Cohort study of SABR combined with anti-PD-1 and targeted therapy versus anti-PD-1 and targeted therapy for recurrent or metastatic renal cell carcinoma patients

开始日期2024-04-01

申办/合作机构

北京大学第一医院

NCT05162755 / Active, not recruiting临床1期IIT

A Phase 1a/1b, Open-label, Multicenter Trial Investigating the Safety, Tolerability, and Preliminary Anti-neoplastic Activity of S095029 (Anti-NKG2A) as Monotherapy and in Combination With Sym021 (Anti-PD-1) in Patients With Advanced Solid Tumor Malignancies Followed by an Expansion Part With Triplet Combinations of S095029 and Sym021 and an Anti-HER2 mAb or Anti-EGFR mAbs (Futuximab/Modotuximab) in Patients With Metastatic Gastric or Colorectal Cancers

The purpose of the study is to investigate the safety, tolerability, and preliminary anti-neoplastic activity of S095029 alone and in combination with Sym021 in patients with advanced solid tumor malignancies followed by an expansion phase of triple combinations.

开始日期2021-10-15

申办/合作机构

Institut de Recherches Intern Servier

[+1]

NCT04195373 / Withdrawn临床1期

A Phase I Open-label, Safety Study of Intra-tumoral Application of TMV-018 in Combination With 5-FC or Anti-PD-1 Therapy in Patients With Tumors of the Gastrointestinal Tract

This study aims to determine the safety and tolerability of TMV-018 when given alone or in combination with the prodrug 5-Fluorocytosine (5-FC) or an anti-PD-1 checkpoint inhibitor in patients with gastrointestinal tumors. Furthermore, the maximum tolerated dose (MTD) and recommended Phase II dose of TMV-018 shall be determined.

开始日期2020-11-23

申办/合作机构

Themis Bioscience GmbH

[+2]

100 项与 Sym-021 相关的临床结果

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100 项与 Sym-021 相关的转化医学

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100 项与 Sym-021 相关的专利（医药）

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项与 Sym-021 相关的文献（医药）

2024-09-20·Nan fang yi ke da xue xue bao = Journal of Southern Medical University

[High RNF7 expression enhances PD-1 resistance of non-small cell lung cancer cells by promoting CXCL1 expression and myeloid-derived suppressor cell recruitment via activating NF-κB signaling].

Article

作者: Geng, B ; Wang, H ; Sun, Z ; Zhong, N ; Zhao, W

OBJECTIVETo investigate the mechanism of RNF7 for regulating myeloid-derived suppressor cells (MDSCs) in nonsmall cell lung cancer (NSCLC).METHODSTIMER2.0 database and immunohistochemistry were used to analyze RNF7 expression level and its correlation with immune cell infiltration in non-small cell lung cancer. The impact of RNF7 expression levels on prognosis of lung cancer patients was analyzed using Kaplan-Meier survival analysis. CMT-167 cells with RNF7 overexpression or knockdown were inoculated subcutaneously in C57BL/6 mice, and the mice in RNF7 knockdown group were treated with anti-PD-1 or IgG isotype control 7 days after the inoculation. The tumor tissues were harvested after 30 days for tumor volume measurement, detection of S100A8+A9 and Gr-1 expressions with immunohistochemistry, and analysis of MDSC infiltration. Gene set enrichment analysis (GSEA) was performed to identify the potential pathways regulated by RNF7 in NSCLC. Western blotting and luciferase assays were used to assess the impact of RNF7 on the NF-κB signaling pathway. ELISA and RT-qPCR were used to measure chemokine (C-X-C motif) ligand 1 (CXCL1) expression.RESULTSRNF7 expression was significantly upregulated in NSCLC, and high RNF7 expression levels were associated with poor prognosis of the patients (P < 0.001). TIMER2.0 analysis revealed a positive correlation between RNF7 expression and MDSC infiltration (P < 0.001). GSEA suggested that RNF7 was enriched in the NF-κB signaling pathway. In NSCLC cells, RNF7 knockdown significantly inhibited NF-κB activation and reduced CXCL1 expression. In the tumor-bearing mice, RNF7 overexpression significantly increased MDSC infiltration in the tumor tissue, and RNF7 knockdown obviously reduced MDSC infiltration and enhanced the efficacy of anti-PD-1 therapy.CONCLUSIONHigh expression of RNF7 in NSCLC cells promotes CXCL1 expression by activating the NF-κB signaling pathway, thus leading to the chemotactic recruitment of MDSCs, which contributes to tumor resistance to antiPD-1 therapy.

