Sintilimab Plus Apatinib and SOX as First-line Treatment in Patients With AFP Gastric or Gastroesophageal Junction Adenocarcinoma: a Single-arm, Multi-center, Phase II Trial

This is a multi-center, prospective, open label phase II study evaluating the safety and efficacy of standard first-line chemotherapy SOX regimen combined with Sintilimab (anti-PD-1 antibody) and Apatinib in the treatment of advanced AFP-positive gastric cancer. This study was conducted in the Department of Anhui Provincial Cancer Hospital. In this study, patients with AFP-positive and HER-2-negative advanced gastric cancer who had not received palliative systematic treatment in the past will be enrolled. Patients who met the inclusion criteria were treated with SOX regimen combined with Sintilimab plus Apatinib every 3 weeks(4 cycles) followed by sintilimab+apatinib until disease progression or intolerable adverse reactions or death(up to 24 months).Patients received regular and periodic reviews, with imaging evaluations every 6 weeks. Safety will be evaluated by AE and laboratory tests.

开始日期2025-07-01

申办/合作机构

安徽省肿瘤医院

NCT07026149

/ Recruiting临床2期IIT

Perioperative Treatment of Combined Radiotherapy With SOX, Apatinib and Camrelizumab for Resectable Locally Advanced Gastric or Esophagogastric Junction Adenocarcinoma: A Phase II Trial

The study is being conducted to evaluate the efficacy, safety and tolerability of radiotherapy and chemotherapy, apatinib with camrelizumab in the neoadjuvant (prior to surgery) and adjuvant (after surgery) treatment of previously untreated adults with gastric and gastroesophageal junction (GEJ) adenocarcinoma.

开始日期2025-06-08

申办/合作机构-

NCT06769425

/ Recruiting临床1期

A Phase I Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Efficacy of HS-10502 Combination Treatment in Subjects With Advanced Solid Tumors

HS-10502 is a PARP1-specific selective inhibitor. The purpose if this study is to assess the safety, tolerability, pharmacokinetics (PK), and efficacy of HS-10502 Combination Treatment in subjects with advanced solid tumors.

开始日期2025-05-07

申办/合作机构

江苏豪森药业集团有限公司

100 项与甲磺酸阿帕替尼相关的临床结果

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100 项与甲磺酸阿帕替尼相关的转化医学

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100 项与甲磺酸阿帕替尼相关的专利（医药）

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2,833

项与甲磺酸阿帕替尼相关的文献（医药）

2025-12-01·Journal of Gastrointestinal Cancer

Third- or Further-Line Treatment in Patients with MSS Type Metastatic Colorectal Cancer

Article

作者: Gou, Miaomiao ; Qian, Niansong ; Dai, Guanghai ; Zhang, Yong ; Wang, Zhikuan

BACKGROUND:

The survival benefit from later-line treatment for patients with metastatic colorectal cancer (mCRC) remains disappointing. Here, in a real-world study, we were aimed to evaluate which choice will affect the survival of mCRC patients after standard treatment in Chinese patients.

METHODS:

A total of 129 patients with refractory mCRC were involved in the study. They received targeted monotherapy or combined with chemo-agents or PD-1 inhibitor before death. Overall survival (OS) and progression-free survival (PFS) were reviewed and evaluated from clinical features and treatment options.

RESULTS:

Among the 129 patients, the median age was 56 years (25-81). The mOS from third-line was 12.5 months. OS of patients who treated with chemo plus targeted therapy group in third-line was shown to be superior to pd-1 inhibitor in combination with antiangiogenic agents or antiangiogenic monotherapy group (15.6 m vs. 10.5 m vs. 8.4 m, p < 0.05). Patients had received triplet-drugs (bevacizumab plus low-dose irinotecan and oxaliplatin) and had prolonged survival compared to those had not (21.3 m vs 10.3 m, p = 0.004). OS between patients who had immunotherapy history or not was not significantly different (p > 0.05). The mPFS was 3.5 months in patients who had administered with antiangiogenic targeted agents plus anti-pd-1 and 4.7 months in chemo plus targeted therapy group and 2.2 months in the other group. In the triplet drugs group, preliminary results showed that ORR was 13.3% and DCR was 80%. The median PFS was 5.1 m, and the median OS was 10.6 m.

