Epidermal growth factor receptor (EGFR) signaling plays a key role in regulating epidermal cell proliferation, survival, and differentiation. Keratins form a scaffold with epidermal desmosomes that involves ErbB/ EGFR signaling and keratin deficiency makes keratinocytes more sensitive to EGFR activation. Erlotinib, an EGFR inhibitor, was approved 20 years ago for cancer treatment and is generally used at 150 mg daily in adults >50 kg. While gastrointestinal and cutaneous side effects commonly occur at doses of 150 mg, adverse events occur less often at lower doses. We first reported erlotinib as effective for Olmsted syndrome, a rare hereditary EDD with painful PPK that results from variants in TRPV3. Erlotinib is now the treatment of choice for children and adults with Olmsted syndrome. Erlotinib is thought to inhibit formation of a complex that includes TRPV3, EGFR, and its primary skin-based ligand, TGF-a, which in turn regulates keratinocyte proliferation and differentiation. High-throughput screening to identify compounds that stabilize keratin filaments have also pointed to the EGFR pathway for targeting. Reviews and recent case reports have suggested the benefit of erlotinib for PC,
Given these preliminary data, we hypothesize that EGFR activation is a characteristic feature of keratinopathies. Further, we expect that oral low-dose erlotinib will improve the scaling and skin thickening of the spectrum of keratinopathies and be tolerated by most patients. For those who experience pain, particularly from plantar involvement, we predict that erlotinib therapy will improve mobility and pain. Finally, we aim to find the mechanism by which erlotinib improves the phenotypes of the various keratinopathies to better understand these disorders and predict response. We will look specifically at the impact on differentiation vs. hyperproliferation and barrier function, as well as the immune modulatory effects of the erlotinib using a multi-omics approach.

开始日期2025-12-01

申办/合作机构

Northwestern University

[+1]

NCT04172779

/ Not yet recruiting临床2期IIT

Phase IIa Single-arm Clinical Trial of Hepatocellular Carcinoma Chemoprevention With Low-dose Erlotinib in Patients With Liver Cirrhosis

This phase IIa trial studies long-term low-dose erlotinib hydrochloride treatment to assess its efficacy and safety to prevent development of hepatocellular carcinoma in patients with liver cirrhosis.

开始日期2025-07-01

申办/合作机构

The University of Texas Southwestern Medical Center

[+1]

NCT06161558

/ Not yet recruiting临床1期IIT

Phase 1 Umbrella Trial of Erlotinib In Combination With Select Tyrosine Kinase Inhibitors In Adult Patients With Advanced Solid Tumors

Cancers that return or spread after their first line of treatment are often difficult to treat with limited next step options. Based on preclinical studies, the EGFR-targeting tyrosine kinase inhibitor (TKI) Erlotinib may be better in stopping or slowing the growth of tumors when given in combination with the multitargeting TKI Lenvatinib or Axitinib. Participants will be screened with a physical exam and tests including urine and blood tests, imaging scans, and a test of their heart function. Erlotinib, axitinib, and lenvatinib are all capsules taken by mouth. All participants will take their drugs at home every day. Some participants will take erlotinib plus lenvatinib once a day. Some participants will take erlotinib once a day and axitinib twice a day. Assignment to one of the treatment arms will be determined by the study. Participants will record their doses in a diary. Treatment is given in 28-day cycles. All participants will have 4 clinic visits during their first treatment cycle. After that, they will have a clinic visit at the start of each new cycle. Imaging scans, blood and urine tests, and other tests will be repeated during various clinic visits. Participants will remain in the study for as long as the treatment is helping them. They will have follow-up phone calls after they stop treatment....

开始日期2025-06-23

申办/合作机构

National Cancer Institute

100 项与盐酸厄洛替尼相关的临床结果

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100 项与盐酸厄洛替尼相关的转化医学

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100 项与盐酸厄洛替尼相关的专利（医药）

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12,069

项与盐酸厄洛替尼相关的文献（医药）

2025-12-31·ANNALS OF MEDICINE

A novel glycogene-related signature for prognostic prediction and immune microenvironment assessment in kidney renal clear cell carcinoma

Article

作者: Zhao, Danni ; Cui, Hanxiao ; Ren, Xueting ; Zhao, Xuyan ; Kang, Huafeng ; Liu, Peinan ; Li, Zihao ; Lin, Shuai ; Zhou, Mingjing

BACKGROUND:

Kidney Renal Clear Cell Carcinoma (KIRC) is a prevalent urinary malignancies worldwide. Glycosylation is a key post-translational modification that is essential in cancer progression. However, its relationship with prognosis, tumour microenvironment (TME), and treatment response in KIRC remains unclear.

METHOD:

Expression profiles and clinical data were retrieved from The Cancer Genome Atlas and Gene Expression Omnibus databases. Consensus clustering, Cox regression, and LASSO regression analyses were conducted to develop an optimal glycogene-related signature. The prognostic relevance of this molecular signature was rigorously analyzed, along with its connections to tumour microenvironment (TME), tumour mutation burden, immune checkpoint activity, cancer-immunity cycle regulation, immunomodulatory gene expression patterns, and therapeutic response profiles. Validation was performed using real-world clinical specimens, quantitative PCR (qPCR), and immunohistochemistry (IHC), supported by cohort analyses from the Human Protein Atlas (HPA) database.

RESULTS:

A glycogene-associated prognostic scoring system was established to categorize patients into risk-stratified subgroups. Patients in the high-risk cohort exhibited significantly poorer survival outcomes (p < 0.001). By incorporating clinicopathological variables into this framework, we established a predictive nomogram demonstrating strong calibration and a concordance index (C-index) of 0.78. The high-risk subgroup displayed elevated immune infiltration scores (p < 0.001), upregulated expression of immune checkpoint-related genes (p < 0.05), and an increased frequency of somatic mutations (p = 0.043). The risk score positively correlated with cancer-immunity cycle activation and immunotherapy-related signals. The high-risk groups also showed associations with T cell exhaustion, immune-activating genes, chemokines, and receptors. Drug sensitivity analysis revealed that low-risk patients were more sensitive to sorafenib, pazopanib, and erlotinib, whereas high-risk individuals responded better to temsirolimus (p < 0.01). qPCR and IHC analyses consistently revealed distinct expression patterns of MX2 and other key genes across the risk groups, further corroborated by the HPA findings.

CONCLUSION:

This glycogene-based signature provides a robust tool for predicting prognosis, TME characteristics, and therapeutic responses in KIRC, offering potential clinical utility in patient management.

