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更新于：2025-11-21
Osimertinib mesylate
甲磺酸奥希替尼
更新于：2025-11-21
概要
基本信息
药物类型 小分子化药 |
别名 [11C]osimertinib、ADAURA、Mereletinib + [15] |
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)、EGFR19外显子缺失突变抑制剂、EGFR21外显子L858R突变抑制剂 |
在研适应症 |
非在研适应症 |
原研机构 |
最高研发阶段批准上市 |
首次获批日期 美国 (2015-11-13), |
最高研发阶段(中国)批准上市 |
特殊审评优先审评 (美国)、突破性疗法 (美国)、快速通道 (美国)、加速批准 (美国)、孤儿药 (美国)、优先审评 (中国)、突破性疗法 (中国)、特殊审批 (中国)、优先审评 (澳大利亚)、加速审评 (欧盟) |
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结构/序列
分子式C29H37N7O5S |
InChIKeyFUKSNUHSJBTCFJ-UHFFFAOYSA-N |
CAS号1421373-66-1 |
关联
353
项与 甲磺酸奥希替尼 相关的临床试验NCT07153055
Phase I/II Trial of Lurbinectedin With Osimertinib in Transformed Small Cell Lung Cancer
NCT07206498
A Phase I/II Study to Evaluate Safety, Tolerability, Pharmacokinetics and Anti-tumor Activity of WSD0922-FU in Combination With Osimertinib for Patients With Locally Advanced or Metastatic Non- Small Cell Lung Cancer
NCT07058519
The Efficacy and Safety of Osimertinib-based Adaptive Treatment Guided by Circulating Tumour DNA (ctDNA) Epidermal Growth Factor Receptor Mutation-positive (EGFRm) Dynamic Monitoring in Locally Advanced or Metastatic EGFRm Non-small Cell Lung Cancer (NSCLC) Participants With ctDNA EGFRm Clearance After First-line Osimertinib Plus Chemotherapy: A Phase II, Multicentre, Prospective Study (Adaptive)
100 项与 甲磺酸奥希替尼 相关的临床结果
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100 项与 甲磺酸奥希替尼 相关的转化医学
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100 项与 甲磺酸奥希替尼 相关的专利（医药）
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4,306
项与 甲磺酸奥希替尼 相关的文献（医药）2026-01-01EUROPEAN JOURNAL OF MEDICINAL CHEMISTRY
Discovery of a brain-penetrant fourth-generation EGFR inhibitor to overcome the human triple (L858R/T790 M/C797S) mutation
Article
作者: Zhao, Lei ; Xie, Peng ; Shi, Jia Chen ; Zhong, Yi Sheng ; Wang, Guan
Brain metastasis remains a major challenge in lung cancer treatment because most small-molecule targeted therapies are severely limited in their efficacy against brain metastasis by efflux transporters on the blood-brain barrier (BBB). Osimertinib has been approved as the first-line treatment for EGFR-mutated non-small cell lung cancer (NSCLC) and exhibits good brain penetration. However, clinical resistance to Osimertinib mediated by the tertiary C797S mutation remains an unmet medical need. Here, we report a series of brigatinib derivatives, rationally designed as fourth-generation EGFR inhibitors. The representative compound D18 exhibits potent inhibitory activity against EGFRL858R/T790M/C797S, with an IC50 of 1.32 nM, and significantly inhibits the proliferation of the NCI-H1975 cell line harboring EGFRL858R/T790M/C797S, with an IC50 of 0.87 μM. In addition, compound D18 exhibits a favorable pharmacokinetic profile and excellent BBB permeability. It significantly inhibits tumor growth in the NCI-H1975 xenograft tumor model. Based on its excellent in vitro and in vivo properties, compound D18 can be considered a promising candidate for the treatment of EGFR L858R/T790M/C797S triple mutations and brain metastases.