2020-12-01·Journal of Hematology & Oncology1区 · 医学

CDK7 inhibitor THZ1 enhances antiPD-1 therapy efficacy via the p38α/MYC/PD-L1 signaling in non-small cell lung cancer

1区 · 医学

ArticleOA

作者: Wang, Jian ; Meng, Rui ; Zhou, Xiaoshu ; Dong, Xiaorong ; Zhang, Sheng ; Yang, Kunyu ; Wu, Gang ; Liu, Li ; Zong, Yan ; Hong, Jiaxin ; Zhang, Ruiguang ; Lin, Zhenyu ; Zhang, Tao ; Chen, Yaobing ; Xu, Yingzhuo ; Tang, Jing ; Xu, Shuangbing

AbstractBackgroundThe cyclin-dependent kinase 7 (CDK7) subunit of TFIIH regulates RNA polymerase-II-based transcription and promotes tumor progression. However, the mechanisms involved in CDK7-mediated immune evasion are unclear in non-small cell lung cancer (NSCLC).MethodsRNA silencing and pharmacologic inhibitors were used to evaluate the functions of CDK7/p38α/MYC/PD-L1 axis in cancer cell proliferation and antiPD-1 therapy resistance. Flow cytometry was performed to detect the status of the immune microenvironment after CDK7 inhibition and antiPD-1 therapy in vivo. CD8 depletion antibodies were used to assess the role of CD8+ T cells in combined CDK7 and PD-1 blockade. The associations among CDK7, p38α, MYC, PD-L1, infiltrating T cells, and survival outcomes were validated in two tissue microarrays and public transcriptomic data of NSCLC.ResultsHigh CDK7 mRNA and protein levels were identified to be associated with poor prognosis in NSCLC. CDK7 silencing and CDK7 inhibitor THZ1 elicited apoptosis and suppressed tumor growth. Moreover, CDK7 ablation specifically suppressed p38α/MYC-associated genes, and THZ1 inhibited MYC transcriptional activity through downregulating p38α. CDK7 inhibition sensitized NSCLC to p38α inhibitor. Further, THZ1 suppressed PD-L1 expression by inhibiting MYC activity. THZ1 boosted antitumor immunity by recruiting infiltrating CD8+ T cells and synergized with antiPD-1 therapy. The CDK7/MYC/PD-L1 signature and infiltrating T cell status collectively stratified NSCLC patients into different risk groups.ConclusionThese data suggest that the combined CDK7 inhibitor THZ1 and antiPD-1 therapy can be an effective treatment in NSCLC.

2019-05-19·mAbs2区 · 医学

Sym021, a promising anti-PD1 clinical candidate antibody derived from a new chicken antibody discovery platform

2区 · 医学

Article

作者: Horak, Ivan D ; Kragh, Michael ; Melander, Maria C ; Pedersen, Mikkel W ; Gad, Monika ; Strandh, Magnus ; Lindsted, Trine ; Bouquin, Thomas ; Lantto, Johan ; Grandal, Michael M ; Koefoed, Klaus ; Uhlenbrock, Franziska ; Galler, Gunther R ; Bhatia, Vikram K ; Dietrich, Nikolaj ; Gjetting, Torben ; Fröhlich, Camilla