2025-10-01·TALANTA

Development of an efficient capillary electrophoresis method for the analysis of salting-out assisted liquid–liquid extracted plasma samples

Article

作者: N'Cho Amin, Christophe ; Montels, Jérôme ; Chouchou, Adrien ; Ladner, Yoann ; Thodhekes Yao, Jean Simon ; Perrin, Catherine

A novel method based on salting-out assisted liquid-liquid extraction (SALLE) combined with capillary electrophoresis coupled to UV detection (CE-UV) was developed for the analysis of anticancer drugs in plasma samples. The SALLE technique allowed efficiently extraction of anticancer drugs from plasma into the organic phase, which was further analyzed by CE-UV. However, first experiments revealed instability in current profiles and UV electropherograms affected the performances of the SALLE-CE-UV method. To address these issues, different background electrolytes (BGEs) were tested to improve the stability and performance of the method. In parallel, microfluidic devices were also used to study the mixing between SALLE-extracted plasma samples and BGEs within the silica capillary. This approach provided key insights into SALLE-CE-UV optimization, highlighting issues such as phase separation, precipitation, and air bubble formation. These were mitigated by introducing an intermediate plug (2-fold diluted BGE) between the SALLE sample and the 100 mM pH 2.0 citric acid/ε-aminocaproic acid BGE, which significantly improved current stability. Further optimization of voltage ramp times (4 min from 0 to +15 kV) and temperature conditions (40 °C) improved method performances. The optimized procedure, applied to three tyrosine kinase inhibitors (TKIs), imatinib mesylate (IMA), axitinib (AXI), and erlotinib hydrochloride (ERL), used for the treatment of malignant tumors, demonstrated excellent linearity (coefficient of determination (R²) ≥ 0.995 from 0.15 to 0.75 mg/L), (R² ≥ 0.994 from 30 to 80 % of the injected volume to the detection window) repeatability (Relative standard deviation (RSD) ≤ 3.2 and 4.3 % on migration times and corrected peak areas), and sensitivity (Limit of detection (LOD) of IMA, ERL and AXI: 40.3, 79.3 and 40.6 ng/mL respectively) with UV detection at 254 nm.

2025-08-01·FREE RADICAL BIOLOGY AND MEDICINE

Exosomal SLC1A5 from senescent endothelial cells promotes gastric cancer progression by dampening ferroptosis via the EGFR/SRC/YAP1/GPX4 signaling

Article

作者: Xiong, Yuyan ; Ren, Yuanyuan ; Li, Xiaofang ; Qian, Lu ; Wang, Zhen ; Yu, Yi ; Zhang, Yan ; Zhang, Xi

A high-fat diet and obesity significantly increase the risk of gastric cancer (GC), with persistent obesity contributing to a notable rise in GC incidence. However, the underlying molecular mechanisms remain largely unclear. In this study, we identified exosomal SLC1A5 (Exo-SLC1A5) as a novel senescence-associated secretory phenotype (SASP) factor that promotes GC malignancy. Exosomal SLC1A5 drives GC progression by suppressing ferroptosis in a GPX4-dependent manner. Mechanistically, in the context of obesity, senescent endothelial cells release exosomal SLC1A5, which engages EGFR on GC cells, triggering SRC phosphorylation at Tyr416 and subsequent YAP1 activation at Tyr357. This leads to YAP1 interaction with MYO1B to enhance the nuclear translocation of YAP1, and subsequent upregulation of GPX4, resulting in ferroptosis suppression and accelerated GC progression. In vivo, depletion of exosomal SLC1A5 from PA-induced senescent ECs attenuated GC tumor growth and metastasis in a xenograft mouse model. These findings reveal a novel mechanism by which exosomal SLC1A5 promotes GC progression through the EGFR/SRC/YAP1/GPX4 signaling axis. Targeting the Exo-SLC1A5/EGFR/SRC/YAP1/GPX4 axis may provide a therapeutic strategy for GC.

