A Phase 1b/2a, Double-blind, Placebo-controlled, Three Arm, Randomized Study Evaluating a Single Intravenous Push Followed by a Continuous Infusion of Certepetide Over 4 Hours When Added to Standard of Care (SoC) Versus Two Intravenous Pushes of Certepetide When Added to SoC, Versus SoC Alone in Subjects With Previously Untreated Metastatic Pancreatic Ductal Adenocarcinoma (FORTIFIDE)

The goal of this clinical trial is to test a new drug plus standard treatment compared with standard treatment alone in people with metastatic pancreatic ductal adenocarcinoma.
The main questions it aims to answer are:
* is the new drug plus standard treatment safe and tolerable
* is the new drug plus standard treatment more effective than standard treatment
Participants will:
* Visit the clinic three times every 28 days for treatment and tests
* Have CT or MRI scans every 8 weeks while on treatment

开始日期2030-01-01

申办/合作机构

Lisata Therapeutics, Inc.

NCT07365306

/ Not yet recruiting临床2期IIT

A Phase 2 Study of Epcoritamab-R-GemOx With Consolidative ASCT and Additional Epcoritamab in Relapsed/Refractory Transplant-Eligible DLBCL

This phase II trial tests how well epcoritamab in combination with rituximab, gemcitabine and oxaliplatin (R-GemOx) works as treatment given after the cancer has not responded to other treatments (salvage therapy) before autologous stem cell transplant in treating patients with diffuse large B-cell lymphoma (DLBCL) that has come back after a period of improvement (relapsed) or that does not respond to treatment (refractory). Epcoritamab is a so-called bispecific antibody, a molecule that can bind simultaneously to two different receptors (proteins present on the cell surface). Epcoritamab binds to a receptor called CD3 with one part of the antibody and to a receptor called CD20 with another part of the antibody. CD3 is expressed on T cells, which are important cells of the immune system that help the body fight cancers and infections. CD20 is expressed on the surface of DLBCL cells. By simultaneous binding to CD3 and CD20, epcoritamab brings T cells and DLBCL cells close together and activates the T cells to kill the lymphoma cells. Rituximab is a so-called monoclonal antibody, a molecule that binds to a single receptor. Like epcoritamab, rituximab binds to CD20. After binding to CD20, rituximab activates the immune system to kill the lymphoma cell through several different mechanisms. Gemcitabine is a chemotherapy drug that blocks the cells from making DNA and may kill cancer cells. Oxaliplatin is in a class of medications called platinum-containing antineoplastic agents. It damages the cell's DNA and may kill cancer cells. Giving epcoritamab-R-GemOx as therapy before an autologous stem cell transplant may help kill cancer cells in the body and help make room in the patient's bone marrow for new blood-forming cells (stem cells) to grow.

开始日期2026-12-30

申办/合作机构

City of Hope National Medical Center

[+1]

NCT07275216

/ Not yet recruiting临床2期IIT

Phase 2 Study of Pembrolizumab With Chemotherapy in Frail Patients With Newly Diagnosed Classical Hodgkin Lymphoma

This phase II trial tests how well pembrolizumab in addition to chemotherapy (gemcitabine, brentuximab vedotin, and dacarbazine) works in treating frail patients with newly diagnosed Hodgkin lymphoma who aren't candidates for standard anthracycline-based treatment. Immunotherapy with monoclonal antibodies, such as pembrolizumab, may help the body's immune system attack the cancer, and may interfere with the ability of cancer cells to grow and spread. Gemcitabine is a chemotherapy drug that blocks the cells from making deoxyribonucleic acid (DNA) and may kill cancer cells. Brentuximab vedotin is in a class of medications called antibody-drug conjugates. It is made of a monoclonal antibody called brentuximab that is linked to a cytotoxic agent called vedotin. Brentuximab attaches to CD30 positive lymphoma cells in a targeted way and delivers vedotin to kill them. Dacarbazine is in a class of medications called alkylating agents. It works by damaging the cell's DNA and may kill cancer cells and slow down or stop cancer growth. Pembrolizumab in combination chemotherapy may be a safe and effective alternative treatment option for frail patients with Hodgkin lymphoma who can't receive standard anthracycline-based treatment.

开始日期2026-07-01

申办/合作机构

City of Hope National Medical Center

[+1]

100 项与盐酸吉西他滨相关的临床结果

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100 项与盐酸吉西他滨相关的转化医学

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100 项与盐酸吉西他滨相关的专利（医药）

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11,849

项与盐酸吉西他滨相关的文献（医药）

2026-03-01·JOURNAL OF CLINICAL ONCOLOGY

Gemcitabine Intravesical System Plus Cetrelimab or Cetrelimab Alone as Neoadjuvant Therapy in Muscle-Invasive Bladder Cancer: SunRISe-4 Primary Analysis and Biomarker Results

Article

作者: Sanchez de Llano, Cristina ; Necchi, Andrea ; Crispen, Paul L. ; Szabados, Bernadett ; Hasan, Mohamad ; Psutka, Sarah P. ; Battaglia, Sebastiano ; Peyton, Charles C. ; Bögemann, Martin ; Stitou, Hind ; Shore, Neal ; Preston, Mark A. ; Ku, Ja Hyeon ; Gong, Cinty ; Pradere, Benjamin ; Guerrero-Ramos, Félix ; Garje, Rohan ; Xylinas, Evanguelos ; Bhanvadia, Sumeet ; Sweiti, Hussein ; Urtishak, Karen ; Herrera-Imbroda, Bernardo

PURPOSE:

Standard of care for muscle-invasive bladder cancer (MIBC) is radical cystectomy (RC) with neoadjuvant cisplatin-based chemotherapy (NAC). However, many patients are ineligible for or refuse cisplatin. SunRISe-4 (ClinicalTrials.gov identifier: NCT04919512 ) is an open-label, multicenter, parallel-cohort phase II study assessing neoadjuvant gemcitabine intravesical system (TAR-200/gem-iDRS) plus cetrelimab or cetrelimab monotherapy in patients with MIBC.

METHODS:

Adults with Eastern Cooperative Oncology Group performance status 0-1, cT2-T4a N0M0, ineligible/refusing NAC, and planned for RC were randomly assigned 5:3, stratified by transurethral resection of bladder tumor completeness (residual tumor ≤3 cm permitted) and T stage, to receive TAR-200 plus cetrelimab (cohort 1) or cetrelimab monotherapy (cohort 2). The primary end point was pathologic complete response (pCR) at RC. Secondary end points included recurrence-free survival (RFS) and safety. Exploratory end points included pathologic overall response (pOR; ≤ypT1N0) and circulating tumor (ct) and urinary tumor (ut) DNA molecular residual disease (MRD). Side-by-side descriptive efficacy summary was planned.

RESULTS:

At the May 9, 2025, data cutoff, 159 patients were treated; 88 in cohort 1 and 46 in cohort 2 underwent RC. pCR, pOR, and 1-year RFS rates were 38%, 53%, and 77% in cohort 1 and 28%, 44%, and 64% in cohort 2, respectively. pCR rates were consistent across subgroups. No new safety signals were observed. Across cohorts, utDNA– status before RC (week 12) and utDNA clearance correlated with pCR ( P < 10 –5 and < 10 –3 , respectively). ctDNA– status at baseline and week 12 was associated with longer RFS compared with ctDNA+ status at the same time point ( P = .04 and 0.01, respectively).

CONCLUSION:

TAR-200 plus cetrelimab provided higher pCR, pOR, and 1-year RFS rates compared with cetrelimab monotherapy, supporting further investigation of the neoadjuvant combination in MIBC. utDNA and ctDNA MRD results support further investigation as biomarkers for residual local and nonlocal disease, respectively.

2026-02-24·Current topics in medicinal chemistry

An Expedition of FDA-Approved Anticancer Drugs in 2024: Synthetic Routes, Mechanisms of Action, and Clinical Indications.

Article

作者: Kurmi, Balak Das ; Priya, Sakshi ; Soni, Reena ; Cherian, Issac V ; Kasana, Shivani ; Islam, Md Mustahidul ; Das, Km Supriya ; Patel, Preeti

The year 2024 witnessed significant advancements in cancer therapy, with the U.S. Food and Drug Administration (FDA) approving 56 anticancer drugs for various malignancies. These approvals encompass 36 organic small molecules and 20 macromolecular monoclonal antibody conjugates, each with distinct mechanisms of action targeting key oncogenic pathways. Among the small molecules, kinase inhibitors such as Ribociclib, Imatinib Mesylate, and Nilotinib Hydrochloride Dihydrate modulate critical signaling cascades, while antimetabolites like Fluorouracil and Pemetrexed Disodium disrupt nucleotide biosynthesis. Other classes include DNA-damaging agents (Mitomycin, Gemcitabine Hydrochloride), immune modulators (Pomalidomide, Lenalidomide), and hormonal antagonists (Abiraterone Acetate, Erleada). The macromolecular therapeutics primarily consist of monoclonal antibody-based agents, such as Keytruda, Tecentriq, and Imfinzi, which enhance immune checkpoint inhibition, and antibody-drug conjugates like Enhertu and Elahere, which deliver cytotoxic payloads with high specificity. This review systematically examines the chemical synthesis, mechanisms of action, and therapeutic indications of these FDAapproved agents, emphasizing their role in improving patient outcomes. By analyzing their structural frameworks and biological targets, we aim to provide insights into current trends in anticancer drug development and potential future directions.

