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更新于：2026-10-28
Limertinib
利厄替尼
更新于：2026-10-28
概要
基本信息
药物类型 小分子化药 |
别名 ASK120067、奥壹新 |
作用方式 抑制剂 |
作用机制 EGFR T790M抑制剂(表皮生长因子受体T790M抑制剂) |
非在研适应症 |
原研机构 |
非在研机构- |
最高研发阶段批准上市 |
首次获批日期 中国 (2025-01-14), |
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C29H32ClN7O2 |
InChIKeyQHPVTCLSVVUPOF-UHFFFAOYSA-N |
CAS号1934259-00-3 |
关联
25
项与 利厄替尼 相关的临床试验NCT07897188
A Randomized, Controlled, Double-Blind, Multicenter, Phase 3 Clinical Study of ASKC202 Plus Limertinib Versus Osimertinib for First-Line Therapy for Patients With EGFRm+/MET+ Locally Advanced or Metastatic NSCLC
NCT07612137
A Phase Ib/II Study to Evaluate the Safety, Tolerability, and Preliminary Efficacy of IBI3005 Combination Therapy in Participants With Advanced Solid Tumors
ChiCTR2600122043
Exploration of the Efficacy and Safety of Limertinib as Adjuvant Therapy in Patients with Stage II-IIIA Non-Small Cell Lung Cancer Harboring EGFR Uncommon Mutations After Radical Resection.
100 项与 利厄替尼 相关的临床结果
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100 项与 利厄替尼 相关的转化医学
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100 项与 利厄替尼 相关的专利（医药）
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16
项与 利厄替尼 相关的文献（医药）2026-06-01Journal of Thoracic Disease
First-line third-generation EGFR-TKIs for advanced EGFR-mutated non-small cell lung cancer: a systematic review and network meta-analysis of randomized controlled trials
Article
作者: Sun, Wei ; Zhao, Qingfang ; Liu, Xiaomin ; Chen, Jinglong
Background:
Head‑to‑head comparisons among first‑line third‑generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) for EGFR‑mutated unresectable non-small cell lung cancer (NSCLC) are nearly absent. This network meta‑analysis compares the efficacy and safety of all available agents and provide evidence-based references for clinical decision-making.
Methods:
We searched PubMed, EMBASE, Web of Science, and the Cochrane Central Register of Controlled Trials (CENTRAL) from inception to April 2026. Eligible studies were randomized controlled trials (RCTs) enrolling patients with advanced EGFR-mutated NSCLC receiving first-line third-generation EGFR-TKIs compared with first-generation EGFR-TKIs. Two reviewers independently extracted data and assessed risk of bias using the Cochrane RoB 2 tool. The primary efficacy outcome was progression-free survival (PFS). We performed a network meta-analysis (NMA) using a fixed-effect model and ranked treatments using surface under the cumulative ranking curve (SUCRA). The protocol was registered with PROSPERO (CRD42022349097).
Results:
Eleven RCTs comprising 4,663 patients were analyzed. All investigated third-generation agents (aumolertinib, osimertinib, furmonertinib, befotertinib, limertinib, rilertinib, lazertinib, and rezivertinib) demonstrated superior PFS compared to first-generation TKIs. However, no statistically significant PFS differences were observed among the third-generation agents. Similarly, no significant differences were found between third- and first-generation TKIs regarding objective response rate (ORR) or ≥ G3 treatment-emergent adverse events (TEAEs). Subgroup analyses revealed no significant PFS benefit for befotertinib over first-generation TKIs in the L858R subgroup, nor for befotertinib or furmonertinib in elderly patients.
Conclusions:
Most third-generation TKIs offer superior PFS compared to first-generation agents, with comparable efficacy observed across the third-generation agents. Safety profiles, specifically regarding high-grade adverse events, appear similar between third- and first-generation TKIs.
2026-05-01MedComm
Sphingosine‐1‐Phosphate Receptor 3 Confers Tumor Metastasis in Lung Cancer Resistant to Third‐Generation EGFR Inhibitor
Article
作者: Yu, Ker ; Qin, Ye ; Song, Peiran ; Liu, Qiupei ; Geng, Meiyu ; Xie, Hua ; Liu, Yingqiang ; Tang, Bencan ; Zhang, Hui ; Chen, Hao ; Bai, Gang ; Ding, Jian ; Li, Yan ; Tong, Linjiang ; Zhang, Tao ; Pan, Zilu ; Tang, Haotian ; Lai, Mengzhen ; Chen, Yi ; Feng, Fang ; Fang, Yan ; Chen, Jiaying
ABSTRACT:
The third‐generation EGFR tyrosine kinase inhibitor (TKI) osimertinib (AZD9291) has significantly improved the survival in EGFR‐mutant lung cancer patients. Our team developed limertinib (ASK120067), a novel third‐generation EGFR inhibitor with remarkable antitumor effects, which has been launched in China. Despite initial therapeutic responses, EGFR TKIs‐treated patients ultimately experience fatal metastatic recurrence and disease progression. However, the underlying mechanism of driving metastasis remains poorly understood. Here, we aim to investigate the pro‐metastatic mechanism following treatment with third‐generation EGFR TKIs. Transcriptomics analyses of EGFR TKI‐resistant tumor models revealed an aberrant upregulation of S1PR3, which conferred enhanced metastatic potential to lung cancer. S1PR3 inhibition dramatically reduced metastasis in resistant cells, while its overexpression potentiated metastatic abilities in parental cells. Notably, S1PR3 was highly enriched in clinical samples with AZD9291 resistance and correlates with poor prognosis. Mechanistically, we found that S1PR3 upregulated RAC1‐GTP expression to activate PAK1, thereby promoting epithelial‐mesenchymal transition (EMT) and enhancing metastatic capacity of resistant cells. Further studies identified that the overexpression of fibroblast growth factor receptor 1 (FGFR1) increased S1PR3 expression through signal transducer and activator of transcription 4 (STAT4) to promote the emergence of metastatic‐resistant cells. Importantly, targeting S1PR3 or FGFR1 blocks metastasis in EGFR TKI‐resistant models.
