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更新于：2026-09-18

Irinotecan Hydrochloride

盐酸伊立替康

更新于：2026-09-18

概要

基本信息

药物类型

小分子化药

别名

ASC-201 - Ascelia Pharma、IHT、irinotecan

+ [39]

靶点

Top I

作用方式

抑制剂

作用机制

TOP1抑制剂(DNA拓扑异构酶I抑制剂)

治疗领域

肿瘤免疫系统疾病消化系统疾病+ [7]

在研适应症

儿童恶性实体瘤肠肿瘤结肠癌+ [29]

非在研适应症

腺癌食管腺癌大肠腺癌+ [64]

原研机构

Yakult Honsha Co., Ltd.

在研机构

Yakult Honsha Co., Ltd.

Daiichi Sankyo Co., Ltd.Valent Technologies LLC

+ [12]

非在研机构

Bristol Myers Squibb Co.

AstraZeneca PLC

Sanofi

+ [15]

权益机构

Hanmi Pharmaceutical Co., Ltd.

Dr. Reddy's Laboratories Ltd.

SAM CHUN DANG PHARM Co., Ltd.

+ [7]

最高研发阶段批准上市

首次获批日期

日本 (1994-01-19),

非小细胞肺癌卵巢癌胰腺癌+ [3]

最高研发阶段(中国)批准上市

特殊审评加速批准 (美国)、优先审评 (中国)

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结构/序列

分子式C33H45ClN4O9

InChIKeyKLEAIHJJLUAXIQ-JDRGBKBRSA-N

CAS号136572-09-3

关联

1,850

项与盐酸伊立替康相关的临床试验

JPRN-UMIN000006999

/ Completed临床2期IIT

Phase II randomized trail of Gemcitabine and Irinotecan in Patients with Platinum Refractory and Resistant Mullerian carcinoma (tailored dose vs optimal dose chemotherapy)

开始日期2046-12-31

申办/合作机构-

NCT07748611

/ Not yet recruiting临床2期IIT

SMART-PANC: SMAD4 Tailored Neoadjuvant Therapy for Pancreatic Cancer, A Phase ll Non-Randomized, Single Center Pilot Study

This phase II trial tests the impact of using SMAD4-mutant status to personalize chemotherapy in treating patients with pancreatic ductal adenocarcinoma (PDAC) that can be removed by surgery (resectable) or that may be between resectable and unresectable (borderline resectable) before undergoing surgery (neoadjuvant). PDAC is one of the most aggressive and fastest growing tumors. SMAD4, a tumor suppressor gene, acts like a brake on cell growth and helps to prevent tumor cells from growing. However, losing it makes the tumor more aggressive and often resistant to standard of care (SOC) treatments regimens, such as gemcitabine with nab-paclitaxel and fluorouracil, leucovorin, irinotecan, and oxaliplatin (FOLFIRINOX). Gemcitabine is a chemotherapy drug that blocks the cells from making deoxyribonucleic (DNA) and may kill tumor cells. Paclitaxel is in a class of medications called antimicrotubule agents. It stops tumor cells from growing and dividing and may kill them. Nab-paclitaxel is an albumin-stabilized nanoparticle formulation of paclitaxel which may have fewer side effects and work better than other forms of paclitaxel. Fluorouracil, a type of antimetabolite, stops cells from making DNA and it may kill tumor cells. Leucovorin is a form of folic acid. It is a type of chemoprotective agent and a type of chemosensitizing agent. Irinotecan is in a class of antineoplastic medications called topoisomerase I inhibitors. It blocks a certain enzyme needed for cell division and DNA repair and may kill tumor cells. Oxaliplatin is in a class of medications called platinum-containing antineoplastic agents. It damages the cell's DNA and may kill tumor cells. Instead of a one-sized fits all treatment approach with SOC therapies, matching therapy based on SMAD4 mutation status may use this specific genetic weakness against the tumor. This approach to neoadjuvant therapy may dramatically alter the path of treatment and improve outcomes, including complete resection rates, in patients with resectable or borderline resectable PDAC.

开始日期2027-02-03

申办/合作机构

Northwestern University

[+1]

NCT07363408

/ Not yet recruiting临床1期IIT

A Phase I Clinical Trial of Ivonescimab and ADG126, Alone, and in Combination With 5-FU/LV or FOLFIRI in MSS Advanced/Metastatic Colorectal Cancer

This phase I trial studies the safety, side effects, and best dose of ADG126, in combination with ivonescimab alone, in combination with ivonescimab, leucovorin, and fluorouracil, or in combination with ivonescimab and leucovorin, fluorouracil, and irinotecan (FOLFIRI regimen) in treating patients with microsatellite stable (MSS) colorectal cancer that may have spread from where it first started to nearby tissue, lymph nodes, or distant parts of the body (advanced) or has spread from where it first started (primary site) to other places in the body (metastatic). Immunotherapy with monoclonal antibodies, such as ivonescimab and ADG126, may help the body's immune system attack the cancer, and may interfere with the ability of tumor cells to grow and spread. Ivonescimab may also stop or slow the cancer by blocking the growth of new blood vessels necessary for tumor growth. Leucovorin calcium is a type of drug called a folic acid analog, which means it is similar to the vitamin folic acid. It is used in combination with certain chemotherapy drugs to enhance their ability to kill tumor cells or to lessen their harmful side effects. Fluorouracil is a type of chemotherapy called an antimetabolite, which is a drug that mimics a natural chemical and prevents its use in cells. It interferes with the production of a key component of deoxyribonucleic acid (DNA), which prevents the DNA from copying itself. This causes tumor cells and other rapidly dividing cells to die. Fluorouracil also gets incorporated into ribonucleic acid (RNA) and DNA, disrupting critical cell functions. Irinotecan is in a class of antineoplastic medications called topoisomerase I inhibitors. It blocks a certain enzyme needed for cell division and DNA repair and may kill cancer cells. Giving ADG126 with ivonescimab, with or without leucovorin and fluorouracil or FOLFIRI regimen, may be safe in treating patients with MSS advanced/metastatic colorectal cancer.