2026-01-01·MOLECULAR BIOTECHNOLOGY

Exploring the Effects of Opioid-Related Drugs on the Clinical Outcome of Prostate Cancer Patients Via Integrated Bioinformatics Analysis

Article

作者: Zhang, Yunxuan ; Cao, Qi ; Liu, Yuenan ; Miao, Qi ; Zhang, Xiaoping ; Chen, Kailei

Opioids are the primary regimens for perioperative analgesia with controversial effects on oncological survival. The underlying mechanism remains unexplored. This study developed survival-related gene co-expression networks based on RNA-seq and clinical characteristics from TCGA cohort. Two survival-related networks were identified, and drug-induced transcriptional profiles were predicted. Immune cell infiltration algorithm, least absolute shrinkage and selection operator (LASSO) regression, and cox proportional models were executed to explore the correlation between opioid-related drugs and prostate cancer patient prognosis. The opioid receptor agonists, represented by tramadol, were evidenced for anti-survival effects on prostate cancer by facilitating the DNA replication and cell cycle, and immune cell infiltration. Conversely, opioid receptor antagonists showed pro-survival effects. A novel prognostic model containing CNIH2, MCCC1, and Gleason scores was established and validated in two independent cohorts. This study revealed opioids' effect on prostate cancer progression, and provided a novel model to predict these regulations in clinical outcomes.