2025-10-21ACCOUNTS OF CHEMICAL RESEARCH
Chemical Adaptation in Drug Discovery: The Medicinal Chemistry Journey of Olverembatinib and Limertinib in Overcoming Kinase Drug Resistance
Article
作者: Weixue Huang ; Ke Ding ; Yupeng Li ; Yang Zhou
Drug resistance remains one of the biggest challenges in kinase inhibitor therapy, particularly in cancers where prolonged treatment fosters the emergence of resistant mutations. These mutations often alter amino acid residues within the kinase active site, reshaping the local chemical environment and disrupting critical drug-target interactions. The resulting changes - such as steric hindrance, loss of key hydrogen bonds, elimination of reactive residues, or other structural incompatibilities - can drastically reduce drug efficacy. To counter these effects, drug molecules must undergo tailored chemical adaptation - strategic modifications that align their molecular features (e.g., geometric shape, stereochemistry, acidity/basicity, and reactivity) with the mutation-altered changes in steric, electronic, and reactivity landscapes within the mutant kinase binding pocket. In this Account, we describe how the principles of chemical adaptation guided our rational design of small molecule kinase inhibitors to overcome clinically relevant resistance. Over the past 18 years, these efforts have culminated in the discovery and approval of two targeted therapies - olverembatinib and limertinib - as well as the advancement of several clinical-stage candidates.Olverembatinib was developed to treat chronic myeloid leukemia patients harboring the gatekeeper Bcr-AblT315I mutation, which confers resistance to first- and second-generation inhibitors. To mitigate steric clashes and restore lost hydrogen bonding, we introduced an alkyne linker to accommodate conformational shifts, and a 1H-pyrazolo[3,4-b]pyridinyl moiety to form new stabilizing hydrogen bonds within the hinge region. For non-small cell lung cancer patients with EGFRT790M-driven resistance, we designed heterocyclic scaffolds bearing electrophilic groups capable of covalently targeting Cys797, enabling high selectivity for EGFR mutants while sparing wild-type EGFR. This approach led to the development of limertinib, a potent and mutant-selective third-generation EGFR inhibitor approved for treating patients with or without EGFRT790M mutations, including those with brain metastases. Building on this success, we are advancing next-generation inhibitors designed to overcome additional resistance mutations such as EGFRL858R/T790M/C797S.In summary, this Account highlights the medicinal chemistry strategies underlying the approvals of olverembatinib and limertinib, illustrating how chemical adaptation can be harnessed to overcome kinase inhibitor resistance. Moving forward, we aim to expand this concept across broader drug modalities and therapeutic targets to address ongoing clinical challenges.
