Clinical Study on the Efficacy and Safety of Radiotherapy Combined With Immunotherapy and Chemotherapy for Pre-treated Patients With Small Cell Lung Cancer and Liver Metastases

This is clinical trial evaluating the safety and efficacy of radiotherapy combined with immunotherapy and chemotherapy in patients with extensive-stage small-cell lung cancer (ES-SCLC) and liver metastases.

开始日期2026-10-31

申办/合作机构

四川大学

NCT07724457

/ Not yet recruiting临床2/3期IIT

A Randomized Phase 2/3 Study the Bispecific Antibody (BsAb), Glofitamab, Plus Chemoimmunotherapy in Newly Diagnosed and Relapsed Burkitt and High-Grade (Double Hit) B-Cell Lymphomas With MYC and BCL2 Rearrangements

This phase II/III trial tests adding glofitamab to standard of care chemoimmunotherapy in patients with Burkitt and high grade (double hit) B- cell lymphomas that are newly diagnosed, that has come back after a period of improvement (relapsed) or that does not respond to treatment (refractory). Glofitamab is a monoclonal antibody. It binds to a protein called CD20, which is found on B cells (a type of white blood cell) and some types of cancer cells. This may help the immune system kill cancer cells. Obinutuzumab and rituximab are also monoclonal antibodies. They bind to a protein called CD20, which is found on B cells (a type of white blood cell) and some types of cancer cells. This may help the immune system kill cancer cells. Etoposide is in a class of medications known as podophyllotoxin derivatives. It blocks a certain enzyme needed for cell division and DNA repair and may kill cancer cells. Doxorubicin is in a class of medications called anthracyclines. Doxorubicin damages the cell's DNA and may kill cancer cells. It also blocks a certain enzyme needed for cell division and DNA repair. Vincristine is in a class of medications called vinca alkaloids. It works by stopping cancer cells from growing and dividing and may kill them. Cyclophosphamide is in a class of medications called alkylating agents. It works by damaging the cell's DNA and may kill cancer cells. It may also lower the body's immune response. Prednisone is in a class of medications called corticosteroids. It is used to reduce inflammation and lower the body's immune response to help lessen the side effects of chemotherapy drugs. Methotrexate is in a class of medications called antimetabolites. It is also a type of antifolate. Methotrexate stops cells from using folic acid to make DNA and may kill cancer cells. Chemotherapy drugs, such as cytarabine and ifosfamide, work in different ways to stop the growth of cancer cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Carboplatin is in a class of medications known as platinum-containing compounds. It works in a way similar to the anticancer drug cisplatin, but may be better tolerated than cisplatin. Carboplatin works by killing, stopping or slowing the growth of cancer cells. Giving glofitamab with standard of care chemotherapy may work well for the treatment of newly diagnosed, relapsed or refractory Burkitt and high grade (double hit) B- cell lymphomas.

开始日期2026-10-30

申办/合作机构

National Cancer Institute

NCT07662928

/ Not yet recruiting临床2期IIT

Epcoritamab in Combination With Dose Adjusted R-EPOCH for High Risk Burkitt Lymphoma (BL) (BEDROCK Study)

This phase II trial studies how well epcoritamab works in combination with the chemotherapy regimen dose adjusted etoposide, prednisone, Oncovin (vincristine), cyclophosphamide, hydroxydaunorubicin-rituximab (DA-EPOCH-R) in treating patients with high risk Burkitt lymphoma. Epcoritamab binds to a protein called CD3, which is found on T cells (a type of white blood cell). It also binds to a protein called CD20, which is found on B cells (another type of white blood cell) and some lymphoma cells. This may help the immune system kill cancer cells. Epcoritamab is a type of bispecific T-cell engager. Etoposide is in a class of medications known as podophyllotoxin derivatives. It blocks a certain enzyme needed for cell division and DNA repair and may kill cancer cells. Vincristine is in a class of medications called vinca alkaloids. It works by stopping cancer cells from growing and dividing and may kill them. Cyclophosphamide is in a class of medications called alkylating agents. It works by damaging the cell's DNA and may kill cancer cells. It may also lower the body's immune response. Doxorubicin is in a class of medications called anthracyclines. Doxorubicin damages the cell's DNA and may kill cancer cells. It also blocks a certain enzyme needed for cell division and DNA repair. Prednisone is in a class of medications called corticosteroids. It is used to reduce inflammation and lower the body's immune response to help lessen the side effects of chemotherapy drugs. Giving epcoritamab in combination with the DA-EPOCH-R regimen may be an effective treatment for patients with high risk Burkitt lymphoma.

开始日期2026-09-17

申办/合作机构

National Cancer Institute

100 项与依托泊苷相关的临床结果

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100 项与依托泊苷相关的转化医学

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100 项与依托泊苷相关的专利（医药）

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30,149

项与依托泊苷相关的文献（医药）

2026-12-31·Gut Microbes

Gut bacterial O -demethylation modulates systemic exposure to oral etoposide

Article

作者: Lee, Seongsoo ; Lee, Hyunwoo ; Sullivan, Peter ; Cooper, Bruce R. ; Ilktach, Giokdjen ; Shin, Jongoh ; Jeong, Hyunyoung ; Cho, Byung-Kwan ; Lee, Wooin ; Kyawt, Toe Ein ; Orjala, Jimmy ; Tripathi, Ashutosh ; Weilbaker, Holly A. ; Won, Kyoung-jae ; Armstrong, Abigail T. ; Ko, Yeonju

Gut microbial O-demethylation has been reported for plant-derived dietary compounds containing O-methylated aromatic(s). However, the significance of gut microbial O-demethylation in drug metabolism and disposition remains unexplored. This study examined 64 clinically used oral drugs containing one or more methoxylated aromatics for gut microbial O-demethylation using high-resolution mass spectrometry (HRMS). For 35 of the tested drugs, including the anticancer agent etoposide, we detected metabolites corresponding to O-demethylation (i.e., a mass difference of -14 and its multiples) when individual drugs were incubated with mouse cecal contents. We confirmed that the O-demethylated metabolite (M1) of the model drug etoposide is etoposide catechol using HRMS and proton nuclear magnetic resonance spectroscopy. By testing an in-house collection of 56 gut bacteria individually, we identified seven previously unknown gut bacterial species that exhibit etoposide O-demethylating activity. Etoposide anticancer therapy has been associated with an increased risk of acute myeloid leukemia. We demonstrated that M1 is more genotoxic to myeloid cells when it is orally administered to mice, whereas M1 is less cytotoxic against MCF-7 and HeLa cancer cells than the parent etoposide, suggesting that the gut microbiota may contribute to the secondary genotoxicity of etoposide via O-demethylation. Comparative pharmacokinetic analysis of orally administered etoposide in control and antibiotic-treated mice showed that systemic exposure to etoposide increased 1.9-fold, while M1 exposure decreased 3.7-fold in antibiotic-treated mice, suggesting that gut microbial O-demethylation is a significant determinant of etoposide metabolism and disposition. Collectively, our study reveals the prevalence of gut bacteria with O-demethylation activity, illustrates the contribution of gut microbial O-demethylation to altering drug efficacy and toxicity with the model drug etoposide, and provides a knowledge basis for in-depth characterization of other drugs identified as being susceptible to gut microbial O-demethylation.