1,288

项与盐酸吉西他滨相关的新闻（医药）

2026-03-06

·腹部外科杂志

专家论坛 · 王坚教授 |靶免时代胆道恶性肿瘤治疗的困境与希望

靶免时代胆道恶性肿瘤治疗的困境与希望余立钦王坚（上海交通大学医学院附属第六人民医院肝胆胰外科，上海 200233） DOI：10.3969/j.issn.1003-5591.2026.01.003 通信作者：王坚，主任医师，博士生导师，主要从事胆道肿瘤的基础与临床方面的研究引用本文：余立钦,王坚.靶免时代胆道恶性肿瘤治疗的困境与希望[J].腹部外科,2026,39(1):17-23. Yu Liqin,Wang Jian.Challenges and prospects for treating biliary tract cancer in the era of targeted therapy and immunotherapy[J].J Abdominal Surg,2026,39(1):17-23. 摘要胆道恶性肿瘤（biliary tract cancer，BTC）发病隐匿，侵袭性强，确诊时多数病人已处于晚期，丧失根治性手术机会。BTC特有的生物学特性是靶向、免疫治疗（简称靶免治疗）疗效差的重要原因，努力提高BTC的早诊早治率和R0切除率是当前突破靶免治疗困境的关键。随着对肿瘤生物学特性和耐药机制研究的不断深入，未来将充分发挥靶向、免疫、化疗的协同效应，探索出具有获益人群更精准、疗效更高、不良反应更低的联合方案，进一步改善BTC病人的长期生存率。关键词胆道恶性肿瘤；免疫治疗；靶向治疗；生物学特性；联合治疗胆道恶性肿瘤（biliary tract cancer，BTC）恶性程度极高，其发病率在全球范围内呈上升趋势。在1990～2021年间，我国BTC新发病例数从1.7万例上升至5.2万例，标准化发病率从2.19/10万上升至2.49/10万，约增长了13.6%［1］。R0切除是目前唯一可能的治愈方式，但由于其发病隐匿、侵袭性强的特点，确诊时多数病人已处于晚期。BTC具有转移侵袭率高、R0切除率低、对放化疗不敏感和5年生存率低的特点。文献报道，肝内胆管癌（intrahepatic cholangiocarcinoma，iCCA）、肝门部胆管癌、远端胆管癌和胆囊癌的R0切除率分别为15%～20%、30%～40%、49.3%～70%和20%～68%，根治性切除术后5年生存率分别为20%～40%、25%～67%、20%～25%、17%～47.5%［2-7］。近年来，恶性肿瘤的系统治疗正从以单一化疗为主的方案逐渐转向化疗、免疫和靶向治疗的联合应用方案，恶性黑色素瘤、非小细胞肺癌和肝细胞癌等癌种在靶向、免疫治疗（简称靶免治疗）方面均取得了不错的疗效，但BTC作为一种“冷肿瘤”对放化疗及靶免治疗的疗效有限。如何在提高根治性切除率、降低手术并发症的基础上，寻找有效的靶免治疗药物，实现外科学与肿瘤学的完美结合是提高BTC疗效的关键。一 BTC特殊的生物学特性是其疗效差的重要原因 BTC疗效差与其特有的生物学特性密切相关。（1）BTC具有高转移性和高侵袭性的特点，肿瘤细胞极易侵犯肝十二指肠韧带内的肝动脉、门静脉与淋巴神经组织，并发生远处淋巴转移和血行转移，加上肝门处空间狭小、解剖变异多，导致其手术难度大和并发症多。（2）BTC的异质性强，分子表型复杂，其基因突变的靶点众多且不恒定，不同病人的突变谱差异明显，缺乏明显的共性特征，导致靶免治疗效果存在明显的个体差异，缺乏有效的靶免药物。（3）BTC属于低增殖型肿瘤，对化疗及靶免药物不敏感。肿瘤间质多、细胞少，肿瘤周围存在大量成纤维细胞和细胞外基质，形成物理屏障，阻碍化疗药物穿透至肿瘤核心区域，导致药物有效浓度不足，同时形成免疫抑制的微环境，影响免疫治疗的效果［8］。如何从BTC的生物学特性出发，加大基础研究的力度，寻找逆转其恶性程度极高的生物学表型的方法，是提高BTC疗效的希望所在。二免疫治疗是突破BTC治疗困境的潜在希望自ABC-02试验［9］结果公布以来，吉西他滨联合顺铂（GC）方案作为BTC标准的化疗方案已有十余年，其中位总生存期（median overall survival，mOS）为11.7个月。近期TOPAZ-1和［10］ KEYNOTE-966［11］两项免疫治疗联合GC方案化疗的Ⅲ期临床试验结果均证实了在化疗基础上联合程序性死亡受体1（programmed death-1， PD-1）或程序性死亡配体1（programmed death-ligand 1， PD-L1）抑制剂（度伐利尤单抗或帕博利珠单抗）带来的生存获益明显优于单用GC化疗的标准方案，且安全性总体可控。在TOPAZ-1试验中，相较于单用GC方案化疗组，度伐利尤单抗联合GC方案组获得了mOS的明显提升（12.9个月比11.3个月），联合治疗组的3年总生存率是GC方案组的2倍多（14.6%比6.9%），这显示出联合治疗在改善病人长期生存方面的优势。在KEYNOTE-966试验中，相较于单用GC方案化疗组，帕博利珠单抗联合GC方案组同样获得了mOS的明显提升（12.7个月比10.9个月，P=0.003 4），联合治疗组2年客观缓解率（objective response rate， ORR）为18%，约为对照组的2.6倍。两项研究的成功标志着BTC一线治疗里程碑式的进步，为晚期或转移性BTC的系统治疗带来了曙光，目前已被中国临床肿瘤学会（CSCO）和美国国立综合癌症网络（NCCN）指南推荐为局部晚期或转移性BTC一线治疗的优选方案［12-13］。虽然TOPAZ-1和KEYNOTE-966这两个Ⅲ期临床试验为BTC的治疗带来了希望，但我们应理性看待这一结果。免疫联合化疗虽然带来了mOS在统计学意义上的明显提升，但这一提升的幅度仅为1.6～1.8个月，综合考虑治疗成本和药物副作用，远未达到真正意义上的延长病人生存的目标，绝大多数病人仍面临着疾病进展的现实问题。肿瘤免疫应答是一个多步骤、高度协调的生物学过程，与免疫细胞的浸润程度和功能状态密切相关。相比对免疫治疗敏感的“热肿瘤”（如黑色素瘤、非小细胞肺癌），BTC是典型的“免疫冷肿瘤”。表现为［8］：（1）低免疫原性和抗原呈递缺陷：BTC肿瘤突变负荷普遍较低，新抗原缺乏，难以被免疫系统有效识别；此外，肿瘤细胞还可干扰抗原加工和呈递通路，使得即使产生新抗原，也无法被有效呈递给T细胞。（2）抑制性的免疫微环境：肿瘤实质内细胞毒性T细胞浸润少且功能处于耗竭状态，M2型肿瘤相关巨噬细胞、调节性T细胞等免疫抑制成分大量富集。（3）纤维化间质形成的免疫微环境进一步抑制免疫系统的激活：BTC免疫微环境的间质是由大量的肿瘤相关成纤维细胞形成的致密间质，且肿瘤相关成纤维细胞还能与肿瘤细胞相互作用，或通过多种趋化因子如CC型趋化因子配体（CCL）2、CXC趋化因子配体（CXCL）12和转化生长因子-β等募集大量免疫抑制细胞，不仅影响药物传递，使药物不能准确渗透至肿瘤中心，还能抑制免疫细胞的激活。因此，如何提高免疫治疗在BTC中的疗效、如何筛选出免疫治疗潜在的获益人群是未来BTC免疫治疗的研究热点。目前虽然已有许多研究分析了相关生物标志物判断免疫治疗疗效的预测作用，但除微卫星高度不稳定（microsatellite instability-high，MSI-H）/错配修复缺陷（defect mismatch repair，dMMR）外，其余如PD-L1表达、肿瘤突变负荷等均没有发挥出理想的预测作用［14-16］。而BTC中MSI-H/dMMR的发生率＜5%，适配人群非常有限。未来多种生物标志物的联合应用能更好地预测免疫治疗的效果，如在KRAS突变，同时具有PD-L1表达的病人相较于PD-L1阴性表达的病人具有更长（10.1个月比2.6个月，P=0.047）的中位无进展生存期（median progression-free survival， mPFS）［17］。综合利用临床数据、放射学和影像组学特征构建临床影像组学的列线图模型也具有较好的预测作用，在晚期胆管癌病人中列线图模型高分组病人的总生存期和无进展生存期均长于列线图模型低分组病人（均P＜0.001）［18］。虽然目前BTC对于免疫治疗的疗效还未达到令人满意的结果，但从肿瘤的发生机制和人体免疫系统对肿瘤的防御与清除机制看，随着人类对免疫治疗的进一步深入研究，免疫治疗应该是最有希望成为治愈肿瘤的有效途径。