Phase 2 Study of 9-ING-41, a Glycogen Synthase Kinase 3 Beta (GSK 3β) Inhibitor, Plus Carboplatin in Patients With Advanced, Metastatic Salivary Gland Carcinoma

9-ING-41 is a small molecule potent selective GSK-3β inhibitor with antitumor activity. This study investigates 9-ING-41 in combination with carboplatin chemotherapy in patients with incurable, recurrent or metastatic salivary gland carcinomas (SGC). Patients with advanced SGC (including all histologic subtypes and adenoid cystic carcinoma [ACC]) will receive 9-ING-41 intravenously (IV) along with carboplatin IV at standard dosing together on Day 1, and 9-ING-41 alone on Day 4 of a 21-day cycle. Participants will be enrolled to two histologic cohorts: Cohort 1 will be comprised of those with ACC, and Cohort 2 will include patients with non-ACC SGC (or all other salivary gland cancer histologies). Treatment will continue until progression of disease, death, or discontinuation of therapy for any reason.

开始日期2030-12-18

申办/合作机构

Actuate Therapeutics, Inc.

NCT07229339

/ Not yet recruiting临床2期IIT

Phase 2 Trial of Zipalertinib in Patients With Resectable Non-Small Cell Lung Cancer With EGFR Exon 20 Insertion or Uncommon/Compound Mutations

This phase II trial tests how well zipalertinib with carboplatin and pemetrexed works in treating stage II-IIIB non small cell lung cancer. that can be removed by surgery (resectable). Zipalertinib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. 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 tumor cells. Pemetrexed is in a class of medications called antifolate antineoplastic agents. It works by stopping cells from using folic acid to make DNA and may kill tumor cells. Giving zipalertinib with carboplatin and pemetrexed may kill more tumor cells in patients with resectable, stage II-IIIB non-small cell lung cancer.

开始日期2027-06-01

申办/合作机构

Jonsson Comprehensive Cancer Center

[+1]

NCT07346196

/ Not yet recruiting临床2期IIT

A Randomized Phase II Trial of Induction Cemiplimab Plus Chemotherapy With or Without Fianlimab in Locoregionally Advanced Squamous Cell Carcinoma of The Head and Neck

The goal of this clinical trial is to learn if the combination of cemiplimab and fianlimab can improve outcomes compared to cemiplimab alone in adults with Human Papillomavirus Positive HPV-positive head and neck cancer.

开始日期2027-02-07

申办/合作机构

The University of Chicago

100 项与卡铂相关的临床结果

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100 项与卡铂相关的转化医学

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100 项与卡铂相关的专利（医药）

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13,495

项与卡铂相关的文献（医药）

2026-12-31·OncoImmunology

A mixed inflammatory peripheral signature defines clinical outcomes in a phase II trial combining pembrolizumab with paclitaxel and carboplatin in melanoma

Article

作者: Cocolakis, Eftihia ; Cailhier, Jean-François ; Lapointe, Réjean ; Thébault, Paméla ; Letendre, Caroline ; Shechtman, Yelena ; Lepage, Stéphanie ; Le, Huy ; Dionne, Jeanne ; Bélanger, Karl ; Jamal, Rahima ; Lambert, Caroline ; Miller Jr, Wilson H.

Checkpoint blockade of PD-1 with pembrolizumab provides long-term survival to a significant proportion of patients with metastatic melanoma. Pembrolizumab has been successfully used in combination with chemotherapy in non-small-cell lung cancer to increase the response rate. This phase II trial combined pembrolizumab with carboplatin/paclitaxel (CP) to assess its safety and efficacy, and to identify correlates of responses. Thirty patients without prior immunotherapy for unresectable/metastatic melanoma were treated with pembrolizumab and CP. Peripheral blood was collected at baseline and after 2 cycles to characterize systemic immune activity by multiplex assays and flow cytometry. Seventy percent of patients received all 4 cycles of CP; 87% received pembrolizumab for 2 y or until progression. Grade 3 and higher adverse events (AEs) occurred in 50% of the patients. The overall response rate (ORR) and disease control rate (DCR) by irRC criteria were 43% and 53%, respectively. Median overall survival (OS) was 23.8 months. Objective response was associated with a lower frequency of naive CD8 T cells and low plasma CCL3 at baseline, along with a larger proportion of mature NK cells and of CD4 T cells expressing BTLA or LAIR-1. Survival rate was higher for patients with lower baseline of IL-6, IL-8, and CD4⁺CD39⁺ T cells. Following treatment, pro-inflammatory soluble factors increased in both responders and non-responders. Addition of CP to pembrolizumab in this study did not appear to result in a response or survival advantage and was less tolerable than immunotherapy alone. Correlative data point to peripheral signals to investigate further as potential biomarkers. Trial registration: clinicaltrials.gov, NCT02617849, registered on December 1st, 2015.

2026-12-31·Human Vaccines & Immunotherapeutics

Durable response of anaplastic thyroid cancer to pembrolizumab combined with chemotherapy: A case report

Article

作者: Zhuang, Yihan ; Chen, Qiongshan ; Lin, Wen ; Chen, Zipei

Anaplastic thyroid cancer is a notoriously aggressive malignancy with a dismal prognosis, typically associated with a median overall survival of less than one year. Therapeutic alternatives are particularly limited for patients without actionable driver mutations. Here, we report a case of BRAF V600E wild-type, PD-L1-positive (tumor proportion score of 80%) anaplastic thyroid cancer with residual/relapsed disease following surgery and subsequent progression on multi-targeted tyrosine kinase inhibitor therapy. The patient was thereafter treated with a combination of pembrolizumab, nab-paclitaxel and carboplatin, resulting in a sustained near-complete response lasting over 30 months, accompanied by a manageable safety profile. The favorable response in this case suggests that further evaluation of this triplet regimen could be considered for anaplastic thyroid cancer, though this remains a speculative premise requiring validation. Further studies are also needed to clarify the underlying mechanisms of this combination and to identify predictive biomarkers for patient selection.

