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更新于：2026-06-03
Zorifertinib
盐酸佐利替尼
更新于：2026-06-03
概要
基本信息
药物类型 小分子化药 |
别名 佐利替尼、AZD-3759、AZD3759 + [1] |
作用方式 抑制剂 |
作用机制 EGFR19外显子缺失突变抑制剂、EGFR21外显子L858R突变抑制剂 |
原研机构 |
在研机构 |
最高研发阶段批准上市 |
首次获批日期 中国 (2024-11-15), |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构/序列
分子式C22H23ClFN5O3 |
InChIKeyMXDSJQHFFDGFDK-CYBMUJFWSA-N |
CAS号1626387-80-1 |
关联
12
项与 盐酸佐利替尼 相关的临床试验NCT07620951
Phase I Clinical Study on Material Balance of [14C]Zorifertinib in Healthy Adult Male Participants in China
NCT07551414
A Prospective Study of Zorifertinib Plus Intra-Ommaya CSF Chemotherapy for Leptomeningeal Progression in NSCLC After Third-Generation EGFR-TKI Therapy
ChiCTR2600121513
Zorifertinib Plus Radiotherapy as First-Line Treatment in EGFR-Mutant NSCLC with Brain Metastases: A Prospective Clinical Study
100 项与 盐酸佐利替尼 相关的临床结果
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100 项与 盐酸佐利替尼 相关的转化医学
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100 项与 盐酸佐利替尼 相关的专利（医药）
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72
项与 盐酸佐利替尼 相关的文献（医药）2026-08-01COMPUTATIONAL BIOLOGY AND CHEMISTRY
A palmitoylation-related prognostic risk scoring model and tumor microenvironment characterization in lung adenocarcinoma, using single-cell RNA sequencing data
Article
作者: Liu, Haixiao ; Wang, Lingyun ; Ren, Juanxia ; Zheng, Guangda ; Li, Changlin ; Bao, Yanju ; Meng, Linghan ; Li, Dongtao ; Hu, Yue ; Shang, Lu
BACKGROUND:
Lung adenocarcinoma (LUAD) is the predominant pathological subtype of non-small cell lung cancer. Its considerable tumor heterogeneity and drug resistance present major clinical obstacles, resulting in unfavorable patient outcomes. Protein palmitoylation is known to be a key factor in tumorigenesis; however, its cell-specific expression patterns and prognostic value in LUAD remain incompletely characterized.
METHODS:
Using two independent datasets, TCGA-LUAD and GSE68465, and scRNA-seq data from 10 LUAD samples, we analyzed the expression of palmitoylation-related genes. Through single-cell clustering, CNV analysis, and palmitoylation activity scoring, malignant epithelial cells were identified. 10 machine learning algorithms were applied to construct prognostic models based on differentially expressed genes. RT-qPCR was used to detect mRNA expression of prognostic marker genes in clinical samples. In vitro experiments validated SEC61G's role in regulating drug sensitivity.
RESULTS:
A subset of malignant epithelial cells with high palmitoylation activity was identified. A 5-gene signature (UBE2S, SEC61G, CCT6A, GAPDH, HLA-DRA) was established by the integrated CoxBoost+SuperPC method, showing robust predictive efficacy in both GSE68465 and TCGA-LUAD. High-risk samples carried higher mutation burden, greater genomic heterogeneity, and a stronger tumor immunosuppressive microenvironment than the low-risk group. Clinical sample testing revealed upregulation of UBE2S, SEC61G, CCT6A, and GAPDH in LUAD patients and downregulation of HLA-DRA. SEC61G expression inversely correlated with AZD3759 sensitivity. In vitro, SEC61G knockdown or AZD3759 alone suppressed LUAD proliferation and induced apoptosis; no synergy was observed with combination therapy, indicating that SEC61G modulates AZD3759 sensitivity in LUAD cells.
CONCLUSION:
Our study comprehensively reveals the cellular heterogeneity of palmitoylation, establishes a robust palmitoylation-related prognostic model, and identifies SEC61G as a promising therapeutic target in LUAD, offering a novel perspective for LUAD precision stratification and treatment studies.