408

项与盐酸厄洛替尼相关的新闻（医药）

2025-06-20

·汇聚南药

“王炸”落地，信立泰将否极泰来？

资本市场的估值法则冷酷而清晰：仿制药企，无论业绩如何，市场都已经不愿意再给高估值；创新药企，即使产品仍在临床，但市场却依然愿意相信BD预期。这道隐形的 “估值鸿沟”，是市场对“增长天花板”与“创新想象空间”的差异化定价。曾几何时，信立泰都是中国仿制药的“典型代表”，凭借一款“泰嘉”而名声鹊起。然而，随着集采的降临，信立泰逐渐遭遇业绩瓶颈，迫于无奈信立泰只得加速转型创新，并先后收获了1类创新药苯甲酸福格列汀片（商品名：信立汀）、恩那度司他片（商品名：恩那罗）及2.3类改良型新药阿利沙坦酯氨氯地平片（商品名：复立坦）。近日，信立泰的创新药矩阵又增加了一款重磅产品。5月27日，信立泰宣布，高血压新药沙库巴曲阿利沙坦钙片（信超妥）获批上市，这是国产原研首款、全球第二款获批的ARNI类药物。而在资本市场中，信立泰的股价也在今年备受投资者认可，单年涨幅接近80%。对于信立泰而言，股价的跃升是市场对于其向创新转型的最佳褒奖。随着创新药收入占比的持续攀升，信立泰不仅走出集采阵痛阴影，更向市场讲述了一个宏伟的“心血管帝国”故事。01“王炸”终于落地作为全球最常见的心血管慢性病之一，高血压影响着全球近10亿人口，甚至每年导致约940万人死于心梗、脑卒中等并发症。在我国，高血压防控形势尤为严峻：《中国心血管健康与疾病报告2022》显示，成人患病率达27.8%，患者规模达2.45亿，其中65岁以上人群发病率逼近50%。庞大的患者基数持续驱动治疗需求扩张。据智研咨询数据，2023年我国抗高血压药物市场规模达544.14亿元，2024年预计增至625.24亿元，同比增长14.9%，市场呈显著扩容趋势。当前临床常用高血压药物超百种，主要分为五大类：利尿剂、β受体阻滞剂（洛尔类）、钙通道阻滞剂（地平类）、血管紧张素转换酶抑制剂（普利类）和血管紧张素Ⅱ受体拮抗剂（沙坦类）。然而，全球范围内高血压原研药专利普遍已到期，仿制药陷入低价竞争红海。与之形成反差的是新药研发进展缓慢，近几年仅日本武田的美阿沙坦钾片、默克的比索洛尔氨氯地平复方制剂及诺华的沙库巴曲缬沙坦（诺欣妥，全球首款ARNI类药物）等少数创新药获批进口。尽管创新步伐缓慢，但却诞生出了诺欣妥这个爆款。诺欣妥是由诺华研发的全球首个血管紧张素受体脑啡肽酶抑制剂（ARNI），它独立于传统五大类高血压药物，被《中国高血压防治指南》列为新一类常用高血压药物，适用于高血压初始和维持治疗。其作用机制为通过抑制脑啡肽酶对利钠肽的降解，发挥利尿、利钠、扩血管及抗交感神经效应，同时其血管紧张素受体阻断作用可避免脑啡肽酶抑制后对 RAS 的代偿激活，从而实现协同降压。依靠ARNI类药物独特的机制，诺欣妥能够显著降低心血管死亡风险，减少患者因心力衰竭而住院的几率‌。因此，在过去五年中，诺欣妥始终保持高速增长趋势。2024年，诺华的诺欣妥全球销售额高达78.22亿美元，同比增长29.61%，稳居全球最畅销药物之列。在国内市场，其表现同样亮眼：2023年公立医疗机构销售额约28.1亿元，同比增长63.66%；2024年销售额进一步攀升至40.73亿元，同比增长44.95%。图：诺华诺欣妥营收与增速，来源：锦缎研究院正是看到了诺欣妥的强势表现，信立泰才决心跟进这一全新靶点，从“信超妥”的名字中也能看到信立泰的雄心。5月27日，信立泰自主研发的信超妥终于获批上市，成为国产原研首款、全球第二款获批的 ARNI 类药物，打破了诺华在该领域的垄断。信超妥并非简单的跟进，而是进一步的优化改良。信立泰公布的III期临床研究显示，信超妥降压疗效显著且呈明确剂量依赖性：240mg、480mg每日一次治疗12周后，平均诊室坐位收缩压降幅分别为25.07mmHg、28.22mmHg；治疗延长至52周时，仍能持续稳定控压，长期安全性和耐受性良好。此外，信超妥支持每日一次口服，而诺欣妥需每日两次，这对需要终身服药的高血压患者而言，依从性提升意味着实际疗效的跨越。目前，信立泰针对信超妥累计登记13项临床试验，其中包括3项III期临床试验。除已获批的轻、中度原发性高血压适应症外，其针对慢性射血分数降低型心衰（HFrEF）的III期临床已在2022年6月完成首例患者入组，目前持续推进中。对标诺华诺欣妥，市场预测信超妥凭借机制创新、用药便利性及本土化研发优势，峰值销售额有望达到47.7亿元，且其化合物专利保护期至2037年，为长期市场独占提供保障。“王炸”终于落地，这堪称信立泰在心血管领域多年研发投入的厚积薄发。信超妥上市后，将与信立坦、复立坦形成战略互补，进一步巩固信立泰在心血管领域的领先地位。02“心血管帝国”浮出水面这些年，信立泰的股价虽然不温不火，但其却在持续布局，悄然之间已经形成了一个“心血管帝国”。在心血管慢病治疗领域，信立泰已构建起降压、心衰、抗凝、降脂、卒中等多领域交叉的产品矩阵。除刚上市的信超妥，信立泰在降压药领域已上市的产品还包括信立坦（阿利沙坦酯片）、复立坦等创新药，以及信达怡（贝那普利片）、信达平（乐卡地平片）、信达悦（奥美沙坦酯片）等仿制药，覆盖几乎所有主流类型的降压药，是拥有国内高血压产品最全面的药企之一。其中，信立坦是信立泰心血管矩阵的基石，引进自艾力斯，是国内首个拥有自主知识产权的血管紧张素Ⅱ受体拮抗剂类降压药，于2013年获批上市，制剂专利保护期至2028年。信立坦降压强效平稳，不仅能显著提升杓型血压比例、改善夜间高血压，更因不经肝脏代谢，药物相互作用风险低，联合用药安全性更优；还有独特的降低尿酸作用，长期使用具有心肾等靶器官保护作用。2024年上市的复立坦作为国产原研 ARB/CCB 复方制剂，针对单药控制不佳的患者，通过“沙坦+地平”的经典组合，在增强降压疗效的同时减少水肿等不良反应。2024年上市后快速进入医保，成为合并动脉粥样硬化、慢性肾病或蛋白尿患者的首选方案之一。另一款同样为复方制剂的SAL0108（阿利沙坦酯吲达帕胺缓释片）已报产，通过“沙坦+利尿剂”的组合，进一步覆盖脑卒中病史患者。此外，信立泰还有S086/CCB类复方制剂、ETA 受体拮抗剂、醛固酮合酶抑制剂、小核酸药物等项目在研，为难治性高血压及复杂合并症提供解决方案。信立泰的产品矩阵不仅覆盖高血压全病程，更向肾病和心衰领域深度延伸。2023年6月获批的恩那罗（恩那度司他片）是一种抗肾性贫血口服小分子HIF-PHI抑制剂，用于治疗非透析成人慢性肾病（CKD）患者的贫血治疗，是国内第二个也是首个国产上市的HIF-PHI抑制剂。全球首款该类药物是阿斯利康罗沙司他，2024年中国销售收入达23亿元。相较之下，恩那度司他在疗效、安全性及用药依从性方面都具有优势。JK07是信立泰美国子公司Salubris Biotherapeutics自主研发的神经调节蛋白-1（NRG-1）融合抗体药物，通过激活心肌细胞ErbB4受体，促进心肌细胞再生与功能修复，为全球首个进入临床的“心肌再生疗法”。目前JK07在美国、加拿大和中国开展国际多中心的II期临床试验，中期分析已显现良好安全性与有效性积极信号，有望成为慢性心衰领域的下一款重磅炸弹。图：信立泰研发产品布局，来源：公司财报在医疗器械领域，信立泰也布局研发，涵盖神经介入、冠脉介入、外周介入、RDN、结构性心脏病等细分领域。其中，Maurora支架已累计植入超过 5 万条，并持续保持高增长态势。通过聚焦化学药、生物医药、医疗器械三条创新主线，信立泰构建了短期、中期、长期的产品研发梯队，形成覆盖不同治疗阶段的竞争优势在研产品。通过药品、器械与服务的战略协同，为患者提供全方位治疗解决方案，持续巩固在心血管慢病领域综合诊疗方案的领先地位。03专注，走出集采阴影创立伊始，信立泰就将心血管领域确立为未来的发展方向，这一干就是27年。1998年3月，赛诺菲与BMS联合研发的抗血凝药物氯吡格雷（波立维）获美国FDA批准上市，用于心血管疾病治疗，这款全球畅销药上市不到五年便创下百亿美元销售额。就在那一年，信立泰正式成立。两年后的2000年，信立泰的氯吡格雷仿制药“泰嘉”抢在原研药之前于国内获批上市，凭借等效疗效与价格优势迅速渗透各级医院，并占据市场主导地位。受当时国内专利制度影响，泰嘉与原研药波立维均获12年市场独占期，直至2012年第二款仿制药才上市。凭借先发与独占优势，泰嘉成为信立泰的核心现金流支柱：2013年销售额突破15亿元，占公司总营收64.46%；2018年达32亿元，占总营收近七成。转折发生在2019年9月的全国集采，赛诺菲爆冷给出了2.54元的全场最低价，国内同类药物也都报出了3元以下的价格，而信立泰的报价3.13元成了全场最高价，导致丢标出局。次年泰嘉销售额同比骤降59.97%，公司营收下滑38.74%，净利润更是断崖式下跌91.49%。集采失利，让信立泰清醒地意识到，中国药企以仿制药暴利赚钱的时代已经过去，必须下定决心转型创新药。但要如何选择创新药赛道呢？当时的行业惯性逻辑指向两条“捷径”：押注短期热门的生物类似药，或是跨界涌入肿瘤领域分羹。然而，信立泰的选择的却是继续押注心血管赛道，哪里跌倒就从哪里爬起来。2020年开始，信立泰陆续打包出售各种低端仿制药项目，盐酸达泊西汀、盐酸厄洛替尼、利伐沙班、甲磺酸伊马替尼统统变卖，其中甚至不乏刚刚获批上市不到一个月的产品。与此同时，信立泰通过引进战略投资者、非公开发行股票、抛售股权等手段，短短两年就募集了超40亿元资金。经历多轮、多省份的集采后，信立泰的仿制药收入逐渐趋于稳定，成为现金流“压舱石”。同时，公司的营收结构也悄然改变，从以仿制药为主，到创新药、仿制药各占半壁江山，再到创新药成为最主要的增长来源。这其中，核心产品信立坦2017年纳入医保后持续放量，2021年销售额破10亿元，2024年达15亿元，占公司营收37.4% 并保持高增长。2024年，信立泰实现营收40.12亿元，同比增长19.22%；归母净利润6.02亿元，同比增长3.71%。创新药收入占制剂收入的比例从2023年的43%提高到48%，随着获批创新药的销量和数量逐渐增加，预计2026年时创新药的收入占比将达到74%。创新药收入占比提高，也让信立泰的销售毛利率得到提升，2024年，毛利率达到72.64%，较2023年提高4.06个百分点，并在2025年一季度达到75.32%。回顾信立泰的发展历程，其转型之路堪称中国药企应对行业变革的教科书案例：从泰嘉断崖到信超妥登顶，其以五年战略定力完成从仿制药依赖到创新驱动的蜕变。当仿制药企在集采红海中沉浮时，唯有专注于创新，方能推开估值窄门。信立泰更是用十年转型揭示了一条铁律：真正的创新不在风口扎堆处，而是在巨头忽略的细分领域持续深耕，终能构筑不可复制的护城河。喜欢我们文章的朋友点个“在看”和“赞”吧，不然微信推送规则改变，有可能每天都会错过我们哦~免责声明“汇聚南药”公众号所转载文章来源于其他公众号平台，主要目的在于分享行业相关知识，传递当前最新资讯。图片、文章版权均属于原作者所有，如有侵权，请在留言栏及时告知，我们会在24小时内删除相关信息。信息来源：医曜往期推荐本平台不对转载文章的观点负责，文章所包含内容的准确性、可靠性或完整性提供任何明示暗示的保证。