Discovery of therapeutic antibodies is a field of intense development, where immunization of rodents remains a major source of antibody candidates. However, high orthologue protein sequence homology between human and rodent species disfavors generation of antibodies against functionally conserved binding epitopes. Chickens are phylogenetically distant from mammals. Since chickens generate antibodies from a restricted set of germline genes, the possibility of adapting the Symplex antibody discovery platform to chicken immunoglobulin genes and combining it with high-throughput humanization of antibody frameworks by "mass complementarity-determining region grafting" was explored. Hence, wild type chickens were immunized with an immune checkpoint inhibitor programmed cell death 1 (PD1) antigen, and a repertoire of 144 antibodies was generated. The PD1 antibody repertoire was successfully humanized, and we found that most humanized antibodies retained affinity largely similar to that of the parental chicken antibodies. The lead antibody Sym021 blocked PD-L1 and PD-L2 ligand binding, resulting in elevated T-cell cytokine production in vitro. Detailed epitope mapping showed that the epitope recognized by Sym021 was unique compared to the clinically approved PD1 antibodies pembrolizumab and nivolumab. Moreover, Sym021 bound human PD1 with a stronger affinity (30 pM) compared to nivolumab and pembrolizumab, while also cross-reacting with cynomolgus and mouse PD1. This enabled direct testing of Sym021 in the syngeneic mouse in vivo cancer models and evaluation of preclinical toxicology in cynomolgus monkeys. Preclinical in vivo evaluation in various murine and human tumor models demonstrated a pronounced anti-tumor effect of Sym021, supporting its current evaluation in a Phase 1 clinical trial. Abbreviations: ADCC, antibody-dependent cellular cytotoxicity; CD, cluster of differentiation; CDC, complement-dependent cytotoxicity; CDR, complementarity determining region; DC, dendritic cell; ELISA, enzyme-linked immunosorbent assay; FACS, fluorescence activated cell sorting; FR, framework region; GM-CSF, granulocyte-macrophage colony-stimulating factor; HRP, horseradish peroxidase; IgG, immunoglobulin G; IL, interleukin; IFN, interferon; mAb, monoclonal antibody; MLR, mixed lymphocyte reaction; NK, natural killer; PBMC, peripheral blood mono-nuclear cell; PD1, programmed cell death 1; PDL1, programmed cell death ligand 1; RT-PCR, reverse transcription polymerase chain reaction; SEB, Staphylococcus Enterotoxin B; SPR, surface Plasmon Resonance; VL, variable part of light chain; VH, variable part of heavy chain.

