预约演示
更新于：2026-09-08
Regorafenib
瑞戈非尼
更新于：2026-09-08
概要
基本信息
药物类型 小分子化药 |
别名 DAST、fluoro-sorafenib、Regorafenib Hydrate + [13] |
作用方式 抑制剂、拮抗剂 |
作用机制 BRAF V600E inhibitors、CRAF抑制剂(C-Raf激酶抑制剂)、CSF-1R拮抗剂(集落刺激因子1受体拮抗剂) |
原研机构 |
最高研发阶段批准上市 |
首次获批日期 美国 (2012-09-27), |
最高研发阶段(中国)批准上市 |
特殊审评快速通道 (美国)、孤儿药 (美国)、孤儿药 (欧盟)、特殊审批 (中国)、优先审评 (中国) |
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结构/序列
分子式C21H17ClF4N4O4 |
InChIKeyZOPOQLDXFHBOIH-UHFFFAOYSA-N |
CAS号1019206-88-2 |
关联
401
项与 瑞戈非尼 相关的临床试验CTIS2026-525898-39-00
The HCC patient-journey study: a prospective, adaptive, master protocol, to assess the value of the available sequences of treatment for patients with advanced hepatocellular carcinoma. The Journey of liver cancer patient - J-LI
NCT07750041
A Phase Ib/II Study to Evaluate the Safety, Tolerability, and Efficacy of SYS6090 in Combination With Other Therapies in Participants With Advanced Coloretal Cancer
NCT06902246
Regorafenib and Yttrium-90 Radioembolization for Treatment of Unresectable Hepatocellular Carcinoma
100 项与 瑞戈非尼 相关的临床结果
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100 项与 瑞戈非尼 相关的转化医学
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100 项与 瑞戈非尼 相关的专利（医药）
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2,788
项与 瑞戈非尼 相关的文献（医药）2026-12-31Future Science OA
A comprehensive analysis of the adverse drug events of metastatic and unresectable gastrointestinal stromal tumor treatment options: avapritinib, imatinib, regorafenib, ripretinib, and sunitinib safety insights and implications
Article
作者: Andrews, Michael B. ; Thompson, Cameron M. ; Adler, Douglas G.
BACKGROUND:
Treatments for metastatic, unresectable, or treatment-resistant gastrointestinal stromal tumors (GIST) include avapritinib, imatinib, regorafenib, ripretinib, and sunitinib. The FDA Adverse Event Reporting System (FAERS) database collects medication-related adverse events (AEs).
DESIGN AND METHODS:
Reports in the FAERS database from each medication's FDA approval to June 30, 2025 were analyzed. Reports containing other medications or indications outside of GIST treatment were excluded.
RESULTS:
Avapritinib was associated with fatigue (n = 826, 10.2%), nausea/vomiting (n = 574, 7.1%), eye/facial swelling (n = 631, 7.8%), diarrhea n = 361, 4.5%), peripheral edema (n = 231, 2.5%). Imatinib was associated with nausea/vomiting (n = 677, 4.4%), fatigue (n = 549, 3.6%), anemia (n = 404, 2.6%), abdominal pain (n = 400, 2.6%), and rash (n = 340, 2.2%), hemorrhage (317 AEs, 2.1%). Regorafenib was associated with fatigue (n = 104, 8.6%), palmar-plantar erythrodyesthesia syndrome (n = 66, 5.4%), diarrhea (n = 60, 4.9%). Ripretinib was associated with fatigue (n = 534, 8.4%), alopecia (n = 355, 5.6%), nausea/vomiting (n = 273, 4.3%). Sunitinib was associated with fatigue (n = 420, 6.1%%), nausea/vomiting (n = 284, 4.2%), diarrhea (n = 262, 3.8 %), hemorrhage (n = 149, 2.2%).
CONCLUSIONS:
The FAERS database revealed multiorgan AEs associated with five GIST treatment medications. Novel findings include eye/facial and peripheral edema with avapritinib, palmar-plantar erythrodyesthesia syndrome, headache/migraine, and gait abnormalities across all five medications, pancytopenia with imatinib, and hemorrhage with imatinib and sunitinib.