专利到期上市批准

2025-06-17

·PRNewswire

Lung Cancer Research Foundation Announces Request for Proposals Focused on Curing EGFR Mutant Lung Cancers

New Team Science Award is $1.5 million Over Three Years NEW YORK, June 17, 2025 /PRNewswire/ -- The Lung Cancer Research Foundation (LCRF) announces today a new funding mechanism: the 2025 LCRF Team Science Award on Advancing Therapies Toward Curing EGFR Mutated Lung Cancers. The Request for Proposals is now open for submissions. Designed to bring together scientific teams to accomplish innovative breakthroughs, this team science award must include at least two projects directed at understanding and treatment of resistant or persistent disease in EGFR mutated lung cancer. Lung cancer is responsible for more deaths worldwide than any other cancer, accounting for an estimated 124,730 deaths annually in the United States alone.1 In the last 10 to 15 years, accelerated clinical trials and FDA approvals of targeted therapies for non-small cell lung carcinoma have been possible in part due to advances in molecular profiling of tumors. Many of these targeted therapies are directed against oncogenic drivers. Epidermal growth factor receptor (EGFR) mutations were the first oncogenic drivers that were successfully targeted with the use of tyrosine kinase inhibitors (TKIs). Subsequently additional oncogenic driver alterations in EML4-ALK, BRAF, RET, KRAS G12C, HER2, MET, NTRK, ROS1 and NRG1 were identified along with corresponding therapeutic options for treatment. Several TKIs including gefitinib, erlotinib, afatinib, dacomitinib, and osimertinib have been approved by the FDA for the treatment of EGFR mutated (EGFRmut+) Non Small Cell Lung Cancer (NSCLC.) Despite substantial progress in the treatment of EGFRmut+ lung cancer, available treatments are not curative, and resistance invariably develops. Sometimes biopsies are repeated to identify the source of resistance to potentially evaluate patients for additional targeted therapy. Usually, at some point in time chemotherapy is employed to treat the disease. Immunotherapy in the form of PD-1/PD-L1 inhibitors has revolutionized the treatment of many forms of lung cancer but has not proven effective in the treatment of most oncogene-driven lung cancers. Given that therapeutic options available to date are not curative, there is a need for novel approaches to treat these lung cancers and improve outcomes for patients with the ultimate intention of cure. This grant mechanism will focus on furthering the development of novel therapies for patients with EGFRmut+ NSCLC. "There has been so much scientific discovery in EGFR mutated lung cancer, and with the development of targeted treatments, patients are living longer," said Benay Taub, lung cancer survivor. "However, even with the best of circumstances, resistance develops and we need patients to have more treatment options. The goal of this award is to support a team of committed researchers in pursuit of improved treatments and outcomes for lung cancer patients and hopefully, one day, a cure." "EGFR discoveries were the start of oncogene-driven treatment and while the science has made great strides, there is still a significant need for more to be discovered," says Dr. Antoinette Wozniak, Chief Scientific Officer for LCRF. "Our commitment to people affected by lung cancer is simple: continue to fund research that pushes the boundaries of what is known to what is possible – toward a cure. This award will hopefully move the science in that direction." "Tomorrow's breakthroughs are made possible by research that happens today," emphasized David Carbone, MD, PhD, Director, Translational Therapeutics Program, The Ohio State University Wexner Medical Center and member of LCRF's Scientific Advisory Board. "Taking a team approach to combatting resistance in EGFR mutant lung cancer promises to accelerate the pace of discovery." This new Team Science Award is made possible by a generous private donation from Benay and Steven Taub. Their visionary support reflects a deep belief in the power of collaboration to drive scientific discovery. Submissions to the Request for Proposals will be reviewed through a two-step process: Letters of Intent will be accepted until midnight on July 29, 2025; if selected, projects will then be chosen to submit full proposals. All applications will be subject to a rigorous review by LCRF's Scientific Advisory Board. More details about the Request for Proposal, along with eligibility, requirements, and deadlines can be found at LCRF.org/FundingOpportunities. Siegel RL, Giaquinto AM, Jemal A. CA: A Cancer Journal for Clinicians, Vol 24,Issue 1, Jan/Feb 2024 About the Lung Cancer Research Foundation (LCRF) The Lung Cancer Research Foundation® (LCRF) is the leading nonprofit organization focused on funding innovative, high-reward research with the potential to extend survival and improve quality of life for people with lung cancer. LCRF's mission is to improve lung cancer outcomes by funding research for the prevention, diagnosis, treatment, and cure of lung cancer. To date, LCRF has funded 429 research grants, totaling nearly $48 million, the highest amount provided by a nonprofit organization dedicated to funding lung cancer research. For more information about the LCRF grant program and funding opportunities, visit lcrf.org/research. Contact: LUNG CANCER RESEARCH FOUNDATION (LCRF) Sheila Sullivan Sr. Director, Marketing & Communications [email protected] SOURCE Lung Cancer Research Foundation WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