项与 Sym-021 相关的新闻（医药）

2024-09-24

·奇点网

又促癌又利好免疫治疗，墙头草啊这是

*仅供医学专业人士阅读参考看多了人体内各种细胞争先恐后给癌细胞当帮凶的研究，奇点糕总有种误入了某全员内鬼酒厂，啊不组织的感觉，哪天真跳出来个助力抗癌的“正面人物”，奇点糕都得看着论文标题愣一下才敢相信，这叫什么个事儿啊。不过奇点糕的这种刻板印象其实也不算错，今天要介绍的助力癌症免疫治疗的“正面人物”也确实不是细胞，而是肠道微生物的一员。近日，香港中文大学医学院于君领衔的研究团队在Cancer Cell期刊发表了最新研究成果[1]，首次揭示常在结直肠癌（CRC）中富集、且可能导致CRC发生发展的具核梭杆菌（Fusobacterium nucleatum），竟然还会助力免疫治疗激活CD8+T细胞，从而使免疫治疗在此前疗效不佳的微卫星稳定型（MSS）CRC中打开突破口，真是意想不到啊。研究发现，具核梭杆菌可产生大量丁酸，抑制CD8+T细胞中的组蛋白去乙酰化酶（HDAC）3/8，由此诱导Tbx21基因启动子的H3K27乙酰化和表达上调，作为转录调节因子的TBX21就能转录抑制CD8+T细胞表达PD-1，从而缓解CD8+T细胞耗竭，恢复它们的效应功能，因此MSS型CRC患者瘤内的具核梭杆菌丰度较高，也与免疫治疗效果较好相关。一图总结论文核心内容MSS型CRC占全部CRC的85%以上，奇点糕都记不清免疫治疗在这里多少次碰得头破血流了，所以能发现具核梭杆菌这个“自己人”内应，确实挺出乎意料的.特别是此前还有研究显示，在免疫治疗已取得突破的微卫星不稳定型（MSI）CRC中，具核梭杆菌丰度可能与CD8+T细胞的浸润呈负相关；但在MSS型CRC中，相关性又掉转成了正相关[2]。于君团队就从这项结论看似有些矛盾性的研究出发，开始探究具核梭杆菌对MSS型CRC的免疫治疗到底有什么影响。对25例患者的初步分析显示，肿瘤组织样本内的具核梭杆菌丰度，与患者接受免疫治疗的生存预后（PFS/OS）呈正相关，乃至与免疫治疗是否对CRC肝转移有效都有关；将瘤内富集具核梭杆菌CRC患者的粪菌移植到荷瘤小鼠体内，也可显著改善小鼠对免疫治疗的应答，且肿瘤内的CD8+T细胞显著增多、耗竭细胞占比则减少。具核梭杆菌丰度可预测MSS型CRC对免疫治疗的应答研究者们又采用先以抗生素处理清除小鼠肠道菌群、再饲喂具核梭杆菌的方法证实，具核梭杆菌确实会加速MSS型CRC在小鼠体内的增殖，与既往研究发现一致，但瘤内存在具核梭杆菌也会使荷瘤小鼠对PD-1抑制剂治疗的应答更好，且瘤内浸润的主要是具有较强细胞毒效应功能的CD8+T细胞（IFN-γ+/TNF-α+/GZMB+），而非耗竭CD8+T细胞（PD-1+）。