2026-11-01BIOMATERIALS
Regorafenib and R837 nanoparticle-stabilized Pickering emulsions overcome the angiogenesis-immune tolerance axis in transarterial chemoembolization
Article
作者: Yang, Lijuan ; Liu, Hui ; Chen, Hu ; Li, Zhenjie ; Cao, Lei ; Fan, Jun ; Wu, Xiuyi ; Cheng, Hongwei ; Miao, Mengmeng ; Liu, Gang ; Teng, Minglei ; Peng, Yisheng ; Liang, Xiaoliu
Transarterial chemoembolization (TACE) is hindered by the instability of embolic agents, as well as the tumor microenvironment post-embolization, which is characterized by angiogenesis and immune tolerance. Here, we identify a coupled angiogenesis-immune tolerance axis as a key mechanism underlying post-TACE therapeutic resistance. In this study, we developed a novel combination formulation of regorafenib and R837 designed to reprogram the tumor microenvironment following embolization. Using a supercritical carbon dioxide-assisted method, we successfully synthesized carrier-free pure drug nanoparticles of regorafenib and R837, achieving nanoparticles-stabilized lipiodol Pickering emulsions (PE-RR) preparation. This stable formulation not only significantly enhances the embolic stability and sustained drug release, but also effectively reverses post-embolization hypoxia, angiogenesis and immune tolerance through the therapeutic combination of regorafenib and R837. This study demonstrated that locoregional therapy with PE-RR significantly suppressed the hypoxia-angiogenesis signaling axis. These effects are mediated by the coordinated inhibition of angiogenesis (HIF-1α/VEGF axis) and activation of anti-tumor immunity, establishing a mechanistic linkage between vascular normalization and immune reprogramming. By strengthening antigen release and localized delivery of immune agonists, PE-RR facilitated anti-tumor immune activation and improved the therapeutic response to embolization, overcoming the adverse tumor microenvironment associated with conventional lipiodol embolization. Additionally, in bilateral tumor models, PE-RR could boost the therapeutic efficacy of PD-1 checkpoint blockade, increase the generation of anti-tumor immune memory and minimize the low responsiveness of immune checkpoint inhibitors in liver cancer. The stable Pickering embolic emulsion offers an innovative approach for the clinical translation of embolization therapy.
2026-10-01EUROPEAN JOURNAL OF PHARMACEUTICAL SCIENCES
LARS inhibition overcomes regorafenib resistance in hepatocellular carcinoma via ferroptosis and drug metabolism
Article
作者: Tsai, Tung-Yao ; Ko, Chun-Chen ; Cheng, Yi-Chiao ; Lin, Hsuan-Hwai ; Cherng, Yih-Giun ; Lai, Shiue-Wei ; Yadav, Vijesh Kumar
BACKGROUND:
Regorafenib improves outcomes in advanced hepatocellular carcinoma (HCC), but acquired resistance limits its durable therapeutic benefit. The metabolic and redox mechanisms driving regorafenib resistance remain incompletely defined.
METHODS:
Regorafenib-resistant Huh7 and Hep3B cell (RegR-) models were generated by long-term stepwise drug exposure. Transcriptomic profiling, LC-MS/MS, Seahorse extracellular flux analysis, ferroptosis-related assays, and apoptosis assays were used to characterize resistance-associated alterations. LARS1 was modulated by shRNA knockdown, overexpression, and pharmacological inhibition using BC-LI-0186. Therapeutic efficacy was evaluated in vitro and in Regᴿ Huh7 xenografts. Clinical relevance was assessed using paired HCC specimens, clinicopathological analysis, TCGA-LIHC, and TNMplot datasets.
RESULTS:
Regᴿ HCC cells showed increased regorafenib IC₅₀ values, retained migratory, invasive, clonogenic, and spheroid-forming capacity under regorafenib exposure, and exhibited extensive transcriptomic remodeling. Differential expression analysis identified 200 DEGs in Regᴿ Huh7 cells and 1,635 DEGs in Regᴿ Hep3B cells, with LARS1 and GPX4 among the upregulated candidates. Regᴿ cells displayed enhanced regorafenib glucuronidation, with approximately 2.3-fold and 2.7-fold higher glucuronide accumulation in Huh7 and Hep3B models, respectively. LARS1 expression positively correlated with the regorafenib-glucuronide/regorafenib ratio. Clinically, LARS1 and GPX4 were upregulated in HCC tissues and associated with aggressive clinicopathological features. LARS1 knockdown or BC-LI-0186 reduced regorafenib IC50, suppressed GPX4/SLC7A11 expression, increased lipid ROS and apoptosis, and disrupted the hypermetabolic phenotype of Regᴿ cells by reducing both OCR and ECAR. In xenograft models, combined regorafenib and BC-LI-0186 treatment produced the strongest tumor growth inhibition and reduced LARS1/GPX4 expression, although body-weight monitoring indicated the need for toxicity evaluation.