2026-12-31·CANCER BIOLOGY & THERAPY

Evaluating carboplatin and PARP inhibitor combination efficacy using high-grade serous carcinoma spheroids and organoids

Article

作者: Tomas, Emily J. ; Davis, Jennifer ; Ramos Valdes, Yudith ; Shepherd, Trevor G.

BACKGROUND:

PARP inhibitors (PARPis) are new targeted agents that exploit homologous recombination DNA repair deficiencies (HRDs), which are present in 50% of high-grade serous carcinoma (HGSC) cases. Currently, olaparib is approved as maintenance therapy for BRCA1/2-mutated HGSC, and niraparib is approved for platinum-sensitive recurrent disease. However, research is currently expanding their potential as front-line agents or in combination with carboplatin, a standard HGSC chemotherapeutic.

METHODS:

Immortalized ovarian cancer (iOvCa) cell lines, developed from HGSC patient ascites, were treated with carboplatin, olaparib and niraparib to determine their sensitivity. Immunofluorescence analysis of RAD51 was conducted for HRD testing of all the cell lines. The cell lines were cultured as three-dimensional organoids and spheroids to mimic tumor growth and metastasis, respectively, and then treated to assess the effects of different drug combinations.

RESULTS:

The half-maximal inhibitory concentrations of olaparib and niraparib varied across our iOvCa cell lines, with iOvCa195 BRCA1-mutant line exhibiting the expected high sensitivity to both PARPis. Direct combination of carboplatin with olaparib or niraparib enhanced cell killing, yet achieved cell viability levels to those of carboplatin alone. In sequential experiments, carboplatin followed by either PARPi or vice versa showed no significant difference in cell viability to carboplatin alone, except in iOvCa195 organoids when treated with a PARPi first.

CONCLUSIONS:

Overall, first-line carboplatin treatment remains ideal, yet there may be select utility for PARPi prior to chemotherapy. Using patient-derived tumor models such as spheroids and organoids may provide insights for on-going and future clinical trials to enhance therapeutic outcomes for HGSC patients.

