预约演示
更新于：2025-12-09
Leflunomide
来氟米特
更新于：2025-12-09
概要
基本信息
药物类型 小分子化药 |
别名 5-Methyl-N-(4-(trifluoromethyl)phenyl)-4-isoxazolecarboxamide、5-Methylisoxazole-4-carboxylic acid (4-trifluoromethyl)anilide、alpha,alpha,alpha-Trifluoro-5-methyl-4-isoxazolecarboxy-p-toluidide + [17] |
靶点 |
作用方式 抑制剂 |
作用机制 DHODH抑制剂(双氢乳清酸酯脱氢酶抑制剂) |
原研机构 |
权益机构- |
最高研发阶段批准上市 |
首次获批日期 美国 (1998-09-10), |
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C12H9F3N2O2 |
InChIKeyVHOGYURTWQBHIL-UHFFFAOYSA-N |
CAS号75706-12-6 |
关联
143
项与 来氟米特 相关的临床试验ChiCTR2500112844
Trastuzumab Combined With Chemotherapy and Leflunomide for HER2-Expressing Unresectable Advanced Biliary Tract Malignancies: An Open-Label, Single-Arm, Phase II Study
NCT07138898
Immunosuppressant Management in Rheumatology Patients Undergoing Elective Total Shoulder Arthroplasty
NCT06923488
Phase I/II Study of Leflunomide in Combination With Decitabine for Treatment of Relapsed or Refractory (R/R) Myelodysplastic Syndromes (MDS)
100 项与 来氟米特 相关的临床结果
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100 项与 来氟米特 相关的转化医学
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100 项与 来氟米特 相关的专利（医药）
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3,828
项与 来氟米特 相关的文献（医药）2026-02-01BIOMATERIALS
Mitocytosis-inducing nanoparticles alleviate gemcitabine resistance via dual disruption of pyrimidine synthesis and redox homeostasis in pancreatic ductal adenocarcinoma
Article
作者: Song, Haolin ; Sun, Tao ; Jiang, Chen ; Fan, Hongrui ; Cheng, Leilei ; Chen, Qinjun ; Su, Boyu ; Wang, Yu ; Li, Xuwen
Metabolic reprogramming in pancreatic ductal adenocarcinoma (PDAC) poses a significant challenge to the efficacy of gemcitabine-based chemotherapy. Aberrant activation of intracellular pyrimidine metabolism is a key factor contributing to the reduced effectiveness of gemcitabine. Combining gemcitabine with metabolic regulators targeting critical pathways may alleviate gemcitabine resistance. In this study, we focus on the abnormal activation of dihydroorotate dehydrogenase (DHODH) in PDAC cells, a pivotal enzyme in the de novo pyrimidine synthesis pathway that diminishes cellular sensitivity to gemcitabine and catalyzes the reduction of ubiquinone to ubiquinol, playing an essential role in maintaining cellular redox homeostasis. To address these challenges, we developed GE11 peptide-modified polyphenol-iron chelate nanoparticles for co-delivery the long carbon chain-modified gemcitabine and the DHODH inhibitor leflunomide, with peptide modification enabling nanoparticles to target PDAC cells with high expression of epidermal growth factor receptor. The nanoparticles demonstrated the ability to induce mitocytosis and achieve deep tumor penetration in PDAC tissues. Upon drug release at the core lesion, the three components, modified gemcitabine, leflunomide and iron ions synergistically enhanced tumor cell killing by alleviating gemcitabine resistance and disrupting cellular redox homeostasis to induce multimodal cell death. In an in situ pancreatic cancer mouse model, this strategy exhibited superior anti-tumor efficacy compared to the standard AG chemotherapy regimen (nab-paclitaxel and gemcitabine), even at a 6.3-fold lower gemcitabine concentration. These findings underscore the potential of this approach as a highly effective therapeutic strategy for PDAC treatment.
2025-12-01CLINICAL IMMUNOLOGY
Ferroptosis in patients with rheumatoid arthritis
Review
作者: Lu, Cui ; Shen, Xian ; Dou, Jingjing ; Zheng, Song Guo ; Shao, Han ; Fan, Xiaoli ; Cai, Yunping ; Zhou, Nihong
BACKGROUND:
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and joint destruction. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has recently emerged as a potential contributor to RA pathogenesis.
METHODS:
A systematic literature review was conducted to explore the mechanisms of ferroptosis in RA, focusing on iron metabolism dysregulation, oxidative stress, and immune cell dysfunction. Databases including PubMed, Embase, and Web of Science were searched for relevant studies.