CONCLUSIONS:

Triplet drugs resulted in significantly longer overall survival, and immunotherapy may have limited benefit in MSS type CRC patients.

2025-12-01·Current gastroenterology reports

Small Bowel Bleeding Due to Vascular Lesions: Pathogenesis and Management

Review

作者: Barkin, Jodie A ; Sandhu, Sunny ; Gross, Jonathan

Abstract:

Purpose of Review:

The purpose of this review is to provide a comprehensive review and recent updates in the understanding of the pathogenesis, diagnosis, and management of small bowel vascular lesions.

Recent Findings:

Recent terminology has shifted from “obscure GI bleeding” to “small bowel bleeding”, with the former reserved for cases when the source of bleeding is not detected despite a thorough evaluation of the entire GI tract, including the small bowel. Recent diagnostic advances including imaging, video capsule endoscopy (VCE), and deep enteroscopy have allowed for the identification of most small bowel bleeding sources.

Summary:

The incidence of small bowel bleeding remains a relatively uncommon event. Vascular lesions remain the most common etiology of small bowel bleeding, with angiodysplasia representing the majority of vascular small bowel lesions. Standard therapeutic approach includes adequate resuscitation and endoscopic evaluation, with consideration of medical therapy (including somatostatin analogues and antiangiogenic agents), endoscopic interventions, radiologic procedures, or surgical therapy in select patients.

2025-11-01·JOURNAL OF COLLOID AND INTERFACE SCIENCE

Tumor microenvironment-responsive nanoregulator CoMnMOF superparticles for enhanced microwave dynamic therapy via multi-pronged amplification of reactive oxygen species

Article

作者: Wang, Dongdong ; Chen, Zengzhen ; Chen, Xiaowei ; Tan, Longfei ; Fu, Changhui ; Meng, Xianwei ; Wu, Qiong ; Ren, Xiangling

Microwave dynamic therapy (MDT) is promising in tumor therapy by generation of toxic reactive oxygen species (ROS), whose therapeutic efficacy is severely compromised by hypoxia and the antioxidant defense in the tumor microenvironment (TME). To address these bottlenecks, we designed a multifunctional nanoregulator CoMnMOF@Apatinib@l-menthol@RBC-HA (denoted as CMALRH) to achieve enhanced MDT via a multi-pronged ROS amplification strategy. We demonstrated that the enhanced ROS generation is attributed to the up-regulate O₂ level, down-regulate vascular endothelial growth factor (VEGF) expression and deplete glutathione (GSH). Meanwhile, CMALRH is verified to perform superior microwave (MW) thermal effect, thus remarkably potentiating the efficacy of anti-tumor therapy. The experiments in vitro and in vivo confirmed the enhanced MDT in combination with microwave thermal therapy can successfully inhibit the proliferation of breast cancer. This TME based ROS amplification strategy provides an avenue for the development of remarkably high efficiency MDT and MW thermal therapy.