3,801

项与卡铂相关的新闻（医药）

2026-05-20

·ioncology

三阴性乳腺癌术前免疫疗效早预测

点击蓝字，关注我们三阴性乳腺癌虽然具有免疫原性，但是仅仅部分患者能对术前免疫检查点抑制剂联合化疗获益。目前缺乏可用于指导医生筛选患者并且根据早期疗效变化动态调整治疗方案的生物学预测指标，而且既往研究大多局限于治疗前单一时间点。 2026年5月19日，欧洲肿瘤内科学会官方期刊《肿瘤学年鉴》在线发表意大利、中国台湾、奥地利、西班牙、美国、德国、俄罗斯、爱尔兰、匈牙利、英国等地学者的NeoTRIP研究报告，通过治疗前后两个时间点的基因转录组分析，探讨了三阴性乳腺癌术前化疗±免疫检查点抑制剂阿替利珠单抗疗效的预测因素。 NeoTRIP / NeoTRIPaPDL1 / NeoTRIP Michelangelo (NCT02620280): Neoadjuvant Therapy in TRIPle Negative Breast Cancer With antiPDL1 Official Title: Neo-Adjuvant Study With the PDL1-directed Antibody in Triple Negative Locally Advanced Breast Cancer Undergoing Treatment With Nab-paclitaxel and Carboplatin 该国际多中心随机对照三期临床研究于2016年5月至2018年12月入组高风险三阴性乳腺癌患者280例，按1比1随机分为两组： CT组142例：术前卡铂＋白蛋白紫杉醇 CT/A组138例：术前卡铂＋白蛋白紫杉醇＋阿替利珠单抗在治疗前和第二个治疗周期第一天采集肿瘤活检样本，采用纵向基因转录测序分析标志基因、免疫相关基因和铁死亡相关基因的特征，通过单因素逻辑回归和多因素人工智能机器学习模型分析与病理完全缓解的相关性。结果发现，治疗前CT/A组增殖水平较高和基质及代谢程序较低与病理完全缓解率较高相关，治疗早期活检样本没有肿瘤细胞是两组患者手术时病理完全缓解的较强预测因素。治疗期间与治疗前样本的比较表明，肿瘤细胞增殖减少、免疫和基质特征增强。病理完全缓解患者这些变化更为显著，尤其化疗联合免疫治疗患者。免疫反卷积分析证实治疗期间肿瘤微环境动态重塑，表现为免疫细胞群富集和肿瘤上皮细胞比例降低。虽然某些代谢特征在治疗前与预后相关，但是大多数在治疗期间失去预测价值，此时免疫相关程序成为疗效的主要相关因素。探索性多因素分析表明，治疗期间细胞毒性免疫活性和铁代谢对影响化疗免疫疗效发挥互补作用。因此，该研究结果表明，纵向转录组分析揭示三阴性乳腺癌术前治疗期间肿瘤及其微环境的动态重塑，治疗前肿瘤内在特征和早期治疗诱导免疫激活可为预测化疗±阿替利珠单抗疗效提供互补信息，治疗期间活检标本早期肿瘤细胞清除是病理完全缓解的有力替代指标，并支持探索根据疗效的术前治疗策略。该研究的优势：纵向设计和随机对照试验背景支撑。与既往大量停留于治疗前单一时间点的静态研究相比，该研究抓住了动态变化这个牛鼻子。癌症治疗不是静止的，而是在不断变化，既往研究大多只看治疗前的肿瘤特征，但是该研究在治疗前和治疗早期的第二个周期都进行活检，该配对设计能够捕捉到药物和免疫系统在肿瘤内部引发的实时交锋，揭示治疗如何一步步改变肿瘤微环境，这在技术上要求极高，但是生物学意义极其深远。多维度交叉验证，结论更扎实。该研究不仅看基因特征，还引入InstaPrism算法进行免疫细胞评分反卷积分析，并特意进行肿瘤纯度校正，这排除了因为肿瘤细胞死得多、免疫细胞占比自然上升的假象，确凿地证明免疫激活是真正的药效反应，而非简单的细胞比例稀释。该严谨逻辑闭环是转化医学非常推崇的。发现潜在的新玩家：铁死亡与代谢。除了大家熟知的免疫信号，该研究还把目光投向铁死亡和代谢重编程，尤其是在多因素模型里提出细胞毒性免疫活性和铁代谢的共同作用影响免疫治疗效果，这为我们将来寻找新药靶点提供了非常有价值的线索。该研究的局限：贵族化的检测，难以普惠大众。该研究核心是根据全转录组测序，这在大型研究中心做科研没有问题，但是对于广大基层医院而言，成本太高、流程太复杂、出结果太慢。临床医生需要像免疫组织化学染色那样简单、快捷、便宜的预测工具，例如三阴性乳腺癌复旦四分型。如何将几十个基因的特征浓缩成几个核心蛋白质的试剂盒，是下一步必须解决的转化问题。缺乏独立的外部验证集。虽然该研究基于NeoTRIP这样优秀的国际多中心三期试验，但是全部的模型构建和验证都在同一个队列内完成，即使是交叉验证，这在统计学上容易产生过拟合。如果能用完全独立的、比如我们中国的三阴性乳腺癌大队列印证该多基因模型，那该结论的分量将呈指数级上升。依然没有回答停药或换药的终极问题。该研究发现第二个治疗周期第一天没有肿瘤细胞是病理完全缓解的较强预测因素，但是临床医生更需要知道如果第二个治疗周期第一天没有肿瘤细胞，我们能不能提前做手术？或者能不能减免后续治疗？反之，如果第二个治疗周期第一天完全没有免疫激活，我们是否应该立刻更换靶向药或参加其他临床试验？该研究提供了预测，但是没有给出明确的干预阈值。该研究的重大意义：打破了基因检测只看一次的传统观念，向我们证明治疗是动态博弈的过程，尤其加入免疫治疗后，肿瘤微环境的觉醒和重塑比肿瘤本身的初始状态更重要，这彻底改变了我们对生物学指标的认知，将来的趋势一定是动态监测。为免疫＋化疗的协同作用提供了完美注解，从基因层面给出了答案，化疗不仅杀死了快速增殖的肿瘤细胞、抑制了增殖特征，还为免疫系统腾出了空间，而免疫治疗的加入，则在该基础上引发了更强烈的抗肿瘤免疫反应，两者在基因表达上的动态变化完美互补。为复旦四分型等中国原创方案提供了国际视角的印证：三阴性乳腺癌不是一种病，而是四种病（管腔雄激素受体型、免疫调节型、基底样免疫抑制型、间质型）。该研究同样发现，治疗前的高增殖、低代谢特征，以及治疗后的免疫微环境转化，是决定疗效的核心。这与复旦四分型的核心理念按亚型精准打击是不谋而合的。这说明，无论是中国人群的独特规律，还是国际多中心的宏观数据，都在指向同一个真理：只有摸清肿瘤的底牌，并在治疗中看透肿瘤的变化，我们才能真正攻克三阴性乳腺癌。总而言之，该研究是极具启发性的前沿探索，没有停留在过去非黑即白的免疫检查点表达上，而是用发展的眼光，为我们展示了疗效产生的动态生物学机制。对于我们临床医生而言，这不仅是研究报告，更是指引未来开展根据早期疗效动态调整术前治疗的蓝图。我们要做的就是沿着这个方向，继续脚踏实地，把实验室的发现转化为患者手中实实在在的救命药。相关链接从空间预测三阴性乳腺癌免疫疗效一张静态快照预测乳腺癌动态变化自然综述：人类乳腺癌免疫学 Ann Oncol. 2026 May 19. IF: 65.4 Longitudinal transcriptomic profiling identifies predictors of response to neoadjuvant chemoimmunotherapy in triple-negative breast cancer: results from the NeoTRIPaPDL1 trial. Dugo M, Huang CS, Egle D, Bermejo B, Seitz RS, Nielsen TJ, Zamagni C, Thill M, Antón-Torres A, Russo S, Sevillano E, Ciruelos EM, Schweitzer BL, Galbardi B, Greil R, Semiglazov V, Colleoni M, Kelly CM, Del Mastro L, Mariani G, Viale Gi, Gyorffy B, Ali HR, Pusztai L, Viale G, Callari M, Gianni L, Bianchini G. IRCCS Ospedale San Raffaele, Milan, Italy; Istituto Europeo di Oncologia IRCCS, Milan, Italy; Fondazione IRCCS Istituto Nazionale dei Tumori, Milan, Italy; Università Vita-Salute San Raffaele, Milan, Italy; Fondazione Michelangelo, Milan, Italy; IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy; Azienda Sanitaria Universitaria Friuli Centrale, Udine, Italy; IRCCS Ospedale Policlinico San Martino, Genova, Italy; Università di Genova, Genova, Italy; National Taiwan University Hospital, College of Medicine, National Taiwan University and Taiwan Breast Cancer Consortium, Taipei City, Taiwan, China; Medical University Innsbruck, Innsbruck, Austria; Paracelsus Medical University Salzburg, Salzburg Cancer Research