2026-04-05CHINESE MEDICAL JOURNAL
Epidermal growth factor receptor tyrosine kinase inhibitor for the treatment of non-small cell lung cancer in the past 30 years (1997–2026)
Review
作者: Han, Xiaohong ; Xie, Zucheng ; Yang, Mengwei ; Gao, Ruyun ; Sun, Yan ; Chen, Xinrui ; Shi, Yuankai
Abstract:
Epidermal growth factor receptor (
EGFR
) is a critical driver gene in non-small cell lung cancer (NSCLC). Since 1997, EGFR tyrosine kinase inhibitors (EGFR-TKIs) have evolved from first-generation agents, such as gefitinib, erlotinib, and icotinib, to second-generation agents like afatinib and dacomitinib, now to third-generation agents, including osimertinib, aumolertinib, furmonertinib, befotertinib, rezivertinib, rilertinib, limertinib, lazertinib, mifanertinib for
EGFR
L858R, sunvozertinib for
EGFR
exon 20 insertion (20ins), and zorifertinib for
EGFR
-sensitive mutation with brain metastases. Throughout this evolution, EGFR-TKIs have become the cornerstone of treatment for
EGFR
-mutant NSCLC, extending beyond advanced stages to encompass the entire disease spectrum, including perioperative and maintenance therapies, with combination therapies further expanding treatment options. These advancements have significantly improved patient survival and quality of life. However, challenges such as acquired resistance remain significant hurdles in achieving long-term disease control. Over the past 30 years, substantial advancements have been made in the comprehensive management of
EGFR
-mutant NSCLC. This systemic review provides the history of the development of EGFR-TKI therapy for NSCLC from 1997 to 2026, highlighting clinical milestones, emerging therapies, and future directions in this rapidly evolving field.
2026-04-01INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
Subtype-specific APOBEC enrichment links genomic instability to predict immunotherapy response in breast cancer subtypes
Article
作者: Zhou, JiaQi ; Ning, ChunLan ; Cao, XuChen ; Zhao, ZeWei ; Xie, Yongjie ; Wang, Xin ; Yu, Yue ; Zhou, Yaoyao ; Jia, WenBin
Breast cancer (BRCA), a prevalent malignancy among women, significantly impacts survival quality and life expectancy, with rising incidence and mortality rates posing substantial psychological and economic burdens on patients and families. Current treatment modalities exhibit considerable variability in efficacy, often hindered by resistance and recurrence, thus emphasizing the urgent need for novel biomarkers and therapeutic targets. This study investigates the genomic characteristics of the APOBEC family genes across different BRCA subtypes and their influence on mutation profiles. Utilizing data from multiple databases, including The Cancer Genome Atlas (TCGA) and the Clinical Proteomic Tumor Analysis Consortium (CPTAC), SMC, and Metabric, we conducted a comprehensive analysis of APOBEC mutation enrichment scores (APMs) and tumor mutational burden (TMB). Our findings reveal that APMs are significantly elevated in BRCA compared to other cancers, with distinct variations among subtypes; specifically, HER2+ breast cancer exhibited the highest APMs while triple-negative breast cancer (TNBC) displayed the lowest. We also observed correlations between APMs and TMB, suggesting differential immune microenvironment interactions, particularly in HER2+ versus TNBC and Luminal subtypes. Furthermore, APMs demonstrated a significant association with DNA damage response pathways, with implications for treatment strategies. Our study subsequently investigates the predictive role of the APOBEC mutagenesis-related prognostic risk score (AMrs) in guiding targeted and immunotherapy combinations for different subtypes of BRCA, specifically TNBC, Luminal, and HER2+ breast cancer. By leveraging a multi-center database, we seek to validate the correlation between AMrs scores and the sensitivity of these BRCA subtypes to immunotherapy. Based on in vivo experiments in mice, our research highlights that the administration of specific agents-AZD3759 for HER2+, Vorinostat for TNBC, and SGC0946 for Luminal-when combined with anti-PD-1 therapy, not only boosts therapeutic effectiveness but also transforms the immunological environment within tumors. This synergistic approach led to notable reductions in tumor volume and an increase in cytotoxic T cell density in in vivo and in vitro experiments, further validating the role of AMrs scores in tailoring treatment modalities across BRCA subtypes. Overall, our study elucidates the critical role of APOBEC family genes in BRCA heterogeneity, highlighting their potential as biomarkers for personalized therapeutic approaches and pointing towards future research directions in integrating APOBEC-related mechanisms with immunotherapy.