737

项与甲磺酸阿帕替尼相关的新闻（医药）

2025-06-13

·医学新视点

北肿沈琳团队研究登《柳叶刀》：胃癌进展或死亡风险降低63%！CAR-T治疗实体瘤新突破

Claudin 18.2是Claudin蛋白质家族成员之一，作为胃癌中特异性高表达的跨膜蛋白质，已成为热门潜在治疗靶点。Satricabtagene autoleucel（satri-cel/CT041）是一种靶向CLDN18.2的CAR-T细胞疗法，有潜力治疗CLDN18.2阳性的晚期消化道肿瘤。近期，《柳叶刀》（The Lancet）发表CT041-ST-01试验的关键2期主要结果，表明satri-cel在晚期胃癌/食管胃结合部腺癌的三线治疗中展现出显著生存获益。与医生选择的标准治疗相比，satri-cel可延长中位无进展生存期（PFS），疾病进展或死亡风险显著降低63%。该研究通信作者为北京大学肿瘤医院沈琳教授。截图来源：The LancetCT041-ST-01试验是一项在中国开展的开放标签、多中心、随机对照2期试验，纳入CLDN18.2阳性、至少接受过二线治疗失败的晚期胃癌/食管胃结合部腺癌患者156例。研究人员以2：1的比例随机将患者分配至satri-cel组或医生选择的标准治疗组：satri-cel组（104例）：每次输注250×106细胞的satri-cel，最多输注3次；医生选择的标准治疗组（52例）：由临床医生决定，选择其中一种标准药物（纳武利尤单抗、紫杉醇、多西他赛、伊立替康或阿帕替尼）。主要终点为独立评审委员会评估的患者PFS。satri-cel组和医生选择的标准治疗组中位随访时间分别为9.07个月和3.45个月。研究结果显示，satri-cel组中位PFS为3.25个月，长于医生选择的标准治疗组的1.77个月，satri-cel组疾病进展或死亡风险显著降低63%（HR=0.37，95%CI：0.24~0.56，P＜0.0001）。此外，satri-cel组中位总生存期（OS）也显示出明显的获益趋势（7.92个月 vs. 5.49个月），satri-cel组死亡风险降低31%（HR 0.69，95%CI：0.46~1.05，P=0.0416）。安全性方面，satri-cel组和医生选择的标准治疗组分别有87例（99%）和30例（63%）的患者发生3级以上治疗相关不良事件，主要为淋巴细胞计数减少（98%）、白细胞计数减少（77%）和中性粒细胞计数减少（66%）。satri-cel组有84例（95%）患者出现细胞因子释放综合征，但整体安全性可控。文章表示，该研究是“首个CAR-T疗法治疗实体瘤的随机对照试验”。基于本次研究结果，satri-cel有望成为CLDN18.2阳性晚期胃癌/食管胃结合部腺癌患者的三线治疗新选择。点击文末“阅读原文/Read more”，即可访问The Lancet官网阅读完整论文。推荐阅读欢迎投稿：学术成果、前沿进展、临床干货等主题均可，点此了解投稿详情。参考资料[1]Zhang, Y, Wei H, Li Z, et al. Claudin-18 isoform 2-specific CAR T-cell therapy (satri-cel) versus treatment of physician's choice for previously treated advanced gastric or gastro-oesophageal junction cancer (CT041-ST-01): a randomised, open-label, phase 2 trial. The Lancet. Advance online publication. https://doi-org.libproxy1.nus.edu.sg/10.1016/S0140-6736(25)00860-8免责声明：本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。版权说明：欢迎个人转发至朋友圈，谢绝媒体或机构未经授权以任何形式转载至其他平台。转载授权请在「医学新视点」微信公众号留言联系。如有其他合作需求，请联系wuxi_media@wuxiapptec.com分享，点赞，在看，传递医学新知

2025-06-12

·癌度

两款前沿CLDN18.2抗体–药物偶联物（ADC），正启动经治胃/食管结合部癌Ⅲ期临床招募！

癌度临床试验病友交流群（点击）胃癌/胃食管结合部腺癌多数患者诊断时已处于中晚期，化疗 + 靶向/免疫治疗是主流。一线中位总生存期（OS）约 12–14 个月，二线后中位总生存期更短。Ⅲ线患者治疗选择少，预后差。免疫治疗虽改善部分群体结局，但仍不足以彻底逆转预后趋势。CLDN18.2 是一种胃肠道肿瘤特异性表位，是靶向胃癌的热门抗原。因此，对抗 CLDN18.2，一种高度特异且在胃癌中广泛表达的靶点，正在成为治疗突破的有效策略。1、LM‑302（抗CLDN18.2 ADC，MMAE偶联）治疗机制：采用人源化抗体特异识别 CLDN18.2，通过可裂解连接子释放 MMAE（微管抑制剂）。直接杀伤表达 CLDN18.2 的肿瘤细胞，并产生“Bystander effect”波及邻近肿瘤细胞，还可能引发 ADCC 免疫效应。疗效数据：在 36 例多次治疗失败胃/GEJ 癌患者中，治疗应答率ORR≈30.6%，疾病控制率DCR≈75%，中位无进展生存时间PFS ≈7.2 个月。安全性良好：Ⅲ/IV期不良事件较少，未发现 ILD。招募信息：CLDN18.2 阳性（IHC ≥2+/3+，≥50%肿瘤细胞）、HER2 阴性、胃/GEJ 癌，≥二线治疗失败。年龄 18–80 岁，ECOG 0–1。目前在中国多中心Ⅰ/Ⅱ期或Ⅲ期试验招募，开放比例 2:1（LM‑302 VS 阿帕替尼/伊立替康）2、IBI343（抗CLDN18.2 ADC，Exatecan偶联）治疗机制：人源抗体特异识别 CLDN18.2，连接拓扑异构酶 I 抑制剂 Exatecan。类似 MMAE ADC，具备靶向细胞毒、Bystander 和潜在的免疫启动能力。疗效数据：在 89 例 CLDN18.2 中高表达（≥40% IHC 2+/3+）胃/GEJ 癌患者中：治疗应答率ORR≈32.6%，疾病控制率DCR≈80.9% ，6 mg/kg 组 ORR≈31.2%，DCR≈89.6%；8 mg/kg 组 ORR≈41.4%，DCR≈82.8%。低表达者疗效不明显。不良事件总体可控，Ⅲ/IV 级治疗相关不良事件约 37.7%，GI 毒性少，没有 ILD 报告。招募信息：标准一线或二线后失败者；IHC ≥40–75% CLDN18.2 阳性；HER2 阴性；年龄 ≥18 岁；体力评分ECOG 0–1。当前 ≥二线患者在推进中的全球Ⅲ期 G‑HOPE‑001 试验。3、如何报名？CLDN18.2的抗体偶联药ADC 正在改变胃癌治疗格局：LM‑302 与 IBI343 两款 ADC 已展现出 30–40% 的显著 ORR 和持续的疾病控制能力，且安全性可控。这两款药都在中国开展临床试验，招募适合患者入组用药。如果你或家人符合条件（CLDN18.2 高表达、HER2 阴性、ECOG 0–1 等），欢迎随时联系癌度咨询。新药名额有限，早一步入组少一步等待。（您也可以点击本文的小程序，和扫描下面图片二维码报名）