开始日期2026-12-01

申办/合作机构

City of Hope National Medical Center

[+1]

100 项与盐酸伊立替康相关的临床结果

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100 项与盐酸伊立替康相关的转化医学

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100 项与盐酸伊立替康相关的专利（医药）

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9,713

项与盐酸伊立替康相关的文献（医药）

2026-12-01·JOURNAL OF PHARMACEUTICAL AND BIOMEDICAL ANALYSIS

In depth study on the mechanism of Xiao-Chai-Hu-Tang in ameliorating irinotecan-induced intestinal toxicity and enhancing antitumor immunity via intestinal microbiota and fecal metabolomics

Article

作者: Hou, Zong ; Liu, Zhiqiang ; Zhang, Yangyang ; Liu, Shu ; Cao, Xia

Irinotecan (CPT-11) is a cornerstone chemotherapeutic for advanced colorectal cancer (CRC), but its clinical use is limited by dose-dependent gastrointestinal (GI) toxicity. Xiao-Chai-Hu-Tang (XCHT), a classical traditional Chinese medicine formula, alleviates CPT-11-induced adverse effects, yet its mechanism remains unclear. This study established a CPT-11-induced intestinal toxicity model in CRC rats, using multi-omics analyses (16S rRNA sequencing, fecal metabolomics, SCFA quantification) and an antibiotic depletion model to explore XCHT's mechanism via the gut microbiota-metabolite axis. XCHT significantly alleviated intestinal toxicity, reduced inflammation, and restored intestinal barrier integrity. It also enhanced antitumor immunity, as evidenced by an increased CD4⁺/CD8⁺ ratio and promoted Th1 polarization, and potentiated CPT-11's antitumor effects. XCHT alleviated CPT-11-induced dysbiosis of key bacterial genera and substantially restored the disturbed metabolome, with the restored metabolites primarily enriched in unsaturated fatty acid biosynthesis and linoleic acid metabolism. It also restored SCFA levels and upregulated colonic SCFA receptors/transporter. Correlation analysis revealed that these microbial and metabolic shifts were closely associated with the improvement of intestinal toxicity and antitumor immunity, and XCHT's protective effects depended on an intact gut microbiota. In conclusion, XCHT mitigates CPT-11-induced intestinal injury and enhances immunity by restoring gut microbiota balance and metabolic reprogramming, providing scientific evidence for its clinical use as a complementary therapy for CRC patients on CPT-11.

2026-10-01·PHYTOMEDICINE

Xiao-Chai-Hu-Tang alleviates irinotecan-induced diarrhea via promoting bile acid reabsorption and decreasing focal adhesion kinase signaling revealed by metabolomics and proteomics

Article

作者: Zhu, Lijun ; Rao, Jinsong ; He, Zhuoru ; Cai, Yu ; Chen, Yongxv ; Liu, Zhongqiu ; Qiu, Huawei ; Yao, Ye ; Zhou, Runze ; Zhou, Jialin ; Ma, Tongyang

BACKGROUND:

Irinotecan (CPT-11) is widely used for colorectal cancer treatment, with delayed-onset diarrhea as its primary side effect. Xiao-Chai-Hu-Tang (XCHT) has been clinically observed to alleviate chemotherapy-induced diarrhea, but its underlying mechanisms remain unclear.

PURPOSE:

This study aimed to elucidate the regulatory mechanisms through which XCHT alleviated CPT-11-induced diarrhea using an integrated multi-omics approach.

METHODS:

The chemical components of XCHT were detected using UHPLC-QE-Orbitrap-MS, and 12 active components were quantified via UHPLC-QQQ-MS/MS to ensure quality stability. CPT-11-induced diarrheal mice were established to evaluate the therapeutic effects of XCHT. Differential metabolites in liver and intestinal tissues among control, CPT-11, and XCHT mice were analyzed by untargeted metabolomics, followed by molecular network analysis using IPA. Bile acids were quantified using targeted UHPLC-QQQ-MS/MS method. Proteomics of colon tissues identified differentially expressed proteins, with functional enrichment conducted via GO and KEGG. Western blot and flow cytometry were used to validate the potential biopathway.

RESULTS:

Total 1108 chemical components were identified in XCHT, mainly including flavonoids, terpenoids and phenylpropanoids. XCHT significantly improved diarrhea symptoms and reduced intestinal inflammation. Metabolomics revealed 117 and 53 differential metabolites in the liver and intestine, respectively, with both tissues showing alterations in bile acid metabolism. Targeted bile acid analysis showed that CPT-11 inhibited the synthesis and uptake of bile acids in the liver and enhanced bile excretion, resulting in an increase in bile acids in the gallbladder. Meanwhile, CPT-11 impaired the reabsorption of bile acids in the intestine, leading to a decrease in total bile acid levels, reduction of circulating bile acids, and accumulation of conjugated bile acids in the colon. XCHT reversed these abnormal phenomena, restoring the intestinal bile acid homeostasis. Proteomics identified 86 differentially expressed proteins in colon tissues, with significant enrichment in 'Focal adhesion' pathway. Further verification indicated that CPT-11 abnormally activated the focal adhesion kinase (FAK) and its downstream RhoA/ROCK pathways, then reduced tight junction proteins ZO-1 and Occludin, damaging the intestinal barrier. XCHT inhibited this pathway, restored the expression of tight junction proteins, balanced Th1/Th2 differentiation, and alleviated intestinal inflammation. Cholestyramine, a bile acid chelator, also alleviated CPT-11-induced diarrhea by reducing the accumulation of bile acids in the intestine, confirming the key role of bile acids in the treatment of CPT-11-induced diarrhea.