Institute-CCCIT; and Cancer Cluster Salzburg, Salzburg, Austria; Hospital Clinico Universitario de Valencia, Valencia, Spain; Hospital Universitario Miguel Servet, Zaragoza, Spain; Instituto de Investigación Sanitaria HM Hospitales, Madrid, Spain; University Hospital 12 de Octubre, Madrid, Spain; Insight Molecular Diagnostics Inc. Nashville, TN, USA; Yale Cancer Center, Yale School of Medicine, New Haven, CT, USA; Kliniken Markus-Krankenhaus, Agaplesion, Frankfurt Am Main, Germany; N. N. Petrov Research Institute of Oncology, St. Petersburg, Russian; Mater Private Hospital, Dublin, Ireland; Semmelweis University, H-1094, Budapest, Hungary; University of Pecs, H-7624, Pecs, Hungary; Institute of Molecular Life Sciences, HUN-REN Research Centre for Natural Sciences, H-1117, Budapest, Hungary; CRUK Cambridge Institute, University of Cambridge, Cambridge, UK; Addenbrookes Hospital, Cambridge, UK. HIGHLIGHTS Baseline proliferation and metabolic signatures predict response to neadjuvant chemotherapy plus atezolizumab in TNBC. Early absence of tumor cells at D1C2 biopsy is a strong surrogate of final pathologic complete response. On-treatment immune activation and reduced proliferation associate with pCR, especially with atezolizumab. Longitudinal transcriptomics reveals treatment-induced microenvironment remodeling linked to response. Multi-signature models improve prediction and identify distinct baseline and on-treatment predictors by arm. BACKGROUND: Triple-negative breast cancer (TNBC) is immunogenic, but only a subset of patients benefits from neoadjuvant immune checkpoint inhibitors (ICIs) combined with chemotherapy. Predictive biomarkers to guide patient selection and treatment adaptation are lacking. PATIENTS AND METHODS: In the randomized phase III NeoTRIPaPDL1 trial, 280 patients with high-risk TNBC received neoadjuvant carboplatin plus nab-paclitaxel (CT, n=142) or the same regimen with atezolizumab (CT/A, n=138). Tumor biopsies were collected at baseline and on the first day of the second cycle (D1C2). Longitudinal RNA sequencing was performed to evaluate hallmark, immune, and ferroptosis-related gene signatures. Associations with pathologic complete response (pCR) were assessed using univariable logistic regression and multivariable XGBoost models. RESULTS: At baseline, in the CT/A arm higher proliferation and lower stromal and metabolic programs were associated with increased pCR rate. Absence of tumor cells in early on-treatment biopsies strongly predicted surgical pCR in both treatment arms. Comparison of on-treatment with baseline samples revealed a reduced proliferation and increased immune and stromal signatures. These changes were more pronounced in tumors achieving pCR, particularly in patients receiving chemoimmunotherapy. Immune deconvolution analyses confirmed dynamic remodeling of the tumor microenvironment during treatment, with response-associated enrichment of immune cell populations and reduction of tumor epithelial fractions. While several metabolic signatures were associated with outcome at baseline, most lost predictive value on-treatment, where immune-related programs became the dominant correlates of response. Exploratory multivariable analyses suggested complementary contributions of on-treatment cytotoxic immune activity and iron metabolism in shaping response to chemoimmunotherapy. CONCLUSIONS: Longitudinal transcriptomic profiling revealed dynamic tumor and microenvironment remodeling during neoadjuvant therapy in TNBC. Baseline tumor-intrinsic features and early treatment-induced immune activation provide complementary information for predicting response to chemoimmunotherapy. Early tumor clearance in on-treatment biopsies represents a strong surrogate of pCR and supports investigation of response-adapted neoadjuvant strategies. KEYWORDS: Triple-negative breast cancer, neoadjuvant therapy, immunotherapy, longitudinal sampling, transcriptomic profiling, predictive biomarker DOI: 10.1016/j.annonc.2026.05.694 （来源：SIBCS）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。