三靶向治疗是突破BTC治疗困境的重要途径靶向治疗是指针对肿瘤细胞特有的分子靶点（如基因突变、基因融合、蛋白过表达等），设计并使用特异性药物，精准阻断肿瘤细胞的信号传导、增殖、侵袭和血管生成通路，从而实现抑制肿瘤生长、诱导肿瘤细胞凋亡的治疗方式。目前表皮生长因子受体（EGFR）、血管内皮生长因子受体（VEGFR）、人表皮生长因子受体2（HER2）和Ras-Raf-MEK-ERK通路（MAPK通路）等已成为肺癌、乳腺癌等肿瘤的一线治疗靶点。例如，在非小细胞肺癌中EGFR是最常见的驱动基因，突变率约为50%，第三代EGFR的酪氨酸激酶抑制剂奥希替尼在不可切除非小细胞肺癌中的mPFS已达39.1个月，ORR高达57%，已成为携带EGFR突变的不可切除的非小细胞肺癌病人的首选治疗方案［19］；在HER2阳性的晚期乳腺癌中，曲妥珠单抗与帕妥珠单抗联合化疗作为一线治疗的mOS也已达57.1个月［20］。在胆道肿瘤中，由于上述基因不是BTC的驱动基因，在其他肿瘤中有效的通路抑制剂，如针对EGFR、VEGFR的靶向药物，在BTC的临床试验中却屡遭失败，凸显了BTC驱动基因谱的独特性与复杂性［21］。目前BTC领域内靶向治疗及其联合免疫治疗方案主要运用于化疗后进展的病人，部分靶向成纤维细胞生长因子受体（FGFR）、异柠檬酸脱氢酶（IDH）、HER2等靶点和信号通路的药物，已在化疗后进展的iCCA或BTC病人中初见成效，现已获批用于治疗化疗后进展的iCCA或BTC病人［22-24］。但上述有效靶点在BTC中的突变率较低（FGFR2：15%的iCCA［25］，IDH：7%～36%的iCCA［25-27］，HER2：15%～30%的胆囊癌、15%～20%的远端胆管癌和3%～5%的iCCA［27］），对于大多数不携带这些突变的病人，仍缺乏有效的靶向治疗方案。即使携带了这些可靶向的突变位点，也不是所有的病人均有效。针对BRAFV600E突变、NTRK融合等基因改变的抑制剂虽也获得了NCCN指南的推荐［28-29］，但前者突变的发生率仅1%～5%，后者突变的发生率＜1%，适配的人群十分有限［12］。产生上述现象的原因为：（1）肿瘤组织学亚型的分子特征和对靶向药物治疗响应存在差异，文献报道［30］， FGFR2融合、IDH1/2和BRAFV600E突变多见于iCCA，而TP53、KRAS和BRCA1突变多见于肝外胆管癌，ERBB2扩增则在胆囊癌中更常见。另外，中国和欧美裔人群中BTC的肿瘤分子特征也存在差异，如IDH1突变发生率在欧美裔的BTC人群中为19%～30%，而在中国BTC人群中仅为6.5%～20%［30］。即使携带了相同的靶点，不同亚型的BTC对同一药物的治疗响应也存在差异。Lee等［31］发现在HER2阳性的胆囊癌和iCCA病人中应用曲妥珠单抗的ORR存在明显差异：胆囊癌的ORR为39%，而iCCA的ORR为0。此外，Javle等［32］也报道了类似的结论。（2）靶点人群占比低且分布不均［33］。胆道肿瘤整体可靶向靶点（如FGFR融合、IDH1突变）的发生率仅为30%～40%，多数病人无明确驱动靶点，且同一肿瘤组织内存在“靶点阳性或阴性”亚克隆，单靶点药物无法覆盖全部肿瘤细胞，导致治疗应答不完全。（3）靶点功能依赖性弱。部分靶点为“协同驱动”而非“核心驱动”，部分突变仅为肿瘤进展的伴随现象，并非关键致癌通路，靶向药物阻断后肿瘤可通过其他通路代偿增殖，难以实现有效抑制。（4）原发性和继发性耐药。FGFR抑制剂治疗后出现的靶点继发突变、旁路信号激活等耐药机制已被证实［34］。当FGFR通路被抑制时，肿瘤细胞通过激活其他受体酪氨酸激酶（如EGFR、MET）或其下游信号（如KRAS、PIK3CA、BRAF）来维持生存和增殖。例如，动物模型显示FGFR2融合的胆管癌细胞可通过上调EGFR信号逃逸FGFR抑制、BRAF抑制剂常通过再激活MAPK通路获得耐药性等。另外，目前基因组检测仍依赖肿瘤活检样本的二代测序（NGS）技术分析，受限于BTC的生长部位、瘤体病灶较多纤维成分和肿瘤组织异质性高等多种因素，通过肿瘤穿刺活检往往难以获得能够满足测序要求的高质量肿瘤组织。如何克服靶向药物的耐药性，开发下一代药物（如高选择性FGFR2抑制剂RLY-4008）和联用其他位点或通路的抑制剂（如：靶向BRAF和MEK的双抑制疗法，针对MAPK通路），这是改善靶向治疗生存获益的关键［35-36］。同时，应针对驱动基因开发新的靶向治疗药物。尽管BTC的靶向治疗尚存在诸多问题，但针对基因突变产生肿瘤的机制，从源头上进行基因修正的靶向治疗应该是攻克BTC的重要途径。随着精准分层+联合治疗+耐药破局的推进，靶向治疗在BTC治疗中的作用将越来越重要。四努力提高BTC的早诊早治率是突破胆道肿瘤治疗困境的前提鉴于BTC极其恶性的生物学特性、较低的R0切除率和缺乏有效的放化疗及靶免治疗手段，提高BTC的早诊早治率是提高BTC病人5年生存率的最有效途径。（1）应重视胆道良性疾病尤其是胆囊良性疾病的规范化诊治，对于符合手术指征的良性疾病，如胆囊腺肌症、胆囊息肉合并结石、萎缩的胆囊、瓷化胆囊、充填型胆囊结石、胆囊腺瘤、胆总管囊肿、胆管腺瘤、合并胆胰合流异常的胆囊等均应及时手术，消除恶变隐患［37］。我们应坚决反对“保胆取石”手术，因为其会遗漏胆囊癌，并导致肿瘤播散，升高肿瘤的TNM分期［38］。（2）应重视高危人群的随访和筛查（如肝内外胆管结石、胆囊息肉、胆管腺瘤、胆管乳头状肿瘤病、先天性肝内胆管扩张症、胆管结石、肝硬化、乙型/丙型肝炎病毒感染、原发性硬化性胆管炎等），定期进行肿瘤标志物［糖类抗原（CA）19-9、CA125、癌胚抗原（CEA）等］检查和B型超声筛查，有异常者进一步行增强CT/MRI检查。（3）以分层筛查为基础，建立多模态联合筛查模式。根据普通人群、高危人群与极高危人群，联合基础血清学（CA19-9+CA125+CEA）+肝功能（谷丙转氨酶+谷草转氨酶+碱性磷酸酶+ γ-谷氨酰转移酶+总胆红素）、B型超声、增强CT与MRI+磁共振胰胆管成像（MRCP）、超声内镜、分子检测，建立分层次、分阶段的多模态筛查体系，并建立随访数据库，以提高早筛的可持续性、可对比性和可追踪性。（4）应革新筛查技术，推动BTC的早诊早治，如近期芝加哥大学团队发现，通过检测血液样本中循环肿瘤RNA早期诊断结直肠癌的准确率高达95%，类似的早期筛查手段在BTC中的应用将显著提高BTC的早诊早治率［39］。五努力提高BTC的R0切除率是突破胆道肿瘤治疗困境的基石制约BTC根治性切除的关键点在于：（1）剩余肝脏体积不足；（2）肿瘤侵犯血管导致无法切除。BTC根治性切除的难点在于肿瘤侵犯肝门部。笔者把侵犯肝门的胆道肿瘤纳入围肝门胆道肿瘤，包括iCCA侵犯肝门、肝门胆管癌和胆囊癌侵犯肝门三大类［5］。其治疗难点在于：（1）肿瘤侵犯肝动脉与门静脉，需联合血管切除重建；（2）难以做到高质量的黏膜对黏膜的胆肠吻合；（3）手术方式的不确定性大，需要术中敞开肝门再评估；（4）手术风险大、并发症多、围手术期死亡率高。为此，笔者近年提出的“围肝门外科技术体系”［5， 40-42］，其以肝门解剖与暴露为核心、以三维数字医学影像评估技术为手段，通过由肝外向肝门和由肝内向肝门顺逆结合的肝门解剖路径，完全敞开肝门后充分显露病灶与肝动脉和门静脉之间的关系，从而制定合理的个体化手术方案，能大大提高进展期累及肝门的胆道肿瘤的R0切除率。 “围肝门外科技术体系”的核心是精确全面的术前评估，充分评估肝动脉、门静脉和胆道的变异、走行与受侵犯程度，充分评估病人的全身重要脏器功能与营养状况，准确测量剩余肝脏体积，以制订合理的手术规划。术中运用顺逆结合的肝门敞开技术，重视肝门敞开后肿瘤与血管及胆管关系的再评估，以修正手术方案。且敞开肝门后对血管切除重建、胆肠吻合和保证胆管足够的切缘提供足够的手术空间。术后运用预判性思维管控并发症。总之，提高BTC的R0切除率的关键是提高围肝门胆道肿瘤的R0切除率，利用“围肝门外科技术体系”能最大程度减少手术并发症和死亡率，提高R0切除率［43］。六破局胆道肿瘤治疗困境的几点思考（一）人工智能（artificial intelligence，AI）助推早筛早诊的精确性与敏感性单纯的CT与MRI等影像学检查对早期微小的胆道肿瘤的检查率不高，不易筛查出早期肿瘤。