CONCLUSION:

This study revealed that the combined administration of XCHT could restore bile acid reabsorption, reduced the accumulation of conjugated bile acids in the colon, inhibited the abnormally activated FAK-RhoA/ROCK pathway, improved intestinal epithelial barrier function and alleviate diarrhea. These findings provide a new entry point for the treatment of chemotherapy-induced diarrhea (CID) and offer data support for the combined medication regimen of XCHT and CPT-11.

2026-07-03·Expert Opinion On Drug Safety

Drug-induced nasal septum perforation: a disproportionality analysis of the FDA adverse event reporting system database

Article

作者: Xie, Chubo ; Wang, Yuewu ; Qiu, Qianhui ; Liu, Yitong ; Jiang, Zhilin ; Cui, Yi ; Sun, Fang ; Zhou, Suizi ; Wang, Keshuang

BACKGROUND:

Nasal septum perforation represents a significant clinical concern, with limited investigations into the role of medications in its etiology. This study utilizes the FDA Adverse Event Reporting System (FAERS) database to identify the drugs associated with nasal septum perforation and assess their risk.

RESEARCH DESIGN AND METHODS:

This retrospective pharmacovigilance study analyzed drug-induced nasal septum perforation data from January 2004 to December 2023. Disproportionality analysis using reporting odds ratio (ROR) assessed drug associations with nasal septum perforation.

RESULTS:

For 552 identified cases, the most commonly reported drugs were bevacizumab (n = 56), fluticasone propionate (n = 50), methotrexate (n = 34), hydrocodone and acetaminophen (n = 22), and paclitaxel (n = 17). Twenty-six drugs showed positive risk signals, with the top five being azelastine hydrochloride and fluticasone propionate (ROR = 173.82), beclomethasone dipropionate (ROR = 90.91), oxymetazoline (ROR = 53.77), desmopressin (ROR = 51.43), and leucovorin (ROR = 42.83). Intriguingly, 18 of these drugs did not list nasal septum perforation as a known side effect.

CONCLUSION:

This study provides a comprehensive overview of drug-induced nasal septum perforation from a pharmacovigilance perspective, highlighting the need for further research to clarify these associations and update drug safety information to reduce patient risk.