2026-12-01·JOURNAL OF COMPUTER-AIDED MOLECULAR DESIGN

Computational study on QSAR modeling, molecular docking, and ADMET profiling of pyrazole-modified catalpol derivatives as prospective dual inhibitors of VEGFR-2/BRAF V600E

Article

作者: Mandal, Manab ; Pal, Sumanta ; Ghosh, Narendra Nath ; Singh, Vivek Dutta ; Pati, Soumen Kumar

Pancreatic and Esophageal cancers are highly aggressive with high mortality and limited treatment, causing over 466,000 and 544,100 deaths worldwide in 2020 respectively. This highlights the urgent need for safer,and effective anticancer agents. Catalpol, a natural iridoid glycoside, shows anticancer potential, but due to its poor drug-like properties it requires structural modification. This study investigates pyrazole-modified catalpol derivatives as dual inhibitors for these cancers using Quantitative Structure Activity Relationship (QSAR) modelling, molecular docking, and pharmacokinetic studies. We analyzed fourteen pyrazole-modified catalpol derivatives with reported IC50values against four cancer cell lines(BxPC-3, PANC-1, Eca109, and EC9706). The molecules were optimized using DensityFunctional Theory (DFT), and 2D molecular descriptors were calculated using PaDEL. QSAR models were developed by utilizing a Genetic Function Algorithm (GFA) and Multiple Linear Regression (MLR) and validated using statistical metrics such as R², Q², R²adj, and R²pred. Docking studies targeted VEGFR-2 and BRAF V600E kinases using AutoDockVina, while ADMET and drug-likeness properties were predicted using SwissADME and pkCSM tools. The external validation R²pred values for BxPC-3, PANC-1, Eca109, and EC9706 cell lines were 0.9412, 0.9535, 0.9981, and 0.9935, respectively. Among the derivatives, compound 3k showed the highest binding affinity for VEGFR-2 (- 8.18 kcal/mol) and BRAF (- 8.64 kcal/mol), surpassing the control drugs etoposide (- 8.00 kcal/mol) and dabrafenib (- 8.15 kcal/mol) respectively. ADMET analysis confirmed good intestinal absorption, limited blood-brain barrier penetration, non-toxicity, acceptable total clearance, and compliance with Lipinski's rule. Overall, the study suggests that pyrazole-modified catalpol derivatives, especially compound 3k, are promising multi-target inhibitors for pancreatic and esophageal cancers, justify further in-vitro and in-vivo studies.

2026-11-01·Biomaterials advances

Supramolecular guest-host composites of adamantane-modified gelatin and β-cyclodextrin polymers, displaying unexpected rheological and bioinert behavior

Article

作者: Prakash, Jai ; Stevens, Christian V ; Vergauwen, Bjorn ; Valoor, Remya ; Raeymaekers, Ruben

Because of their strong complexation behavior, guest-host interactions between adamantane (Ad) and β-cyclodextrin (CD) are often used to create physically crosslinked, reversible supramolecular networks. In this work, scalable syntheses of adamantane-modified gelatin (GelAd) and high molecular weight, water-soluble β-cyclodextrin polymers (CDPs) are presented. Despite confirmed Ad-CD complexation, guest-host combinations of GelAds and CDPs resulted in viscous liquids with viscosities up to tens of Pa.s in all cases at physiological temperature. The resulting viscous composites showed strong shear-thinning and excellent self-healing behavior, but consistently higher loss moduli than storage moduli (G″ > G'), even at high polymer concentrations, high degrees of GelAd modification, and with CDPs near the solubility-limited molecular weight. The addition of laponite enabled true solid hydrogel formation at physiological temperature, but the resulting solid hydrogel was not completely self-healing. The GelAd-CDPs composites exhibited improved resistance to degradation by collagenase. Surprisingly, the composites exhibited no cellular attachment by NIH/3T3 fibroblasts despite the presence of native RGD motifs on gelatin. In addition, the NIH/3T3 fibroblasts remained viable near the gel interface over 12 days, indicating no cytotoxicity and making them highly bioinert. These results reveal that Ad-CD guest-host interactions were in this case not sufficient to form truly solid hydrogels at physiological temperature. Instead, strongly viscous soft composites were formed. The unique combination of shear-thinning, self-healing, improved collagenase resistance, cytocompatibility and bioinertness highlights these GelAd-CDP composites as promising materials for biomedical applications requiring cell-repellent and mechanically adaptive interfaces.