RESULTS:
RA patients exhibit paradoxical iron distribution, with systemic deficiency but synovial overload, promoting ferroptosis. Key findings include: (1) Iron accumulation and lipid peroxidation exacerbate synovial inflammation; (2) Ferroptosis differentially affects immune cells (M1/M2 macrophages, T cells) and fibroblast-like synoviocytes (FLS); (3) Antioxidant defenses (GPX4) are impaired in RA, while some disease-modifying drugs (leflunomide, sulfasalazine) may modulate ferroptosis.
CONCLUSION:
Ferroptosis plays a critical role in RA progression by disrupting synovial homeostasis. Targeting ferroptosis pathways offers promising therapeutic potential, though further research is needed to clarify cell-specific effects and optimize interventions.
2025-12-01CANCER CHEMOTHERAPY AND PHARMACOLOGY
Non-oncologic to oncologic drug: A systematic review of drug repurposing in cancer
Review
作者: Ganesh, Vakkalagadda Siva ; Dhanush, Yarava
PURPOSE:
This systematic review investigates drug repurposing as a strategy to accelerate and improve cancer treatment by specifically examining how existing medications can effectively target the established hallmarks of cancer. The research explores how repurposed drugs can address the challenges of conventional cancer drug development, including high costs, lengthy development timelines, and frequent clinical failures.
METHODS:
The review systematically analyzes repurposed drugs with their ability to target specific cancer hallmarks, including oncogenic signaling pathways, cell death regulation, metabolic reprogramming, growth suppressor reactivation, phenotypic plasticity, antitumor immunity, telomerase activity, angiogenesis, inflammation, cellular senescence, invasion and metastasis, DNA damage response, microbiome modulation, and epigenetic regulation.
RESULTS:
The analysis identified several promising repurposed medications targeting specific cancer hallmarks: artemisinin derivatives for oncogenic signalling, niclosamide for cell death pathways, leflunomide for metabolic dysregulation, statins for tumour suppressor reactivation, metformin for phenotypic plasticity, liothyronine for immune activation, PARP inhibitors for replication, itraconazole for angiogenesis, celecoxib for inflammation, BCL-2 inhibitors for senescence, fluoroquinolones for metastasis, spironolactone for DNA damage, isoliquiritigenin for microbiome modulation, and various agents targeting non-mutational epigenetic regulation.
CONCLUSION:
Drug repurposing represents an intriguing approach for addressing the limitations of traditional cancer drug development while effectively targeting the fundamental hallmarks of cancer. By leveraging existing medications with established safety profiles, this strategy offers potential for more rapid translation to clinical applications and may enhance the therapeutic arsenal against various cancer types.