3,112

项与盐酸伊立替康相关的新闻（医药）

2026-09-17

·今日头条

【ADCXDC论坛 | BioCon2026】9月15日精彩演讲摘要

来源：市场资讯（来源：商图药讯） 9月15日，BioCon China Expo 2026 第十三届国际生物药技术年会在上海盛大启幕！六大高规格平行论坛重磅开启，百余项前沿议题深度研讨，汇聚 100 + 顶尖行业专家领衔开讲，覆盖创新药出海BD、双多/单抗、ADC/XDC、体内细胞治疗、核酸药物、iPSC干细胞、AI新药研发全赛道。3000 +行业精英齐聚一堂，35+优质展商同台亮相，全场座无虚席、热度拉满，共绘生物医药产业高质量发展新蓝图。本篇ADCXDC专场报道，带您直击第十三届BioCon上海站首日不容错过的精彩内容！演讲话题：双payload ADC创新技术平台与临床前开发演讲嘉宾：刘辰，亚飞医药/亲合力生物，创始人、董事长、CEO、CMO 刘总介绍亚飞医药 TMEA 肿瘤微环境酶激活平台，依靠莱古酶可在肿瘤局部特异性激活药物，降低全身毒性。核心产品莱古比星 III 期临床疗效显著，解决蒽环类药物心脏毒性难题。平台拓展出 TMEA‑ADC、TMEA‑IO 等多条管线，开发双载荷 ADC，同时搭载细胞毒素与免疫激动剂，实现化疗联合原位免疫激活。AI 贯穿靶点筛选、分子设计、PK/PD 预测、患者分层全流程，形成闭环数据飞轮。报告展示 CLDN6、ROR1、EGFR/TROP2 等双载荷 ADC 临床前优异药效，同时布局遮蔽型细胞因子、TCE 等免疫分子，面向实体瘤寻求合作开发。演讲话题：基于多元临床需求的多特异性多载荷ADC药物研发演讲嘉宾：闫树德，多禧生物CSO 闫总分享多禧生物多特异性、双载荷 ADC 研发成果。DXC006 靶向 CD56，在小细胞肺癌临床展现突出抗肿瘤响应，整体安全性可控。公司布局多款差异化分子：DXC008 为 STEAP1/PSMA 双靶点 ADC，应对前列腺癌抗原异质性；DXC018 是 HER2 双表位双载荷 ADC，2026 年 3 月递交 IND，临床前药效优于对标药物。建立 GAC、TAC、PAC 等多种双载荷技术组合，通过不同毒性载荷协同杀伤，降低耐药风险。同时解析双抗 ADC 设计要点，依托专有毒素、定点偶联与完整 CMC 能力，推进十余款临床阶段 ADC 项目，覆盖多类实体瘤。圆桌讨论：双抗双载荷ADC创新下一程：机遇与挑战演讲嘉宾：刘宁姝，亚虹医药，首席科学官刘辰，亚飞医药/亲合力生物创始人、董事长、CEO、CMO 黄长江，靶联生物，创始人兼首席科学家符策雄，翎泰天润创始人兼CEO 讨论方向： 1.与传统ADC对比的优势，双抗、双载荷能解决临床的哪些挑战和需求？特别是复发或难治的适应症 2.双靶点的选择，双载荷的选择，靶点-载荷组合的协同逻辑 3.根据载荷的MoA, 在时序设计和错配的逻辑及解决路径 4.研发投入(设计和成药性的复杂性) vs 临床价值 5.差异化与内卷破局讨论嘉宾围绕以上主题方向展开了热烈且有深度的讨论，详情敬请关注后续专题文章。演讲话题：双特异性ADC与双载荷ADC开发的洞见与思考演讲嘉宾：Mr. Dowdy Jackson, Antigenix Therapeutics CSO，前信达生物执行总监 Dowdy分享全球 ADC 行业现状，目前已有 22 款 ADC 获批，四百余款处于临床阶段，但 82% ADC 早期临床失败。肿瘤抗原异质性、靶点丢失、Payload 耐药是单靶点 ADC 核心瓶颈。双特异性 ADC 可识别两个抗原，提升肿瘤细胞覆盖，降低逃逸；双载荷 ADC 搭载两种作用机制毒素，协同杀伤、延缓耐药。报告梳理双特异 ADC 主流分子格式、晚期管线与已上市产品，对比不同技术优劣势，解析靶点筛选、分子构型、偶联工艺、CMC 及临床转化关键考量，为下一代 ADC 差异化设计提供参考。演讲话题：破解ADC耐药困局：从载荷源头创新到双载荷协同设计演讲嘉宾：党群，河南真实生物科技有限公司，总裁党总剖析 Topo‑1 类 ADC 临床交叉耐药问题，靶点突变、BCRP 药物外排是喜树碱类 Payload 耐药关键诱因。真实生物依托 AIDD 技术开发非喜树碱类 Topo1 抑制剂平台，代表分子 ZSSW‑136，可应对 Topo1 突变，规避 BCRP 外排。在伊立替康原发、继发耐药的类器官及 PDX 模型展现强效抗肿瘤活性，骨髓毒性更低。该新母核毒素具备多样偶联位点，可适配 ADC、PDC 等 XDC 开发，拥有完整自主专利，有望破解现有 Topo‑1 ADC 耐药难题，对外寻求项目联合开发合作。演讲话题：CRO视角下的偶联药物研发发展趋势演讲嘉宾：陈春麟，美迪西，创始人、董事长&CEO 陈总从 CRO 视角解析 XDC 行业格局，全球已有 22 款 ADC 获批，靶点扎堆，载荷成为差异化关键。技术向着定点偶联、双特异 / 双载荷 ADC、DAC、AOC 等新模态演进。重点介绍肿瘤微环境激活型 TMALIN 连接子，兼顾血浆稳定性与肿瘤局部释放。新型载荷突破传统细胞毒素范畴，拓展至降解剂、免疫刺激分子。阐述 XDC 药理毒理评价要点，分析脱靶毒性产生诱因，强调 PK/TK 研究的重要性。美迪西具备完整 XDC 一站式服务，覆盖连接子‑payload 演讲话题：双载荷ADC开发的挑战与技术壁垒演讲嘉宾：黄长江，靶联生物创始人兼首席科学家黄总指出双载荷 ADC 可借助两种不同作用机制毒素，克服肿瘤异质性与耐药，提升治疗窗口，但开发存在多重壁垒。难点包含两种 payload 的配比控制、定点偶联工艺难度大、DAR 均一性难以保障，杂质增多带来 CMC 与分析检测压力。分子层面需考量 linker 兼容性、payload 理化相容性，避免互相干扰。同时会增加药理毒理评估复杂度。分享主流双载荷实现技术路径，对比不同策略优劣。提出要平衡分子设计、偶联工艺、质控分析，做好早期成药性评估，才能推进双载荷 ADC 从概念走向临床。以上内容由组委会整理编辑而成，未全经本人审阅，