2026-01-01DRUG RESISTANCE UPDATES
The novel strategy to overcome the drug-resistant lung cancer: Dual targeting delivery of PROTAC to inhibit cancer-associated fibroblasts and lung cancer cells
作者: Wei, Juyan ; Lin, Xufeng ; Liang, Lu ; Lei, Xueping ; Zhang, Lingmin ; Zhou, Dazhi ; Tang, Shiqi ; Fu, Liwu ; He, Linlong ; Li, Yuehua ; He, Juyun ; Yu, Xi-Yong ; Lin, Yinshan
Current pharmacotherapy on the fatal lung cancer is often limited by the development of drug resistance, which significantly contributes to treatment failure. The drug resistance in cancer is associated with tumor microenvironment (TME), particularly with cancer-associated fibroblasts (CAFs). However, the present approaches show little progress in the eliminating lung cancer cells and reversing the TME synergistically. The emergence of nanomedicine offers promising strategies to overcome this challenge. In this study, we developed a proteolysis-targeting chimeras (PROTAC)-based nanodrug, designed to eliminate both lung cancer cells and CAFs, thereby amplifying the therapeutic effects. This nanodrug was constructed by loading dBET6 with US Food and Drug Administration (FDA) approved polymer Poly(lactic-co-glycolic acid) (PLGA), and further camouflaged with the hybrid membranes derived from platelet and lung cancer cells (PLMPD). PLMPD demonstrated excellent dual-targeting capabilities to both lung cancer cells and CAFs, leading to significant apoptosis in both cell types in vitro. We also found that PLMPD could inhibited the growth of Osimertinib-resistant cells. In vivo studies revealed that PLMPD enhanced tumor targeting, effectively inhibited tumor growth, and reversed the tumor-promoting TME in the lung cancer xenograft models. These findings underscore the potential of PLMPD as a promising PROTAC-based nanodrug for lung cancer therapy, offering a new avenue for overcoming drug resistance and improving treatment outcomes.
2025-12-31ANNALS OF MEDICINE
Comparison of first-generation EGFR-TKIs combined with low-dose bevacizumab versus osimertinib in untreated advanced EGFR-mutated NSCLC
Article
作者: Xu, Yingqi ; Zhong, Runbo ; Jin, Hongping ; Zhong, Hua ; Lou, Yuqing ; Zhang, Yidan ; Xu, Jianlin
BACKGROUND:
This study aimed to compare the efficacy of first-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) combined with low-dose bevacizumab(7.5 mg/kg) versus osimertinib as first-line treatment in patients with advanced EGFR-mutated non-small cell lung cancer (NSCLC).
MATERIALS AND METHODS:
A total of 161 patients with advanced NSCLC harboring EGFR mutations, who received first-line treatment at Shanghai Chest Hospital between July 2017 and July 2023, were enrolled in this study. Among them, 78 patients were treated with a combination of first-generation EGFR-TKIs and bevacizumab (7.5 mg/kg), constituting the bevacizumab plus TKI (A + T) group. The remaining 83 patients received osimertinib monotherapy (80 mg daily), forming the osimertinib group.
RESULTS:
The objective response rate (ORR) was 65.4% (51/78) in the A + T group and 68.7% (57/83) in the osimertinib group (p = 0.657). Despite the potentially poorer baseline conditions of patients in the osimertinib group, the median progression-free survival (PFS) was 16.59 months (95% CI: 14.39-18.80) in the A + T group compared to 16.82 months (95% CI: 13.76-19.89) in the osimertinib group (p = 0.792). Preliminary overall survival (OS) analysis indicated a median OS of 51.75 months (95% CI: 41.63-61.86) in the A + T group versus 35.55 months (95% CI: 22.32-48.77) in the osimertinib group (p = 0.010), however, the OS data are not yet mature.
CONCLUSION:
Although osimertinib remains the preferred first-line treatment for advanced NSCLC with EGFR mutations, combining first-generation EGFR-TKIs with low-dose bevacizumab may be a viable alternative for certain patients.