具核梭杆菌是如何激活CD8+T细胞主导的免疫应答，就是接下来要明确的问题了，研究者们认为奥秘可能与具核梭杆菌的某种分泌物质有关，并在实验中证实具核梭杆菌的条件培养液（CM）就足以增敏PD-1抑制剂治疗，而且还能直接作用于CD8+T细胞；研究者们又按分泌物分子质量进行了分层分析，证实关键物质的分子量<3 kDa。而在37种分子量符合<3 kDa条件的候选物质中，富集程度受具核梭杆菌存在与否影响最大的就是丁酸，用它单独处理CD8+T细胞就能起到改善细胞毒效应功能、缓解耗竭状态的作用，并在细胞/类器官/小鼠实验中都对免疫应答有正向激活作用，下一步研究的主要对象当然就是它啦。丁酸是具核梭杆菌外分泌影响CD8+T细胞状态和功能的关键物质通过单细胞RNA测序，研究者们发现具核梭杆菌CM处理或丁酸直接处理，都会上调CD8+T细胞的Tbx21基因表达，它编码的TBX21是对CD8+T细胞激活有关键作用的细胞因子；接下来的实验则揭示，具核梭杆菌外分泌丁酸调控Tbx21基因表达的机制，是经典的表观遗传套路启动子H3K27乙酰化，丁酸会通过抑制HDAC3/8的功能来推动这个进程，从而促进TBX21表达上调，以此不让CD8+T细胞表达PD-1，这样就能保住CD8+T细胞的抗癌积极性了。具核梭杆菌外分泌的丁酸，主要通过表观遗传机制上调Tbx21表达，下调CD8+T细胞的PD-1表达所以说，看似对免疫治疗极为抗拒的MSS型CRC里，其实也有免疫治疗可以利用的机会，至少瘤内具核梭杆菌丰度就有可能成为临床可用的Biomarker。不过，直接补充丁酸这招可能不灵，因为丁酸正常情况下在体内的半衰期只有6分钟，而具核梭杆菌是在瘤内产生丁酸，投递距离太近了才能避开这个问题，基于具核梭杆菌设计治疗策略或许才是正解。------奇点糕近期推出了《2024ASCO年会深度盘点》课程，为大家系统盘点了2024ASCO年会上实体瘤领域的重磅进展，让您在100分钟内迅速深入把握前沿。长按识别下图中的二维码即可购买，购买后您可以在「奇点网小程序」收听，或下载奇点网「医学奇点」苹果客户端收听。如果遇到任何技术问题，大家可以戳我们下图中的客服小伙伴来解决~~参考文献：[1]Wang X, Fang Y, Liang W, et al. Fusobacterium nucleatum facilitates anti-PD-1 therapy in microsatellite stable colorectal cancer[J]. Cancer Cell, 2024.[2]Hamada T, Zhang X, Mima K, et al. Fusobacterium nucleatum in colorectal cancer relates to immune response differentially by tumor microsatellite instability status[J]. Cancer Immunology Research, 2018, 6(11): 1327-1336.本文作者丨谭硕