AI时代可以利用多模态筛查方式如生化指标+影像学+液体活检等与AI结合，通过AI赋能影像学检查，提升微小癌灶的检出率，运用多模态影像AI融合分析技术，提升影像学诊断的敏感性与准确性。如Jeong等［44］利用卷积神经网络设计了一种辅助识别胆囊息肉性质的AI模型，该模型能在术前预测息肉的性质，并显著提升了超声科医生的诊断能力。除此之外，利用AI优化血清学与分子检测，挖掘早期生物标志物和助推高危人群精确分层与全流程管理也是未来的发展方向之一。（二）深入研究肿瘤的生物学特性，提高靶免治疗的有效性通过深入研究肿瘤异质性、微环境特征及分子调控机制，开展大样本BTC全基因组测序、全外显子测序及转录组测序，结合单细胞测序技术，明确不同病理类型（iCCA、肝外胆管癌、胆囊癌）的特异性驱动基因突变谱。研究表观遗传调控机制，针对无明确基因突变的“冷肿瘤”，开展表观遗传靶向治疗方案，解析免疫微环境的异质性，靶向重塑免疫微环境，如联合抗血管生成药物，降低肿瘤组织间质压力，促进T细胞浸润，将“冷肿瘤”转化为“热肿瘤”，阐明靶免治疗的耐药的机制，实现耐药逆转［45-46］。（三）依据胆道肿瘤的病理类型开展多中心临床研究目前，靶免治疗的大部分临床研究都是针对所有的胆道肿瘤，没有区分不同的病理类型。但是iCCA、肝外胆管癌、胆囊癌的生物学特性是不同的，其基因突变的靶点和对药物的敏感性也是不同的，不区分病理类型的临床研究所得出的结论不能有效地针对特定病理类型的肿瘤，比如对iCCA中有效的靶免药物，不一定对胆囊癌有效，反之亦然。鉴于胆道肿瘤发病率相对较低，只有开展全国多中心研究，才能建立较大的样本库，实现从临床研究的真实数据出发，结合临床样本的基础研究，彻底厘清不同病理类型肿瘤的分子机制，找到真正有效的突变靶点与驱动基因，开发有效治疗靶点与预测靶点。（四）探索靶向、免疫、化疗的不同组合治疗的效果要探索靶向、免疫、化疗的协同效应，利用化疗的细胞毒作用、靶向治疗的精准抑制和免疫治疗的长效杀伤实现对胆道肿瘤的“三重打击”。化疗可诱导肿瘤细胞凋亡、降低肿瘤负荷，同时改善肿瘤间质纤维化，提升靶向药物穿透性。靶向药物可逆转化疗耐药、抑制肿瘤细胞增殖的同时，上调PD-L1的表达，增加肿瘤浸润淋巴细胞的密度，将“冷肿瘤”转化为“热肿瘤”。联合用药还可通过多通路阻断，降低耐药克隆的生存概率。在探索组合治疗过程中，应优化联用方案，降低不良反应，并筛选获益人群。（五）寻找转化治疗的有效方案，实现肿瘤学与外科学的完美结合目前根治性手术仍是BTC治疗的核心手段，如何将外科学与肿瘤学完美结合，对于局部进展期BTC及不可切除BTC实现转化治疗，是目前实现BTC疗效突破的重要抓手。最近，由复旦大学附属中山医院牵头开展的一项针对局部进展期BTC的Ⅱ期临床研究已揭示了“靶向+免疫+化疗”三联四药方案在转化治疗中的应用潜力，其转化率为68.3%，转化后的R0切除率为63.4%［47］。总体来说，胆道肿瘤目前仍缺乏明确有效的转化治疗方案，同时受限于病人术前肝功能状态、全身营养状况、体能状况和药物的不良反应，能承受有效转化治疗的病人比例不高。因此通过多中心临床研究，根据不同病理类型的胆道肿瘤，试验不同靶向、免疫与化疗药物的组合，寻找转化效率与病人耐受性的平衡点，提高转化治疗的有效性，是未来的突破方向。同时筛选出手术获益的分子标志物，以精确指导哪些病人适用于转化治疗，最大程度发挥手术的有效性与必要性。七结语 BTC的治疗在靶免时代迎来了希望的曙光，但受限于由肿瘤自身生物学特性，免疫与靶向治疗带来的生存获益仍不容乐观。我们面对的是一个具有“冷”免疫特性和分子特征高度异质的复杂疾病。当前治疗所取得的进步，是突破重围的第一步。未来研究重点在于如何筛选出更有效的人群、如何提高免疫应答率从而削弱BTC“冷肿瘤”的特性、如何延缓耐药性，以及如何减少不良反应等，而这些突破必将依赖于对疾病本质更深刻的理解、对耐药机制更清晰的认识和对治疗策略更智慧的联合设计。这是一场需要基础科学家、临床研究者、药物研发者共同参与的持久战。唯有通过持续不断的协同创新，实现从早期筛查、精准手术到个体化辅助治疗的全程管理，方能为BTC病人点燃更具生命力的希望之火，最终实现从延长生存到追求高质量的长期生存的跨越。利益冲突声明所有作者均声明不存在利益冲突 1. 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Challenges and prospects for treating biliary tract cancer in the era of targeted therapy and immunotherapy Yu LiqinWang Jian （Department of Hepatobiliary and Pancreatic Surgery， Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine， Shanghai 200233， China） Abstract: Biliary tract cancer（BTC） is characterized by insidious onset and high invasiveness， with most patients diagnosed at an advanced stage， thereby losing the opportunity for curative resection. The distinct biological features of BTC significantly contribute to the limited efficacy of targeted and immunotherapeutic approaches. Enhancing early diagnosis and treatment rates， as well as improving R0 resection rates， represents a critical strategy to overcome current therapeutic challenges. With advancing research into tumor biology and resistance mechanisms， future efforts should focus on harnessing the synergistic effects of targeted therapy，immunotherapy，and chemotherapy.This will facilitate the development of combined regimens with more precise patient selection，improved efficacy， and reduced toxicity， ultimately leading to better long-term survival outcomes for patients with biliary tract malignancies. Key words: Biliary tract cancer；Immunotherapy；Targeted therapy；Biological features；Combination therapy 基金信息：国家自然科学基金面上项目（82273411）中图分类号： R735.8 文章编号：1003-5591（2026）01-0017-07 文献标识码： A 收稿日期：2026-01-12 出版日期：2026-02-22 网刊发布日期：2026-02-27 点击蓝字关注我们版权声明本文为《腹部外科》杂志原创文章，版权归中华医学会武汉分会所有。其他媒体、网站、公众号等如需转载，请联系本刊编辑部获得授权，并在文章下醒目位置注明“原文刊发于《腹部外科》杂志，卷（期）：起止页码”。官方网站解锁更多精彩官方网址：http://www.fbwk.net 电话：027-82789737 Email：fubuwaike@vip.163.com 扫描二维码关注我们微信公众号