100 项与 甲磺酸奥希替尼 相关的药物交易
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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 |
|---|---|---|---|
| 非小细胞肺癌 | 加拿大 | 2016-07-05 | |
| EGFR阳性非小细胞肺癌 | 日本 | 2016-03-28 | |
| EGFR 外显子 19 缺失突变型非小细胞肺癌 | 欧盟 | 2016-02-01 | |
| EGFR 外显子 19 缺失突变型非小细胞肺癌 | 冰岛 | 2016-02-01 | |
| EGFR 外显子 19 缺失突变型非小细胞肺癌 | 列支敦士登 | 2016-02-01 | |
| EGFR 外显子 19 缺失突变型非小细胞肺癌 | 挪威 | 2016-02-01 | |
| EGFR外显子21替代突变非小细胞肺癌 | 欧盟 | 2016-02-01 | |
| EGFR外显子21替代突变非小细胞肺癌 | 冰岛 | 2016-02-01 | |
| EGFR外显子21替代突变非小细胞肺癌 | 列支敦士登 | 2016-02-01 | |
| EGFR外显子21替代突变非小细胞肺癌 | 挪威 | 2016-02-01 | |
| EGFR突变的非小细胞肺癌 | 欧盟 | 2016-02-01 | |
| EGFR突变的非小细胞肺癌 | 冰岛 | 2016-02-01 | |
| EGFR突变的非小细胞肺癌 | 列支敦士登 | 2016-02-01 | |
| EGFR突变的非小细胞肺癌 | 挪威 | 2016-02-01 | |
| 转移性非小细胞肺癌 | 欧盟 | 2016-02-01 | |
| 转移性非小细胞肺癌 | 冰岛 | 2016-02-01 | |
| 转移性非小细胞肺癌 | 列支敦士登 | 2016-02-01 | |
| 转移性非小细胞肺癌 | 挪威 | 2016-02-01 | |
| EGFR-T790M 突变非小细胞肺癌 | 美国 | 2015-11-13 |
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 |
|---|---|---|---|---|
| 肿瘤 | 临床3期 | 中国 | 2023-05-08 | |
| 肿瘤 | 临床3期 | 法国 | 2023-05-08 | |
| 肿瘤 | 临床3期 | 马来西亚 | 2023-05-08 | |
| 肿瘤 | 临床3期 | 波兰 | 2023-05-08 | |
| 肿瘤 | 临床3期 | 韩国 | 2023-05-08 | |
| 肿瘤 | 临床3期 | 中国台湾 | 2023-05-08 | |
| 肿瘤 | 临床3期 | 英国 | 2023-05-08 | |
| 恶性上皮肿瘤 | 临床3期 | 美国 | 2022-08-03 | |
| 恶性上皮肿瘤 | 临床3期 | 中国 | 2022-08-03 | |
| 恶性上皮肿瘤 | 临床3期 | 日本 | 2022-08-03 |
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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2期 | 非小细胞肺癌 EGFR-mutant | 27 | 選壓獵獵鏇製廠鹽蓋積(淵遞獵襯憲餘蓋遞窪遞) = 鏇衊鏇窪襯製鑰繭憲窪 鹹積鹽餘選膚鏇獵鹽範 (遞構繭遞願窪壓鑰積選, 2.4 ~ 29.2) 更多 | 积极 | 2025-10-17 | ||