100 项与 来氟米特 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 |
|---|---|---|---|
| 银屑病关节炎 | 欧盟 | 1999-09-02 | |
| 银屑病关节炎 | 冰岛 | 1999-09-02 | |
| 银屑病关节炎 | 列支敦士登 | 1999-09-02 | |
| 银屑病关节炎 | 挪威 | 1999-09-02 | |
| 类风湿关节炎 | 美国 | 1998-09-10 |
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 |
|---|---|---|---|---|
| 肾移植排斥反应 | 临床2期 | 美国 | 2012-07-01 | |
| 病毒血症 | 临床2期 | 美国 | 2012-07-01 | |
| 系统性红斑狼疮 | 临床2期 | 中国香港 | 2003-01-01 |
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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4期 | 192 | (Standard Care) | 醖憲廠鹹繭積鹹遞鹹遞(鬱簾廠夢糧廠製鑰廠鏇) = 醖構蓋觸衊壓簾鬱網齋 顧壓糧衊齋觸鬱餘簾齋 (蓋廠願繭簾簾網鏇築選, 1.5) 更多 | - | 2025-11-26 | ||
(Combination csDMARD) | 醖憲廠鹹繭積鹹遞鹹遞(鬱簾廠夢糧廠製鑰廠鏇) = 壓獵憲選齋網網艱壓糧 顧壓糧衊齋觸鬱餘簾齋 (蓋廠願繭簾簾網鏇築選, 1.5) 更多 | ||||||
N/A | 100 | 簾壓遞壓衊鑰鹹醖鹽齋(餘夢選衊簾鏇鑰憲餘積) = Frequency of Transaminitis was higher in MTX + LEF group. See Figure 1 for detailed comparison of adverse events between both combinations. 憲願鑰鹽鑰醖鹽鑰繭廠 (襯積淵顧窪選網夢鹽製 ) | 积极 | 2025-06-11 | |||
N/A | 62 | - | 不佳 | 2025-06-11 | |||
選襯鑰製衊構鑰餘齋簾(構壓鏇餘衊艱範築遞選) = 壓廠憲壓築願襯鹹壓艱 壓顧構觸夢鹹鏇鬱廠衊 (鬱遞糧製範鬱獵遞鏇積 ) | |||||||
N/A | 83 | 築壓餘網繭衊糧餘糧憲(醖蓋築構簾憲觸範鏇鬱): P-Value = 0.0001 更多 | 积极 | 2025-06-11 | |||
临床4期 | 32 | Lab Work (DMARD's Responder and Non-Responder) | 夢簾憲顧憲醖網鬱鏇壓(艱夢襯構觸衊艱簾襯築) = 鏇製繭淵獵繭蓋觸顧顧 獵襯襯夢醖鏇衊蓋遞願 (夢壓糧鑰選選憲選選構, 構選顧憲構鹽窪築遞製 ~ 築網築積獵膚壓積餘壓) 更多 | - | 2024-07-10 | ||
Naproxen+Medrol+Hydroxychloroquine+humira+prednisone+Lab Work+Triamcinolone+Methotrexate+Sulfasalazine+CDP870+Leflunomide (DMARD's Plus Cimzia (Certolizumab Pegol)) | 網糧窪艱選鏇簾積夢膚(願鏇齋簾夢淵繭衊醖顧) = 範鹽鏇鏇觸齋鏇網網壓 衊艱選餘襯鹽齋製窪鏇 (淵築衊網繭衊鏇觸顧獵, 0.132) 更多 | ||||||
临床1/2期 | 2 | Best Practice+Leflunomide | 鏇憲繭築構餘壓築艱顧 = 遞選顧艱鬱齋淵鏇製選 觸鹽夢構糧顧膚餘積窪 (觸艱餘築顧膚網艱簾鹽, 選鹽艱襯壓觸襯獵醖網 ~ 鹹鬱顧顧鹽繭鑰願餘簾) 更多 | - | 2024-07-03 | ||
临床1期 | 18 | Leflunomide 20mg | 夢鏇憲鹽鹽鏇壓壓壓憲(憲齋鬱鬱觸鬱顧窪鹽遞) = GI (diarrhea: 27%, nausea/vomiting: 5%, abdominal pain: 5%), cytopenias (anemia: 16%, leukopenia: 11%), hepatic failure (5%), lab abnormalities (AST/ALT increase: 11%, bilirubin increase: 5%), fatigue (11%), and headache (5%). 積鑰積衊蓋醖憲醖餘襯 (餘糧獵鏇憲獵廠餘積繭 ) 更多 | 积极 | 2024-02-01 | ||
临床2期 | 1 | 願襯襯鬱憲醖廠製鏇選 = 壓積餘襯襯範簾鑰鏇艱 壓壓廠夢網獵鹹鏇簾繭 (壓憲淵蓋積窪鑰選繭獵, 繭選簾憲遞醖網糧鏇餘 ~ 襯積網鏇衊積築鬱遞鑰) 更多 | - | 2023-12-05 | |||
临床1/2期 | 12 | Pharmacological Study+Leflunomide (Arm 1: 20 mg Leflunomide) | 觸蓋廠夢廠壓蓋膚獵構 = 壓鬱築艱顧糧築淵夢廠 構鑰壓網淵蓋範膚窪醖 (構窪製遞鹹醖憲淵構壓, 淵廠蓋醖網鹹積糧範鏇 ~ 襯構獵製蓋餘餘齋遞醖) 更多 | - | 2023-10-10 | ||
Pharmacological Study+Leflunomide (Arm 2: 40 mg Leflunomide) | 觸蓋廠夢廠壓蓋膚獵構 = 衊夢鹽鑰網積簾餘衊鏇 構鑰壓網淵蓋範膚窪醖 (構窪製遞鹹醖憲淵構壓, 醖鹽窪蓋淵網鬱鹹製餘 ~ 淵壓餘簾衊鹽艱艱膚積) 更多 | ||||||
临床2期 | 11 | 繭製壓選醖醖顧築膚選(襯廠鏇襯窪獵蓋夢憲壓) = 遞築餘艱鹹觸廠製選艱 範蓋簾顧構醖選壓顧壓 (壓餘築願簾齋窪鹹憲壓 ) 更多 | - | 2023-09-26 |
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