抗体药物偶联物临床3期临床结果

2025-06-11

·ioncology

前沿速递丨靶向HER2治疗的耐药机制盘点

点击上方蓝字关注我们编者按：HER2是乳腺癌或胃癌的明确治疗靶点之一。随着研究进展，尤其对于乳腺癌患者而言，治疗获益已经从HER2阳性患者扩展至HER2低表达人群。然而，随着HER2靶向药物的应用，部分患者会出现耐药情况。哪些机制会导致靶向HER2的治疗出现耐药？靶向耐药和脱靶耐药又会影响哪些基因或通路，如何解决？本文特别总结相关内容，以期为读者提供相关参考。HER2靶向耐药机制1. HER家族蛋白表达突变HER家族蛋白的表达突变是HER2靶向治疗获得性耐药的潜在机制之一。临床前研究发现，在使用靶向HER2的ADC（如T-DM1）治疗过程中，相比于敏感性癌细胞，耐药性癌细胞表面的HER2表达显著降低[1,2]。此外，在接受曲妥珠单抗治疗的患者中，比较治疗前和治疗后的肿瘤组织样本发现，疾病进展过程中的HER2表达显著降低[3-5]。为了克服这种耐药机制，目前已经开发出新型有效载荷和/或更高DAR的强效第二代ADC，如T-DXd和ARX788等，临床前和临床实践中的数据均表明，此类药物对HER2低表达的肿瘤也具有良好活性[2,6]，因此也扩大了HER2靶向治疗的范围。2. HER2靶点丢失或掩蔽产生HER2靶向耐药性的另一种获得性机制涉及靶表位的丢失或掩蔽。例如，细胞表面粘蛋白或HER2结合蛋白（如t-DARPP）的上调或HER2蛋白糖基化等，会干扰曲妥珠单抗与其结合，从而会影响疗效[7-9]。此外，在接受HER2靶向治疗患者的肿瘤组织和液体活检样本中发现，ERBB2中也会出现阻止药物结合的二次突变，临床前研究表明，HER2蛋白的酪氨酸激酶结构域中的二次突变会降低对HER2 TKI的疗效并导致获得性耐药[10]。3. 瘤内HER2表达差异瘤内异质性决定了肿瘤在空间和时间上的演变，其中瘤内HER2表达差异是HER2靶向药物疗效不佳的主要原因[11]。有研究评估了ADC药物T-DXd在3种不同HER2表达水平的异体移植模型的疗效，发现该靶向药物及其曲妥珠单抗部分的分布取决于肿瘤组织HER2表达水平的高低；然而其有效载荷也会出现在HER2阳性肿瘤附近的HER2阴性区域，表明存在一种“旁观者效应”，即DXd能够穿过细胞膜从HER2阳性细胞扩散到邻近的肿瘤细胞[12]。这种“旁观者效应”可能是改善实体瘤HER2异质表达的关键机制。HER2脱靶耐药机制1. HER2下游信号通路突变HER2下游信号通路突变也会抵消HER2靶向药物的抗肿瘤作用；而其中的典型案例为PTEN缺失和PI3K通路其他成分的激活突变。临床前研究表明，PTEN功能缺失会重新激活MAPK和PI3K信号通路[13]，从而降低肿瘤细胞对HER2靶向药物的敏感性。通过对肿瘤患者抗HER2治疗前后的游离DNA进行分析，发现RAS和/或RAF基因存在新突变，并且获得了PIK3CA突变，这些突变在疾病进展时会激活MAPK和PI3K信号传导。除PTEN外，在拉帕替尼耐药和曲妥珠单抗耐药的胃癌细胞系中还发现了SRC激活突变；干细胞因子可结合酪氨酸激酶KIT并增强MAPK和PI3K信号传导，以促进细胞增殖和侵袭，并且在对HER2靶向药物产生耐药性的细胞系中观察到干细胞因子水平上调[14]。PI3K或MEK的单独抑制或与抗HER2疗法联合使用，或可干扰这种旁路信号传导并增强抗肿瘤活性。2. 补偿信号通路激活事实上，激活补偿信号通路同样是一种重要的脱靶耐药机制，研究者已经对该信号通路进行了分析。对HER2阳性食管癌患者在疾病进展过程中的不同时间点的多个转移部位进行分析，发现了新发EGFR或MET扩增。临床前研究发现，MET的旁路激活会重新刺激HER2下游的信号通路，从而解除HER2靶向药物对细胞的生长抑制[15]。因此，MET抑制剂和HER2靶向药物联合治疗，可在体外和体内抑制获得性耐药细胞的生长。此外，普遍认为成纤维细胞生长因子受体（FGFR）信号传导的激活也是赋予HER2靶向药物耐药性的旁路途径；FGFR2或FGFR3表达增加与HER2阳性胃癌患者HER2靶向治疗的反应不佳相关，而在临床前模型中通过下调FGFR信号传导可恢复HER2靶向药物的敏感性[16]。3. HER2阳性伴细胞周期基因扩增HER2阳性G/GEJC患者同时伴有调节细胞周期基因（如CCNE1和CDK6）扩增，则对HER2靶向治疗的疗效不佳，联合参与DNA损伤修复（DDR）的药物有望克服这种耐药性[17]。临床前研究的数据表明，PARP1在曲妥珠单抗耐药细胞中上调，以增强DDR通路的功能，从而解决曲妥珠单抗诱导的双链断裂，PARP1抑制剂可以部分克服这种断裂，而ATM抑制剂的加入会进一步损害基因组完整性并导致合成致死。在具有CCNE1扩增的HER2阳性和HER2低表达实体瘤患者的异种移植模型中，WEE1抑制剂adavosertib与ADC药物联合使用时表现出协同作用。HER2通过过度激活SHC SH2结构域结合蛋白1（SHCBP1）和Polo样激酶（PLK1）信号，参与促进肿瘤形成过程中的细胞有丝分裂，据报道，SHCBP1表达增加与曲妥珠单抗治疗HER2阳性胃癌患者的疗效不佳相关。而临床前模型发现，通过药理学抑制SHCBP1-PLK1的相互作用，可使HER2阳性胃癌细胞对曲妥珠单抗敏感[18]。