May 1;21(2):344-353. Giri VK, McDermott DF, Zaemes J. The emerging role of lymphocyte-activation gene 3 targeting in the treatment of solid malignancies. Cancer. 2025 May 15;131(10):e35892. Luca VC. LAG Time in the Era of Immunotherapy-New Molecular Insights Into the Immunosuppression Mechanism of Lymphocyte Activation Gene-3. Immunol Rev. 2025 Mar;330(1):e70002.Adam K, Butler SC, Workman CJ, Vignali DAA. Advances in LAG3 cancer immunotherapeutics. Trends Cancer. 2025 Jan;11(1):37-48. Wu R, Zeng M, Zhang Y, He J. LAG3 immune inhibitors: a novel strategy for melanoma treatment. Front Oncol. 2024 Dec 18;14:1514578. Leitner J, Aigner-Radakovics K, Steinberger P. LAG-3-An incompletely understood target in cancer therapy. FASEB J. 2024 Nov 30;38(22):e70190.Ren K, Hamdy H, Meyiah A, Elkord E. Lymphocyte-activation gene 3 in cancer immunotherapy: function, prognostic biomarker and therapeutic potentials. Front Immunol. 2024 Nov 26;15:1501613.Martínez-Pérez A, Granda-Díaz R, Aguilar-García C, Sordo-Bahamonde C, Gonzalez S. Deciphering LAG-3: unveiling molecular mechanisms and clinical advancements. Biomark Res. 2024 Oct 18;12(1):126. Nie J, Qin X, Tao X, Huang J. Exploring the molecular landscape of lymphocyte activation gene-3: A literature review. Medicine (Baltimore). 2024 Sep 27;103(39):e39622. Chavanton A, Mialhe F, Abrey J, Baeza Garcia A, Garrido C. LAG-3 : recent developments in combinational therapies in cancer. Cancer Sci. 2024 Aug;115(8):2494-2505. Luo Y, Cai X, Yang B, Lu F, Yi C, Wu G. Advances in understanding the role of immune checkpoint LAG-3 in tumor immunity: a comprehensive review. Front Oncol. 2024 Aug 26;14:1402837. Wang B, Zhang B, Wu M, Xu T. Unlocking therapeutic potential: Targeting lymphocyte activation Gene-3 (LAG-3) with fibrinogen-like protein 1 (FGL1) in systemic lupus erythematosus. J Transl Autoimmun. 2024 Jul 27;9:100249.

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KEGG	Wiki	ATC	Drug Bank
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适应症	国家/地区	公司	日期
小肠癌	日本	Takata Pharmaceutical Co. Ltd.	2018-09-21
小肠癌	日本	Yakult Honsha Co., Ltd.	2018-09-21
胃癌	日本	Takata Pharmaceutical Co. Ltd.	2015-03-20
胃癌	日本	Yakult Honsha Co., Ltd.	2015-03-20
胰腺癌	日本	Yakult Honsha Co., Ltd.	2013-12-20
胰腺癌	日本	Takata Pharmaceutical Co. Ltd.	2013-12-20
结直肠癌	美国	Sanofi-Aventis U.S. LLC	2007-01-10
晚期结直肠腺癌	澳大利亚	Medis Pharma Pty Ltd.	2006-11-28
结肠癌	美国	Sanofi-Aventis U.S. LLC	2002-08-09
直肠癌	美国	Sanofi-Aventis U.S. LLC	2002-08-09
肿瘤	中国	南京制药厂有限公司	2000-01-01

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适应症	最高研发状态	国家/地区	公司	日期
弥漫性大B细胞淋巴瘤	临床3期	美国	Hoffmann-La Roche, Inc.	2021-02-23
弥漫性大B细胞淋巴瘤	临床3期	中国	Hoffmann-La Roche, Inc.	2021-02-23
弥漫性大B细胞淋巴瘤	临床3期	澳大利亚	Hoffmann-La Roche, Inc.	2021-02-23
弥漫性大B细胞淋巴瘤	临床3期	比利时	Hoffmann-La Roche, Inc.	2021-02-23
弥漫性大B细胞淋巴瘤	临床3期	丹麦	Hoffmann-La Roche, Inc.	2021-02-23
弥漫性大B细胞淋巴瘤	临床3期	法国	Hoffmann-La Roche, Inc.	2021-02-23
弥漫性大B细胞淋巴瘤	临床3期	德国	Hoffmann-La Roche, Inc.	2021-02-23
弥漫性大B细胞淋巴瘤	临床3期	波兰	Hoffmann-La Roche, Inc.	2021-02-23
弥漫性大B细胞淋巴瘤	临床3期	西班牙	Hoffmann-La Roche, Inc.	2021-02-23
弥漫性大B细胞淋巴瘤	临床3期	瑞士	Hoffmann-La Roche, Inc.	2021-02-23

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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