2026-09-17

·网易号

【ADCXDC论坛 | BioCon2026】9月15日精彩演讲摘要

来源：市场资讯（来源：商图药讯）9月15日，BioCon China Expo 2026 第十三届国际生物药技术年会在上海盛大启幕！六大高规格平行论坛重磅开启，百余项前沿议题深度研讨，汇聚 100 + 顶尖行业专家领衔开讲，覆盖创新药出海BD、双多/单抗、ADC/XDC、体内细胞治疗、核酸药物、iPSC干细胞、AI新药研发全赛道。3000 +行业精英齐聚一堂，35+优质展商同台亮相，全场座无虚席、热度拉满，共绘生物医药产业高质量发展新蓝图。本篇ADCXDC专场报道，带您直击第十三届BioCon上海站首日不容错过的精彩内容！演讲话题：双payload ADC创新技术平台与临床前开发演讲嘉宾：刘辰，亚飞医药/亲合力生物，创始人、董事长、CEO、CMO刘总介绍亚飞医药 TMEA 肿瘤微环境酶激活平台，依靠莱古酶可在肿瘤局部特异性激活药物，降低全身毒性。核心产品莱古比星 III 期临床疗效显著，解决蒽环类药物心脏毒性难题。平台拓展出 TMEA‑ADC、TMEA‑IO 等多条管线，开发双载荷 ADC，同时搭载细胞毒素与免疫激动剂，实现化疗联合原位免疫激活。AI 贯穿靶点筛选、分子设计、PK/PD 预测、患者分层全流程，形成闭环数据飞轮。报告展示 CLDN6、ROR1、EGFR/TROP2 等双载荷 ADC 临床前优异药效，同时布局遮蔽型细胞因子、TCE 等免疫分子，面向实体瘤寻求合作开发。演讲话题：基于多元临床需求的多特异性多载荷ADC药物研发演讲嘉宾：闫树德，多禧生物CSO闫总分享多禧生物多特异性、双载荷 ADC 研发成果。DXC006 靶向 CD56，在小细胞肺癌临床展现突出抗肿瘤响应，整体安全性可控。公司布局多款差异化分子：DXC008 为 STEAP1/PSMA 双靶点 ADC，应对前列腺癌抗原异质性；DXC018 是 HER2 双表位双载荷 ADC，2026 年 3 月递交 IND，临床前药效优于对标药物。建立 GAC、TAC、PAC 等多种双载荷技术组合，通过不同毒性载荷协同杀伤，降低耐药风险。同时解析双抗 ADC 设计要点，依托专有毒素、定点偶联与完整 CMC 能力，推进十余款临床阶段 ADC 项目，覆盖多类实体瘤。圆桌讨论：双抗双载荷ADC创新下一程：机遇与挑战演讲嘉宾：刘宁姝，亚虹医药，首席科学官刘辰，亚飞医药/亲合力生物创始人、董事长、CEO、CMO黄长江，靶联生物，创始人兼首席科学家符策雄，翎泰天润创始人兼CEO讨论方向：1.与传统ADC对比的优势，双抗、双载荷能解决临床的哪些挑战和需求？特别是复发或难治的适应症2.双靶点的选择，双载荷的选择，靶点-载荷组合的协同逻辑3.根据载荷的MoA, 在时序设计和错配的逻辑及解决路径4.研发投入(设计和成药性的复杂性) vs 临床价值5.差异化与内卷破局讨论嘉宾围绕以上主题方向展开了热烈且有深度的讨论，详情敬请关注后续专题文章。演讲话题：双特异性ADC与双载荷ADC开发的洞见与思考演讲嘉宾：Mr. Dowdy Jackson, Antigenix Therapeutics CSO，前信达生物执行总监Dowdy分享全球 ADC 行业现状，目前已有 22 款 ADC 获批，四百余款处于临床阶段，但 82% ADC 早期临床失败。肿瘤抗原异质性、靶点丢失、Payload 耐药是单靶点 ADC 核心瓶颈。双特异性 ADC 可识别两个抗原，提升肿瘤细胞覆盖，降低逃逸；双载荷 ADC 搭载两种作用机制毒素，协同杀伤、延缓耐药。报告梳理双特异 ADC 主流分子格式、晚期管线与已上市产品，对比不同技术优劣势，解析靶点筛选、分子构型、偶联工艺、CMC 及临床转化关键考量，为下一代 ADC 差异化设计提供参考。演讲话题：破解ADC耐药困局：从载荷源头创新到双载荷协同设计演讲嘉宾：党群，河南真实生物科技有限公司，总裁党总剖析 Topo‑1 类 ADC 临床交叉耐药问题，靶点突变、BCRP 药物外排是喜树碱类 Payload 耐药关键诱因。真实生物依托 AIDD 技术开发非喜树碱类 Topo1 抑制剂平台，代表分子 ZSSW‑136，可应对 Topo1 突变，规避 BCRP 外排。在伊立替康原发、继发耐药的类器官及 PDX 模型展现强效抗肿瘤活性，骨髓毒性更低。该新母核毒素具备多样偶联位点，可适配 ADC、PDC 等 XDC 开发，拥有完整自主专利，有望破解现有 Topo‑1 ADC 耐药难题，对外寻求项目联合开发合作。演讲话题：CRO视角下的偶联药物研发发展趋势演讲嘉宾：陈春麟，美迪西，创始人、董事长&CEO陈总从 CRO 视角解析 XDC 行业格局，全球已有 22 款 ADC 获批，靶点扎堆，载荷成为差异化关键。技术向着定点偶联、双特异 / 双载荷 ADC、DAC、AOC 等新模态演进。重点介绍肿瘤微环境激活型 TMALIN 连接子，兼顾血浆稳定性与肿瘤局部释放。新型载荷突破传统细胞毒素范畴，拓展至降解剂、免疫刺激分子。阐述 XDC 药理毒理评价要点，分析脱靶毒性产生诱因，强调 PK/TK 研究的重要性。美迪西具备完整 XDC 一站式服务，覆盖连接子‑payload 演讲话题：双载荷ADC开发的挑战与技术壁垒演讲嘉宾：黄长江，靶联生物创始人兼首席科学家黄总指出双载荷 ADC 可借助两种不同作用机制毒素，克服肿瘤异质性与耐药，提升治疗窗口，但开发存在多重壁垒。难点包含两种 payload 的配比控制、定点偶联工艺难度大、DAR 均一性难以保障，杂质增多带来 CMC 与分析检测压力。分子层面需考量 linker 兼容性、payload 理化相容性，避免互相干扰。同时会增加药理毒理评估复杂度。分享主流双载荷实现技术路径，对比不同策略优劣。提出要平衡分子设计、偶联工艺、质控分析，做好早期成药性评估，才能推进双载荷 ADC 从概念走向临床。以上内容由组委会整理编辑而成，未全经本人审阅，