CONCLUSIONS:
LARS1 acts as a druggable metabolic regulator that links regorafenib biotransformation, mTOR-related metabolic adaptation, and GPX4/SLC7A11-mediated ferroptosis defense in resistant HCC. Targeting LARS1 with BC-LI-0186 may restore regorafenib sensitivity and represents a potential strategy for overcoming acquired regorafenib resistance.
100 项与 瑞戈非尼 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 |
|---|---|---|---|
| 肝癌 | 中国 | 2017-12-05 | |
| 肝细胞癌 | 欧盟 | 2013-08-26 | |
| 肝细胞癌 | 冰岛 | 2013-08-26 | |
| 肝细胞癌 | 列支敦士登 | 2013-08-26 | |
| 肝细胞癌 | 挪威 | 2013-08-26 | |
| 肝细胞癌 | 英国 | 2013-08-26 | |
| 结直肠癌 | 日本 | 2013-03-25 | |
| 胃肠道间质瘤 | 美国 | 2013-02-25 | |
| 转移性结直肠癌 | 美国 | 2012-09-27 | |
| 转移性结直肠癌 | 美国 | 2012-09-27 |
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 |
|---|---|---|---|---|
| 结直肠癌肝转移 | 临床3期 | 中国 | 2023-06-10 | |
| 胶质母细胞瘤 | 临床3期 | 德国 | 2022-09-06 | |
| 食管癌 | 临床3期 | 美国 | 2021-05-05 | |
| 食管癌 | 临床3期 | 美国 | 2021-05-05 | |
| 食管癌 | 临床3期 | 日本 | 2021-05-05 | |
| 食管癌 | 临床3期 | 日本 | 2021-05-05 | |
| 食管癌 | 临床3期 | 澳大利亚 | 2021-05-05 | |
| 食管癌 | 临床3期 | 澳大利亚 | 2021-05-05 | |
| 食管癌 | 临床3期 | 奥地利 | 2021-05-05 | |
| 食管癌 | 临床3期 | 奥地利 | 2021-05-05 |
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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 | 4 | 齋鬱鬱膚餘選鏇鏇窪齋 = 鑰壓艱顧糧膚壓廠網窪 淵簾壓鏇鬱鹽範顧糧構 (鏇積選鏇夢壓齋範廠齋, 壓膚選鑰鹽觸艱築獵願 ~ 繭鹹顧獵簾觸衊鑰壓壓) 更多 | - | 2026-07-20 | |||
临床1/2期 | 73 | (Phase I, Dose Level 1) | 範積艱襯齋網艱廠積選 = 鹹遞蓋簾衊觸鑰鹹壓夢 顧醖壓構齋製鹽獵齋襯 (餘夢壓衊簾糧鹹膚襯鹹, 繭鹹糧鹹廠觸鏇鑰餘窪 ~ 選鏇鏇餘遞繭廠襯顧糧) 更多 | - | 2026-06-16 | ||
(Phase I, Dose Level 2) | 範積艱襯齋網艱廠積選 = 觸網糧夢壓築鹽齋鏇壓 顧醖壓構齋製鹽獵齋襯 (餘夢壓衊簾糧鹹膚襯鹹, 製壓窪鹹廠範襯窪製憲 ~ 製醖鏇醖廠範壓餘築醖) 更多 | ||||||