免疫疗法临床研究

2025-06-17

·今日头条

肺癌患者自救指南：2025肺癌患者需知道的四大前沿技术+饮食调理

肺癌是全球死亡率最高的癌症，长期以来都是人类健康的劲敌。但医学的发展让我们看到希望：早期肺癌患者有着较高的长期生存率；即便处于中晚期，借助前沿治疗手段，也能有效延缓肿瘤进展，降低复发转移风险，延长生存时间。当患者身体状态稳定后，甚至可以回归正常工作生活，以“带癌生存” 的状态继续拥抱人生。然而，不少患者对肺癌治疗的认知，仍局限于传统的手术、放化疗。当面临无法耐受手术或放化疗、缺乏靶向药，以及术后预防复发转移等困境时，是否还有其他选择？答案是肯定的。为帮助患者坚定抗癌信心，全球肿瘤医生网小编整合各国最新文献数据与长生存患者的抗癌经验，精心梳理出“2025 肺癌患者自救指南”，聚焦五大前沿技术，助力患者成功抗癌，跨过一个又一个五年！认识免疫细胞疗法：激活身体的抗癌“部队” 人体的免疫系统本就是抵御癌症的天然防线，而免疫细胞疗法的核心，就是激活并强化这道防线。其中，CAR - T 细胞疗法、NK细胞疗法、TIL细胞疗法等是目前较为热门的免疫细胞治疗方式。 C-13-X：国内首个获得临床新药IND批准的CEA CAR-T，肺癌疾病控制率高达87% PART 1 CAR-T细胞疗法主要针对血液肿瘤，但在肺癌领域的研究也在逐步深入。它通过对患者自身的T细胞进行基因改造，使其能够精准识别并攻击癌细胞表面的特定抗原，经过体外扩增后回输到患者体内，形成强大的抗癌力量。而2025 ASCO大会上，一款中国自研的CAR-T疗法——C-13-X引起了广泛关注，并公布了C-13-X治疗晚期转移性非小细胞肺癌（NSCLC）Ⅰ期临床研究“的惊艳数据。C-13-X是国内首个获得新药临床默示许可（IND）的CEA靶向CAR-T疗法，适用于成人CEA阳性晚期恶性肿瘤（包括非小细胞肺癌、胃癌、胰腺癌、结直肠癌、食管癌、乳腺癌、胆管癌等）。在本次Ⅰ期临床研究中，共纳入15例病情极为棘手、经多线治疗均失败的晚期患者参与研究，接受了C-13-X输注。结果显示：接受C-13-X治疗的患者 1年总生存率（OS）高达71.1%，整体疾病控制率（DCR）达到87% （13/15），其中肺部靶病灶的DCR更是高达 93%，客观缓解率（ORR）达到47% （7/15）。 NY-ESO-1 TCR-T：助多线失败治疗失败的晚期肺腺癌患者症状减轻，肿瘤显著缩小76% PART 2 在非小细胞肺癌（NSCLC）领域，NY-ESO-1抗原在11.8%-21%的患者肿瘤组织中表达，这使其成为癌症免疫治疗的关键靶点。基于这一发现，科研团队成功研发出针对NY-ESO-1的TCR-T细胞疗法，为多线治疗失败的患者带来了新的希望与选择。《Oncology Letters》发布的临床研究（NCT02457650）数据令人振奋，该研究聚焦HLA-A2阳性且NY-ESO-1表达的转移性非小细胞肺癌患者。其中，一名44岁的晚期肺腺癌（LADC）女性患者的治疗经历极具代表性。她不仅携带EGFR突变，确诊时卡氏功能状态评分（KPS）仅50分，长期受咯血、胸痛等症状困扰。此前，她先后接受6个周期的多西他赛联合卡铂化疗，以及吉非替尼、厄洛替尼靶向治疗，但病情仍持续进展。2015年9月的CT检查显示，肿瘤已广泛转移至右肺门、纵隔、右胸膜、右肝叶及肝包膜，常规治疗手段已难以奏效。转机出现在进一步检查中，医生发现其右肺肿瘤NY-ESO-1抗原呈强阳性，这一结果使她获得参与NY-ESO-1 TCR-T细胞治疗临床试验的资格。首次TCR-T细胞输注43天后，CT复查带来惊喜：肺原发灶从95×86×54mm缩小至64×44×54mm，体积缩减约56% ；肝转移灶由19.8×19.6×20mm缩小至10×10×10mm，体积减少达76% 。同时，胸水完全吸收，肺组织恢复正常形态。根据RECIST1.1标准，患者达到部分缓解（PR）。此外，她的 KPS评分从50分提升至90分，咯血、胸痛症状显著缓解，生活质量得到极大改善。 ▲图源“Oncology Letters”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除这一临床案例充分验证了NY-ESO-1 TCR-T细胞疗法在晚期肺癌治疗中的显著疗效，为晚期肺癌患者的治疗策略提供了重要参考，也为攻克肺癌难题带来了新的曙光。 Lifileucel TIL细胞：改写转移性非小细胞肺癌结局，近八成患者肿瘤负荷下降，“无药可治”者肿瘤骤缩81% PART 3 TIL 细胞疗法则是从肿瘤组织中分离出浸润的淋巴细胞，在体外进行培养和扩增，筛选出对肿瘤细胞具有高杀伤力的 TIL 细胞，然后回输到患者体内。这种疗法能够更精准地识别肿瘤细胞，对部分肺癌患者展现出良好的治疗效果。 Lifileucel 作为全球首款获批上市的自体肿瘤浸润淋巴细胞（TIL）疗法，在转移性非小细胞肺癌（mNSCLC）的治疗领域展现出巨大潜力。《Cancer Discovery》杂志公布的 Ⅱ 期临床数据表明，它为免疫检查点抑制剂（ICI）耐药的转移性非小细胞肺癌（mNSCLC）患者带来了新的治疗希望。结果显示：客观缓解率（ORR）达21.4% （6/28），近八成患者（79.2%，19例）肿瘤负荷显著降低；部分缓解率（PR）达17.9% （5/28），其中 1例达完全缓解（CR），42.9%（12/28）患者病情稳定（SD）。值得特别关注的是一名41岁的IV期KRASG12D突变型黏液性肺腺癌患者，其肿瘤突变负荷（TMB）仅3.3mut/Mb，且PD-L1表达为0%，按照传统认知，属于从免疫治疗中获益可能性极低的人群。然而，在接受Lifileucel治疗12周后，依据RECISTv1.1标准评估，其肿瘤缩小率高达81%，达到部分缓解（PR）。这一突破性案例有力证明，Lifileucel疗法能够打破传统免疫治疗的局限，为难治性肿瘤患者带来显著的临床获益。 ▼该患者接受TIL治疗前、治疗后6周的CT扫描对比 ▲图源“Cancer Discov”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除 CCCR-NK92疗法：助肺癌脑转移患者，肿瘤病灶显著缩小 PART 4 CAR-NK细胞疗法融合了NK细胞天然的实体肿瘤浸润能力与CAR靶向技术，可精准识别癌细胞，相比传统疗法，能显著降低移植物抗宿主病（GvHD）、细胞因子释放综合征（CRS）风险，为肺癌患者开辟了全新治疗选择。我国近期公布的自研CCCR-NK92（改良版CAR-NK细胞）临床案例（NCT03656705）令人瞩目，该疗法在晚期非小细胞肺癌（NSCLC）脑转移治疗方面展现出良好疗效。一位69岁女性患者的经历极具代表性。基因检测显示，其肺组织存在Exon-1919-del与T790突变，且PD-L1表达≥1%，影像学检查确诊颅内转移。尽管此前已接受吉非替尼、奥希替尼等靶向治疗，以及头部和局部放疗，但病情依旧进展。出于对化疗副作用的顾虑，她选择参与CCCR-NK92细胞治疗临床试验。