免疫疗法引进/卖出临床结果

2026-03-06

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恒瑞创新药卡瑞利珠单抗治疗高危局晚期鼻咽癌Ⅲ期研究成果发表于《英国医学杂志》

近日，恒瑞医药创新药卡瑞利珠单抗（PD-1抑制剂）一项高危局晚期鼻咽癌Ⅲ期临床研究成果重磅发表于国际顶级医学期刊《英国医学杂志》（The BMJ，IF：43）[1]。该研究由中山大学附属第五医院陈明远教授团队领衔，评估了“卡瑞利珠单抗（PD-1抑制剂）联合同步放化疗并序贯辅助治疗”的疗效与安全性。结果显示[1]，该研究达到了主要研究终点。对于经吉西他滨联合顺铂诱导化疗后未达到影像学或生物学缓解的Ⅱ-Ⅲ期（AJCC第八版），或基线为T4/N3期的高危局晚期鼻咽癌患者，在同步放化疗基础上联用卡瑞利珠单抗并序贯卡瑞利珠单抗辅助治疗可显著改善患者的无进展生存期，3年无进展生存率从71.3%显著提升至83.4%（HR=0.51，P=0.001），且安全性良好，有望为更多“高复发风险”局晚期鼻咽癌患者点亮生存新希望。研究发表于The BMJ01研究背景鼻咽癌尤其高发于我国南方地区及东南亚国家，2022年全球新发病例超12万，而中国新发病例约占全球总量的50%[2]。对于局晚期鼻咽癌患者而言，即便采用诱导化疗联合同步放化疗的强化治疗方案，仍有20%-30%的患者会面临疾病复发或转移的困境。目前，诱导化疗序贯同步放化疗（CCRT）虽为临床主流治疗策略，但患者耐受性欠佳，临床上亟需更安全有效且能“精准靶向人群”的治疗方案以突破这一瓶颈。近年来，以PD-1单抗为代表的免疫检查点抑制剂，在鼻咽癌治疗领域展现出令人瞩目的潜力。CAPTAIN研究[3]证实，针对二线化疗失败的晚期鼻咽癌患者，卡瑞利珠单抗单药治疗的客观缓解率（ORR）达28.2%，中位总生存期（OS）延长至17.4个月，且安全性表现良好。CAPTAIN-1st研究[4]显示，卡瑞利珠单抗联合化疗一线治疗复发/转移性鼻咽癌时，客观缓解率（ORR）高达88.1%，中位无进展生存期（PFS）达10.8个月，较传统方案提升近4个月，疾病进展及死亡风险降低49%，中位OS长达34.5个月，5年OS率绝对差异达13.6%，为晚期鼻咽癌患者带来了生存希望。此外，DIPPER研究[5]也证实，卡瑞利珠单抗单药用于局晚期鼻咽癌（Ⅲ-Ⅳa期）的辅助治疗，可显著改善患者的无事件生存期（EFS），3年EFS率达86.9%，3年OS率达96.4%，已呈现获益趋势。综上，卡瑞利珠单抗在复发/转移性鼻咽癌及局晚期鼻咽癌患者研究中均展现出治疗获益，且安全性可控。然而，针对高危局晚期鼻咽癌患者的临床应用，卡瑞利珠单抗的最佳使用时机、适宜疗程，仍值得更多临床研究进一步探索和明确，以实现“精准治疗”。02研究设计该研究于2020年8月至2022年6月在中国7家医院开展，入组了390例年龄18-70岁、经组织病理学确诊为非角化型鼻咽癌（分化型或未分化型）、Ⅳa期（T4或N3，AJCC第八版）或Ⅱ-Ⅲ期(经诱导化疗后影像学评估为疾病稳定/疾病进展或外周血可检测到EBV-DNA）、KPS≥70分的高危局晚期鼻咽癌患者。患者按照1:1随机分为卡瑞利珠单抗组（194例）和标准治疗组（196例）。标准治疗组使用顺铂为基础的标准同步放化疗（顺铂100mg/m2，第1天3周/次*2次；调强放疗69.96Gy/33次，每天1次）；卡瑞利珠单抗组使用标准治疗（同步放化疗）联合卡瑞利珠单抗（200mg静脉输注，每3周1次，2周期），序贯卡瑞利珠单抗辅助治疗17周期。研究的主要终点为PFS，次要终点包括OS、无远处转移生存期（DMFS）、无局部区域复发生存期（LRFS）、安全性及生活质量。图1. 研究设计03研究结果1患者基线两组基线特征均衡匹配：两组均以非角化未分化型病理为主，诊断时EBV-DNA负荷水平相近（拷贝数1237.0 vs 1130.0）；T3或T4期肿瘤占比超87%、N2/N3期占比超72%，Ⅳa期患者占比均超72%。同时纳入了诱导化疗后未达到肿瘤缓解的Ⅱ-Ⅲ期“隐性高危”患者，两组诱导化疗后肿瘤未缓解比例（51.5% vs 53.6%）几乎持平。表1. 患者基线情况2患者依从性两组患者均在完成3周期吉西他滨联合顺铂诱导化疗、完成2周期顺铂同步化疗均无明显差异，两组放疗处方剂量、放疗时长及剂量学参数均无明显差异。卡瑞利珠单抗组94.8%患者在同步放化疗阶段完成2周期卡瑞利珠单抗治疗；61.9%的患者（120例）在放疗结束后完成了研究方案规定的17周期辅助治疗，辅助治疗阶段卡瑞利珠单抗的中位治疗周期为17周期。 3临床疗效● 中位随访39.9个月的结果显示，卡瑞利珠单抗组36个月无进展生存率高达83.4%（95% CI：78.3%-88.8%），显著高于标准治疗组的71.3%（95% CI：65.2%-77.9%），疾病复发或死亡风险降低49%（HR=0.51，95% CI：0.34-0.77，P=0.001），达到了主要研究终点。 ● 次要终点中，卡瑞利珠单抗组36个月率LRFS为92.8%，标准治疗组为83.2%，局部区域复发风险降低62%（HR=0.38，P=0.001），且两组复发均以野内复发为主（92.9% vs 93.8%）；卡瑞利珠单抗组36个月DMFS率为88.9%，标准治疗组为80.7%，远处转移风险降低46%（HR=0.54，P=0.02）；卡瑞利珠单抗组36个月OS率为94.8%，标准治疗组为92.2%，虽未达到统计学显著差异（HR=0.59，P=0.19），但已呈现出获益趋势，需延长随访时间。 ● 肿瘤缓解情况方面，完成诱导化疗后两组肿瘤部分缓解率分别为71.1%（卡瑞利珠单抗组）和68.4%（标准治疗组）；放疗结束16周后，两组完全缓解率均达到90%以上（90.2% vs 90.3%）。图2. 无事件生存率（左）与无远处转移生存率（右）图3. 无局部区域复发生存率（左）与总生存率（右） 4安全性研究结果显示，卡瑞利珠单抗联合方案的安全性良好，未出现新增或不可控的不良事件，且生活质量不受影响。该研究还采用EORTC QLQ-C30问卷评估，结果显示两组患者在躯体功能、角色功能、认知功能、情绪功能等维度的评分无显著差异，卡瑞利珠单抗未加重患者症状负担。图4. 生活质量 04总结该研究作为全球首个将“动态影像评估+EBV-DNA动态变化”双指标纳入多中心Ⅲ期随机对照试验风险分层的里程碑式研究，首次证实了在同步放化疗基础上联用卡瑞利珠单抗并序贯卡瑞利珠单抗辅助治疗，可显著提高高危局晚期鼻咽癌患者的无进展生存期，这一成果有望重塑临床治疗实践，为更多“高复发风险”局晚期鼻咽癌患者点亮生存新希望。卡瑞利珠单抗是恒瑞医药自主研发的一款人源化PD-1单克隆抗体，于2019年5月获批在中国上市。目前已在肺癌、肝癌、食管癌、鼻咽癌以及宫颈癌等瘤种中获批多项适应症，为获批适应症和覆盖瘤种数量领先的国产PD-1产品。其相关研究此前多次刊登于《柳叶刀》《美国医学会杂志》等国际顶级学术期刊。本次高危局晚期鼻咽癌研究的发表，再次彰显卡瑞利珠单抗作为中国创新药在实体瘤领域的竞争力。未来，恒瑞医药将继续坚持“以患者为中心”的理念，针对中国高发肿瘤领域持续推进创新研发，力争研制出更多更好的新药、好药，服务健康中国，惠及全球患者。参考文献： [1]You R, Xu GQ, Ding X, et al. Standard chemoradiotherapy with concurrent and adjuvant camrelizumab in patients with high risk nasopharyngeal carcinoma: multicentre, randomised, open label, phase 3 trial. BMJ. 2026;392:e085863. Published 2026 Feb 10. doi:10.1136/bmj-2025-085863 [2]胡晨,薛继尧,龚洪立,等. 鼻咽癌放射治疗或放射化学治疗后颈淋巴结残留或复发的颈淋巴结清扫术[J]. 中国眼耳鼻喉科杂志,2020,20(5):352-355,385. [3]Fang W, Yang Y, Ma Y, et al. Camrelizumab (SHR-1210) alone or in combination with gemcitabine plus cisplatin for nasopharyngeal carcinoma: results from two single-arm, phase 1 trials. Lancet Oncol. 2018;19(10):1338-1350. doi:10.1016/S1470-2045(18)30495-9 [4]YANG Y, OU S, LIJ, et al. Camrelizumab versus placebo in combination with gemcitabine and cisplatin as first-linetreatment for recurrent or metastatic nasopharyngeal carcinoma (CAPTAIN-1st): A multicentre, randomised, doubleblind,phase 3 trial.Lancet Oncol,2021,22(8):1162-1174. [5]Liang Y, Liu X, Shen L, et al. Adjuvant PD-1 Blockade With Camrelizumab for Nasopharyngeal Carcinoma: The DIPPER Randomized Clinical Trial. JAMA. Published online March 13, 2025. doi:10.1001/jama.2025.1132（恒瑞医药）