4. 其他相关通路在对曲妥珠单抗或拉帕替尼耐药的G/GEJC细胞系中观察到波形蛋白上调、E-钙粘蛋白和上皮标志物表达下调[19]，这是通过YAP1或WNT-TGFβ信号通路诱导上皮-间质转化的结果。使用小干扰RNA或YAP1-TEAD抑制剂维替泊芬破坏YAP1表达和/或活性可降低YAP1过表达、曲妥珠单抗耐药的G/GEJC或BTC细胞系的生长和迁移能力，这也是一种克服HER2靶向药物耐药性的潜在策略。此外，抑制WNT-β-catenin通路（使用小分子抑制剂ICG-001）已被证明可以逆转上皮-间质转化-间充质转化，并优先减少曲妥珠单抗耐药胃细胞系的增殖和侵袭。5. 肿瘤代谢可塑性癌细胞具有动态重新编程其代谢的能力，以支持肿瘤进展、转移和对治疗产生耐药；因此，开发抵消癌细胞代谢可塑性的治疗策略是一个重要的研究目标。一项临床前研究表明，曲妥珠单抗耐药胃癌细胞系中谷氨酰胺酶1（GLS1）的谷氨酰胺代谢增加，并且GLS1微泡分泌增加通过巨噬细胞的M2极化促进免疫抑制性TME[20]。此外，研究发现，脂肪酸合酶（FASN）的上调与HER2阳性胃癌患者的高干细胞评分和预后不良相关，并且HER2和FASN的共同靶向治疗（分别使用曲妥珠单抗和TVB3166）可减少小鼠模型中曲妥珠单抗耐药细胞的生长[21]。参考文献上下滑动查看更多内容[1]. Le Joncour, V. et al. A novel anti-HER2 antibody–drug conjugate XMT-1522 for HER2-positive breast and gastric cancers resistant to trastuzumab emtansine. Mol. Cancer Ther. 18, 1721–1730 (2019).[2]. Skidmore, L. et al. ARX788, a site-specific anti-HER2 antibody–drug conjugate, demonstrates potent and selective activity in HER2-low and T-DM1-resistant breast and gastric cancers. Mol. Cancer Ther. 19, 1833–1843 (2020).[3]. Pietrantonio, F. et al. HER2 loss in HER2-positive gastric or gastroesophageal cancer after trastuzumab therapy: implication for further clinical research. Int. J. Cancer 139, 2859–2864 (2016).[4]. Saeki, H. et al. Re-evaluation of HER2 status in patients with HER2-positive advanced or recurrent gastric cancer refractory to trastuzumab (KSCC1604). Eur. J. Cancer 105, 41–49 (2018).[5]. Seo, S. et al. Loss of HER2 positivity after anti-HER2 chemotherapy in HER2-positive gastric cancer patients: results of the GASTric cancer HER2 reassessment study 3 (GASTHER3). Gastric Cancer 22, 527–535 (2019).[6]. Modi, S. et al. Trastuzumab deruxtecan in previously treated HER2-low advanced breast cancer. N. Engl. J. Med. 387, 9–20 (2022).[7]. Hong, J. et al. Regulation of ERBB2 receptor by t-DARPP mediates trastuzumab resistance in human esophageal adenocarcinoma. Cancer Res. 72, 4504–4514 (2012).[8]. Shi, M. et al. Catecholamine-induced beta2-adrenergic receptor activation mediates desensitization of gastric cancer cells to trastuzumab by upregulating MUC4 expression. J. Immunol. 190, 5600–5608 (2013).[9]. Duarte, H. O. et al. ST6Gal1 targets the ectodomain of ErbB2 in a site-specific manner and regulates gastric cancer cell sensitivity to trastuzumab. Oncogene 40, 3719–3733 (2021).