2026-05-20

·求实药社

历史性一夜！中国ADC在子宫内膜癌告捷，后面还压着近20个III期临床

昨夜是中国ADC历史性的一夜！科伦博泰与默沙东宣布，sac-TMT（SKB264）在子宫内膜癌（EC）后线治疗的全球III期注册性研究TroFuse-005中，同时达到OS（总生存期）和PFS（无进展生存期）双主要终点，ORR（客观缓解率）关键次要终点同样阳性。安全性与既往研究一致，未观察到新的安全信号。很多人把这件事情只当成是“SKB264又多了一个妇瘤后线适应症”，真正的里程碑意义在于：这是SKB264在全球注册性临床中首个达到临床终点的适应症，而之后它还有快二十个三期临床正在推进。一款百亿美元大药的金字塔，底座已经打好了。 01 一线越强，后线越空——子宫内膜癌的治疗悖论子宫内膜癌从来都不是小适应症。在女性生殖系统肿瘤中，子宫内膜癌是欧美发病率最高的病种之一。晚期或复发性子宫内膜癌总体预后仍然偏差：这是一个拥有真实临床需求、真实患者群体、真实商业空间的妇科大适应症，不该被「小瘤种」的标签轻易打发。治疗格局的变化，在过去三五年里发生得相当快。过去，晚期或复发性子宫内膜癌的一线方案相对固定：卡铂+紫杉醇的铂类化疗组合，在部分分子分型中辅以激素治疗。二线则以仑伐替尼+K药为核心选择，尤其对pMMR/MSS人群而言，这个组合一度是标准。然后IO前移了。随着K药+卡铂/紫杉醇（CP方案），多塔利单抗+CP方案，度伐利尤单抗+CP方案等疗法在一线子宫内膜癌中相继取得阳性结果，IO-chemo组合正在成为晚期子宫内膜癌一线治疗的新标准。这一变化对整个治疗序列的影响，造成了序贯治疗非常大的影响，虽然给一线治疗带来了更长的无进展生存期，但同样带来了一个大问题——前线都用完了，后线用啥药呢？说白了，问题出在这里：当PD-1/PD-L1抑制剂前移到一线，二线的逻辑就被改写了。患者一线已经接受过铂类，一线也已经接受过PD-1/PD-L1。进展之后，再用K药-based therapy的意义明显减弱；传统单药化疗（紫杉醇、多柔比星、脂质体多柔比星等）在经治人群里疗效本就有限。这个时候，post-platinum + post-IO的患者进展了，该用什么？这就是子宫内膜癌的治疗悖论：一线越强，后线患者越难治；免疫治疗越早使用，post-IO时代的治疗真空就越需要新的机制来填补。 TroFuse-005出现在这个空白里，拿到了一个OS级别的答案。 02 同为TROP2 ADC，但证据等级已经拉开在讨论TroFuse-005之前，得先确认一件事：SKB264在子宫内膜癌中的三期成功，到底有多大意义？在既往经治子宫内膜癌的早期临床数据中，SKB264显示出约30%的ORR，mPFS大约在5至7个月区间，DCR较高，安全性以血液学毒性、胃肠道反应和口腔炎为主，均属于TOP1 inhibitor载药ADC的已知毒性谱，未观察到明显不可管理的新安全信号。这是一次从早期信号到注册性验证的连续兑现。两者之间那段距离，是四到五年的全球临床执行力，也是默沙东全球临床执行力的最好体现。把SKB264放到同靶点竞品的坐标里看，局面会更清楚。 Trodelvy在子宫内膜癌的TROPHY-EC单臂研究中显示出约22-23%的ORR，mPFS约5个月左右——这可以说明TROP2这个靶点在EC中的生物学活性。Trodelvy的全球III期ASCENT-GYN-01目前仍在推进中，尚未报出注册性结果。Datroway（datopotamab deruxtecan）在乳腺癌和肺癌中有较大布局，EC方向暂无公开的专项注册性数据。这样放在一起看，局面就清楚了：Trodelvy证明了TROP2在子宫内膜癌中有活性，SKB264进一步证明了TROP2 ADC在post-platinum + post-IO子宫内膜癌中能够转化为生存获益。在两者之间，就是一个III期OS阳性和一个单臂早期数据之间的距离。同一个靶点，但临床成果的证据等级，已经被无限拉开。从sac-TMT自身机制看，它采用的是抗TROP2抗体加可裂解连接子加贝洛替康衍生物（TOP1抑制剂）的结构。与Trodelvy同为TROP2 ADC、同为TOP1 inhibitor载药，但在DAR、连接子设计和具体载药分子上存在差异。但现在SKB264比trodelvy强（非头对头横向比较），或许是行业内大多数人的共同认知。销售峰值上，对子宫内膜癌后线适应症的单独销售峰值，估值上需要保持谨慎。后线EC的患者群体受到体能状态、前线治疗可及性和地区医疗水平的多重折损；ADC的定价在不同地区差异显著；此外，TroFuse-005对应的是既往接受过铂类和IO的人群，这个口径在未来可能随治疗指南的演变而调整。综合来看，EC后线适应症的全球销售峰值保守估算约为6-8亿美元，base case约10-15亿美元，若后续向pMMR EC一线或维持治疗前移成功，这个数字可以显著上修。但子宫内膜癌给了SKB264第一个确定性支点。它真正的意义是SKB264第一次在全球III期中证明了自己。 03 四个战场决定百亿美元叙事理解SKB264的全部价值，需要一张铺满房间的地图。把SKB264正在推进的全球III期按商业价值和战略意义拆分，可以归纳为四个战场：肺癌、乳腺癌、妇瘤、泛实体瘤。 NSCLC是全球实体瘤中最大的商业市场之一。SKB264+K药联合一线治疗NSCLC，是目前最值得密切关注的临床方向。在默沙东的肿瘤战略框架里，K药+ADC的联合逻辑在多个瘤种同步推进，而SKB264是其中推进速度最快、全球布局最系统的ADC搭档之一。中国人群的III期数据将在ASCO 2026上以口头报告形式披露——这是市场验证SKB264肺癌潜力的重要窗口。肺癌的结果，将很大程度上决定这个资产能否从me better变成game changing。如果说TroFuse-005证明了SKB264在全球注册性研究中可以跑出OS级别的确定性，那么肺癌的数据才是决定百亿美元弹性空间的那场大考。乳腺癌上，TROP2 ADC在乳腺癌领域的商业价值已经有Trodelvy的成功路径作为先例。Trodelvy在mTNBC中率先拿到OS阳性、完成商业化，随后进入HR+/HER2-乳腺癌；Datroway紧随其后，AZ当初引进交易金额总包超过60亿美元，已经说明了这个市场的体量。 SKB264在乳腺癌中的布局覆盖mTNBC和HR+/HER2-乳腺癌，以及潜在的早期TNBC场景。这个大适应症领域的优势在于，市场对TROP2 ADC的接受度和支付路径已经相对成熟。但有一说一：乳腺癌赛道的竞争也是最激烈的。Trodelvy和Datroway已经占据了大量临床和商业空间，SKB264能否从中切出足够的份额，还需要等头对头或间接对比数据来回答。疗效断层领先是SKB264的核心筹码。妇科肿瘤上，TroFuse-005是妇瘤战场的第一声炮响，但SKB264的妇瘤布局远不止后线EC：pMMR EC一线或维持治疗的探索、宫颈癌、卵巢癌——这是一张系统性铺开的妇瘤地图。如果pMMR EC一线或维持治疗同样取得成功，适应症人群将从经治后线大幅扩展，峰值销售的天花板也随之上移。宫颈癌和卵巢癌作为TROP2高表达的妇科肿瘤，是值得持续关注的潜在适应症。 SKB264的妇瘤叙事，是从EC后线、pMMR EC一线、宫颈癌、卵巢癌多个方向系统性铺开的。TroFuse-005是第一张牌，但不是最重的一张牌。除上述三个主战场外，SKB264在胃癌、膀胱癌/尿路上皮癌等TROP2高表达实体瘤中也有布局。这部分目前不是核心叙事，但在管线深度和平台宽度上构成了补充性的估值支撑。 Jefferies曾将sac-TMT视为超过100亿美元的潜在机会。这其中或许有很大一部分，是给默沙东全球临床执行力以及与K药联用的溢价。 EC后线一个适应症虽然只有10-20亿刀。但如果没有TroFuse-005的OS阳性，那个100亿刀的峰值预测始终没有迈出第一步验证，有了TroFuse-005，这个叙事第一次才有了注册性临床成功的支点。结语：医学史上有一个反复出现的规律：真正改变疾病格局的药物，往往是在一个看起来不够大的适应症里先证明自己，然后才在更大的战场上展开。 TroFuse-005的意义，不在于子宫内膜癌后线这个具体的市场空间，而在于它是SKB264第一次在全球多中心注册性III期中，用OS+PFS双阳性证明了自己跑得通。这个先例一旦建立，整个管线矩阵的叙事分量就变了。肺癌的那场考试还没开始——ASCO 2026的数据才是真正意义上的压力测试。乳腺癌的战场竞争更激烈，需要数据说话。妇瘤的平台还在扩展，EC后线只是第一块砖。子宫内膜癌给了SKB264一个全球注册性成功的起点，肺癌、乳腺癌和妇瘤矩阵，才决定它能不能真正走向那个百亿美元的位置。免责声明：文章内容仅供参考，不构成投资建议。投资者据此操作，风险自担, 关于对文中陈述、观点判断保持中立，不对所包含内容的准确性、可靠性或完整性提供任何明示或暗示的保证。请读者仅作参考，并请自行承担全部。联系我们国内规模最大的类器官领域盛会！ ISO 2026 类器官报名仅剩3周！扫码立即咨询电话：13816031174 （同微信）赞助形式包括但不仅限于演讲席位、会场展位、会刊彩页、晚宴赞助、会议用品宣传等。点击此处“阅读全文”咨询更多精彩！