临床结果临床3期临床成功ASCO会议

2026-03-06

·BioSpace

Immuneering Reports Fourth Quarter and Full Year 2025 Financial Results and Provides Business Updates

- 64% overall survival observed at 12 months in ongoing Phase 2a trial of atebimetinib + mGnP in first-line pancreatic cancer patients, well above the standard of care benchmark from GnP of 35% overall survival; On track for expanded pancreatic cancer cohort data readout in first half of 2026 - - On track to dose first patient in p ivotal Phase 3 MAPKeeper 301 trial of atebimetinib + mGnP in patients with first-line metastatic pancreatic cancer in mid-2026 - - Dosing in Phase 2 trial of atebimetinib + Libtayo ® in patients with first-line RAS-mutant non-small cell lung cancer expected to begin in second half of 2026 - - Ended 2025 with $217 million in cash, cash equivalents and marketable securities with anticipated runway into 2029 - NEW YORK, March 06, 2026 (GLOBE NEWSWIRE) -- Immuneering Corporation (Nasdaq: IMRX), a late-stage clinical oncology company focused on keeping cancer patients alive and helping them thrive, today reported financial results for the fourth quarter and full year ended December 31, 2025, and provided business updates. “2025 was a transformative year for Immuneering. We reported 64% overall survival at 12 months in first-line pancreatic cancer patients treated with atebimetinib + mGnP, well above the benchmark for GnP standard of care. We designed atebimetinib with three mechanisms well-established to improve survival, and we believe these survival gains are driven by atebimetinib shrinking tumors durably with less resistance, preserving body mass by countering cachexia, and minimizing side effects to maximize combinability and performance status," said Ben Zeskind, Ph.D., Chief Executive Officer of Immuneering. “We also made rapid progress in preparation for our pivotal Phase 3 trial in first-line pancreatic cancer patients, MAPKeeper 301, having secured alignment with both the FDA and EMA on our trial design, and we are on track to dose the first patient mid-year. With cash runway expected into 2029, uniquely encouraging clinical data, and a solid pipeline, we are strongly positioned to deliver on our mission to help patients live longer and feel better.” Recent Corporate Highlights Reported 64% Overall Survival at 12 Months in First-Line Pancreatic Cancer Patients Treated with Atebimetinib + mGnP: In January, the Company announced positive updated survival and safety data from its ongoing Phase 2a trial of atebimetinib in combination with mGnP in first-line pancreatic cancer patients (N=34), with 13.4 months median follow up. Immuneering reported 64% overall survival (OS) observed at 12 months as of the December 15, 2025 data cutoff date. Atebimetinib (320mg dosed once daily) + mGnP was observed to demonstrate a favorable tolerability profile, with only two categories of adverse events observed at or above the grade 3 level in more than 10% of patients (neutropenia and anemia, both of which are categories commonly observed with standard of care chemotherapy), in comparison to toxicity profiles for other combinations in the front line pancreatic cancer setting, which demonstrate significantly more grade 3 and higher adverse events. No head-to-head clinical trial has been conducted evaluating atebimetinib and other candidates or products. Differences exist between trial designs, subject characteristics and other factors, and caution should be exercised when comparing data across studies. Secured Alignment with FDA and EMA on pivotal Phase 3 Atebimetinib Trial for First-Line Metastatic Pancreatic Cancer Patients: In December, Immuneering announced that it expected to dose the first patient in its planned global pivotal Phase 3 registrational trial, MAPKeeper 301, in first-line pancreatic cancer patients in mid-2026, evaluating atebimetinib (320 mg QD) in combination with modified gemcitabine and nab-paclitaxel (mGnP), compared with gemcitabine and nab-paclitaxel (GnP) alone. The Company remains on track with this guidance. Notably, the Company completed its End-of-Phase 2 (EOP2) interactions with the U.S. Food and Drug Administration (FDA) and received scientific advice from the European Medicines Agency (EMA). Immuneering achieved alignment with both agencies on the key elements of the proposed Phase 3 trial. Added to the Nasdaq Biotechnology Index (NBI): On December 22, 2025, Immuneering was added to the Nasdaq Biotechnology Index. Anticipated Near-Term Milestones Immuneering is planning for several near-term anticipated milestones related to atebimetinib, including: Q2 2026: Report updated circulating tumor DNA data on acquired alterations at a major scientific meeting. 1H 2026: Report updated survival data from over 50 first-line pancreatic cancer patients treated with atebimetinib + mGnP. Mid-2026: Dose first patient in pivotal Phase 3 MAPKeeper clinical trial of atebimetinib + mGnP in first-line pancreatic cancer. 2H 2026: Dose first patient in trial of atebimetinib + Libtayo® in RAS-mutant first-line non-small cell lung cancer. Fourth Quarter and Full Year 2025 Financial Highlights Cash Position: Cash, cash equivalents and marketable securities as of December 31, 2025 were $217.0 million, compared with $36.1 million as of December 31, 2024. Research and Development (R&D) Expenses: R&D expenses for the fourth quarter of 2025 were $9.3 million compared to $14.9 million for the fourth quarter of 2024. Full year 2025 R&D expenses were $42.0 million compared to $48.0 million for full year 2024. R&D expenses for the fourth quarter and full year 2025 decreased compared to the same respective periods in 2024, primarily driven by reduced spend related to the Company's product candidate envometinib (IMM-6-415) and certain pre-clinical activities, in addition to decreased personnel related costs. This was partially offset by increased clinical and regulatory consulting resources utilized during the period to support atebimetinib's ongoing development and regulatory readiness activities. General and Administrative (G&A) Expenses: G&A expenses for the fourth quarter of 2025 were $4.5 million compared to $3.7 million for the fourth quarter of 2024. Full year 2025 G&A expenses were $17.3 million compared to $16.1 million for full year 2024. G&A expenses for the fourth quarter and full year 2025 increased compared to the same respective periods in 2024, primarily driven by increased employee-related costs and external professional fees, in addition to increased public filing costs associated with the Company's various financing efforts. Net Loss: Net loss attributable to common stockholders was $11.6 million, or $0.18 per share, for the quarter ended December 31, 2025, compared to $18.1 million, or $0.58 per share, for the quarter ended December 31, 2024. Net loss attributable to common stockholders for full year 2025 was $56.0 million, or $1.27 per share, compared to $61.0 million, or $2.04 per share, for full year 2024. 2026 Financial Guidance Based on cash, cash equivalents and marketable securities as of December 31, 2025, and current operating plans, the Company expects its cash runway to be sufficient to fund operations into 2029. About Atebimetinib Atebimetinib is the first in a new category of oral drug candidates, Deep Cyclic Inhibitors (DCIs), designed to improve overall survival by three mechanisms: shrinking tumors durably with less resistance, preserving body mass by countering cachexia, and minimizing side effects to maximize performance status and combinability. Each of these mechanisms has been well established to improve survival in published studies. DCIs challenge the conventional model of sustained or continuous inhibition in oncology. Whereas most therapies are designed for sustained inhibition, driving cancer to adapt and develop resistance so tumors shrink quickly but temporarily, DCIs are designed to pulse faster than tumors can adapt, so tumors shrink slowly but durably. Moreover, DCIs aim to restore full transient signaling to healthy cells, with the goal of leading to fewer adverse events. Atebimetinib targets MEK, a key control point in the MAPK pathway (RAS-RAF-MEK-ERK), which is pathologically activated in a majority of cancers, including approximately 97% of pancreatic cancers. Targeting MEK blocks a broader range of MAPK pathway alterations because it is further downstream, creating the potential for more durable benefit. About Immuneering Corporation Immuneering is a late-stage clinical oncology company focused on keeping cancer patients alive and helping them thrive. The Company is developing an entirely new category of cancer medicines, Deep Cyclic Inhibitors, designed to improve overall survival by three mechanisms: shrinking tumors durably with less resistance, preserving body mass by countering cachexia, and minimizing side effects to maximize performance status and combinability. Immuneering’s lead product candidate, atebimetinib, is an oral, once-daily Deep Cyclic Inhibitor of MEK, designed to improve survival across many cancer indications, including MAPK pathway-driven tumors such as pancreatic cancer. The company expects to dose the first patient in mid-2026 in MAPKeeper 301, a globally randomized pivotal Phase 3 trial evaluating atebimetinib in combination with chemotherapy in first-line pancreatic cancer patients. The Company’s development pipeline also includes additional combination opportunities and early-stage programs. For more information, please visit Forward-Looking Statements This press release contains forward-looking statements, including within the meaning of the Private Securities Litigation Reform Act of 1995. All statements contained in this press release that do not relate to matters of historical fact should be considered forward-looking statements, including, without limitation, statements regarding: the treatment potential of atebimetinib, alone or in combination with other agents to treat cancer, including modified Gemcitabine/nab-paclitaxel (mGnP) in first-line pancreatic cancer and its potential to deliver overall survival with both durability and tolerability; the ability of the three design mechanisms of atebimetinib to improve overall survival; the timing of commencing dosing in the Phase 3 trial; the ability of atebimetinib + mGnP to deliver a more durable and compounding benefit, including compared to standard of care; the timing, venue and content of future data releases and presentations and for the phase 2 results to continue to trend positively; and the timing for the initiation of additional atebimetinib clinical trial combination arms, including in non-small cell lung cancer. These forward-looking statements are based on management’s current expectations. These statements are neither promises nor guarantees, but involve known and unknown risks, uncertainties and other important factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements, including, but not limited to, the following: the risks inherent in oncology drug research and development, including target discovery, target validation, lead compound identification, and lead compound optimization; we have incurred significant losses, are not currently profitable and may never become profitable; our projected cash runway; our need for additional funding; our unproven approach to therapeutic intervention; our ability to address regulatory questions and the uncertainties relating to regulatory filings, reviews and approvals; the lengthy, expensive, and uncertain process of clinical drug development, including potential delays in or failure to obtain regulatory approvals; our reliance on third parties and collaborators to conduct our clinical trials, manufacture our product candidates, and develop and commercialize our product candidates, if approved; failure to compete successfully against other drug companies; protection of our proprietary technology and the confidentiality of our trade secrets; potential lawsuits for, or claims of, infringement of third-party intellectual property or challenges to the ownership of our intellectual property; our patents being found invalid or unenforceable; costs and resources of operating as a public company; and unfavorable or no analyst research or reports. These and other important factors discussed under the caption “Risk Factors” in our Annual Report on Form 10-K for the period ended December 31, 2025, and our other reports filed with the U.S. Securities and Exchange Commission, could cause actual results to differ materially from those indicated by the forward-looking statements made in this press release. Any such forward-looking statements represent management's estimates as of the date of this press release. While we may elect to update such forward-looking statements at some point in the future, except as required by law, we disclaim any obligation to do so, even if subsequent events cause our views to change. These forward-looking statements should not be relied upon as representing our views as of any date subsequent to the date of this press release. Investor Contacts: Courtney Dugan Cdugan@immuneering.com Media Contact: Gina Nugent gina@nugentcommunications.com IMMUNEERING CORPORATION CONSOLIDATED STATEMENTS OF OPERATIONS AND COMPREHENSIVE LOSS (Unaudited) Three Months Ended December 31, Twelve Months Ended December 31, 2025 2024 2025 2024 Operating expenses Research and development $ 9,254,626 $ 14,857,166 $ 42,048,461 $ 47,964,388 General and administrative 4,490,776 3,693,672 17,298,241 16,077,746 Amortization of intangible asset 7,317 7,317 29,267 29,267 Total operating expenses 13,752,719 18,558,155 59,375,969 64,071,401 Loss from operations (13,752,719 ) (18,558,155 ) (59,375,969 ) (64,071,401 ) Other income (expense) Interest income 1,861,044 415,240 3,039,406 2,593,300 Other income, net 311,665 91,430 311,665 441,493 Net loss $ (11,580,010 ) $ (18,051,485 ) $ (56,024,898 ) $ (61,036,608 ) Net loss per share attributable to common stockholders, basic and diluted $ (0.18 ) $ (0.58 ) $ (1.27 ) $ (2.04 ) Weighted-average common shares outstanding, basic and diluted 64,590,066 31,050,448 44,011,830 29,981,565 Other comprehensive income: Unrealized gain from marketable securities 81,332 (7,846 ) 81,332 778 Comprehensive Loss $ (11,498,678 ) $ (18,059,331 ) $ (55,943,566 ) $ (61,035,830 ) IMMUNEERING CORPORATION CONSOLIDATED BALANCE SHEETS December 31, 2025 December 31, 2024 Assets Current assets: Cash and cash equivalents $ 128,645,025 $ 36,144,720 Marketable securities, current 44,186,244 — Prepaids and other current assets 3,414,685 3,442,849 Total current assets 176,245,954 39,587,569 Marketable securities, non-current 44,183,186 — Property and equipment, net 938,481 1,122,865 Goodwill 6,690,431 6,690,431 Intangible asset, net 321,147 350,413 Right-of-use assets, net 3,322,249 3,667,352 Other assets 283,562 1,295,783 Total assets $ 231,985,010 $ 52,714,413 Liabilities and stockholders' equity Current liabilities: Accounts payable $ 1,542,737 $ 1,958,536 Accrued expenses 7,842,367 4,973,129 Other liabilities 291,513 233,665 Lease liabilities 397,104 338,438 Total current liabilities 10,073,721 7,503,768 Long-term liabilities: Lease liabilities, net of current portion 3,427,321 3,824,419 Total liabilities 13,501,042 11,328,187 Commitments and contingencies Stockholders’ equity: Preferred stock, $0.001 par value; 10,000,000 shares authorized at December 31, 2025 and December 31, 2024; 0 shares issued or outstanding at December 31, 2025 and December 31, 2024 — — Class A common stock, $0.001 par value, 200,000,000 shares authorized at December 31, 2025 and December 31, 2024; 64,648,230 and 31,050,448 shares issued and outstanding at December 31, 2025 and December 31, 2024, respectively 64,648 31,050 Class B common stock, $0.001 par value, 20,000,000 shares authorized at December 31, 2025 and December 31, 2024; 0 shares issued and outstanding at December 31, 2025 and December 31, 2024 — — Additional paid-in capital 498,658,072 265,650,362 Accumulated other comprehensive income 81,332 — Accumulated deficit (280,320,084 ) (224,295,186 ) Total stockholders' equity 218,483,968 41,386,226 Total liabilities and stockholders' equity $ 231,985,010 $ 52,714,413

临床3期临床2期临床结果财报

100 项与盐酸吉西他滨相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D01155	盐酸吉西他滨	L01BC05	DB00441

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
非肌层浸润性膀胱肿瘤	美国	Janssen Biotech, Inc.	2025-09-09
局部晚期非小细胞肺癌	澳大利亚	Sandoz Pty Ltd.	2008-12-02
局部晚期胰腺腺癌	澳大利亚	Sandoz Pty Ltd.	2008-12-02
转移性非小细胞肺癌	澳大利亚	Sandoz Pty Ltd.	2008-12-02
转移性胰腺腺癌	澳大利亚	Sandoz Pty Ltd.	2008-12-02
复发性卵巢癌	澳大利亚	Sandoz Pty Ltd.	2008-12-02
尿路上皮癌	日本	Eli Lilly & Co.	2008-11-25
膀胱癌	巴西	Libbs Farmacêutica Ltda.	2008-05-26
胆道癌	日本	Eli Lilly & Co.	2001-08-31
淋巴瘤	日本	Eli Lilly & Co.	2001-08-31
卵巢癌	日本	Eli Lilly & Co.	2001-08-31
乳腺癌	美国	Eli Lilly & Co.	1996-05-15
转移性乳腺癌	美国	Eli Lilly & Co.	1996-05-15
非小细胞肺癌	美国	Eli Lilly & Co.	1996-05-15
胰腺腺癌	美国	Eli Lilly & Co.	1996-05-15
胰腺癌	美国	Eli Lilly & Co.	1996-05-15