免疫疗法临床研究微生物疗法

2024-09-15

·微信

乳酸真是特容易坏事做尽啊

*仅供医学专业人士阅读参考提问：各位如果听到一种蛋白的名字是“剪接因子”，对它功能的第一反应会是什么？至少以奇点糕的想象力，绝对不会想到表观遗传、调控代谢、教唆巨噬细胞促癌这些方面去，但人体内偏偏真就有这么“不务正业”的家伙，你说可气不可气？近日，复旦大学附属中山医院肝癌研究所代智研究员团队在《癌症通讯》（Cancer Communications）期刊发表的最新研究成果，就揭示了丝氨酸/精氨酸剪接因子10（SRSF10）在肝细胞癌（HCC）中的又一重促癌机制：SRSF10能够通过调节糖酵解和乳酸代谢，帮助癌细胞将巨噬细胞导向促癌的M2表型（M2-TAMs），介导免疫逃逸和免疫治疗耐药[1]！具体来说，SRSF10会与经典癌基因MYB RNA的3′非翻译区结合增强其稳定性，从而经由MYB上调葡萄糖转运蛋白1（GLUT1）、乳酸脱氢酶A（LDHA）等糖酵解过程关键酶的表达，在细胞内外积聚更多乳酸，而乳酸增多诱导的组蛋白乳酸化修饰又会上调SRSF10表达，并导致巨噬细胞组蛋白广泛发生H3K18乳酸化（H3K18la），使它们转变为抑制免疫细胞的促癌表型，因此SRSF10有着成为增敏HCC免疫治疗靶点和临床实用Biomarker的潜力。论文首页截图其实在一年多以前，SRSF10就在奇点糕这儿露过脸，而且很巧的是同样是我国学者的研究，同样在HCC中开展，但当时SRSF10还只能算是做了点本职工作以外的拓展，影响的对象是细胞周期调节因子CDC25A，这回跨界到影响糖酵解和乳酸代谢，还是挺让人意外的。中山医院团队此次的研究，出发点则是寻找影响HCC免疫治疗效果的关键基因，在对6例HCC患者（4例对免疫治疗无应答）进行单细胞测序，并比对既往测序数据后，研究者们发现无应答患者的恶变肝细胞，普遍存在糖酵解通路关键基因的表达显著富集（对比应答患者），Srsf10就是这些基因中的一员，且它是唯一仅在癌细胞中表达上调的基因。外部数据库资料还显示，SRSF10的表达上调往往与免疫抑制性肿瘤微环境同时出现，研究者们也通过敲除HCC模型小鼠的Srsf10证实了这一点，敲除Srsf10使HCC微环境内的CD4+/CD8+T细胞数量显著增多，而典型巨噬细胞亚群减少，说明巨噬细胞大概率是受SRSF10影响，在肿瘤微环境中导致免疫抑制的具体执行人。对巨噬细胞组分的分析显示，敲除或沉默Srsf10显著减少了促癌的M2-TAMs占比，使有利抗癌的M1型TAMs占比上升，且SRSF10表达水平与M2-TAMs典型标志物正相关；研究者们还专门进行了共培养实验，证实未敲除Srsf10的HCC细胞确实有使巨噬细胞向M2型极化促癌的能力，且巨噬细胞也是抑制CD8+T细胞免疫功能时必不可缺的。SRSF10可通过使巨噬细胞向M2型极化，介导免疫抑制性肿瘤微环境既然前面的单细胞测序已经显示，SRSF10与糖酵解通路相关，乳酸又是糖酵解的产物，下一步的机制探索自然就要看乳酸：共培养实验首先显示，乳酸可逆转敲除HCC细胞Srsf10导致的M2-TAMs减少等影响，而环境中缺少葡萄糖时，是否敲除或沉默Srsf10也不会产生明显影响，说明糖酵解产生乳酸是必要条件；乳酸调控巨噬细胞的具体机制则是组蛋白H3K18la修饰，这会使多个M2-TAMs的关键基因，如CD206、ARG1和IL10转录激活。同时，研究者们还明确了SRSF10在HCC细胞中能够对糖酵解正向调控，并证实与此前在乳腺癌中的发现[2]类似，SRSF10使糖酵解增强产生的更多乳酸，还会通过乳酸化修饰转录激活SRSF10，正反馈通路就此形成，促癌效应也就停不下来了。而导致上面一切改变的源头事件，就是SRSF10与MYB这个强力转录因子RNA的3′非翻译区结合，增强了RNA的稳定性，随后MYB就会激活GLUT1等参与糖酵解的关键酶，使乳酸增多导致免疫抑制；沉默Srsf10或使用专门抑制剂阻断这个“罪恶链条”，就能与PD-1抑制剂协同增效，患者来源类器官实验也初步证实了可行性。此外，HCC患者的SRSF10表达水平也与免疫治疗耐药和不良预后相关，提示SRSF10或可作为Biomarker。SRSF10与MYB RNA结合，从而上调糖酵解来实现后续免疫抑制------奇点糕近期推出了《2024ASCO年会深度盘点》课程，为大家系统盘点了2024ASCO年会上实体瘤领域的重磅进展，让您在100分钟内迅速深入把握前沿。长按识别下图中的二维码即可购买，购买后您可以在「奇点网小程序」收听，或下载奇点网「医学奇点」苹果客户端收听。如果遇到任何技术问题，大家可以戳我们下图中的客服小伙伴来解决~~参考文献：[1]Cai J, Song L, Zhang F, et al. Targeting SRSF10 might inhibit M2 macrophage polarization and potentiate anti-PD-1 therapy in hepatocellular carcinoma[J]. Cancer Communications, 2024.[2]Pandkar M R, Sinha S, Samaiya A, et al. Oncometabolite lactate enhances breast cancer progression by orchestrating histone lactylation-dependent c-Myc expression[J]. Translational oncology, 2023, 37: 101758.本文作者丨谭硕