结果显示： CCCR-NK92细胞展现出强大的抗肿瘤活性，肿瘤病灶明显缩小。CT影像数据显示，患者左肺包裹性胸腔积液厚度从46.22mm降至33.59mm （详见下图A/C）；前气管-后腔静脉间质区域的淋巴结直径，也由11.3mm缩小至8.55mm （详见下图B/C）。这一案例为晚期肺癌治疗提供了重要临床依据，证实了CCCR-NK92疗法对肿瘤病灶的有效控制能力 ▼CCCR-NK92细胞治疗前后CT图像对比 ▲图源“Sage Journals”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除癌症疫苗：点燃免疫系统的“烽火台” 癌症疫苗与传统的预防传染病疫苗不同，它主要用于治疗已发生的癌症，通过激活人体免疫系统，使其主动识别并攻击癌细胞。肺癌领域的癌症疫苗研究主要集中在肿瘤抗原疫苗、树突状细胞疫苗、古巴肺癌疫苗、mRNA癌症疫苗等。以古巴肺癌疫苗CIMAvax-EGF为例，III期随机对照研究数据极具说服力。研究表明，晚期非小细胞肺癌患者在一线化疗后使用该疫苗，生存结局能得到显著改善——令人振奋的是，其五年生存率从常规治疗的0%大幅提升至23%。具体数据显示，疫苗接种组患者的中位总生存期（OS）达12.43个月，而对照组仅为9.43个月；长期生存率对比更为显著，疫苗接种组的2年生存率为37%，远超对照组的20% ；五年生存率更是实现了从无到有的突破，疫苗接种组为23%，而对照组为0% 。为更直观展现CIMAvax-EGF疫苗对肺癌的长期控制效果，特选取2例代表性患者治疗前后的影像学变化，以便直观地展示该疫苗对肺癌的长期控制效果。 ▼两例代表性患者接受CIMAvax-EGF治疗前后的CT对比 ▲图源“frontiers”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除益生菌：守护肠道微生态的抗癌“盟友” 肠道是人体最大的免疫器官，而益生菌作为肠道微生态的重要组成部分，对肺癌患者的健康有着不可忽视的作用。一方面，益生菌能够调节肠道菌群平衡，改善因手术、放化疗导致的肠道功能紊乱，缓解腹泻、便秘等不良反应，促进营养物质的吸收，为患者提供充足的能量支持。例如，双歧杆菌和乳酸杆菌等常见益生菌，可通过产生短链脂肪酸，维持肠道黏膜屏障的完整性，减少有害物质的吸收。另一方面，益生菌能够激活肠道免疫系统，增强机体的免疫功能。研究发现，益生菌可以促进免疫细胞的分化和成熟，调节细胞因子的分泌，从而提升机体对癌细胞的识别和杀伤能力。此外，部分益生菌还具有抗氧化和抗炎特性，有助于减轻炎症反应对身体的损害，降低肿瘤发生发展的风险。肺癌患者可以通过食用富含益生菌的食物，如酸奶、发酵豆制品等补充益生菌，也可在医生指导下服用益生菌补充剂，但要注意选择质量可靠、活性有保障的产品。《Cancer Control》发表的首个益生菌联合免疫检查点抑制剂（ICI）治疗晚期肺癌的大规模真实世界研究，带来令人振奋的成果。研究数据显示，总体人群客观缓解率（ORR）高达58.0% （详见下图B），中位无进展生存期（PFS）达12.0个月（95%CI：10.4-13.6个月）。值得关注的是，益生菌组展现出显著优势：其患者中位PFS为13.3个月（95%CI：8.5-18.4个月），相比对照组的12.0个月（95%CI：9.9-14.1个月），在延缓疾病进展上呈现明显优势趋势（详见下图C）。这一发现为晚期肺癌治疗策略提供了重要参考依据。 ▲图源“Sage Journals”，版权归原作者所有，如无意中侵犯了知识产权，请联系我们删除饮食及生活方式调整：为身体注入抗癌能量 1、饮食调理：除了依靠先进的医疗技术，肺癌患者还需从生活细节入手，为身体创造良好的抗癌环境。在饮食方面，应保证营养均衡，多摄入富含蛋白质的食物，如鱼肉、鸡肉、豆类等，为身体修复和免疫细胞的生成提供充足的原料；同时，多吃新鲜的蔬菜水果，补充维生素和膳食纤维，增强机体的抗氧化能力。避免食用高盐、高脂、加工肉类等可能加重身体负担的食物。 2、生活方式调整：规律作息同样关键，充足的睡眠有助于免疫系统的修复和调节，患者应尽量保证每天7-8小时的高质量睡眠，避免熬夜。适当的运动也不可或缺，可根据自身身体状况选择散步、太极拳、瑜伽等低强度运动，既能增强体质，又能改善心情，提高生活质量。此外，心理调节也不容忽视。肺癌的诊断和治疗过程往往给患者带来巨大的心理压力，负面情绪会影响免疫系统功能。患者可以通过与家人朋友交流、参加抗癌互助小组、进行冥想等方式缓解压力，保持积极乐观的心态，这对治疗效果和身体康复有着重要的促进作用。新药临床试验：探索抗癌新希望的前沿之路新药临床试验是抗癌治疗的前沿阵地，为肺癌患者带来新的治疗可能。当传统治疗手段效果不佳或无药可用时，参与新药临床试验或许能让患者提前用上尚未上市的创新药物和疗法。这些试验旨在评估新药的安全性和有效性，患者有机会获得新的治疗方案，同时也为癌症治疗的发展贡献力量。参与新药临床试验需要遵循严格流程。患者首先要符合试验设定的入组标准，如癌症类型、分期、既往治疗情况等。之后需详细了解试验的目的、方法、可能的风险与获益，并签署知情同意书。在试验过程中，患者会接受密切的医疗监测，医生会及时评估药物效果和不良反应。好消息是，目前有多款肺癌新药的临床试验正在进行中。感兴趣的患者可点击原文了解详情：2025非小细胞肺癌有哪些治疗新方案？17款“续命”新药临床招募中小编寄语与肺癌的斗争是一场持久战，免疫细胞疗法和癌症疫苗为患者带来了新的曙光，而生活方式的调整与科学的治疗管理则是这场战斗的坚实后盾。肺癌患者应积极了解前沿医疗技术，结合自身情况选择合适的治疗方案，保持良好的生活习惯和乐观的心态，与医生并肩作战，坚定战胜病魔的信念，为自己争取更美好的未来。参考资料 [1]Xia Y,et al.Treatment of metastatic nonsmall cell lung cancer with NYESO1 specific TCR engineeredT cells in a phase I clinical trial: A case report[J]. Oncology letters, 2018, 16(6): 6998-7007. https://www-spandidos-publications-com.libproxy1.nus.edu.sg/10.3892/ol.2018.9534 [2]Zhang X,et al.Cytokine release syndrome after modified CAR-NK therapy in an advanced non-small cell lung cancer patient: a case report[J]. Cell Transplantation, 2022, 31: 09636897221094244. https://journals-sagepub-com.libproxy1.nus.edu.sg/doi/full/10.1177/09636897221094244 本文为全球肿瘤医生网原创，未经授权严禁转载