2026-09-17

·百度百家

「ADCXDC论坛｜BioCon2026」9月15日精彩演讲摘要

（来源：商图药讯） 9月15日，BioCon China Expo 2026 第十三届国际生物药技术年会在上海盛大启幕！六大高规格平行论坛重磅开启，百余项前沿议题深度研讨，汇聚 100 + 顶尖行业专家领衔开讲，覆盖创新药出海BD、双多/单抗、ADC/XDC、体内细胞治疗、核酸药物、iPSC干细胞、AI新药研发全赛道。3000 +行业精英齐聚一堂，35+优质展商同台亮相，全场座无虚席、热度拉满，共绘生物医药产业高质量发展新蓝图。本篇ADCXDC专场报道，带您直击第十三届BioCon上海站首日不容错过的精彩内容！演讲话题：双payload ADC创新技术平台与临床前开发演讲嘉宾：刘辰，亚飞医药/亲合力生物，创始人、董事长、CEO、CMO 刘总介绍亚飞医药 TMEA 肿瘤微环境酶激活平台，依靠莱古酶可在肿瘤局部特异性激活药物，降低全身毒性。核心产品莱古比星 III 期临床疗效显著，解决蒽环类药物心脏毒性难题。平台拓展出 TMEA‑ADC、TMEA‑IO 等多条管线，开发双载荷 ADC，同时搭载细胞毒素与免疫激动剂，实现化疗联合原位免疫激活。AI 贯穿靶点筛选、分子设计、PK/PD 预测、患者分层全流程，形成闭环数据飞轮。报告展示 CLDN6、ROR1、EGFR/TROP2 等双载荷 ADC 临床前优异药效，同时布局遮蔽型细胞因子、TCE 等免疫分子，面向实体瘤寻求合作开发。演讲话题：基于多元临床需求的多特异性多载荷ADC药物研发演讲嘉宾：闫树德，多禧生物CSO 闫总分享多禧生物多特异性、双载荷 ADC 研发成果。DXC006 靶向 CD56，在小细胞肺癌临床展现突出抗肿瘤响应，整体安全性可控。公司布局多款差异化分子：DXC008 为 STEAP1/PSMA 双靶点 ADC，应对前列腺癌抗原异质性；DXC018 是 HER2 双表位双载荷 ADC，2026 年 3 月递交 IND，临床前药效优于对标药物。建立 GAC、TAC、PAC 等多种双载荷技术组合，通过不同毒性载荷协同杀伤，降低耐药风险。同时解析双抗 ADC 设计要点，依托专有毒素、定点偶联与完整 CMC 能力，推进十余款临床阶段 ADC 项目，覆盖多类实体瘤。圆桌讨论：双抗双载荷ADC创新下一程：机遇与挑战演讲嘉宾：刘宁姝，亚虹医药，首席科学官刘辰，亚飞医药/亲合力生物创始人、董事长、CEO、CMO 黄长江，靶联生物，创始人兼首席科学家符策雄，翎泰天润创始人兼CEO 讨论方向： 1.与传统ADC对比的优势，双抗、双载荷能解决临床的哪些挑战和需求？特别是复发或难治的适应症 2.双靶点的选择，双载荷的选择，靶点-载荷组合的协同逻辑 3.根据载荷的MoA, 在时序设计和错配的逻辑及解决路径 4.研发投入(设计和成药性的复杂性) vs 临床价值 5.差异化与内卷破局讨论嘉宾围绕以上主题方向展开了热烈且有深度的讨论，详情敬请关注后续专题文章。演讲话题：双特异性ADC与双载荷ADC开发的洞见与思考演讲嘉宾：Mr. Dowdy Jackson, Antigenix Therapeutics CSO，前信达生物执行总监 Dowdy分享全球 ADC 行业现状，目前已有 22 款 ADC 获批，四百余款处于临床阶段，但 82% ADC 早期临床失败。肿瘤抗原异质性、靶点丢失、Payload 耐药是单靶点 ADC 核心瓶颈。双特异性 ADC 可识别两个抗原，提升肿瘤细胞覆盖，降低逃逸；双载荷 ADC 搭载两种作用机制毒素，协同杀伤、延缓耐药。报告梳理双特异 ADC 主流分子格式、晚期管线与已上市产品，对比不同技术优劣势，解析靶点筛选、分子构型、偶联工艺、CMC 及临床转化关键考量，为下一代 ADC 差异化设计提供参考。演讲话题：破解ADC耐药困局：从载荷源头创新到双载荷协同设计演讲嘉宾：党群，河南真实生物科技有限公司，总裁党总剖析 Topo‑1 类 ADC 临床交叉耐药问题，靶点突变、BCRP 药物外排是喜树碱类 Payload 耐药关键诱因。真实生物依托 AIDD 技术开发非喜树碱类 Topo1 抑制剂平台，代表分子 ZSSW‑136，可应对 Topo1 突变，规避 BCRP 外排。在伊立替康原发、继发耐药的类器官及 PDX 模型展现强效抗肿瘤活性，骨髓毒性更低。该新母核毒素具备多样偶联位点，可适配 ADC、PDC 等 XDC 开发，拥有完整自主专利，有望破解现有 Topo‑1 ADC 耐药难题，对外寻求项目联合开发合作。演讲话题：CRO视角下的偶联药物研发发展趋势演讲嘉宾：陈春麟，美迪西，创始人、董事长&CEO 陈总从 CRO 视角解析 XDC 行业格局，全球已有 22 款 ADC 获批，靶点扎堆，载荷成为差异化关键。技术向着定点偶联、双特异 / 双载荷 ADC、DAC、AOC 等新模态演进。重点介绍肿瘤微环境激活型 TMALIN 连接子，兼顾血浆稳定性与肿瘤局部释放。新型载荷突破传统细胞毒素范畴，拓展至降解剂、免疫刺激分子。阐述 XDC 药理毒理评价要点，分析脱靶毒性产生诱因，强调 PK/TK 研究的重要性。美迪西具备完整 XDC 一站式服务，覆盖连接子‑payload 演讲话题：双载荷ADC开发的挑战与技术壁垒演讲嘉宾：黄长江，靶联生物创始人兼首席科学家黄总指出双载荷 ADC 可借助两种不同作用机制毒素，克服肿瘤异质性与耐药，提升治疗窗口，但开发存在多重壁垒。难点包含两种 payload 的配比控制、定点偶联工艺难度大、DAR 均一性难以保障，杂质增多带来 CMC 与分析检测压力。分子层面需考量 linker 兼容性、payload 理化相容性，避免互相干扰。同时会增加药理毒理评估复杂度。分享主流双载荷实现技术路径，对比不同策略优劣。提出要平衡分子设计、偶联工艺、质控分析，做好早期成药性评估，才能推进双载荷 ADC 从概念走向临床。以上内容由组委会整理编辑而成，未全经本人审阅，