100 项与 盐酸佐利替尼 相关的药物交易
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外链
| KEGG | Wiki | ATC | Drug Bank |
|---|---|---|---|
| - | - | - |
研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| EGFR 外显子 19 缺失突变型非小细胞肺癌 | 中国 | 2024-11-15 | |
| EGFR外显子21替代突变非小细胞肺癌 | 中国 | 2024-11-15 |
未上市
10 条进展最快的记录, 后查看更多信息
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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 | 中国 | 2018-10-29 | |
| EGFR-T790M 突变非小细胞肺癌 | 临床3期 | 新加坡 | 2018-10-29 | |
| EGFR-T790M 突变非小细胞肺癌 | 临床3期 | 韩国 | 2018-10-29 | |
| EGFR-T790M 突变非小细胞肺癌 | 临床3期 | 中国台湾 | 2018-10-29 | |
| EGFR突变的非小细胞肺癌 | 临床3期 | 中国 | 2018-10-18 | |
| EGFR突变的非小细胞肺癌 | 临床3期 | 新加坡 | 2018-10-18 | |
| EGFR突变的非小细胞肺癌 | 临床3期 | 韩国 | 2018-10-18 | |
| EGFR突变的非小细胞肺癌 | 临床3期 | 中国台湾 | 2018-10-18 | |
| 软脑膜转移性恶性肿瘤 | 临床2期 | 中国 | 2026-05-30 | |
| EGFR阳性非小细胞肺癌 | 临床2期 | 中国 | 2017-10-19 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床3期 | 439 | 網繭獵築願壓廠網鬱窪(選遞窪簾廠鑰齋糧繭願): HR = 0.467 (95% CI, 0.352 ~ 0.619) 更多 | 积极 | 2024-10-01 | |||
临床3期 | 439 | 壓簾艱齋齋夢網範衊鑰(鹹獵遞獵獵憲網鹹憲製) = 窪觸壓齋鏇淵鏇蓋積鹽 選齋壓繭鹽窪糧顧淵築 (製窪窪廠構構憲壓鹹糧, 8.2 ~ 9.7) 更多 | 优效 | 2023-05-26 | |||
Gefitinib 250 mg or Erlotinib Hydrochloride 150 mg | 壓簾艱齋齋夢網範衊鑰(鹹獵遞獵獵憲網鹹憲製) = 願壓廠醖蓋衊壓憲顧艱 選齋壓繭鹽窪糧顧淵築 (製窪窪廠構構憲壓鹹糧, 6.3 ~ 8.0) 更多 | ||||||
临床2期 | 30 | 壓構壓淵蓋觸製構夢廠(鬱觸膚齋獵膚顧衊鬱餘) = 廠窪醖艱蓋範淵築蓋鹽 簾鑰積構餘艱簾鏇廠淵 (膚膚糧窪顧餘遞鬱願餘 ) 更多 | 积极 | 2023-03-31 | |||
临床1期 | EGFR突变的非小细胞肺癌 EGFR Mutation | 67 | (dose-escalation) | 選製鹽蓋遞廠鹹觸廠遞(觸餘襯蓋築餘醖範製鏇) = led to treatment discontinuation in one (4%) patient treated with 200 mg twice a day (grade 3 increase of alanine aminotransferase and aspartate aminotransferase) and two (13%) patients given 300 mg twice a day (grade 3 diarrhoea [n=1] and grade 3 skin rash [n=1]). 構範顧顧範夢淵窪鑰製 (淵構壓製膚獵繭繭窪築 ) 更多 | 积极 | 2017-11-01 | |
(dose-expansion) | |||||||
临床1期 | 38 | 範鑰糧築積壓廠製築餘(顧窪簾鏇鏇壓觸構醖選) = above pEGFR IC90 淵繭鏇襯遞選鑰鹽鹹鹽 (壓襯壓觸鏇鬱獵餘構築 ) 更多 | - | 2017-05-30 | |||
临床1期 | 38 | 壓壓網鏇鏇繭選糧壓繭(艱鑰糧築鏇艱糧衊遞膚) = 67% (12 out of 18) patients had drug-related dose interruption and/or reduction, however, there were no drug-related discontinuations 獵遞鹹繭憲積壓顧憲襯 (觸壓遞鑰網鏇餘淵餘鏇 ) 更多 | 积极 | 2017-05-30 | |||
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