2026-05-20

·BioSpace

Continuity Biosciences Announces First-in-Human Clinical Trial of Precision Drug Delivery Platform for Pancreatic Cancer

Study now open for enrollment at leading academic medical centers CARY, N.C. and BRADENTON, Fla. , May 20, 2026 /CNW/ -- Continuity Biosciences, LLC, a clinical-stage biotechnology company advancing precision drug delivery platforms, today announced the initiation of a Phase I, first-in-human clinical trial evaluating gemcitabine delivered via its iontophoretic oncology platform (IOP) for the treatment of pancreatic cancer. The study, listed on ClinicalTrials.gov (NCT07481383), is now open for enrollment at leading academic medical centers, including WVU Medicine J.W. Ruby Memorial Hospital, West Virginia University's academic medical center (Morgantown, WV), and Taubman Ctr Univ Michigan Medicine, the University of Michigan's academic medical center (Ann Arbor, MI). Designed to enable localized, controlled delivery of therapeutics directly into pancreatic tumors, Continuity Biosciences' proprietary IOP platform aims to address longstanding challenges in drug penetration and systemic toxicity that have limited the effectiveness of conventional treatment approaches. By increasing intratumoral drug concentration while minimizing systemic exposure, the IOP platform is intended to support more effective use of both existing and emerging oncology therapies. "This first-in-human study represents an important milestone in our mission to transform how therapies are delivered to solid tumors," said Ramakrishna "Krishna" Venugopalan, Chief Executive Officer of Continuity Biosciences. "By enabling precise, localized delivery, we believe our platform has the potential to enhance the effectiveness of existing therapies and serve as a foundation for combination treatment approaches across multiple tumor types." Pancreatic cancer remains one of the leading causes of cancer-related mortality, with five-year survival rates remaining in the low double digits. Despite advances in systemic therapies, effective drug delivery to pancreatic tumors continues to be a major barrier to improved outcomes. "Pancreatic cancer remains one of the most difficult cancers to treat, and patients urgently need better options," said Jen Jen Yeh, MD, Director of the Pancreatic Cancer Center of Excellence at the University of North Carolina Lineberger Comprehensive Cancer Center. "Approaches that effectively deliver therapy precisely to the tumor while sparing the rest of the body could meaningfully change outcomes for patients." "This trial is a critical step toward safer, more effective delivery of gemcitabine for pancreatic cancer patients," said Brian Boone, M.D., surgical oncologist at the WVU Cancer Institute and principal investigator for the WVU Medicine trial. "By targeting therapy directly to the tumor, we hope to improve outcomes while reducing the side effects that so often limit treatment in advanced disease." "One of the central challenges in treating pancreatic cancer is getting enough drug into the tumor without harming the rest of the body," said Dr. Benjamin Ferguson, M.D., PhD, Clinical Assistant Professor of Surgery and surgical oncologist at the University of Michigan Medical Center. "This study will tell us whether targeted, localized delivery can overcome that barrier for gemcitabine and potentially open the door to better treatment strategies for patients with limited options." Beyond pancreatic cancer, Continuity Biosciences is exploring the broader applicability of its IOP platform across additional oncology settings, including localized delivery of carboplatin in oral head and neck cancers. About Continuity Biosciences Continuity Biosciences is a clinical-stage biotechnology company developing precision drug delivery platforms designed to enable targeted, localized therapy across a range of diseases. The company's technologies are intended to overcome key translational barriers by improving how therapies are delivered, distributed, and sustained -- with applications spanning oncology, endocrinology, and beyond -- translating precision delivery innovation into practical therapeutic solutions for patients worldwide. Learn more at View original content to download multimedia: SOURCE Continuity Biosciences LLC