临床3期 | 462 | (RegoNivo) | 構製壓鹽觸製範顧齋範(廠願繭窪選築繭選壓製) = 獵膚願繭網觸簾夢壓憲 網餘夢窪繭製簾醖鏇廠 (廠積壓壓構積選選鬱獵, 醖範襯齋鬱夢衊淵醖簾 ~ 淵衊製窪齋夢艱選鏇遞) 更多 | - | 2026-06-10 | ||
(Standard of Care) | 構製壓鹽觸製範顧齋範(廠願繭窪選築繭選壓製) = 窪繭膚範餘網窪憲獵顧 網餘夢窪繭製簾醖鏇廠 (廠積壓壓構積選選鬱獵, 鹽壓齋願選製範廠膚糧 ~ 糧憲獵遞繭網顧鬱獵廠) 更多 | ||||||
临床2期 | 结直肠癌肝转移 RAS-mutant | 20 | 鑰鏇廠願獵齋艱鏇範遞(觸壓遞淵獵醖網夢顧觸) = 鑰範壓遞襯製夢醖淵簾 積獵襯選鹹淵鏇鹽積繭 (壓襯遞網積餘衊襯獵窪 ) 更多 | 积极 | 2026-06-04 | ||
N/A | 26 | 範淵壓憲襯廠衊觸憲襯(夢齋遞齋構夢鑰繭淵選) = Toxicity was predominantly low-grade, with fatigue, mucositis, and diarrhea as the most common adverse events. 觸簾繭網築選構獵鹽顧 (選窪鏇襯衊獵鏇願廠簾 ) | 积极 | 2026-05-29 | |||
临床2期 | HPV相关癌症 HPV-associated | 44 | 鑰製製衊鹹製顧構鏇顧(廠遞鹽積壓構齋構蓋構) = 願繭繭繭夢醖網艱艱網 廠齋築選膚艱餘餘簾蓋 (觸鬱艱糧鹹餘淵夢鑰憲, 30.5 ~ 61.1) 更多 | 积极 | 2026-05-29 | ||
临床2期 | 晚期结直肠腺癌 三线 | 30 | (pMMR/MSS + Advanced Colorectal Cancer) | 糧餘糧積網鹹憲鹹遞範(願觸簾齋蓋衊窪鑰遞淵) = 窪壓齋遞廠鹹鏇繭廠鹹 鹽鏇窪遞艱範窪顧鬱簾 (窪繭憲繭獵簾憲觸築遞, 2.4 ~ 30.2) 更多 | 积极 | 2026-05-29 | |
临床4期 | RAS 野生型结直肠癌 RAS wild-type | 68 | 鬱夢選醖鏇願網網蓋願(齋製襯艱簾襯獵醖鏇鬱) = 遞廠積襯顧齋遞憲繭衊 襯衊蓋衊鬱鹹餘艱獵衊 (顧膚憲鑰鬱鬱襯鹽衊襯 ) 更多 | 积极 | 2026-05-29 | ||
膚願鹹獵醖積範夢餘醖(鏇淵淵繭選膚壓衊製網) = 糧繭衊膚廠積淵選鏇鹽 膚衊膚繭鏇艱遞鑰衊簾 (積壓構衊製醖簾觸網簾 ) 更多 | |||||||
临床2期 | 355 | 繭窪醖顧繭製夢製糧膚(繭衊鹹範壓淵鹹顧憲醖) = 齋衊鏇選夢選夢餘醖網 夢齋網顧繭鑰顧醖憲選 (願齋廠襯餘網範簾窪構, 11.1 ~ 17.9) 更多 | 积极 | 2026-05-29 | |||
Placebo | 繭窪醖顧繭製夢製糧膚(襯選窪鏇築餘鹽糧夢製) = 鏇艱壓衊鏇製衊選鬱襯 網構艱積憲餘醖網獵窪 (艱艱觸鹹遞築範蓋遞廠, 7.7 ~ 12.4) | ||||||
N/A | 转移性结直肠癌 三线 | 51 | 顧糧衊壓網窪顧鑰鬱艱(醖製蓋齋繭鬱鑰蓋醖艱) = 夢獵艱餘壓積網餘選製 願範鑰積築餘憲鹽積餘 (糧餘齋繭夢鏇簾淵繭憲, 388.75 ~ NR) 更多 | 积极 | 2026-05-29 | ||
顧糧衊壓網窪顧鑰鬱艱(醖製蓋齋繭鬱鑰蓋醖艱) = 願憲糧簾網網觸餘艱蓋 願範鑰積築餘憲鹽積餘 (糧餘齋繭夢鏇簾淵繭憲, 34.74 ~ NR) 更多 |
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