免疫疗法细胞疗法临床申请ASCO会议临床1期

100 项与盐酸厄洛替尼相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D04023	盐酸厄洛替尼	L01XE03	DB00530

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
EGFR阳性非小细胞肺癌	日本	CHEPLAPHARM Arzneimittel GmbH	2013-06-14
EGFR阳性非小细胞肺癌	日本	Chugai Pharmaceutical Co., Ltd.	2013-06-14
胰腺癌	欧盟	CHEPLAPHARM Arzneimittel GmbH	2005-09-19
胰腺癌	冰岛	CHEPLAPHARM Arzneimittel GmbH	2005-09-19
胰腺癌	列支敦士登	CHEPLAPHARM Arzneimittel GmbH	2005-09-19
胰腺癌	挪威	CHEPLAPHARM Arzneimittel GmbH	2005-09-19
非小细胞肺癌	美国	OSI Pharmaceuticals, Inc.	2004-11-18

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
EGFR-T790M 突变非小细胞肺癌	临床3期	美国	Eli Lilly & Co.	2015-05-06
EGFR-T790M 突变非小细胞肺癌	临床3期	日本	Eli Lilly & Co.	2015-05-06
EGFR-T790M 突变非小细胞肺癌	临床3期	加拿大	Eli Lilly & Co.	2015-05-06
EGFR-T790M 突变非小细胞肺癌	临床3期	法国	Eli Lilly & Co.	2015-05-06
EGFR-T790M 突变非小细胞肺癌	临床3期	德国	Eli Lilly & Co.	2015-05-06
EGFR-T790M 突变非小细胞肺癌	临床3期	希腊	Eli Lilly & Co.	2015-05-06
EGFR-T790M 突变非小细胞肺癌	临床3期	中国香港	Eli Lilly & Co.	2015-05-06
EGFR-T790M 突变非小细胞肺癌	临床3期	意大利	Eli Lilly & Co.	2015-05-06
EGFR-T790M 突变非小细胞肺癌	临床3期	罗马尼亚	Eli Lilly & Co.	2015-05-06
EGFR-T790M 突变非小细胞肺癌	临床3期	西班牙	Eli Lilly & Co.	2015-05-06