临床1期

100 项与卡铂相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D01363	卡铂	L01XA02	DB00958

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
复发性卵巢癌	美国	Avyxa Pharma	2025-08-08
子宫内膜癌	日本	Clinigen KK	2024-06-24
子宫癌	日本	CHEPLAPHARM Arzneimittel GmbH	2024-06-24
乳腺癌	日本	CHEPLAPHARM Arzneimittel GmbH	2011-11-25
乳腺癌	日本	Clinigen KK	2011-11-25
乳腺癌	日本	Bristol-Myers Squibb KK	2011-11-25
卵巢上皮癌	巴西	Libbs Farmacêutica Ltda.	2006-11-20
小儿生殖细胞肿瘤	日本	CHEPLAPHARM Arzneimittel GmbH	2005-09-15
尤文肉瘤	日本	Bristol-Myers Squibb KK	2005-09-15
尤文肉瘤	日本	Clinigen KK	2005-09-15
肝母细胞瘤	日本	CHEPLAPHARM Arzneimittel GmbH	2005-09-15
肝母细胞瘤	日本	Bristol-Myers Squibb KK	2005-09-15
肝母细胞瘤	日本	Clinigen KK	2005-09-15
神经母细胞瘤	日本	CHEPLAPHARM Arzneimittel GmbH	2005-09-15
神经母细胞瘤	日本	Bristol-Myers Squibb KK	2005-09-15
神经母细胞瘤	日本	Clinigen KK	2005-09-15
复发性尤文肉瘤	日本	CHEPLAPHARM Arzneimittel GmbH	2005-09-15
难治性尤文肉瘤	日本	CHEPLAPHARM Arzneimittel GmbH	2005-09-15
视网膜母细胞瘤	日本	Clinigen KK	2005-09-15
视网膜母细胞瘤	日本	Bristol-Myers Squibb KK	2005-09-15

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
多形性胶质母细胞瘤	临床3期	美国	CarThera SAS	2024-01-29
多形性胶质母细胞瘤	临床3期	奥地利	CarThera SAS	2024-01-29
多形性胶质母细胞瘤	临床3期	比利时	CarThera SAS	2024-01-29
多形性胶质母细胞瘤	临床3期	丹麦	CarThera SAS	2024-01-29
多形性胶质母细胞瘤	临床3期	法国	CarThera SAS	2024-01-29
多形性胶质母细胞瘤	临床3期	德国	CarThera SAS	2024-01-29
多形性胶质母细胞瘤	临床3期	意大利	CarThera SAS	2024-01-29
多形性胶质母细胞瘤	临床3期	荷兰	CarThera SAS	2024-01-29
多形性胶质母细胞瘤	临床3期	西班牙	CarThera SAS	2024-01-29
多形性胶质母细胞瘤	临床3期	瑞士	CarThera SAS	2024-01-29

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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