[10]. Ding, X. et al. Systematic molecular profiling of inhibitor response to the clinical missense mutations of ErbB family kinases in human gastric cancer. J. Mol. Graph. Model. 96, 107526 (2020).[11]. Bang, K. et al. Association between HER2 heterogeneity and clinical outcomes of HER2-positive gastric cancer patients treated with trastuzumab. Gastric Cancer 25, 794–803 (2022).[12]. Haffner, I. et al. HER2 expression, test deviations, and their impact on survival in metastatic gastric cancer: results from the prospective multicenter VARIANZ study. J. Clin. Oncol. 39, 1468–1478 (2021).[13]. Ning, G. et al. A novel treatment strategy for lapatinib resistance in a subset of HER2-amplified gastric cancer. BMC Cancer 21, 923 (2021).[14]. Su, B. et al. Apatinib exhibits synergistic effect with pyrotinib and reverses acquired pyrotinib resistance in HER2-positive gastric cancer via stem cell factor/c-kit signaling and its downstream pathways. Gastric Cancer 24, 352–367 (2021).[15]. Chen, C. T. et al. MET activation mediates resistance to lapatinib inhibition of HER2-amplified gastric cancer cells. Mol. Cancer Ther. 11, 660–669 (2012).[16]. Piro, G. et al. An FGFR3 autocrine loop sustains acquired resistance to trastuzumab in gastric cancer patients. Clin. Cancer Res. 22, 6164–6175 (2016).[17]. Jin, M. H. et al. WEE1 inhibition reverses trastuzumab resistance in HER2-positive cancers. Gastric Cancer 24, 1003–1020 (2021).[18]. Shi, W. et al. Hyperactivation of HER2–SHCBP1–PLK1 axis promotes tumor cell mitosis and impairs trastuzumab sensitivity to gastric cancer. Nat. Commun. 12, 2812 (2021).[19]. Kim, H. P. et al. Testican-1-mediated epithelial–mesenchymal transition signaling confers acquired resistance to lapatinib in HER2-positive gastric cancer. Oncogene 33, 3334–3341 (2014).[20]. Hu, X. et al. Glutamine metabolic microenvironment drives M2 macrophage polarization to mediate trastuzumab resistance in HER2-positive gastric cancer. Cancer Commun. 43, 909–937 (2023).[21]. Castagnoli, L. et al. Fatty acid synthase as a new therapeutic target for HER2-positive gastric cancer. Cell Oncol. 46, 661–676 (2023).（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。