1,854

项与依托泊苷相关的新闻（医药）

2026-09-14

·ioncology

中国之声问鼎首尔！SCLC二线治疗标准或迎历史性格局更替：PFS 7.4个月、死亡风险降低54%——TAISHAN-302闪耀WCLC全体会议并同步登顶NEJM

编者按 2026年9月13日，由中山大学肿瘤防治中心张力教授牵头开展的TAISHAN-302研究（PL02.03）亮相世界肺癌大会（WCLC 2026）全体大会。作为本届大会入选全体会议的两项中国研究之一，备受瞩目。 TAISHAN-302研究是一项多中心、随机、开放标签的III期注册临床试验，旨在评估国产靶向B7-H3的ADC药物依康坦博妥塔单抗（Tam-Peli，YL201）对比标准化疗药物盐酸托泊替康，在经一线含铂治疗进展SCLC患者中的有效性与安全性。结果显示，YL201在无进展生存期（PFS）和总生存期（OS）上均较化疗组实现了具有统计学意义的显著延长，疾病进展或死亡风险大幅降低，且≥3级治疗相关不良事件发生率低于化疗对照组。该研究结果的公布不仅为SCLC二线治疗提供了全新且高级别的循证依据，更是国创ADC在全球肺癌顶级学术舞台上一次里程碑式的亮相。从靶点确证到临床突破 TAISHAN-302研究为SCLC二线治疗再添力证研究背景：SCLC二线治疗的未竟之路小细胞肺癌（SCLC）是肺癌中侵袭性最强、预后最差的亚型，约占所有肺癌确诊病例的15%[1]。该疾病进展迅速，约70%的患者在初诊时已处于广泛期（ES-SCLC）[2]。长期以来，ES-SCLC的一线治疗主要依赖铂类联合依托泊苷的化疗方案，初始客观缓解率（ORR）可达60%–65%，中位PFS为4.7–5.5个月，中位OS为9.9–10.6个月。近年来，IMpower133和CASPIAN等III期研究证实，在化疗基础上联合免疫检查点抑制剂（ICIs）可进一步改善患者结局，ORR提升至60%–80%，中位PFS延长至5.1–6.3个月，但中位OS较单纯化疗仅延长约2–3个月，获益幅度仍十分有限。进入二线治疗后，拓扑替康、芦比替定和塔拉妥单抗的ORR仅约20%–40%，中位PFS约为3–5个月，仍难以显著改善患者的长期生存[3]。因此，SCLC二线治疗亟需探索全新策略，以突破现有疗效局限。抗体偶联药物（ADC）的兴起为这一困境提供了新的治疗选择。与传统化疗不同，其通过将高活性细胞毒性载荷精准递送至表达特定抗原的肿瘤细胞，真正契合了“精准靶向、高效低毒”的治疗理念[1]，从而有效避开SCLC对铂类药物跨膜转运效率改变、DNA修复能力增强等经典耐药机制。基于这一逻辑，SCLC领域的ADC研发近年来进展迅速，针对DLL3、B7-H3、TROP2、SEZ6等靶点的多种ADC已进入不同阶段的临床试验[4]。其中，B7-H3凭借其在SCLC中的高表达频率与广谱覆盖特征，已成为当前最受关注的靶点之一。TAISHAN-302研究的阳性结果，正是为该靶点在SCLC二线治疗中的临床价值提供了最高级别的循证医学证据。研究方法：严谨框架下的科学验证 TAISHAN-302（YL201-CN-302-01）是一项多中心、随机对照、开放标签的III期注册临床研究，旨在评价YL201对比注射用盐酸托泊替康在经一线含铂治疗进展的局限期或广泛期SCLC患者中的有效性和安全性。入组患者按1:1随机分配至试验组（YL201）和对照组（托泊替康）。试验组接受YL201 2.0 mg/kg静脉输注，每3周一次（Q3W）；对照组接受注射用盐酸托泊替康静脉输注，每周期第1至第5天给药，每3周为一个治疗周期。研究预设主要终点为OS，关键次要终点包括研究者评估的PFS和ORR。统计学方法采用固定序贯检验，检验顺序为OS→PFS→ORR，即仅在前一终点达到统计学优效后方可进行下一终点的检验，从而将总体I类错误率严格控制在单侧α=2.5%的水平。疗效数据：三个终点、序贯检验、完整证据链人群基线特征均衡截至2026年5月20日数据截止，共451例患者完成随机分配，其中试验组225例，对照组226例。两组基线特征均衡可比：中位年龄均为62岁；广泛期患者占比分别为96.9%和95.6%；无化疗间隔期<90天患者占比分别为48.9%和48.7%；基线脑转移患者占比分别为34.7%和34.1%。中位随访时间分别为9.2个月和9.5个月，两组随访时长均衡。 OS：期中分析达到预设优效界值，死亡风险降低54% 在主要终点OS方面，本次期中分析的事件数已达到方案预设的优效性判定标准。经IDMC评估确认，YL201组OS较托泊替康组达到了预设的统计学优效界值，YL201组中位OS为13.3个月（95% CI：12.1 - NE），托泊替康组为9.4个月（95% CI：7.7 - 10.5）；HR 0.46（95% CI：0.35 - 0.62），p<0.0001，死亡风险降低54%。亚组分析显示，所有预设亚组中YL201均显示出优于托泊替康的持续OS获益，包括年龄≥65岁、基线脑转移、肝转移及不同无化疗间隔期患者。最终OS分析仍在持续随访中。图1.依康坦博妥塔单抗组与托泊替康组OS Kaplan-Meier曲线 PFS与ORR：均达到预设统计学显著性标准，疾病进展风险或死亡风险降低71% 在完成OS优效性检验后，按固定序贯策略依次对PFS和ORR进行检验，两者同样均达到统计学优效。 PFS：YL201组中位PFS为7.4个月（95% CI：6.1-7.6），托泊替康组为2.8个月（95% CI：1.8 - 3.0）；HR 0.29（95% CI：0.23 - 0.37），p<0.0001，疾病进展或死亡风险降低71%。所有亚组均从YL201治疗中获得一致的PFS获益。图2.依康坦博妥塔单抗组与托泊替康组PFS Kaplan-Meier曲线 ORR：YL201组确认ORR为59.1%（95% CI：52.4 - 65.6），托泊替康组为9.7%（95% CI：6.2 - 14.4），p<0.0001。YL201组疾病缓解率（DCR）为91.1%（95% CI：86.6 - 94.5），中位缓解持续时间（DoR）为6.3个月（95% CI：6.0 - 8.0），中位至缓解时间（TTR）为1.5个月（范围：1.1 - 4.5）。图3.依康坦博妥塔单抗组与托泊替康组肿瘤缓解（研究者评估）瀑布图及汇总数据颅内疗效：在基线脑转移患者中，YL201组颅内PFS中位为6.1个月（95% CI：5.7 - 7.8），托泊替康组为4.2个月（95% CI：2.8 - 5.6）；HR 0.43（95% CI：0.27 - 0.68），p=0.0002。颅内cORR为32.4%（95% CI：22.0 - 44.3）vs 2.9%（95% CI：0.4 - 10.1），p<0.0001；颅内DCR为90.5%（95% CI：81.5 - 96.1）vs 59.4%（95% CI：46.9 - 71.1），p<0.0001。图4.依康坦博妥塔单抗组与托泊替康组颅内疗效（研究者评估）Kaplan-Meier曲线及汇总数据三个疗效终点按预设顺序逐一通过统计学检验，形成了从“近期疗效（ORR）”到“远期生存（PFS、OS）”的完整证据链，从多个维度验证了YL201的临床获益。安全性与可及性：独特优势赋能临床实践在安全性方面，YL201同样展现出区别于传统化疗和T细胞衔接抗体的独特优势。血液学毒性为主，发生率低于化疗试验组≥3级治疗相关不良事件（TRAE）发生率为46.4%，化疗对照组为74.7%。最常见的≥3级TRAE为血液学毒性，YL201组发生率均低于托泊替康组：贫血（10.7% vs 23.5%）、血小板减少（12.5% vs 54.8%）、白细胞减少（19.2% vs 32.3%）、中性粒细胞减少（21% vs 35.5%），均为临床管理经验成熟的毒性类型，易于监测和控制。图5.依康坦博妥塔单抗组与托泊替康组安全性总结无CRS/ICANS，ILD风险低尤为值得关注的是，YL201治疗组未报告细胞因子释放综合征（CRS）或免疫效应细胞相关神经毒性综合征（ICANS）事件。