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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	晚期头颈部鳞状细胞癌	97	Dual Oral Metronomic Therapy (OMT)	構衊範製襯簾壓鏇製範(顧鏇壓廠襯遞齋構鹹膚) = 鹹窪範糧憲築膚壓蓋網鹹糧遞構遞憲獵顧鏇繭 (遞獵齋製鹹鹽艱餘網醖 ) 更多	积极	2025-05-30
				Triple Oral Metronomic Therapy (OMT)	構衊範製襯簾壓鏇製範(顧鏇壓廠襯遞齋構鹹膚) = 淵顧憲積蓋網製醖鑰壓鹹糧遞構遞憲獵顧鏇繭 (遞獵齋製鹹鹽艱餘網醖 ) 更多
NCT00448240 (CTgov)	临床2/3期	晚期头颈部鳞状细胞癌	6	Erlotinib	鏇醖網顧鏇鏇構願廠蓋 = 餘蓋構顧鹽淵襯襯鹽遞願廠顧鑰顧壓壓鬱觸鑰 (糧膚壓膚遞獵鹽鬱齋顧, 積鹽鹽衊築齋積窪構壓 ~ 夢遞積遞鑰齋淵襯憲鹹) 更多	-	2025-03-18
NCT03137771 (NRG-LU002, CTgov)	临床2期	转移性非小细胞肺癌 \| 复发性非小细胞肺癌	218	Erlotinib Hydrochloride+Gemcitabine+Docetaxel+pembrolizumab+Pemetrexed Disodium (Arm 1 (Systemic Maintenance Chemotherapy))	艱餘淵簾範衊淵築選淵(夢糧選鏇夢餘齋觸鏇簾) = 醖繭蓋窪襯鹹遞選襯醖製夢餘夢鏇繭鹹繭製製 (窪積廠積願繭醖鬱糧衊, 窪網顧選鹹顧糧網鹽顧 ~ 膚齋築淵遞廠衊選窪膚) 更多	-	2025-03-11
				Stereotactic Body Radiation Therapy (SBRT)+Erlotinib Hydrochloride+Gemcitabine+Docetaxel+pembrolizumab+Pemetrexed Disodium (Arm 2 (LCT + Systemic Maintenance Chemotherapy))	艱餘淵簾範衊淵築選淵(夢糧選鏇夢餘齋觸鏇簾) = 糧鏇範膚鏇簾夢襯顧膚製夢餘夢鏇繭鹹繭製製 (窪積廠積願繭醖鬱糧衊, 餘構鬱窪構餘夢淵鏇獵 ~ 襯築鹹構製積積顧鹹選) 更多
NCT00446225 (EURTAC, CTgov)	临床3期	晚期非小细胞肺癌	174	Erlotinib (A: Erlotinib Group)	夢顧膚構醖壓廠繭憲夢(網遞艱壓築艱糧蓋築鏇) = 鬱製醖願選齋憲廠繭顧範觸鏇襯遞構選構艱觸 (鹹夢鏇簾膚鬱繭願鑰製, 窪醖鏇獵衊憲選願糧鏇 ~ 願構夢廠餘壓積遞選遞) 更多	-	2025-03-05
				Carboplatin+gemcitabine+Docetaxel+Cisplatin (B: Standard Chemotherapy Group)	夢顧膚構醖壓廠繭憲夢(網遞艱壓築艱糧蓋築鏇) = 繭構網網壓鹹夢製窪鏇範觸鏇襯遞構選構艱觸 (鹹夢鏇簾膚鬱繭願鑰製, 糧餘簾範顧積獵觸積遞 ~ 顧選構構襯鬱齋構範構) 更多
NCT01887795 (ENTER, Pubmed \| Transl Lung Cancer Res)	临床3期	脑转移瘤 epidermal growth factor receptor (EGFR)-mutant	-	Whole-brain radiotherapy (WBRT)	鹹壓鬱廠蓋鬱齋獵製淵(製餘窪繭範廠艱鑰製獵) = 餘壓窪築醖願憲齋襯淵選網壓積築鹽鬱艱鬱築 (壓鬱艱廠遞鬱糧衊壓獵 ) 更多	积极	2024-12-01
				WBRT + Erlotinib	鹹壓鬱廠蓋鬱齋獵製淵(製餘窪繭範廠艱鑰製獵) = 鬱憲願簾網網糧積獵鬱選網壓積築鹽鬱艱鬱築 (壓鬱艱廠遞鬱糧衊壓獵 ) 更多
NCT02411448 (RELAY, Pubmed \| J Thorac Oncol)	临床3期	EGFR突变的非小细胞肺癌 EGFR exon 19del \| L858R mutation \| TP53 co-mutation ... 更多	449	Erlotinib + Ramucirumab	糧製獵鏇衊醖繭願繭遞(網廠壓膚夢鹽壓積範製) = 廠觸憲壓艱鹽構築壓襯製網鏇醖獵鹽積簾壓醖 (顧製廠獵蓋鑰憲鑰鏇衊 ) 更多	不佳	2024-11-01
				Placebo + Erlotinib	糧製獵鏇衊醖繭願繭遞(網廠壓膚夢鹽壓積範製) = 壓顧鏇夢鹽遞鑰膚願淵製網鏇醖獵鹽積簾壓醖 (顧製廠獵蓋鑰憲鑰鏇衊 ) 更多
CTRI/2020/03/023943 (BEER BTC, Pubmed \| J Clin Oncol)	临床2/3期	晚期胆管癌维持	98	Erlotinib (Active Surveillance)	構憲獵艱鏇觸夢築顧築(築窪襯夢艱顧獵鏇鑰鏇) = 1 (2%) with erlotinib 蓋顧觸範糧壓憲鹽願觸 (醖醖獵齋構襯衊鹹網壓 ) 更多	积极	2024-09-20
				Bevacizumab-Erlotinib
JPRN-UMIN000026197 \| JPRN-jRCTs031180404 (ESMO2024) 人工标引	临床2期	EGFR突变的非小细胞肺癌 EGFR Exon 19 Deletion \| EGFR L858R	25	Erlotinib	鏇膚遞壓鏇網願醖觸鏇(憲憲鹹鏇獵願繭夢膚簾) = 簾醖鬱餘膚糧網構鑰鹹淵窪鹹鬱蓋鑰製窪糧糧 (繭簾壓願製憲膚衊蓋襯, 6.6 ~ 30.8) 未达到更多	不佳	2024-09-14
				Erlotinib (EGFR exon 19 deletions)	鏇膚遞壓鏇網願醖觸鏇(憲憲鹹鏇獵願繭夢膚簾) = 鑰蓋觸齋膚襯餘簾齋鹽淵窪鹹鬱蓋鑰製窪糧糧 (繭簾壓願製憲膚衊蓋襯 ) 未达到更多
WCLC2024 人工标引	N/A	转移性非小细胞肺癌 EGFR Mutation	3	EGFR-TKIs + Thoracic Radiation Therapy	遞鬱簾夢襯遞齋壓憲選(鑰鏇網醖築廠築築積築) = 醖鑰齋餘願遞簾憲醖廠範艱餘選鹹襯鹽築淵鏇 (網餘襯鑰壓衊齋繭夢衊, 7 ~ 33) 更多	积极	2024-09-08
WCLC2024 人工标引	N/A	EGFR阳性非小细胞肺癌一线 EGFR Mutation	355	erlotinib	構齋廠願鬱獵襯構願醖(憲築餘積觸繭襯憲鹹憲) = 壓顧遞構淵廠構衊鏇窪糧艱窪構鹽構簾遞襯齋 (簾繭淵夢鏇蓋窪廠鹹鹹, 3 ~ 65) 更多	积极	2024-09-07
				erlotinib (Asian)	構齋廠願鬱獵襯構願醖(憲築餘積觸繭襯憲鹹憲) = 顧製鏇夢範襯選鹹鏇獵糧艱窪構鹽構簾遞襯齋 (簾繭淵夢鏇蓋窪廠鹹鹹, 27 ~ 82) 更多