免疫疗法

2024-09-09

·泽璟制药

2024 ESMO I 泽璟制药多项临床研究成果入选2024年欧洲肿瘤内科学会年会

2024年欧洲肿瘤内科学会（ESMO）年会将于当地时间9月13日至17日在西班牙巴塞罗那召开。ESMO年会作为全球规模最大、学术水平最高、最具权威的肿瘤学会议之一，汇集来自世界各地肿瘤学领域的一流专家、临床医生以及临床研究人员，共同探讨全球肿瘤诊疗先进治疗理念和前沿临床及转化研究热点。在本次年会上，泽璟制药将发布抗体新药注射用ZG006、甲苯磺酸多纳非尼片的多项临床相关研究成果。中文标题：一项在晚期小细胞肺癌或神经内分泌癌患者中针对CD3与Delta样配体3的三特异性抗T细胞衔接器抗体ZG006单药首次人体I期临床研究英文标题：A Phase I First-in-human Study of ZG006, A Trispecific Anti-T Cell Engager Targeting CD3/DLL3/DLL3, as Monotherapy in Patients with Advanced Small Cell Lung Cancer or Neuroendocrine Carcinoma 讲者：河南省肿瘤医院王启明教授摘要编号：686TiP 展示形式：壁报展示当地时间：2024年9月14日星期六北京时间：2024年9月14日星期六中文标题：替雷利珠单抗+多纳非尼联合经动脉化疗栓塞辅助治疗切除后高危复发肝细胞癌(TIDE)：一项前瞻性、单臂、2期研究英文标题：Tislelizumab plus donafenib combined with transarterial chemoembolization in patients with resected high-riskl hepatocellular carcinoma (TIDE): a prospective, single-arm, phase II trial Leading PI：四川大学华西医院文天夫教授讲者：四川大学华西医院彭伟教授摘要编号：976P 展示形式：壁报展示当地时间：2024年9月16日星期一北京时间：2024年9月16日星期一中文标题：经动脉化疗栓塞联合多纳非尼加或不加免疫检查点抑制剂治疗不可切除肝细胞癌的疗效和安全性分析:一项前瞻性、单臂、单中心、Ⅱ期临床研究英文标题：Efficacy and Safety Analysis of Transarterial Chemoembolization Plus Donafenib With or Without Immune Checkpoint Inhibitors for Unresectable Hepatocellular Carcinoma: A Prospective, Single-Arm, Single-Center, Phase II Clinical Study Leading PI：山东省肿瘤医院宋金龙教授讲者：山东省肿瘤医院李金鹏教授摘要编号：978P 展示形式：壁报展示当地时间：2024年9月16日星期一北京时间：2024年9月16日星期一中文标题：酪氨酸激酶抑制剂或抗VEGF抗体联合抗PD-1抑制剂及TACE在肝细胞癌转化治疗中的比较:一项回顾性、多中心真实世界研究英文标题：Tyrosine kinase inhibitors vs. anti-VEGF antibody, combined with anti-PD-1 inhibitors and TACE in the conversion therapy for hepatocellular carcinoma: a retrospective multicenter real-world study 讲者：浙江大学医学院附属第一医院凌琪教授摘要编号：981P 展示形式：壁报展示当地时间：2024年9月16日星期一北京时间：2024年9月16日星期一

临床2期临床1期临床结果

100 项与 Sym-021 相关的药物交易

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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
淋巴瘤	临床2期	美国	Symphogen A/S	2017-11-20
复发性实体肿瘤	临床1期	法国	Symphogen A/S	2020-10-12
复发性实体肿瘤	临床1期	加拿大	Symphogen A/S	2020-10-12
复发性实体肿瘤	临床1期	西班牙	Symphogen A/S	2020-10-12
复发性实体肿瘤	临床1期	美国	Symphogen A/S	2020-10-12
晚期恶性实体瘤	临床1期	加拿大	Symphogen A/S	2017-11-20
晚期恶性实体瘤	临床1期	美国	Symphogen A/S	2017-11-20
肿瘤转移	临床1期	加拿大	Symphogen A/S	2017-11-20
肿瘤转移	临床1期	美国	Symphogen A/S	2017-11-20
淋巴瘤	临床前	加拿大	Symphogen A/S	2017-11-20

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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


