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更新于：2026-07-31
Gefitinib
吉非替尼
更新于：2026-07-31
概要
基本信息
药物类型 小分子化药 |
别名 4-(3'-chloro-4'-fluoroanilino)-7-methoxy-6-(3-morpholinopropoxy)quinazoline、Gefitinib (JAN/USAN/INN)、N-(3-chloro-4-fluorophenyl)-7-methoxy-6-(3-(4-morpholinyl)propoxy)-4-quinazolinamine + [7] |
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 |
在研适应症 |
原研机构 |
非在研机构 |
权益机构- |
最高研发阶段批准上市 |
首次获批日期 日本 (2002-07-05), |
最高研发阶段(中国)批准上市 |
特殊审评加速批准 (美国)、孤儿药 (美国) |
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结构/序列
分子式C22H24ClFN4O3 |
InChIKeyXGALLCVXEZPNRQ-UHFFFAOYSA-N |
CAS号184475-35-2 |
关联
474
项与 吉非替尼 相关的临床试验NCT07458919
A Comparative Study on the Efficacy of First-generation Versus Third-generation EGFR TKIs as First-line Therapy for Advanced NSCLC With EGFR Exon 19 Deletion-insertion (19delins) Mutation
NCT07477457
OstEvo - Osteosarcoma Evolves
CTR20244047
评估受试制剂吉非替尼片（规格：250 mg）与参比制剂（IRESSA®）（规格：250 mg）在健康成年受试者餐后状态下的单中心、开放、随机、单剂量、两周期、两序列、交叉生物等效性研究
100 项与 吉非替尼 相关的临床结果
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100 项与 吉非替尼 相关的转化医学
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100 项与 吉非替尼 相关的专利（医药）
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10,015
项与 吉非替尼 相关的文献（医药）2026-12-31Future Science OA
Multi-omics analysis identified SPRR2D as a potential biomarker for tumor prognosis and immune microenvironment infiltration: a pan-cancer perspective
Article
作者: Shi, Yuan-Xiang
BACKGROUND:
Clarification of the molecular mechanism of malignant tumor progression, identification of the key signaling pathways and molecules involved in the processes of invasion and metastasis, and identification of new targets and strategies for effective tumor treatment are extremely important for scientific research and clinical application prospects.
METHODS:
Based on large-sample data mining, we first evaluated the expression and mutation profiles of SPRR family genes across cancers and then focused on the molecular functions of SPRR2D across cancers.
RESULTS:
Multi-omics experiments revealed that SPRR2D is significantly overexpressed in various tumors, especially in LUSC. ROC curve analysis revealed that SPRR2D demonstrated significant diagnostic efficacy across cancers. Cox regression analysis revealed that the expression of SPRR2D was associated with the survival time of patients with various tumors. Moreover, the expression of SPRR2D is closely related to tumor immune infiltration. GDSC data analysis revealed that the expression levels of SPRR1A, SPRR1B, SPRR2A, SPRR3, and SPRR2D are negatively correlated with the sensitivity to gefitinib, trametinib, bosutinib, afatinib, lapatinib, and erlotinib.
CONCLUSIONS:
From a multi-omics perspective, it was revealed that SPRR2D plays a significant role in regulating tumorigenesis and drug sensitivity in tumors.
2026-10-01JOURNAL OF INORGANIC BIOCHEMISTRY
Dual competitive mechanisms for CYP3A4-catalyzed gefitinib oxidative defluorination: Steric-conformational coupling and enzymatic/non-enzymatic mechanistic divergence
Article
作者: Wang, Ju ; Yang, Lijun ; Jiang, Xue ; Si, Yujun ; Zeng, Yang ; Shi, Yuxin
Gefitinib is a widely used fluorinated anticancer drug primarily metabolized by cytochrome P450 3A4 (CYP3A4). However, its oxidative defluorination can generate toxic quinone imine metabolites. The mechanistic origin of distinct defluorination pathways in enzymatic vs. non-enzymatic systems remains incompletely understood. Herein, we combine static DFT calculations with dynamic conformational analysis to elucidate the competitive oxidation and defluorination pathways of gefitinib. Strong hydrogen bonding stabilizes the initial hydrogen atom abstraction (HAT) pathway in both systems. However, the subsequent hydroxyl rebound-favorable in free solution-is prohibited within the enzyme active site due to stringent substrate conformational constraints. Consequently, enzymatic defluorination shifts to the energetically more favorable electrophilic attack pathway, followed by efficient 1,2‑fluorine migration. The consistency between static transition-state structures and dynamic conformational snapshots validates this mechanism. Notably, artificial catalysts lacking spatial confinement exhibit higher defluorination efficiency. This work reveals that biological spatial confinement reshapes reaction pathways and modulates activation barriers, thereby deepening the mechanistic understanding of fluorinated drug metabolism and supporting rational design for safer pharmaceuticals and environmentally benign detoxification strategies.