100 项与盐酸伊立替康相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D01061	盐酸伊立替康	L01XX19	DBSALT000103

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
儿童恶性实体瘤	日本	Yakult Honsha Co., Ltd.	2013-03-25
儿童恶性实体瘤	日本	Daiichi Sankyo Co., Ltd.	2013-03-25
肠肿瘤	中国	江苏恒瑞医药股份有限公司	1998-01-01
结肠癌	美国	Pfizer Inc.	1996-06-14
直肠癌	美国	Pfizer Inc.	1996-06-14
乳腺癌	日本	Alfresa Pharma Corp.	1995-09-29
乳腺癌	日本	Daiichi Sankyo Co., Ltd.	1995-09-29
乳腺癌	日本	Yakult Honsha Co., Ltd.	1995-09-29
结直肠癌	日本	Yakult Honsha Co., Ltd.	1995-09-29
结直肠癌	日本	Alfresa Pharma Corp.	1995-09-29
结直肠癌	日本	Daiichi Sankyo Co., Ltd.	1995-09-29
淋巴瘤	日本	Alfresa Pharma Corp.	1995-09-29
非霍奇金淋巴瘤	日本	Alfresa Pharma Corp.	1995-09-29
非霍奇金淋巴瘤	日本	Daiichi Sankyo Co., Ltd.	1995-09-29
非霍奇金淋巴瘤	日本	Yakult Honsha Co., Ltd.	1995-09-29
鳞状细胞癌	日本	Alfresa Pharma Corp.	1995-09-29
鳞状细胞癌	日本	Daiichi Sankyo Co., Ltd.	1995-09-29
鳞状细胞癌	日本	Yakult Honsha Co., Ltd.	1995-09-29
胃癌	日本	Alfresa Pharma Corp.	1995-09-29
胃癌	日本	Daiichi Sankyo Co., Ltd.	1995-09-29

未上市

10 条进展最快的记录,

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
RAS 野生型结直肠癌	临床3期	法国	Hoffmann-La Roche, Inc.	2013-10-30
RAS 野生型结直肠癌	临床3期	爱尔兰	Hoffmann-La Roche, Inc.	2013-10-30
RAS 野生型结直肠癌	临床3期	以色列	Hoffmann-La Roche, Inc.	2013-10-30
食管癌	临床3期	加拿大	Pfizer Inc.	2009-04-01
结直肠癌肝转移	临床3期	法国	Sanofi	2004-04-01
结直肠癌肝转移	临床3期	法国	Pfizer Inc.	2004-04-01
结直肠癌肝转移	临床3期	法国	Chugai Pharmaceutical Co., Ltd.	2004-04-01
肝转移	临床3期	法国	Sanofi	2004-04-01
肝转移	临床3期	法国	Chugai Pharmaceutical Co., Ltd.	2004-04-01
肝转移	临床3期	法国	Pfizer Inc.	2004-04-01

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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