此外，与部分其他ADC药物相比，YL201的间质性肺病（ILD）风险较低，本研究中，ILD和非感染性肺炎发生率仅为4.9%。图6.依康坦博妥塔单抗组与托泊替康组治疗相关不良事件（发生率≥20%）上述安全性特征提示YL201可采用常规门诊静脉输注方式给药，无需额外住院监测或特殊毒性管理设施，可有效降低对医疗资源的依赖，也极大改善了患者的用药便利性和治疗依从性。研究结论：B7-H3靶点临床价值的首次III期确证 TAISHAN-302研究首次在III期试验层面确证了B7-H3靶向ADC药物YL201在复发性SCLC二线治疗中的显著临床获益——同时实现了OS、PFS和ORR三个维度的统计学优效，且安全性显著优于标准化疗，无CRS/ICANS等特殊毒性管理要求。这一成果为复发性SCLC患者提供了全新的、具有高级别证据支持的治疗选择。从B7-H3的生物学特征到临床价值的靶点确证重构SCLC二线治疗路径 B7-H3：一个“理想”靶点基于生物学基础的价值解析 B7-H3（又称CD276）是B7免疫调节家族的成员，是一种在正常组织中表达水平极低的跨膜糖蛋白，但在多种实体瘤中呈显著过表达。在SCLC中，约65%的肿瘤组织呈现B7-H3阳性表达[4]；在非小细胞肺癌（NSCLC）中，约80%呈阳性[5]；而在前列腺癌中，这一比例可超过90%[6]。这种肿瘤组织与正常组织之间的巨大表达差异，构成了B7-H3作为优选治疗靶点的前提条件。在功能层面，B7-H3扮演着双重促癌角色。它不仅是免疫检查点分子，可抑制T细胞和自然杀伤（NK）细胞的活化，介导肿瘤免疫逃逸[2]；还可直接促进肿瘤细胞的迁移、侵袭和血管新生，并与化疗耐药的发生密切相关[7-8]。这意味着靶向B7-H3在恢复抗肿瘤免疫应答的同时，可直接抑制肿瘤的恶性生物学行为。与DLL3等其他SCLC靶点在不同分子亚型中表达差异显著不同，B7-H3在SCLC的四种主要转录亚型（ASCL1、NEUROD1、POU2F3、YAP1）中均呈现高度且一致的表达水平，瘤内及患者间异质性更低，覆盖人群更广[9-10]。同时，大量研究证实B7-H3的过表达与肿瘤分期升高、淋巴结及远处转移、患者生存期缩短显著相关，是SCLC独立的不良预后因子[11-12]。由此可见，B7-H3兼具了理想治疗靶点的多重属性：在肿瘤组织中广泛且稳定地高表达，在正常组织中近乎沉默，其表达水平直接关乎疾病进展与预后，且覆盖所有主要分子亚型。 ADC：精准靶向机制驱动疗效突破理想的靶点识别能力需要通过恰当的药物形式转化为实际的抗肿瘤疗效。ADC药物通过其独特的三组分结构——特异性靶向抗体、高细胞毒性载荷，以及连接抗体与载荷的化学连接子精准实现了这一转化[1]。ADC经抗体部分识别并结合肿瘤细胞表面抗原后，通过内吞作用进入细胞，连接子在溶酶体或肿瘤微环境中裂解，释放载荷诱导肿瘤细胞凋亡[1]。可裂解连接子的设计使ADC具备“旁观者效应”，即释放的载荷可穿透细胞膜杀伤邻近抗原阴性或低表达的肿瘤细胞[1]。对于B7-H3表达存在异质性的SCLC而言，这一效应尤为关键，可使ADC克服因抗原下调导致的肿瘤逃逸。此外，YL201所携带的拓扑异构酶I抑制剂是SCLC领域最具前景的ADC载荷类型[4]，其通过与拓扑异构酶I-DNA裂解复合物结合诱导不可修复的DNA双链断裂，可有效避开SCLC对铂类药物的经典耐药路径。正是抗体、连接子与载荷三者的协同配合，构成了ADC从靶点识别到肿瘤杀伤的完整逻辑链条。中国智造：TMALIN®平台的技术优势与临床转化 TMALIN®平台的技术突破：我国自主研发的TMALIN®（Tumor Microenvironment Activable LINker）平台，围绕连接子结构、裂解机制与载荷性能三个维度进行了系统性设计，为YL201的优异表现奠定了技术基础。在体循环稳定性方面，TMALIN®平台采用甲磺酰基嘧啶类连接头实现与抗体的不可逆偶联，从分子层面规避了传统马来酰亚胺连接头因可逆交换反应导致的连接子-载荷提前脱落问题。临床前研究显示，该平台所设计的连接子-载荷在模拟生理条件的血浆中孵育28天后，载荷脱落率仍低于2%，体现了优异的体循环稳定性[13]。在裂解机制方面，TMALIN®平台采用基于缬氨酸-赖氨酸-甘氨酸（VKG）序列等特定三肽基序的连接子。研究表明，该类连接子可被肿瘤微环境中的酶裂解释放有效载荷，其中组织蛋白酶L（Cathepsin L）可能参与该裂解过程。该设计使ADC能够在肿瘤微环境中实现胞外裂解，从而克服了传统上对细胞内吞作用的依赖[14]。由此，载荷释放路径从单一的“细胞内溶酶体释放”拓展为“肿瘤微环境胞外释放”与“细胞内溶酶体释放”并行的双重机制[14-15]。临床前研究显示，采用TMALIN平台开发的ADC在肿瘤组织中能高效释放载荷并发挥显著的抗肿瘤活性，验证了该胞外释放路径的有效性[13]。临床转化验证——B7-H3表达与疗效的非线性关系：TMALIN®平台的双重裂解机制在临床转化层面产生了一个值得关注的现象。在YL201的I期临床试验中，研究者对152例具有基线肿瘤组织样本的晚期实体瘤患者进行了B7H3膜表达水平（H-score）与客观缓解率的相关性分析，结果显示在总体人群及各肿瘤亚型中，B7H3表达高低组间的客观缓解率均无统计学显著差异[15]。这一发现与TMALIN®平台“非内吞依赖”的胞外裂解机制设计相一致[14]。传统ADC依赖内吞-溶酶体途径释放载荷，其疗效通常与靶抗原表达水平呈正相关；而TMALIN®平台通过肿瘤微环境中的胞外裂解路径，绕过了内吞效率的限制[14]，使得即便B7H3表达水平较低的肿瘤细胞，只要处于具有蛋白酶裂解活性的肿瘤微环境中，仍可能暴露于有效浓度的载荷之下。这一发现为两项关键的临床观察提供了解释：其一，YL201在B7-H3表达存在异质性的SCLC人群中仍能取得较高的ORR；其二，YL201的适用人群可能不受靶点表达水平的刚性限制，意味着更多患者可能从中获益。 B7-H3靶点从生物学走向临床 B7-H3作为抗肿瘤靶点的潜力已在实验室研究和早期临床试验中得到初步提示，但其临床获益此前始终缺乏高级别随机对照研究的直接验证。TAISHAN-302研究的阳性结果，首次在III期试验层面证实了B7-H3靶向治疗可为复发性SCLC患者带来确切的生存获益，标志着该靶点的临床价值已从“生物学相关”迈入“临床可获益”的确证阶段。在2026年WCLC全体大会上，除TAISHAN-302外，另一项中国B7-H3靶向ADC的III期研究亦公布了阳性结果。两项研究同时亮相全体大会，标志着B7-H3作为SCLC治疗靶点的临床价值已获最高级别循证医学共识的认可，也意味着中国创新药在这一领域的探索正在从“跟跑”走向“并跑”乃至“领跑”。对于一线治疗失败的SCLC患者而言，靶向B7-H3的ADC治疗提供了一种有别于传统化疗和T细胞衔接抗体的全新选择——不依赖患者的免疫状态，无需复杂的毒性管理，可在门诊完成常规输注。这一治疗策略正在从概念走向现实，并有望成为SCLC二线治疗的新基石。从创新平台到全球认可国创ADC的崛起与SCLC治疗格局的重塑从双BTD到顶刊WCLC：YL201的国际认可之路依康坦博妥塔单抗已相继获得中国NMPA和美国FDA的突破性疗法认定（BTD），用于经含铂治疗失败的复发性SCLC。2026年9月13日，张力教授在WCLC全体大会环节口头汇报TAISHAN-302核心数据；与此同时，研究登顶全球医学界顶刊《新英格兰医学杂志》（NEJM）。从中美双BTD到WCLC全体大会汇报再到国际顶刊收录，依康坦博妥塔单抗以扎实循证证据赢得全球医学界认可。从技术突破到临床转化：中国创新ADC的未来征程 TAISHAN-302研究以III期随机对照试验的最高级别证据，首次确证了B7-H3作为SCLC治疗靶点的临床价值——在二线治疗中，YL201同时覆盖OS、PFS和ORR三个终点且全面优于化疗，为复发性SCLC患者提供了一种兼顾疗效与生活质量的新选择。