抗体药物偶联物临床结果

100 项与甲磺酸阿帕替尼相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	甲磺酸阿帕替尼	L01XE	DB14765

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
gBRCA突变/HER2阴性乳腺癌	中国	江苏恒瑞医药股份有限公司	2024-12-01
肝细胞癌	中国	江苏恒瑞医药股份有限公司	2021-01-07
胃食管交界处腺癌	中国	江苏恒瑞医药股份有限公司	2014-10-17
胃腺癌	中国	江苏恒瑞医药股份有限公司	2014-10-17

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
转移性肝细胞癌	申请上市	美国	Elevar Therapeutics, Inc.	2024-10-21
不可切除的肝细胞癌	申请上市	美国	Elevar Therapeutics, Inc.	2023-05-17
胃癌	申请上市	中国	江苏恒瑞医药股份有限公司	2011-08-09
晚期胃食管交界处腺癌	临床3期	中国	江苏恒瑞医药股份有限公司	2020-09-21
晚期非小细胞肺癌	临床3期	中国	江苏恒瑞医药股份有限公司	2020-09-16
晚期三阴性乳腺癌	临床3期	中国	江苏恒瑞医药股份有限公司	2020-07-06
乳腺癌	临床3期	中国	江苏恒瑞医药股份有限公司	2020-07-03
转移性乳腺癌	临床3期	中国	江苏恒瑞医药股份有限公司	2020-07-03
PD-L1阳性肺癌	临床3期	-	江苏恒瑞医药股份有限公司	2020-06-15
PD-L1阳性非小细胞肺癌	临床3期	-	江苏恒瑞医药股份有限公司	2020-06-15

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临床结果

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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