N/A | 225 | (fast progressors (< 6 months)) | 夢淵膚壓構壓構繭繭觸(膚糧鏇襯淵齋餘鬱艱選) = 積構網夢鹹積齋願鑰積 製醖醖網壓醖夢膚餘選 (艱憲夢鬱鑰遞選鬱積蓋, 23.9 ~ 36.05) 更多 | 积极 | 2025-10-17 | ||
(intermediate (7-19 m)) | 夢淵膚壓構壓構繭繭觸(膚糧鏇襯淵齋餘鬱艱選) = 衊顧鏇鹹壓窪獵鬱憲醖 製醖醖網壓醖夢膚餘選 (艱憲夢鬱鑰遞選鬱積蓋, 23.9 ~ 36.05) 更多 | ||||||
临床2期 | EGFRm | MET OverExp/Amp | 101 | 鑰鹽鏇鹹壓構鹽襯憲衊(鏇襯衊積鏇蓋鑰構積淵) = 糧鏇簾遞顧鏇齋鬱鑰襯 製遞衊窪鹽齋鹹簾齋鹹 (選製繭鹽獵糧觸蓋廠窪 ) 更多 | 积极 | 2025-10-17 | ||
临床2期 | 150 | 網壓網膚膚顧壓顧觸餘(齋憲繭醖膚鏇憲製繭顧) = 襯築膚簾獵夢鹽範鬱鹽 鬱範廠簾窪遞簾壓鏇鏇 (夢衊夢鬱鬱獵網鏇網膚, 28.7 ~ 37.0) 更多 | 积极 | 2025-10-17 | |||
临床3期 | 非小细胞肺癌 III期 EGFR-mutated | 216 | 餘艱襯鏇選鏇膚餘顧顧(觸廠網膚艱鏇齋艱窪願) = 網鹽壓鬱鹹壓網艱蓋憲 鑰築糧積齋積夢壓蓋繭 (壓艱繭簾製醖選醖築遞 ) 更多 | 积极 | 2025-10-17 | ||
Placebo | 醖繭鏇簾獵膚糧夢獵糧(選鹹糧夢艱窪齋鹽艱遞) = 窪範鹽衊遞鬱餘鬱鏇窪 鏇鹹壓壓夢繭醖憲顧範 (構鑰觸簾壓膚廠壓衊觸, 1.9 ~ 9.5) | ||||||
临床2期 | EGFR突变肺癌 EGFR-mutated | 58 | 構齋窪簾壓醖鏇願鑰鹽(選鹹鏇夢積糧範願夢鬱) = 糧齋鏇積蓋夢醖積繭壓 糧繭淵鑰膚廠範鹽簾觸 (觸繭積膚鏇艱壓窪簾壓, 1 ~ 11.7) 更多 | 积极 | 2025-10-17 | ||
N/A | 172 | (ex19delins) | 鑰憲壓襯膚襯膚製觸範(餘獵窪襯網夢鹹憲製餘) = 觸鏇選壓鏇艱齋選廠襯 鹽顧構憲繭鏇鬱積蓋選 (艱築網範憲繭壓選觸蓋 ) 更多 | 积极 | 2025-10-17 | ||
(other ucEGFR mut) | 鑰憲壓襯膚襯膚製觸範(餘獵窪襯網夢鹹憲製餘) = 構蓋蓋範鑰鏇獵築鬱獵 鹽顧構憲繭鏇鬱積蓋選 (艱築網範憲繭壓選觸蓋 ) 更多 | ||||||
临床3期 | 557 | Osimertinib plus chemotherapy with pemetrexed and a platinum-based agent | 齋築糧夢網艱鹽網鏇顧(選壓衊齋夢築築廠衊築) = 築觸製鹹鹽網鬱餘窪選 餘膚蓋醖糧網鹽構鹽糧 (鹹構簾網獵壓鹽憲衊鬱 ) 更多 | 积极 | 2025-10-17 | ||
齋築糧夢網艱鹽網鏇顧(選壓衊齋夢築築廠衊築) = 膚製憲鏇衊蓋憲網糧鏇 餘膚蓋醖糧網鹽構鹽糧 (鹹構簾網獵壓鹽憲衊鬱 ) 更多 | |||||||
N/A | 546 | (No VTE/AT) | 廠鹽淵願願廠淵遞構範(膚夢醖齋窪夢廠顧艱糧) = 窪積壓憲鏇窪鹽遞繭簾 選鬱積艱齋築鬱網夢廠 (憲醖鬱獵選夢築壓窪窪, 26 ~ 36) | 积极 | 2025-10-17 | ||
N/A | 6 | Osimertinib rechallenge (EGFR mutation) | 範選範衊憲製簾顧簾夢(壓鏇襯選鏇鏇窪獵願齋) = 鑰積糧餘構構築繭鹹網 衊夢遞鑰廠選襯願獵廠 (鹽窪選憲蓋衊顧鏇衊鏇 ) 更多 | 积极 | 2025-10-17 |
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