这一突破性成果同时展现了我国在ADC药物研发领域从靶点发现、分子设计到临床验证的完整创新体系的逐步成熟，标志着我国自主研发体系在ADC领域已具备与国际先进水平同台竞争的实力。基于TMALIN®平台，已有15款ADC药物进入临床阶段，覆盖B7-H3、HER3、NaPi2b、c-MET、DLL3、VEGF、PD-L1/VEGF等多个靶点，该技术路径在跨瘤种中的临床转化潜力值得持续关注。以YL201为代表的本土创新ADC药物，有望在SCLC及更多实体瘤的治疗格局演进中发挥积极作用，使基础研究的突破最终转化为患者生存获益与生活质量的切实改善。免责声明：在研产品，尚未获批。依康坦博妥塔单抗用于治疗复发性小细胞肺癌的上市申请已于2026年9月2日获国家药监局正式受理。全球首个基于III期临床数据的B7-H3靶向ADC鼻咽癌上市申请26年7月18日已获CDE受理。参考文献：（上下滑动可查看） 1. CHEN X, ZHOU C. Antibody-drug Conjugates in Lung Cancer: Current Landscape and Future Perspectives.[J]. Current opinion in oncology, 2025, 38(1): 71-82. 2. HAO Z, VILLANO J, ARNOLD S M, et al. Current and Emerging Therapies Targeting Cell Surface Antigens and Epigenetics in Extensive Stage Small Cell Lung Cancer: Primer for Clinicians[J]. Therapeutic advances in medical oncology, 2026, 18: 17588359261458324-17588359261458324. 3. LI Y, CHEN K, LI H, et al. Targeted Precision Strike in Extensive-Stage Small Cell Lung Cancer: Current Advances and Future Perspectives for Antibody–Drug Conjugates[J]. Cancer treatment reviews, 2026, 143: 103091-103091. 4. MONACA F, GOMEZ-RANDULFE I, TORRES-JIMÉNEZ J, et al. Antibody-Drug Conjugates in SCLC: DLL3, B7-H3, TROP2, and Beyond.[J]. Journal of thoracic oncology official publication of the International Association for the Study of Lung Cancer, 2026: 103726-103726. 5. Altan M, Pelekanou V, Schalper KA, et al. B7-H3 Expression in NSCLC and Its Association with B7-H4, PD-L1 and Tumor-Infiltrating Lymphocytes. Clin Cancer Res. 2017;23(18):5202-5209. 6. Guo C, Figueiredo I, Gurel B, et al. B7-H3 as a Therapeutic Target in Advanced Prostate Cancer. Eur Urol. 2023;83(3):224-238. 7. Chapoval AI, Ni J, Lau JS, et al. B7-H3: a costimulatory molecule for T cell activation and IFN-γ production. Nat Immunol. 2001;2(3):269-274.8. Prasad DV, Nguyen T, Li Z, et al. Murine B7-H3 is a negative regulator of T cells. J Immunol. 2004;173(4):2500-2506.9. Ajay A, Wang H, Rezvani A, et al. Assessment of targets of antibody drug conjugates in SCLC[J]. NPJ Precision Oncology, 2025, 9(1): 1.10. Gay CM, Owonikoko TK, Byers LA, et al. Multidimensional Analysis of B7 Homolog 3 RNA Expression in Small Cell Lung Cancer Molecular Subtypes. Clin Cancer Res. 2025;31(16):3476-3482.11. Carvajal-Hausdorf D, Altan M, Velcheti V, et al. Expression and clinical significance of PD-L1, B7-H3, B7-H4 and TILs in human small cell lung Cancer (SCLC)[J]. Journal for immunotherapy of cancer, 2019, 7(1): 65.12. KUROSAKI T, KANEMURA H, OTANI T, et al. Impact of B7-H3 and DLL3 Expression on the Efficacy of PD-L1 Blockade Therapy in Extensive-Stage Small Cell Lung Cancer.[J]. Lung cancer (Amsterdam, Netherlands), 2025, 207: 108723-108723. 13. CAI J, SONG S, ZONG Q, et al. Development and Assessment of a Novel Tumor Microenvironment Activable Linker (TMALIN) ADC Platform for Solid Tumor Treatments[J]. Cancer Research, 2023, 83(7). 14. YANG L, MA J, LIU B, et al. Recent Advances in Peptide Linkers of Antibody-Drug Conjugates.[J]. Journal of medicinal chemistry, 2025, 68(17): 18099-18113. 15. MA Y, YANG Y, HUANG Y, et al. A B7H3-targeting Antibody–drug Conjugate in Advanced Solid Tumors: a Phase 1/1b Trial[J]. Nature medicine, 2025, 31(6): 1949-1957. 16. Yuanyuan Zhao, Hongxu Liu, et al.Tambotatug Pelitecan in Small-Cell Lung Cancer after Platinum-Based Therapy. NEJM. doi:10.1056/NEJMoa2610229. https://www.nejm.org/doi/full/10.1056/NEJMoa2610229 （来源：《肿瘤瞭望》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。