ESMO_GI2026 \| ESMO_GCC2026	N/A	转移性胰腺癌一线 BRCA1 \| BRCA2	26	Gemcitabine plus nab-paclitaxel (GnP)	窪積範積遞製範壓願淵(壓糧淵獵選齋範齋鑰獵) = 憲齋艱衊襯夢廠餘醖築鬱繭網觸淵觸製夢蓋夢 (蓋齋衊艱鬱憲憲憲鬱構 ) 更多	积极	2026-07-02
ESMO_GI2026 \| ESMO_GCC2026	N/A	转移性胰腺癌一线 BRCA1 \| BRCA2	26	modified FOLFIRINOX (mFFX)	窪積範積遞製範壓願淵(壓糧淵獵選齋範齋鑰獵) = 選廠衊齋憲齋製憲淵構鬱繭網觸淵觸製夢蓋夢 (蓋齋衊艱鬱憲憲憲鬱構 ) 更多	积极	2026-07-02
ESMO_GI2026	N/A	转移性结直肠癌	16	oral capecitabine + irinotecan (CapIRI)	網遞鹹築範醖壓醖鏇鬱(網膚簾廠齋構願獵繭襯): HR = 1.03 (95.0% CI, 0.81 ~ 1.3) 更多	相似	2026-07-02
ESMO_GI2026	N/A	转移性结直肠癌	16	5-fluorouracil + irinotecan (FOLFIRI)	網遞鹹築範醖壓醖鏇鬱(網膚簾廠齋構願獵繭襯): HR = 1.03 (95.0% CI, 0.81 ~ 1.3) 更多	相似	2026-07-02
ESMO_GI2026	N/A	结直肠癌肝转移	30	TACE using a combination of oxaliplatin and irinotecan	淵鹽積鹹艱網顧夢淵築(製膚構廠選鬱廠糧餘壓) = Most adverse events were mild and consistent with post-embolization syndrome 鏇淵鏇製鹽餘鬱範糧窪 (鑰衊範糧鏇餘觸醖網壓 )	积极	2026-07-02
NCT07381764 (ROMANCE, ESMO_GI2026)	临床2期	转移性结直肠癌三线 RAS/BRAF wild-type \| pMMR	150	Irinotecan plus cetuximab	網鹹獵網鏇艱夢顧壓夢(獵窪簾淵築選構網壓鑰) = 餘簾網艱繭齋築醖艱鏇築築窪構鹹選齋夢襯齋 (範壓憲願簾鬱鏇襯醖齋 ) 更多	积极	2026-07-02
NCT07381764 (ROMANCE, ESMO_GI2026)	临床2期	转移性结直肠癌三线 RAS/BRAF wild-type \| pMMR	150	trifluridine/tipiracil plus bevacizumab	網鹹獵網鏇艱夢顧壓夢(獵窪簾淵築選構網壓鑰) = 顧餘壓製鹽範膚糧顧壓築築窪構鹹選齋夢襯齋 (範壓憲願簾鬱鏇襯醖齋 )	积极	2026-07-02
ESMO_GI2026	N/A	小肠腺癌二线	34	Irinotecan	繭顧襯築築鹽鬱遞繭獵(憲糧網繭膚鑰選餘鑰簾) = diarrhoea (23.5%), neutropenia (14.7%), and febrile neutropenia (14.7%). 繭憲構簾淵網廠餘簾衊 (顧選獵壓鏇衊鹽襯艱積 ) 更多	积极	2026-07-02
NCT04251715 (HELIX-1, CTgov)	临床2期	不可切除的肝内胆管癌	5	Quality-of-Life Assessment+leucovorin+Dexamethasone+Floxuridine+Irinotecan+oxaliplatin	廠淵壓選獵窪膚壓鬱鬱 = 廠鏇顧齋壓構網窪鑰壓夢鑰齋鑰壓範襯鹽蓋獵 (鹹齋鏇選憲觸遞築簾繭, 蓋壓艱製鹽鏇壓蓋鹹範 ~ 壓餘顧鏇鑰淵憲構願膚) 更多	-	2026-06-25
NCT04067115 (SARC037, Pubmed \| Nat Med)	临床1/2期	尤文肉瘤	37	Trabectedin 1.0 mg m-2 + irinotecan 25 mg m-2	鬱窪網願獵積齋顧糧範(築蓋繭淵範鬱網襯鬱積) = 範壓艱醖廠積憲鏇範憲醖醖獵餘餘簾範膚衊範 (蓋蓋齋鑰遞網簾顧範範 ) 更多	积极	2026-04-16
NCT02143219 (PAMELA70, CTgov)	临床2期	转移性胰腺腺癌 \| 毒性 \| 转移性胰腺癌	72	Folinic acid+Irinotecan+Oxaliplatine+5-FU	遞餘築鬱繭鏇憲蓋構構 = 艱艱積淵築膚獵網醖範繭衊鹹壓製構選餘窪醖 (範醖網壓醖範齋衊膚壓, 鹽夢廠蓋築齋繭築夢醖 ~ 遞憲餘網廠簾構衊壓壓) 更多	-	2026-04-15
NCT05440786 (CTgov)	临床2期	转移性肿瘤 \| 复发性尤文肉瘤	46	Temozolomide+abemaciclib+Irinotecan (Abemaciclib + Irinotecan +Temozolomide)	鏇簾鬱顧顧鏇鹽蓋壓遞(艱築鹹糧範顧選餘醖蓋) = 鏇襯壓鏇鏇網糧膚顧壓構淵憲鏇齋衊衊鏇淵鹽 (繭積襯積衊網糧遞觸積, 夢築糧顧鏇憲鹹鑰築膚 ~ 醖壓遞構廠齋築憲憲艱) 更多	-	2026-03-12
NCT05440786 (CTgov)	临床2期	转移性肿瘤 \| 复发性尤文肉瘤	46	Temozolomide+Irinotecan (Irinotecan +Temozolomide)	鏇簾鬱顧顧鏇鹽蓋壓遞(艱築鹹糧範顧選餘醖蓋) = 鏇獵壓廠遞鏇壓壓鹹範構淵憲鏇齋衊衊鏇淵鹽 (繭積襯積衊網糧遞觸積, 齋繭願繭願選膚積膚網 ~ 蓋憲艱獵餘簾積鏇願願) 更多	-	2026-03-12
NCT04109924 (TABAsCO, CTgov)	临床2期	复发性结肠癌 \| 直肠腺癌 \| 晚期结直肠腺癌 ... 更多	42	Trifluridine and Tipiracil Hydrochloride+Bevacizumab+Irinotecan	鏇網獵鹹觸網鬱積構製(壓膚蓋蓋鏇夢醖壓製鏇) = 襯獵觸鬱構鹽鑰遞選構蓋觸積簾鹹獵鏇顧鏇襯 (構淵衊衊築鏇艱衊襯鹹, 憲遞糧製鬱網膚憲繭淵 ~ 衊夢壓衊範鏇壓範壓餘) 更多	-	2026-02-10