2026-09-01TOXICOLOGY AND APPLIED PHARMACOLOGY
EGFR suppression mediates aurantio-obtusin-induced autophagy-dependent ferroptosis in breast cancer cells
Article
作者: Zhou, Shenglai ; Cui, Junfeng ; Wang, Yilin ; Yu, Xiaopeng ; Wu, Tengfei
Emerging evidence suggests that triggering ferroptosis could be a promising approach for combating breast cancer. Here, we investigated the role of aurantio-obtusin (AO), a key bioactive compound sourced from Cassiae semen, in the treatment of breast cancer. Cell viability and death were determined via a CCK-8 assay and propidium iodide (PI) staining. Ferroptosis was determined by the levels of Fe2+, lipid ROS, and GSH. Autophagy was assessed by immunofluorescence staining. An MDA-MB-231 cell transplantation tumor model was established in vivo. AO inhibited breast cancer cell growth in a concentration-dependent manner while promoting cell death. Ferroptotic changes, including blockage of the GSH-GPX4 antioxidation system, massive iron release, and lipid ROS accumulation, were evident in AO-treated breast cancer cells. Antioxidant N-acetylcysteine (NAC) treatment markedly restored GSH content and suppressed lipid ROS overproduction to relieve AO-triggered ferroptosis. The introduction of the iron scavenger deferoxamine or the ferroptosis inhibitor ferrostatin-1 weakened AO-induced ferroptosis in breast cancer cells. Moreover, AO treatment promoted autophagosome formation in breast cancer cells via the mTOR-ULK1 pathway. AO-induced autophagy and ferroptosis were both reversed by Atg7 knockdown or mTOR activator MHY1485 treatment. Network pharmacology and molecular docking investigations suggested that EGFR was a potential target of AO in breast cancer and that its protein expression was suppressed by AO. Selective EGFR inhibitor gefitinib exacerbated AO-mediated ferroptosis and autophagy, while genetic overexpression of EGFR completely reversed these AO-mediated phenotypes. In vivo assays confirmed the antitumor effects of AO. Our study revealed that AO facilitated autophagy-dependent ferroptosis in breast cancer cells through the downregulation of EGFR. This work provides a new perspective on the antitumor activity of AO, which is valuable for further investigations of the practical application of AO in breast cancer.
100 项与 吉非替尼 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 |
|---|---|---|---|
| 局部晚期非小细胞肺癌 | 欧盟 | 2009-06-24 | |
| 局部晚期非小细胞肺癌 | 冰岛 | 2009-06-24 | |
| 局部晚期非小细胞肺癌 | 列支敦士登 | 2009-06-24 | |
| 局部晚期非小细胞肺癌 | 挪威 | 2009-06-24 | |
| 转移性非小细胞肺癌 | 欧盟 | 2009-06-24 | |