2026-09-14

·ioncology

2026 WCLC 全体大会丨王洁教授：18.5m OS 刷新纪录！Ris-Rez 改写复发 SCLC 治疗格局

✩ 本文仅供医疗卫生等专业人士参考审批码：HS-NP-A107-2609-01918 本资料仅供中国境内医疗卫生专业人士参阅，旨在分享研发前沿资讯，非推广用途，不应被理解为对特定药物的推荐或者建议。请勿参考或倚赖本平台下的任何内容，有关疾病或药品的相关问题，请咨询有资质的医疗专业人员参考文献 [1] J Wang, et al. Risvutatug Rezetecan (a B7-H3-Directed ADC) Versus Topotecan in Relapsed SCLC: Primary Results of Phase 3 ARTEMIS-008. 2026 WCLC. PL02.04. [2] Lu Y, Fan Y. Research Progression of Maintenance Therapy in Small Cell Lung Cancer[J]. Zhongguo Fei Ai Za Zhi. 2015 Sep 20;18(9):559-64. [3] Jazz Pharmaceuticals Provides Update on Zepzelca® (lurbinectedin) Phase 3 LAGOON Trial in Second-Line Small Cell Lung Cancer. [4] Carboplatin plus etoposide versus topotecan as second-line treatment for patients with sensitive relapsed small-cell lung cancer: an open-label, multicentre, randomised, phase 3 trial. Lancet Oncology. 2020;21(9):1224-1233. [5] Tarlatamab in Small-Cell Lung Cancer after Platinum-Based Chemotherapy.New England journal of Medicine. 2025;393:349-361. [6] Carvajal-Hausdorf D, Altan M, Velcheti V, et al. Expression and clinical significance of PD-L1, B7-H3, B7-H4 and TILs in human small cell lung cancer (SCLC). J Immunother Cancer. 2019;7(1):65. [7] Campisi M, Stornante C, Dryg ID, et al. Targeting B7-H3 in the small cell lung carcinoma tumor-immune microenvironment. Cancer Res. 2026;86(7 Suppl):Abstract 5603. [8] Zhou WT, Jin WL. B7-H3/CD276: an emerging cancer immunotherapy. Front Immunol. 2021;12:701006. [9] World Health Organization. Rezetecanum. In: International Nonproprietary Names for Pharmaceutical Substances (INN): Proposed INN List 127. WHO Drug Information. 2022;36(2). [10] Waight J, Zhou Y, Sun D, et al. Abstract 7097: Non-clinical characterization of GSK5764227, a novel B7-H3-directed antibody-drug conjugate (ADC). Cancer Res. 2026;86(7 Suppl):7097. doi:10.1158/1538-7445.AM2026-7097. [11] Duan J, Sun Y, Wang Q, et al. HS-20093, a B7-H3-targeted antibody-drug conjugate in lung cancer: results from the ARTEMIS-001 phase 1a/b trial. Cancer Cell. 2026;44(4):846-857.e3. [12] Zhong H, et al. CT038-Combination of risvutatug rezetecan and adebrelimab in previously treated advanced nsq-NSCLC without actionable genomic alterations: Results from ARTEMIS-101, a phase 1 study.2026 AACR. [13] ClinicalTrials.gov. Study NCT07464327. https://clinicaltrials.gov/study/NCT07464327. 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。