100 项与 利厄替尼 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 | 2025-04-22 | |
| EGFR外显子21替代突变非小细胞肺癌 | 中国 | 2025-04-22 | |
| EGFR-T790M 突变非小细胞肺癌 | 中国 | 2025-01-14 |
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 |
|---|---|---|---|---|
| 局部晚期非小细胞肺癌 | 临床3期 | 中国 | 2026-10-30 | |
| 非鳞状非小细胞肺癌 | 临床3期 | 中国 | 2026-10-30 | |
| EGFR阳性非小细胞肺癌 | 临床3期 | 中国 | 2019-10-30 | |
| EGFR阳性非小细胞肺癌 | 临床3期 | 中国 | 2019-10-30 | |
| EGFR阳性非小细胞肺癌 | 临床3期 | 中国 | 2019-10-30 | |
| 转移性非小细胞肺癌 | 临床3期 | 中国 | 2019-07-23 | |
| 局部晚期恶性实体瘤 | 临床1期 | 中国 | 2022-08-08 | |
| EGFR突变MET阳性非小细胞肺癌 | 临床申请批准 | 中国 | 2026-09-17 | |
| MET基因扩增非小细胞肺癌 | 临床申请批准 | 中国 | 2023-11-20 |
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临床结果
临床结果
适应症
分期
评价
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临床3期 | 337 | 構蓋鹽窪鏇淵觸艱膚製(獵夢鹹餘鬱膚觸衊範糧) = 艱願壓繭夢憲鑰願鏇艱 鹽艱醖餘醖遞鑰築蓋壓 (齋夢鑰壓顧構選遞繭構, 35.9 ~ 48.2) 更多 | 积极 | 2026-03-25 | |||
Gefitinib 250 mg QD | 構蓋鹽窪鏇淵觸艱膚製(獵夢鹹餘鬱膚觸衊範糧) = 鏇觸艱鹽蓋齋膚顧顧齋 鹽艱醖餘醖遞鑰築蓋壓 (齋夢鑰壓顧構選遞繭構, 28.7 ~ 39.3) 更多 | ||||||
临床1期 | EGFR突变MET阳性非小细胞肺癌 EGFR Mutation | MET Overexpression | MET Amplification | 54 | (all doses) | 鹽製獵鬱衊鏇蓋觸襯膚(艱艱壓鑰範膚構淵齋構) = 製觸壓網窪壓夢膚構壓 憲糧鑰鏇製窪積廠簾鹽 (鑰憲繭網築製蓋鹹簾餘 ) 更多 | 积极 | 2025-10-17 | |
(ASKC202 150mg QD + Limertinib 80mg BID) | 鹽製獵鬱衊鏇蓋觸襯膚(艱艱壓鑰範膚構淵齋構) = 範淵遞鏇獵簾構醖壓膚 憲糧鑰鏇製窪積廠簾鹽 (鑰憲繭網築製蓋鹹簾餘 ) | ||||||
临床3期 | 337 | 夢繭鹹積願夢鬱築構製(鏇衊遞觸糧範網構窪壓) = 壓選築構鹹鹽憲糧築鏇 鏇蓋蓋淵壓顧遞憲積窪 (鏇鏇鑰鑰鬱鏇鏇膚選構, 15.2 ~ 22.1) 更多 | 积极 | 2025-06-01 | |||
夢繭鹹積願夢鬱築構製(鏇衊遞觸糧範網構窪壓) = 廠獵餘襯艱襯顧網衊艱 鏇蓋蓋淵壓顧遞憲積窪 (鏇鏇鑰鑰鬱鏇鏇膚選構, 8.3 ~ 11.1) 更多 | |||||||
临床3期 | 337 | 窪齋齋簾顧廠選餘鏇簾(鹹積醖廠壓顧鹽壓顧餘) = 觸醖艱觸積鑰遞築鬱壓 鏇襯鏇獵顧積選廠網鹹 (遞廠蓋艱簾壓遞鏇齋窪 ) 更多 | 积极 | 2025-04-26 | |||
窪齋齋簾顧廠選餘鏇簾(鹹積醖廠壓顧鹽壓顧餘) = 構淵繭夢衊製繭獵醖選 鏇襯鏇獵顧積選廠網鹹 (遞廠蓋艱簾壓遞鏇齋窪 ) 更多 | |||||||
临床2期 | EGFR-T790M 突变非小细胞肺癌 EGFR T790M mutations | 301 | 餘範醖構繭選構鹹艱窪(鹹築築簾憲鹽構積淵壓) = 50.6% 鑰鬱襯鑰顧衊製網衊願 (鹹鹽壓選鹽觸齋艱壓餘 ) 更多 | 积极 | 2025-03-26 | ||
| - | - | 淵獵願淵醖糧壓壓廠醖(願鏇鏇構艱鹽選餘積鏇) = Clinical results have reached the endpoint 範鏇壓糧鬱齋襯網窪壓 (積餘繭網製壓觸糧廠廠 ) | 优效 | 2024-08-13 | |||
临床2期 | EGFR突变的非小细胞肺癌 EGFR T790M Mutation | 301 | 窪糧壓餘鏇獵獵鏇淵憲(鏇艱範蓋淵窪鏇鬱鬱鏇) = 築廠製獵鏇獵築築構襯 積糧顧鬱廠範窪鏇艱淵 (窪廠遞鹽觸範繭糧鹹鬱, 63.2 ~ 74.0) 更多 | 积极 | 2022-06-02 | ||
(CNS metastases) | 窪糧壓餘鏇獵獵鏇淵憲(鏇艱範蓋淵窪鏇鬱鬱鏇) = 窪築鏇廠窪選蓋糧觸醖 積糧顧鬱廠範窪鏇艱淵 (窪廠遞鹽觸範繭糧鹹鬱, 54.4 ~ 74.0) 更多 | ||||||
临床2期 | 301 | 網醖膚餘鹽積糧顧壓構(鹹蓋遞齋網糧憲鏇廠窪) = 膚獵艱選觸製遞築網選 餘壓窪廠糧顧淵鹹廠選 (繭鏇製網膚簾鏇艱憲壓, 39.7% ~ 71.5%) 更多 | 积极 | 2022-06-02 |
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