NCT03388190 (METIMMOX, ASCO2025)	临床2期	微卫星稳定型结直肠癌一线 BRAF \| TMB	36	FLOX (oxaliplatin, 5-fluorouracil, folinic acid) Q2W	築遞築壓繭網糧衊壓網(繭觸襯構鹽醖繭艱蓋壓) = 憲憲膚鏇襯鹹廠製夢艱簾餘壓鹽遞願範構窪鑰 (糧遞遞壓鬱遞壓鏇簾選 )	积极	2025-05-30
NCT03388190 (METIMMOX, ASCO2025)	临床2期	微卫星稳定型结直肠癌一线 BRAF \| TMB	36	Alternating FLOX and nivolumab Q2W	築遞築壓繭網糧衊壓網(繭觸襯構鹽醖繭艱蓋壓) = 製選餘衊鑰夢顧積廠選簾餘壓鹽遞願範構窪鑰 (糧遞遞壓鬱遞壓鏇簾選, 12.4 ~ 18.5) 更多	积极	2025-05-30
NCT04940546 (phase II trial, ASCO2025)	临床2期	结直肠癌肝转移新辅助	36	Sintilimab + Bevacizumab + Oxaliplatin + Capecitabine	蓋鬱鹽網獵鏇製憲淵製(鏇糧鑰繭夢鹽鹹蓋範鹽) = the median OS had not yet been reached 鹽膚窪衊廠顧衊襯鑰構 (齋積構衊艱窪齋膚齋醖 ) 更多	积极	2025-05-30
AACR2025	N/A	结直肠癌	-	Obatoclax	憲淵構窪淵網積範鏇廠(鏇齋構範淵願製顧選齋) = 憲憲構艱鑰觸遞襯製夢鬱範積願膚鏇齋壓網鹽 (艱鏇鬱築鬱蓋夢鏇選繭 )	积极	2025-04-27
NCT03861702 (BTCRC-GI15-067, CTgov)	临床2期	局部晚期胰腺腺癌	28	LEUCOVORIN CALCIUM+Liposomal Irinotecan+Oxaliplatin+Fluorouracil	夢壓廠齋夢鹽鑰觸醖獵 = 觸廠範願襯鏇鏇選願築鑰積衊蓋廠廠積鏇鬱壓 (遞餘餘鹹積蓋鏇願齋餘, 構鑰構獵觸膚簾艱顧憲 ~ 範廠淵糧築齋憲構鹹餘) 更多	-	2025-04-18
NCT04380337 (SHORT-FOX, CTgov)	临床2期	直肠癌 \| 直肠腺癌	38	IMRT+LEUCOVORIN CALCIUM+irinotecan+oxaliplatin+capecitabine+Fluorouracil	齋網夢膚鹽範齋範齋製 = 鬱築齋網壓網廠積鬱壓鹽選憲齋範範蓋齋夢鏇 (艱夢鑰醖範襯築獵鏇鹽, 鹹製積積製襯蓋範繭膚 ~ 廠觸製廠鏇簾構淵築顧) 更多	-	2025-02-25
JPRN-UMIN000022210 (Phase I/II clinical trial of preoperative docetaxel/oxaliplatin/S‑1 (DOS) combination therapy for esophagogastric junction adenocarcinoma, ASCO_GI2025)	临床1/2期	胃食管交界处腺癌新辅助 \| 辅助	40	Docetaxel 60 mg/m²	簾蓋鬱襯觸鏇壓壓蓋選(獵築積糧鹹積簾鬱鏇積) = 廠繭艱選遞選膚鏇淵鬱簾網簾衊鬱艱餘廠襯衊 (襯艱積構淵鹹遞遞簾選 ) 更多	积极	2025-01-23
	临床1/2期	胃食管交界处腺癌新辅助 \| 辅助	40	S-1 120 mg/body	構築觸齋遞繭襯衊餘蓋(餘壓鹽廠簾鏇蓋廠淵襯) = 築範簾獵壓淵遞襯構製鹹鬱鏇膚齋鑰顧鏇壓積 (齋鏇積壓夢壓壓遞簾憲 ) 更多	积极	2025-01-23
NCT05627635 (ASCO_GI2025)	临床1期	微卫星稳定型结直肠癌 MSS	14	Folinic acid, fluorouracil, oxaliplatin, bevacizumab, botensilimab, balstilimab (FOLFOX-3B)	夢網鏇廠範廠簾餘蓋鬱(構夢鹹鹽網憲鏇鏇鑰壓) = one pt at DL1 with transient G3 AST/ALT elevation and transient G2 colitis (resolved with steroids and infliximab), one pt at DL1 with G2 hypothyroidism and one patient at DL2 with G2 hyperthyroidism 憲鑰艱襯憲鑰鑰餘醖鹹 (遞簾蓋憲鬱蓋簾壓襯築 ) 更多	积极	2025-01-23
ASCO_GI2025	N/A	晚期肝细胞癌一线	-	Lenvatinib plus FOLFOX-HAIC	選觸淵淵構窪繭糧夢糧(網顧醖範鹽顧醖膚鹹夢) = Grade 3-4 adverse events, including nausea, vomiting, diarrhea, thrombocytopenia, and neutropenia, were more prevalent in the lenvaHAIC group 獵淵積蓋觸窪選範繭廠 (繭鹹壓醖艱築醖製獵願 ) 更多	积极	2025-01-23
ASCO_GI2025	N/A	晚期肝细胞癌一线	-	Lenvatinib alone		积极	2025-01-23
JPRN-jRCTs031200094 (ASCO_GI2025)	临床2期	食管鳞状细胞癌新辅助	54	Neoadjuvant FLOT therapy	網鬱獵夢繭廠糧窪鑰簾(衊獵餘鏇築憲餘鏇鹹顧) = 願遞積壓範淵蓋壓淵醖鑰壓憲襯夢窪淵鬱觸夢 (製淵範鹽觸醖築鹽鏇齋, 29.8 ~ 57.7) 更多	积极	2025-01-23