Lenvamel (ASCO2024)	N/A	局部晚期黑色素瘤	67	Lenvatinib and anti-PD-1 combination	(顧獵襯鹽糧顧鏇鑰鏇願) = 糧顧糧遞夢遞遞窪夢齋廠顧淵積鹹蓋鏇網窪醖 (繭遞觸艱醖構願範憲簾, 18 ~ 41) 更多	积极	2024-05-24
ASCO2024	N/A	复发性头颈部鳞状细胞癌 PD-L1 positive (CPS≥1)	89	anti-PD-1	餘窪壓憲齋鬱遞蓋窪膚(願膚鑰獵繭顧齋糧觸鹹) = 10% 鏇獵淵網鬱獵鹹壓願衊 (鑰簾築鹽觸膚鑰衊襯窪 ) 更多	积极	2024-05-24
				anti-PD-1
AACR2024 人工标引	临床1期	胆道癌	35	S095018+Sym021	(鹽願獵範壓願獵襯繭製) = 膚膚製廠廠壓選願廠鏇醖製蓋簾鑰衊積壓齋鏇 (鬱糧膚繭範顧膚願鏇顧 ) 更多	积极	2024-04-05
Pubmed \| Front Oncol	N/A	晚期非小细胞肺癌 EGFR mutation positive	67	Anti-PD-1 plus Anlotinib	(壓鏇蓋範願觸壓齋顧鹽) = 齋襯繭壓選觸繭簾繭獵憲衊鹹鏇齋餘醖鹽選憲 (繭簾鑰膚構願鑰簾憲憲 ) 更多	-	2021-03-15
NCT03489343 \| NCT03311412 \| NCT03489369 (ESMO2020)	临床1期	肿瘤转移 \| 晚期恶性实体瘤 \| 淋巴瘤	-	Sym021	構襯製廠廠網構積築壓(憲淵淵鏇廠願憲憲廠鹹) = Sym021, Sym022 and Sym023 alone and Sym021 in combination with either Sym022 or Sym023 were well tolerated with AE profiles typical of immune checkpoint inhibitors 鹽製窪築蓋繭衊鹹構蓋 (鹽構夢觸鬱襯夢顧廠窪 )	-	2020-09-20
				Sym022
ASCO2020	N/A	不可切除的黑色素瘤二线 \| 三线	-	Anti-PD-1 plus Temozolomide	簾願鏇蓋築鏇餘鏇淵築(築夢積壓積齋製醖鏇製) = and hepatotoxicity (0%, 4.8%, 6.9%) 襯顧蓋窪醖餘獵鏇餘鹹 (簾淵夢壓簾遞簾鏇製鑰 ) 更多	积极	2020-05-25
				Temozolomide/DTIC
AUA2020	N/A	泌尿生殖系统肿瘤	51	anti-PD-1 drugs (HLA-A2 supertype)	(糧齋積衊夢鏇獵製繭憲) = 鏇願淵蓋簾窪築選範艱憲糧鏇觸顧製艱繭鬱範 (積憲醖鑰獵窪鹽觸醖糧 )	-	2020-04-01
				anti-PD-1 drugs (Patients without HLA-A2 supertype)	(糧齋積衊夢鏇獵製繭憲) = 窪鏇鑰範鹹膚壓構廠範憲糧鏇觸顧製艱繭鬱範 (積憲醖鑰獵窪鹽觸醖糧 )
Phase I clinical trial (AACR2017)	临床1期	结直肠癌	-	BNC101 + anti-PD-1	窪糧淵顧蓋蓋鏇壓齋構(願遞遞餘簾鑰築蓋繭糧) = 繭簾夢蓋鑰壓膚鹽獵餘夢鏇範鏇蓋鏇憲餘積壓 (獵鹹齋鬱齋願鏇蓋餘廠 )	积极	2017-07-01
WCLC2016	N/A	-	-	Nintedanib	鹹鏇窪製顧齋築製鑰遞(製鑰蓋夢糧醖繭膚鏇簾) = 構獵夢淵選積壓餘壓鑰繭製鹹觸窪觸蓋築襯簾 (鹽積獵鬱築廠顧鏇廠窪 )	-	2016-12-06
				Anti PD-1	鹹鏇窪製顧齋築製鑰遞(製鑰蓋夢糧醖繭膚鏇簾) = 積顧獵壓獵願廠艱築窪繭製鹹觸窪觸蓋築襯簾 (鹽積獵鬱築廠顧鏇廠窪 )