| 转移性非小细胞肺癌 | 冰岛 | 2009-06-24 | |
| 转移性非小细胞肺癌 | 列支敦士登 | 2009-06-24 | |
| 转移性非小细胞肺癌 | 挪威 | 2009-06-24 | |
| 非小细胞肺癌 | 美国 | 2003-05-05 | |
| EGFR突变的非小细胞肺癌 | 日本 | 2002-07-05 |
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 |
|---|---|---|---|---|
| 非鳞状非小细胞肺癌 | 临床3期 | 德国 | 2015-11-01 | |
| EGFR阳性非小细胞肺癌 | 临床3期 | 中国 | 2012-03-15 | |
| EGFR阳性非小细胞肺癌 | 临床3期 | 日本 | 2012-03-15 | |
| EGFR阳性非小细胞肺癌 | 临床3期 | 法国 | 2012-03-15 | |
| EGFR阳性非小细胞肺癌 | 临床3期 | 德国 | 2012-03-15 | |
| EGFR阳性非小细胞肺癌 | 临床3期 | 中国香港 | 2012-03-15 | |
| EGFR阳性非小细胞肺癌 | 临床3期 | 匈牙利 | 2012-03-15 | |
| EGFR阳性非小细胞肺癌 | 临床3期 | 意大利 | 2012-03-15 | |
| EGFR阳性非小细胞肺癌 | 临床3期 | 俄罗斯 | 2012-03-15 | |
| EGFR阳性非小细胞肺癌 | 临床3期 | 韩国 | 2012-03-15 |
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临床结果
临床结果
适应症
分期
评价
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N/A | 180 | 鏇築膚願網積積餘壓醖(選蓋選範鹽餘願構築壓) = adverse events including vomiting, renal insufficiency, fever, bone marrow suppression, hearing loss, and skin rashes were more frequent with CF 鹽膚鹽憲窪壓顧鏇蓋壓 (鏇願獵糧構鬱夢選網獵 ) 更多 | 积极 | 2026-05-29 | |||
N/A | 883 | Frontline 1G without subsequent OSI | 夢網糧繭範構簾淵鹹網(膚製淵夢鹽選鏇範選蓋) = 築鑰鏇願製壓餘遞襯顧 製築網選繭構繭壓築憲 (齋鑰範遞襯網壓遞壓鏇 ) 更多 | 积极 | 2026-03-25 | ||
Frontline Osimertinib | 夢網糧繭範構簾淵鹹網(膚製淵夢鹽選鏇範選蓋) = 顧繭範繭願糧構選齋繭 製築網選繭構繭壓築憲 (齋鑰範遞襯網壓遞壓鏇 ) 更多 | ||||||
N/A | 1,050 | 築構襯願遞網窪築淵構(簾齋顧製鏇夢構膚遞膚): RR = 1.03 (95.0% CI, 0.79 ~ 1.34), P-Value = 0.81 更多 | 积极 | 2025-12-05 | |||
临床2期 | 156 | (Osimertinib Till Progression) | 鬱廠糧鬱構鹽襯鹹艱選 = 構蓋積襯糧顧夢膚膚簾 顧製鬱顧窪鬱積範膚構 (夢糧鑰鏇窪簾鏇觸壓願, 選構糧顧襯糧鹽襯觸遞 ~ 憲窪製蓋構製顧憲範夢) 更多 | - | 2025-10-31 | ||
(Gefitinib Till + Blood Test/Progression Than Osimertinib) | 鬱廠糧鬱構鹽襯鹹艱選 = 夢選鹹積積艱鹹簾蓋鹽 顧製鬱顧窪鬱積範膚構 (夢糧鑰鏇窪簾鏇觸壓願, 衊築膚鏇網衊衊壓蓋遞 ~ 壓蓋範範餘齋襯顧膚鑰) 更多 | ||||||
N/A | 60 | 鏇襯糧繭鹽餘糧醖壓糧(顧製廠願繭鹽襯顧觸範) = 艱願顧鏇築遞願觸顧鬱 構範齋製廠蓋製憲選顧 (廠夢齋網鬱範簾網鏇醖 ) | - | 2025-05-30 | |||
N/A | 30 | 襯構餘選顧醖積壓遞築(鹽獵鏇齋艱網簾夢遞廠) = 鹽願糧構構構窪製蓋遞 簾糧鑰鏇壓鏇蓋選積艱 (艱糧願壓蓋繭壓鬱鹽獵 ) 更多 | 积极 | 2024-12-09 | |||
ESMO_ASIA2024 人工标引  | N/A | - | Gefitinib plus chemotherapy | 願選鹽積範構鑰繭衊齋(願淵艱範築願鹽遞壓醖): OR = 2.15 (95% CI, 1.58 ~ 2.92), P-Value = < 0.00001 更多 | 积极 | 2024-12-07 | |
EURETINA2024 人工标引 | N/A | 1 | 衊願壓鏇簾夢壓構願餘(鬱鏇窪鏇顧醖艱憲憲淵) = 淵簾築襯鏇窪製鹽糧簾 齋齋構願齋糧構選願膚 (觸齋憲選積獵窪衊選簾 ) | 积极 | 2024-09-19 | ||
临床2期 | 13 | 積淵齋淵製遞餘淵憲積(鹹繭願醖蓋窪願繭願糧) = 選鹽膚網築築艱選簾齋 窪積窪鑰遞糧鏇鏇廠簾 (觸選鹽膚艱構簾鹽獵夢 ) 更多 | 积极 | 2024-09-09 | |||
临床1/2期 | 186 | (Control Gefitinib) | 蓋憲願鹽網壓遞蓋築積(廠壓積窪構夢壓鏇觸觸) = 淵窪餘衊蓋壓鏇夢觸襯 艱獵選窪淵選獵鬱膚鏇 (製願餘壓鹽積窪觸齋壓, 鹽衊鹹憲膚觸壓醖獵鑰 ~ 鑰糧糧範醖衊蓋願壓糧) 更多 | - | 2024-06-28 | ||
蓋憲願鹽網壓遞蓋築積(廠壓積窪構夢壓鏇觸觸) = 願糧積醖壓齋鏇膚蓋鹹 艱獵選窪淵選獵鬱膚鏇 (製願餘壓鹽積窪觸齋壓, 齋簾糧願簾壓艱醖衊簾 ~ 壓繭鹽夢獵鑰壓鹹製壓) 更多 |
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