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
晚期胆道癌	临床3期	中国台湾	因华生技制药股份有限公司	2025-07-01
复发性膀胱癌	临床3期	美国	Janssen Research & Development LLC	2024-04-09
复发性膀胱癌	临床3期	中国	Janssen Research & Development LLC	2024-04-09
复发性膀胱癌	临床3期	日本	Janssen Research & Development LLC	2024-04-09
复发性膀胱癌	临床3期	阿根廷	Janssen Research & Development LLC	2024-04-09
复发性膀胱癌	临床3期	比利时	Janssen Research & Development LLC	2024-04-09
复发性膀胱癌	临床3期	巴西	Janssen Research & Development LLC	2024-04-09
复发性膀胱癌	临床3期	法国	Janssen Research & Development LLC	2024-04-09
复发性膀胱癌	临床3期	德国	Janssen Research & Development LLC	2024-04-09
复发性膀胱癌	临床3期	意大利	Janssen Research & Development LLC	2024-04-09

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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


ASCO_GU2026	N/A	非肌层浸润性膀胱肿瘤	133	BCG	觸糧淵積窪鹽衊壓糧鑰(廠構膚夢窪鑰艱選範鬱) = 繭壓襯獵構鏇簾鹽構餘蓋膚壓網遞膚蓋築醖鏇 (鹹顧製鏇壓顧網蓋積範 ) 更多	不佳	2026-02-26
				sequential gemcitabine and docetaxel (Gem/Doce)	觸糧淵積窪鹽衊壓糧鑰(廠構膚夢窪鑰艱選範鬱) = 網窪夢憲壓範襯廠鹽構蓋膚壓網遞膚蓋築醖鏇 (鹹顧製鏇壓顧網蓋積範 ) 更多
NCT04628767 (EA8192, ASCO_GU2026)	临床2期	肾盂和输尿管尿路上皮癌新辅助	30	Gemcitabine/Durvalumab	襯範範夢淵鹹襯選鹽蓋(鬱顧憲衊簾獵願憲窪衊) = 鬱餘網積繭襯獵製衊選艱齋糧願醖鬱餘網夢選 (艱膚窪襯築淵積願網衊, 3.0 ~ 25.2) 更多	积极	2026-02-26
ASCO_GU2026	N/A	肌层浸润性膀胱癌新辅助	517	Gemcitabine 800 mg/m2	膚淵範襯選鹽選選範廠(積繭壓遞觸蓋鹽糧夢遞): P-Value = 0.012 更多	积极	2026-02-26
				Gemcitabine 1000 mg/m2
NCT04179162 (ALLIANCE A032303, ASCO_GU2026)	临床1/2期	复发性膀胱癌	52	Gemcitabine + BCG	鏇衊鬱範顧鬱範鹹鬱膚(糧衊窪選醖願齋廠膚構) = 鬱簾簾選遞夢齋範遞願襯醖繭夢膚衊構壓鹹網 (餘簾淵鹽範鬱繭淵獵夢 ) 更多	积极	2026-02-26
ASCO_GU2026	N/A	肌层浸润性膀胱癌	98	Cisplatin	鬱製顧顧繭夢遞鏇網憲(繭簾淵憲鬱鹽遞鏇鹹積) = 簾網積構憲鏇網憲襯觸構壓廠繭膚顧顧淵築繭 (選範築積衊糧遞簾築鹽 ) 更多	积极	2026-02-26
				5-FU+MMC	鬱製顧顧繭夢遞鏇網憲(繭簾淵憲鬱鹽遞鏇鹹積) = 醖醖遞鹽醖鏇鏇醖鏇衊構壓廠繭膚顧顧淵築繭 (選範築積衊糧遞簾築鹽 ) 更多
NCT03366766 (CTgov)	临床2期	非小细胞肺癌Ⅰ期 \| 可切除非小细胞肺癌 \| 非小细胞肺癌IIIA期 ... 更多	14	Nivolumab+cisplatin+Pemetrexed Disodium (Cohort I (Nivolumab, Cisplatin, Pemetrexed Disodium))	廠顧範積製蓋觸構鹹願 = 襯鑰製製餘積觸鹹遞艱衊廠廠襯鹽醖襯選艱壓 (網選壓繭遞選構簾艱壓, 積艱蓋糧築遞醖範蓋鏇 ~ 遞齋艱積鑰夢網膚繭廠) 更多	-	2026-02-20
				nivolumab+Gemcitabine Hydrochloride (Cohort I (Nivolumab, Cisplatin, Gemcitabine Hydrochloride))	構鬱餘簾鏇簾願鹹遞憲 = 選積構淵願壓範鏇襯顧遞糧製醖構選製膚鏇鏇 (壓窪構遞壓膚壓積顧築, 壓窪遞獵衊鏇膚衊顧觸 ~ 鏇製顧鏇膚醖願構願遞)
NCT04919512 (SunRISe-4, CTgov)	临床2期	肌层浸润性膀胱尿路上皮癌 \| 肌层浸润性膀胱癌 \| 膀胱癌	163	Cetrelimab (TAR-200 + Cetrelimab)	簾鹹遞齋廠膚鬱醖窪齋 = 蓋積遞壓觸遞壓鹽窪網鏇壓願構憲築醖鹹顧網 (築願憲襯鑰製壓願築築, 範繭淵襯鹹夢餘襯醖淵 ~ 願餘選願糧襯網糧憲鬱) 更多	-	2026-02-17
				Cetrelimab (Cetrelimab Alone)	簾鹹遞齋廠膚鬱醖窪齋 = 鏇膚獵構範鏇衊獵襯積鏇壓願構憲築醖鹹顧網 (築願憲襯鑰製壓願築築, 餘齋鏇齋襯蓋構鑰壓窪 ~ 鹹鹹繭糧範遞積鬱鹹襯)
NCT03693807 (CTgov)	临床2期	结直肠癌肝转移 \| 结直肠癌 \| 胆管癌	35	Cetuximab+Gemcitabine+Floxuridine (FUDR)+Oxaliplatin+Irinotecan (CPT-11)+Panitumumab+Fluorouracil (Group 1: Unresectable Liver Metastases From Colorectal Cancer)	鏇淵獵廠獵積簾願餘積(壓觸襯膚廠夢簾艱襯積) = 憲壓襯鹽鏇糧糧構窪鹽繭鏇壓齋選鬱壓餘壓齋 (獵遞鬱鹽構壓構廠選醖, 築襯糧選壓襯餘遞淵製 ~ 糧願製齋壓廠構鹹願顧) 更多	-	2026-02-06
				Cetuximab+Gemcitabine+Floxuridine (FUDR)+Oxaliplatin+Irinotecan (CPT-11)+Panitumumab+Fluorouracil (Group 2: Resectable Liver Metastases From Colorectal Cancer)	鏇淵獵廠獵積簾願餘積(壓觸襯膚廠夢簾艱襯積) = 觸襯淵鑰齋築簾構獵憲繭鏇壓齋選鬱壓餘壓齋 (獵遞鬱鹽構壓構廠選醖, 積獵鏇襯選鬱夢糧廠繭 ~ 鹹積獵獵繭齋廠顧顧襯) 更多
NCT04524702 (CTgov)	临床2期	转移性胰腺腺癌 \| 晚期胰腺腺癌	10	Hydroxychloroquine+Nab-paclitaxel+Gemcitabine+Paricalcitol	願餘積願鏇構鏇顧衊網 = 製醖繭遞積憲窪餘膚鹹鏇鏇積遞窪積築壓餘壓 (蓋糧鑰餘鹹餘製夢獵範, 遞鏇憲窪鑰鏇蓋蓋範積 ~ 鏇簾觸鹹顧鹹範觸構網) 更多	-	2026-01-23
NCT03377491 (PANOVA-3, CTgov)	临床3期	胰腺腺瘤 \| 局部晚期胰腺腺癌	571	Nab-paclitaxel+Gemcitabine (TTFields + Standard of Care)	鹽淵繭艱壓醖衊窪鏇積(簾鹹獵繭鹽廠簾衊網壓) = 鏇構簾遞遞構壓醖餘鏇醖範積構鏇憲鏇衊獵製 (遞憲範積醖鏇餘鏇構選, 範膚鑰淵觸糧蓋範獵齋 ~ 淵鬱獵選憲選築鏇淵繭) 更多	-	2026-01-21
				Nab-paclitaxel+Gemcitabine (Standard of Care)	鹽淵繭艱壓醖衊窪鏇積(簾鹹獵繭鹽廠簾衊網壓) = 選積顧壓築製網衊鑰夢醖範積構鏇憲鏇衊獵製 (遞憲範積醖鏇餘鏇構選, 願鑰夢製餘壓顧構鬱觸 ~ 鹽憲鬱醖構憲餘襯蓋窪) 更多