ASCO2025	N/A	转移性头颈部鳞状细胞癌	-	Camrelizumab + Docetaxel + Cisplatin/Carboplatin	夢觸蓋夢鑰選範膚積願(鑰鏇獵網鑰製獵淵餘鏇) = 顧膚築選觸壓齋製製選願衊鏇憲蓋蓋遞糧壓繭 (膚憲顧製鏇壓簾糧廠憲, 32.0 ~ 61.0) 更多	-	2025-05-30
ASCO2025	N/A	转移性头颈部鳞状细胞癌	-	Camrelizumab + Apatinib	夢觸蓋夢鑰選範膚積願(鑰鏇獵網鑰製獵淵餘鏇) = 製製選選築築壓簾選鬱願衊鏇憲蓋蓋遞糧壓繭 (膚憲顧製鏇壓簾糧廠憲, 35.0 ~ 65.0) 更多	-	2025-05-30
ASCO2025	N/A	广泛期小细胞肺癌一线	-	ICI + Chemotherapy	-	积极	2025-05-30
ASCO2025	N/A	广泛期小细胞肺癌一线	-	ICI + Antiangiogenic agent + Chemotherapy	-	积极	2025-05-30
NCT03612219 (phase 2 study, ASCO2025)	临床2期	鼻咽癌辅助	86	CCRT plus Apatinib	簾廠鏇糧齋製衊廠壓願(襯壓醖鏇淵遞觸鏇憲遞) = 獵蓋襯鏇鹽醖築襯醖顧簾鑰簾蓋齋衊廠鬱壓鬱 (鹹憲構淵壓衊淵構憲鏇, 66.3 ~ 90.9) 更多	积极	2025-05-30
NCT03612219 (phase 2 study, ASCO2025)	临床2期	鼻咽癌辅助	86	apatinib (CCRT)	簾廠鏇糧齋製衊廠壓願(襯壓醖鏇淵遞觸鏇憲遞) = 遞壓糧顧願蓋簾鑰艱淵簾鑰簾蓋齋衊廠鬱壓鬱 (鹹憲構淵壓衊淵構憲鏇, 39.8 ~ 69.2) 更多	积极	2025-05-30
PB2973 (EHA2025)	临床1期	复发性多发性骨髓瘤	4	Apatinib	糧構襯鹹網鑰顧襯襯鑰(廠觸衊鏇網構製鏇廠衊) = All patients died due to disease progression 獵製鹽衊艱憲衊壓壓築 (簾憲艱願齋憲齋壓餘鏇 ) 更多	积极	2025-05-14
PB2973 (EHA2025)	临床1期	复发性多发性骨髓瘤	4	Anti-BCMA/GPRC5D bispecific CAR T-cell therapy		积极	2025-05-14
RM-202 (AACR2025)	临床2期	腺样囊性癌	72	Rivoceranib 700 mg	憲餘鹹壓簾構獵鑰製顧(範齋壓膚衊簾衊積糧遞) = 糧鏇製構憲範齋鬱淵蓋觸觸窪壓鏇鬱願齋觸鏇 (顧廠顧網繭齋夢鑰蓋範, 7.9 ~ 25.7) 更多	积极	2025-04-28
NCT04609176 (CAP 06, NEWS \| Pubmed) 人工标引	临床2期	胃癌 \| 胃食管交界处腺癌一线	36	卡瑞利珠单抗+阿帕替尼+SOX	顧蓋選廠廠網遞醖醖鑰(製糧衊獵廠窪簾鹹製鏇) = 築齋醖憲觸餘艱製遞窪鹽淵觸蓋衊夢衊醖醖齋 (築鬱鏇衊網廠鹽鹽願觸, 49.0 ~ 81.4) 达到更多	积极	2025-04-18
ChiCTR2000029082 (ESMO_TAT2025)	临床2期	转移性肝细胞癌二线	-	Apatinib + HAIC	獵簾遞遞鹹鏇襯壓艱簾(餘膚糧齋顧積鏇築獵艱) = 衊觸積壓簾膚築繭壓積鏇鏇鑰衊鏇網願簾窪顧 (製膚廠憲獵淵憲艱製憲 ) 更多	积极	2025-03-03
NCT05001412 (Signal Transduct Target Ther) 人工标引	临床1期	广泛期小细胞肺癌一线	40	2 cycles of etoposide and carboplatin (EC) as induction treatment followed by 2-4 cycles of camrelizumab, apatinib plus EC, then maintenance camrelizumab plus apatinib.	網選齋夢衊衊膚構願醖(獵窪顧艱鏇艱壓淵餘積) = 範衊壓窪餘範鑰廠餘繭願衊築獵襯鏇蓋膚鑰衊 (壓鹽繭選鏇壓淵憲憲觸, 73.9 ~ 96.9) 更多	积极	2025-02-18
ASCO_GU2025 人工标引	临床2期	阴茎鳞状细胞癌	23	Apatinib 500 mg	觸鑰餘鹹餘鹹構築衊簾(選構襯願淵糧顧網構衊) = 艱襯鏇網齋製餘艱獵鏇襯廠築網夢醖艱膚膚淵 (鬱鬱窪鏇膚糧餘觸簾壓, 10 ~ 42) 更多	不佳	2025-02-13
NCT04722718 (NeoSAC, Signal Transduct Target Ther) 人工标引	临床2期	三阴性乳腺癌新辅助 HER2 Negative \| PR Negative \| ER Negative	34	Apatinib + sintilimab + nab-paclitaxel + carboplatin	艱鹽繭夢觸選齋膚憲顧(糧蓋鏇鹹願願範糧衊觸) = 網鏇夢遞願衊鹹憲艱窪糧築糧鏇鹽網選壓鹽淵 (積廠襯襯衊餘膚醖網夢, 53.0 ~ 85.3) 更多	积极	2025-02-07