2026-09-14

·ioncology

遇见WCLC·研究者说｜张凌云教授：ES-SCLC维持治疗新策略，免疫联合抗血管“加法”能否改写生存曲线？

编者按 2026年9月12日至15日，由国际肺癌研究协会（IASLC）主办的2026世界肺癌大会（WCLC 2026）在韩国首尔隆重召开。作为全球胸科肿瘤学领域规模最大、影响力最广的学术盛会，本届大会以“Science Without Boundaries”为主题，汇聚全球顶尖研究者、临床医生及患者倡导者，集中呈现肺癌诊疗领域的前沿突破与未来图景。本届大会，来自中国医科大学附属第一医院张凌云教授团队主持开展的CLOG2402-ADAPT研究结果入选，该研究旨在探索阿得贝利单抗联合阿帕替尼作为广泛期小细胞肺癌（ES-SCLC）一线诱导后的维持治疗方案。《肿瘤瞭望》特邀张凌云教授解读该项研究进展，特此整理，以飨读者。研究介绍研究背景肺癌是全球发病率和死亡率最高的恶性肿瘤，其中小细胞肺癌（SCLC）约占肺癌的15%，50%-80%的患者在初诊时已是广泛期（ES-SCLC），预后极差。当前一线标准治疗为含铂化疗联合免疫检查点抑制剂（ICI），但相较单纯化疗，中位总生存期（OS）的延长不超过5个月，生存获益仍远未满足临床需求。ETER701研究证实，在化疗基础上叠加小分子抗血管生成药物可将中位OS从11.9个月提升至19.3个月，但四药联合的严重不良事件和出血风险显著增加（≥3级不良事件发生率54.9%，咯血发生率13.4% vs 7.3%）；BEAT-SC研究则发现，大分子抗血管药物贝伐珠单抗联合ICI+化疗并未改善OS，提示小分子TKI可能是ICI联合化疗的更优"搭档"。此外，ASTRUM-005研究提示免疫跨线治疗可能改善OS，但抗血管生成药物联合ICI跨线治疗的疗效尚不明确。基于此，提出"诱导后维持加法"的治疗策略，开展CLOG2402-ADAPT 试验。研究方法 CLOG2402-ADAPT是一项多中心、单臂Ⅱ期临床研究，旨在评估阿得贝利单抗（PD-L1 抑制剂）联合阿帕替尼（VEGFR-2 酪氨酸激酶抑制剂）作为维持治疗的疗效与安全性。截至 2026年3月，共计纳入21 例经 4～6 周期阿得贝利单抗联合铂类 + 依托泊苷一线诱导治疗后疾病未发生进展的广泛期小细胞肺癌患者，患者进入维持阶段的治疗：阿得贝利单抗 1200 mg，静脉输注，每 3 周 1 次；联合阿帕替尼 250 mg，口服，每日 1 次，持续用药直至疾病进展、出现不可耐受毒性或受试者退出研究。主要研究终点为无进展生存期（PFS），定义为自维持治疗启动至首次记录到疾病进展的时间。次要研究终点包括总生存期（OS）、客观缓解率（ORR）、疾病控制率（DCR）、至第二次疾病进展时间（PFS2）。研究结果截至 2026 年 3 月，中位随访时间 7.2 个月（范围 4.8～17.2 个月）。患者中位年龄 65 岁（49～77 岁）；男性占 62%，女性占 38%。57% 的患者存在当前吸烟或既往吸烟史。肝转移发生率 14%，脑转移发生率 19%。诱导治疗的中位时长为 3.8 个月（范围 2.3～6.2 个月）。图 1. 肿瘤病灶最佳缩小比例 85.7%的患者在诱导治疗后达到部分缓解。维持治疗阶段的肿瘤疗效基于维持治疗基线进行评估（表1）。表1 维持治疗阶段的肿瘤疗效维持治疗阶段，21 例患者均接受了至少 1 次肿瘤疗效评估。ORR为 9.5%，DCR76%（包括 2 例部分缓解、14 例疾病稳定、5 例疾病进展）。维持治疗阶段的中位PFS为 6.01 个月，而自首次给药起计算的中位无进展生存期为 9.03 个月。OS数据尚不成熟（图2）。图2 维持治疗阶段的无进展生存期（PFS）所有患者（100%）均发生治疗相关不良事件（TRAEs），3 级治疗相关不良事件发生率为 19%，包括脂肪酶升高、间质性肺炎、免疫性肠炎、γ- 谷氨酰转肽酶（GGT）升高。未发生治疗相关死亡。研究结论该研究初步证实了，ES-SCLC经阿得贝利单抗联合化疗诱导后未进展的患者，采用阿得贝利单抗联合阿帕替尼维持治疗的可行性与可接受的安全性。未来，本项研究继续随访并收集总生存期成熟后的长期获益，回答ES-SCLC的维持治疗或许不再只是"延续"，而是真正成为可改写生存曲线的起点。专家简介张凌云教授中国医科大学附属第一医院肿瘤内科三级教授，主任医师，硕士生导师中国抗癌协会肿瘤临床化疗专委会委员中国抗癌协会罕见突变及罕见肿瘤专委会委员中国抗癌协会骨与软组织肿瘤整合康复专委会常委中国医药教育协会肿瘤化疗专委会常委 CSCO小细胞肺癌专委会委员北京整合医学会肺癌专委会副主任委员北京整合医学会胸部肿瘤转化医学会常委辽宁省抗癌协会肿瘤MDT专业委员会副主任委员辽宁省细胞生物学学会肺癌细胞靶向和免疫治疗专委会副主任委员辽宁省红十字基金会骨转移瘤医学专委会副主任委员辽宁省预防医学会肿瘤防治专委员会常委辽宁省免疫学会肿瘤免疫分会常委兼秘书中国癌症基金会科普与健康传播全国协作组专家《中华肿瘤杂志》青年编委；《肿瘤临床与康复》编委；《中国医科大学学报》编委参考文献：Lingyun Zhang, et al. Adebrelimab Plus Apatinib for Maintenance Treament of ES‑SCLC After First‑Line Induction With Adebrelimab Plus Chemotherapy (CLOG2402‑ADAPT). 2026 WCLC. P3.312 （来源：《肿瘤瞭望》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。

100 项与依托泊苷相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D00125	依托泊苷	L01CB01	DB00773

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
膀胱癌	日本	Clinigen Ltd.	1987-04-30
白血病	日本	Clinigen Ltd.	1987-04-30
淋巴瘤	日本	Nippon Kayaku Co., Ltd.	1987-03-31
卵巢癌	日本	Nippon Kayaku Co., Ltd.	1987-03-31
宫颈癌	日本	Nippon Kayaku Co., Ltd.	1987-03-31
小细胞肺癌	美国	Corden Pharma Latina SpA	1983-11-10
小细胞肺癌	美国	Corden Pharma International GmbH	1983-11-10
睾丸肿瘤	美国	Corden Pharma International GmbH	1983-11-10
睾丸肿瘤	美国	Corden Pharma Latina SpA	1983-11-10

未上市

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
铂耐药性卵巢癌	临床3期	中国	江苏恒瑞医药股份有限公司	2019-08-16
原发部位不明恶性肿瘤	临床3期	美国	Pharmacia & Upjohn, Inc.	2003-09-01
原发部位不明恶性肿瘤	临床3期	美国	Eli Lilly & Co.	2003-09-01
原发部位不明恶性肿瘤	临床3期	美国	AstraZeneca PLC	2003-09-01
广泛期小细胞肺癌	临床3期	美国	GSK Plc	2001-04-01
广泛期小细胞肺癌	临床3期	中国	GSK Plc	2001-04-01
广泛期小细胞肺癌	临床3期	奥地利	GSK Plc	2001-04-01
广泛期小细胞肺癌	临床3期	比利时	GSK Plc	2001-04-01
广泛期小细胞肺癌	临床3期	巴西	GSK Plc	2001-04-01
广泛期小细胞肺癌	临床3期	保加利亚	GSK Plc	2001-04-01