NCT04163432 (STAGGER, CTgov)	临床2期	转移性非小细胞肺癌 \| 转移性非鳞状非小细胞肺癌	43	Carboplatin+Durvalumab+Pemetrexed (Arm A: Chemo-Immuno)	衊遞顧範夢繭餘淵構積 = 窪齋鏇鬱襯餘淵鹽築醖醖簾選齋遞醖窪繭製築 (糧鹽憲鹹糧簾窪簾簾鏇, 艱構淵壓積製糧願夢鹹 ~ 構顧遞艱鑰選衊製窪膚) 更多	-	2026-05-19
				Carboplatin+Durvalumab+Pemetrexed (Arm B: Immuno-Chemo)	衊遞顧範夢繭餘淵構積 = 鏇觸餘窪繭願糧窪窪獵醖簾選齋遞醖窪繭製築 (糧鹽憲鹹糧簾窪簾簾鏇, 選艱遞遞獵廠襯壓獵鏇 ~ 壓遞鏇觸鑰鹽願鹽鹽廠) 更多
NCT04042558 (GFPC 06-2018, CTgov)	临床2期	非小细胞肺癌IIIB期 \| 转移性非小细胞肺癌 \| 非鳞状非小细胞肺癌	150	Carboplatin+Atezolizumab+Bevacizumab+Pemetrexed (Cohort With Bevacizumab)	築範糧鏇鬱獵鏇選簾淵 = 選獵願鹽廠繭願積淵範製蓋夢範壓鹽衊築觸糧 (窪網醖願築齋壓窪選淵, 鬱憲餘製選構獵餘繭遞 ~ 餘鬱齋簾鏇鬱遞廠鹽壓) 更多	-	2026-05-12
				Carboplatin+Atezolizumab+Pemetrexed (Cohort Without Bevacizumab)	築範糧鏇鬱獵鏇選簾淵 = 襯網範遞鹹廠憲觸壓膚製蓋夢範壓鹽衊築觸糧 (窪網醖願築齋壓窪選淵, 鹹製網顧齋夢獵窪鑰窪 ~ 蓋獵憲觸淵鬱淵選蓋簾) 更多
NCT04245085 (ETOP 15-19 ABC-lung \| ETOP ABC-lung \| ABC-lung, CTgov)	临床2期	EGFR突变的非小细胞肺癌	95	Carboplatin+Paclitaxel+Atezolizumab+Bevacizumab (Arm A)	餘獵膚窪齋餘襯遞遞壓 = 鹽憲遞艱範餘築壓製鑰選積選廠鹽鹹範夢顧襯 (餘願夢廠襯築艱鑰遞壓, 壓範範夢範製願糧網繭 ~ 鏇網繭夢鏇構獵餘網遞) 更多	-	2026-05-12
				Atezolizumab+Bevacizumab+Pemetrexed (Arm B)	餘獵膚窪齋餘襯遞遞壓 = 鑰範襯膚觸艱蓋鬱鹹簾選積選廠鹽鹹範夢顧襯 (餘願夢廠襯築艱鑰遞壓, 廠築鬱鹹築觸繭選壓廠 ~ 範繭選餘築網壓夢鹽構) 更多
NCT01507428 (CTgov)	临床2期	非小细胞肺癌IIIA期 \| 非小细胞肺癌IIIB期 \| 局部晚期非小细胞肺癌	138	External Beam Radiation Therapy+18F-Fluoromisonidazole+Fludeoxyglucose F-18+Carboplatin+Paclitaxel (Arm I (Standard Chemoradiotherapy))	鹹獵廠鑰顧網糧壓顧廠(積膚繭鏇繭艱鏇膚積艱) = 襯壓遞廠艱簾構顧窪鹹淵網壓醖選餘鏇築膚夢 (醖顧簾築蓋襯鏇願廠艱, 0.17) 更多	-	2026-04-21
				Computed Tomography+18F-Fluoromisonidazole+Fludeoxyglucose F-18+Carboplatin+Paclitaxel (Arm II (Experimental Chemoradiotherapy))	鹹獵廠鑰顧網糧壓顧廠(積膚繭鏇繭艱鏇膚積艱) = 積範範齋艱齋襯襯鹽蓋淵網壓醖選餘鏇築膚夢 (醖顧簾築蓋襯鏇願廠艱, 0.39) 更多
SWOG S0819 (AACR2026)	临床3期	非小细胞肺癌 Serial CTRS	1,275	Cetuximab + carboplatin/paclitaxel	衊膚遞網製壓膚衊積餘(積餘構蓋膚鏇網積繭衊) = BOR achieved 35% (33–37%) power 觸積鹹鏇構壓鏇製製窪 (積齋齋憲範觸夢顧膚鹽 ) 更多	积极	2026-04-20
				Bevacizumab + cetuximab + carboplatin/paclitaxel
NCT02402920 (CTgov)	临床1期	局限期小细胞肺癌 \| 广泛期小细胞肺癌 \| 神经内分泌肿瘤	83	platinum+etoposide+pembrolizumab (LS-SCLC (Limited-Stage Small Cell Lung Cancer))	選繭鏇築製窪膚鏇衊鬱 = 壓窪廠鑰醖醖壓窪壓淵壓餘糧齋範構鹽醖鹽齋 (艱鬱膚獵淵夢壓壓構艱, 築範顧夢衊淵襯獵蓋選 ~ 構衊積網鹹鹹製齋築網) 更多	-	2026-03-10
				pembrolizumab (ES-SCLC (Extended-Stage Small Cell Lung Cancer))	選繭鏇築製窪膚鏇衊鬱 = 鑰觸積艱製醖餘蓋選蓋壓餘糧齋範構鹽醖鹽齋 (艱鬱膚獵淵夢壓壓構艱, 願鏇衊衊築壓積選範膚 ~ 觸繭製糧選簾衊蓋淵繭) 更多
NCT02031250 (CTgov)	临床2期	头颈部鳞状细胞癌 \| 局部晚期头颈部鳞状细胞癌	106	IMRT (Intensity-Modulated Radiation Therapy)+Carboplatin+cisplatin (Control Arm)	艱餘廠鏇範鬱鏇糧襯積(繭醖顧齋遞淵鏇遞鏇鹹) = 範築廠襯襯糧範遞蓋範壓壓蓋構齋鹽鹽淵積蓋 (鑰築醖繭淵網膚餘窪夢, 齋醖願範製衊膚艱艱糧 ~ 齋餘廠願廠願繭繭鏇鬱) 更多	-	2026-03-02
				IMRT (Intensity-Modulated Radiation Therapy)+Carboplatin+cisplatin (Boost Arm)	艱餘廠鏇範鬱鏇糧襯積(繭醖顧齋遞淵鏇遞鏇鹹) = 窪膚繭顧壓遞顧窪顧蓋壓壓蓋構齋鹽鹽淵積蓋 (鑰築醖繭淵網膚餘窪夢, 顧壓選襯願獵襯鹹鹹醖 ~ 糧淵淵窪蓋膚膚鑰願願) 更多
INTERLACE (ESGO2026)	N/A	局部晚期宫颈癌	32	CarboplatinCisplatinin + Paclitaxel + CarboplatinCisplatinPaclitaxel	鬱齋窪蓋觸醖憲觸膚選(繭鏇憲襯齋網範衊艱積) = 顧願積衊壓襯齋淵積選簾鹽鹹觸築鏇壓鹽顧觸 (壓繭夢積襯餘繭簾衊憲 )	积极	2026-02-28
ESGO2026	N/A	子宫内膜癌辅助	63	Carboplatin with paclitaxel (CP)	遞壓窪願窪窪鑰糧廠壓(鬱簾壓糧簾壓鬱顧繭糧) = 醖鏇壓淵願積顧網觸積衊網簾夢繭鬱壓鏇糧鑰 (蓋積齋積築範選網鏇鏇 ) 更多	积极	2026-02-28
ESGO2026	N/A	子宫内膜癌	36	Weekly carboplatin-paclitaxel (TC) (Frail patients unsuitable for 3-weekly chemotherapy)	醖憲壓衊鑰壓蓋顧艱壓(範襯醖醖艱鹹糧築鹹壓) = Weekly TC was overall well tolerated, with low rates of neutropenia(11%), anaemia(22%), thrombocytopenia(3%), fatigue(6%), neurotoxicity(8%) and gastrointestinal toxicity(3%), and no cutaneous events 遞憲憲壓顧觸壓繭積憲 (淵選膚淵廠淵顧膚艱餘 )	积极	2026-02-28