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临床结果

适应症

分期

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


WCLC2026	N/A	生殖细胞和胚胎肿瘤	114	Bleomisin-etoposide-cisplatin chemotherapy (Nonseminomatous)	範觸衊鏇醖網顧獵襯鹹(簾鏇構鑰艱蓋製遞襯襯) = 夢獵選憲獵製衊築遞構鹹襯襯艱窪蓋鬱憲簾廠 (窪窪構齋選選餘遞網遞, 7.37)	不佳	2026-09-12
WCLC2026	N/A	广泛期小细胞肺癌一线 \| 二线	4,470	Cisplatin-based or carboplatin-based therapy + Cisplatin-basedapiecarboplatin-based therapy	鏇積構醖範憲窪選廠製(鹽繭齋築壓顧鏇衊襯襯) = 顧鬱襯積鏇膚鹽繭範艱鬱艱膚鏇觸鹽餘憲簾糧 (鑰糧淵繭獵範蓋範觸網 ) 更多	积极	2026-09-12
				Etoposide-based regimensTopotecan-based regimens + Etoposide-based regimensTopotecan-based regimens + Etoposide-based regimensTopotecan-based regimens	鏇積構醖範憲窪選廠製(襯壓簾衊窪構顧鏇鏇鬱) = 製艱鏇獵憲鏇製窪淵衊齋鬱壓壓齋鏇鹹鬱遞構 (糧鹹襯鏇顧襯憲築觸鏇 ) 更多
WCLC2026	N/A	广泛期小细胞肺癌一线	97	Carboplatin-Etoposide-Atezolizumab	鹹艱鑰壓憲壓廠鏇鑰繭(願簾壓鹹蓋窪繭膚鏇衊) = 簾憲夢願淵膚築繭襯鹹衊願膚積夢壓繭壓齋壓 (夢範夢願餘顧醖遞夢衊 ) 更多	积极	2026-09-12
ChiCTR1800015883 (Pubmed \| Blood)	临床3期	急性髓性白血病	224	Low-dose cytarabine, mitoxantrone or idarubicin, and granulocyte colony-stimulating factor	網範觸網鹽齋餘獵遞觸(獵範願齋餘遞遞獵衊襯) = 壓憲顧獵構膚構遞構繭積選膚繭願範淵簾遞襯 (製觸構鏇淵簾獵願艱淵 ) 更多	非劣	2026-07-02
				Cytarabine, daunomycin, and etoposide	網範觸網鹽齋餘獵遞觸(獵範願齋餘遞遞獵衊襯) = 築壓鹹憲膚範繭壓餘簾積選膚繭願範淵簾遞襯 (製觸構鏇淵簾獵願艱淵 ) 更多
NCT01783535 (CTgov)	临床2期	单侧视网膜母细胞瘤 \| 视网膜母细胞瘤	174	focal therapy+carboplatin+PEG-filgrastim+filgrastim+vincristine+Topotecan (Stratum A)	壓觸鹽鹹顧襯壓製衊鹽(憲獵醖築壓鹽製糧鬱鹽) = 範膚糧衊餘蓋鑰積遞醖顧淵窪觸齋遞築繭艱鬱 (觸構蓋襯廠積鹹觸醖遞, 鹽夢糧觸網餘齋鏇鹽願 ~ 艱鹹遞構網鹽積鹹窪糧) 更多	-	2026-06-29
				focal therapy+etoposide+carboplatin+PEG-filgrastim+Filgrastim+vincristine+Topotecan (Stratum B)	壓觸鹽鹹顧襯壓製衊鹽(憲獵醖築壓鹽製糧鬱鹽) = 齋範製鹽範鹽鹽夢衊壓顧淵窪觸齋遞築繭艱鬱 (觸構蓋襯廠積鹹觸醖遞, 窪構襯觸鹹鹽廠壓衊衊 ~ 積觸壓遞鹹築憲顧糧製) 更多
ASCO_Breakthrough2026	N/A	神经内分泌癌	37	Definitive chemoradiotherapy (limited-stage disease)	製積鹹獵鬱糧衊鏇遞淵(築繭構壓憲餘廠鹽鹹築) = 衊襯齋齋憲鏇餘壓餘鏇壓艱衊廠網衊繭顧鹽衊 (獵簾壓淵壓築窪願鑰構 ) 更多	积极	2026-06-25
				Platinum-etoposide chemotherapy (extensive-stage disease)	網窪膚壓衊遞窪顧襯夢(顧壓淵鹹憲襯製襯製網) = 淵繭醖網願積鹽遞鹹築獵願餘築蓋築簾膚夢艱 (構鹹鏇膚選獵鬱憲構鑰 ) 更多
NCT07398560 (CAPSTONE-1, ASCO_Breakthrough2026)	临床2期	小细胞肺癌一线	47	Adebrelimab + oral etoposide	衊選衊醖艱夢糧廠壓鏇(餘遞齋醖糧鹽鏇糧糧鹽) = 顧構夢糧夢鏇觸蓋獵範顧鏇憲蓋鬱鬱壓蓋鏇顧 (鏇鏇廠憲獵觸夢蓋衊構 )	积极	2026-06-25
ASCO2026	N/A	广泛期小细胞肺癌一线	87	carboplatin + etoposide + (durvalumab or atezolizumab)	鹽築觸範醖鹹願鹽艱選(壓憲鑰築鏇簾選選壓窪) = 鬱淵製壓積網糧膚廠繭窪衊鬱製壓蓋艱餘簾醖 (鏇衊艱積願艱積糧鬱簾 ) 更多	积极	2026-05-29
NCT05006664 (CHEPA, ASCO2026)	临床2期	外周T细胞淋巴瘤 CD30-positive	33	Brentuximab vedotin plus CHEPA	顧淵壓鬱艱夢醖觸網製(製夢製簾觸顧範窪襯鑰) = 顧鬱糧衊鬱構鏇簾餘餘製網鬱獵糧網餘襯網積 (簾選齋鑰膚獵鬱窪糧鏇 ) 更多	积极	2026-05-29
				Brentuximab vedotin plus CHEPA (ALCL)	顧淵壓鬱艱夢醖觸網製(製夢製簾觸顧範窪襯鑰) = 夢壓獵夢鏇淵鏇鹽鏇遞製網鬱獵糧網餘襯網積 (簾選齋鑰膚獵鬱窪糧鏇 ) 更多
NCT02583893 (CTgov)	临床2期	成人急性髓性白血病	39	Etoposide+Sirolimus+Mitoxantrone+Cytarabine	齋顧鬱廠獵鏇蓋襯選選 = 糧製糧糧鬱艱網艱構顧製蓋願顧範願膚繭壓壓 (鹹憲繭遞顧簾醖觸網鬱, 繭艱窪夢簾鬱遞獵壓壓 ~ 糧觸觸淵鹽鹽鑰壓膚鏇) 更多	-	2026-05-29