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更新于：2025-07-15
Fenofibrate
非诺贝特
更新于：2025-07-15
概要
基本信息
简介非诺贝特是一种小分子药物，具有靶向过氧化物酶体增殖物激活受体α (PPARα) 作为激动剂的独特能力。自 1974 年 11 月法国著名制药企业 Fournier Pharma SA 首次批准该药物以来，该药物已广泛用于治疗血液中的高胆固醇和甘油三酯水平。非诺贝特通过调用 PPARα 发挥作用，PPARα 熟练地调节脂质代谢，最终大幅减少肝脏内胆固醇和甘油三酯的产生。这种强效药物有多种剂型，从胶囊到片剂，通常口服。尽管非诺贝特具有悠久的历史，但它仍然是一种非常有效的治疗选择，可以满足全世界患有血脂异常和相关疾病的患者的需求，因此继续被医疗保健提供者开具处方。 |
药物类型 小分子化药 |
别名 2-(4-(4-Chlorobenzoyl)phenoxy)-2-methylpropanoic acid 1-methylethyl ester、Fenofibrate (JAN/USP/INN)、Finofibrate + [28] |
靶点 |
作用方式 激动剂 |
作用机制 PPARα激动剂(过氧化物酶体增长因子活化受体α激动剂) |
非在研适应症 |
最高研发阶段批准上市 |
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C20H21ClO4 |
InChIKeyYMTINGFKWWXKFG-UHFFFAOYSA-N |
CAS号49562-28-9 |
关联
246
项与 非诺贝特 相关的临床试验NCT07025005
Clinical Study to Evaluate the Possible Role of Fenofibrate in the Prophylaxis From Peripheral Neuropathy Induced by Bortezomib, Lenalidomide and Dexamethasone Protocol in the Treatment of Patients With Multiple Myeloma
NCT06905054
Peroxisome Proliferator-Activated Receptor Agonists to Prevent Primary Sclerosing Cholangitis Recurrence After Liver Transplantation
NCT06858332
Lipoprotein(a) Levels in Patients With Atherosclerotic Cardiovascular Diseases in Russia
100 项与 非诺贝特 相关的临床结果
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100 项与 非诺贝特 相关的转化医学
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100 项与 非诺贝特 相关的专利（医药）
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7,159
项与 非诺贝特 相关的文献（医药）2025-10-01Ocular Surface
Fenofibrate ameliorates ocular surface inflammation in diabetic keratopathy
Article
作者: Lam, Thomas Chuen ; Tan, Hong Chang ; Liu, Yu-Chi ; Liu, Fengyi ; Toh, Charmaine Jan Li ; Zhou, Lei ; Mansoor, Hassan ; Lee, Isabelle Xin Yu ; Liu, Chang ; Yu, Mingyi ; Hsu, Victor Wei-Tsu ; Lu, Daqian
PURPOSE:
To investigate the efficacy of oral fenofibrate in the amelioration of ocular surface inflammation in diabetes mellitus (DM).
METHODS:
In this open-label interventional study, 41 participants with type 2 DM received oral fenofibrate for 30 days. Forty age-matched healthy controls were recruited. Ocular surface objective and subjective assessment, in-vivo confocal microscopy (IVCM) imaging and quantification for corneal dendritic cells (DCs), epithelium and neuromas were performed. Tear inflammatory markers and proteomics were analyzed with enzyme-linked immunosorbent assay (ELISA) and Data Independent Acquisition experiments before and after treatment.
RESULTS:
Oral fenofibrate treatment significantly improved tear film breakup time (p = 0.004), corneal staining evaluated with National Eye Institute-Corneal Fluorescein Staining scores (p = 0.005), and ocular surface symptoms assessed with the Ocular Surface Disease Index scores (p = 0.003), in DM patients. On IVCM, fenofibrate significantly reduced mean DC area (p = 0.01) and mean DC density (p = 0.02), while increasing mean DC elongation (p = 0.004) and length (p = 0.01), suggesting less DC activities. Fenofibrate also significantly increased corneal epithelial cell density (p = 0.04). 192 tear proteins were significantly altered after treatment. Fenofibrate significantly up-regulated the expression of anti-inflammatory interleukin-1 receptor antagonist, while significantly reduced the concentrations of pro-inflammatory and inflammatory proteins, including tumour necrosis factor α, nuclear factor kappa B, complement 4 B, cytochrome B5 Type A, and cytochrome B5 Type B (all p < 0.05) in tears, via regulation of tricarboxylic acid cycle, oxidative phosphorylation and liver X receptor/retinoid X receptor activation.
CONCLUSION:
This first clinical trial demonstrated that oral fenofibrate ameliorates diabetic ocular surface inflammation, providing a novel therapeutic option for diabetic keratopathy.
2025-09-01ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
PPARα activation attenuated heat-induced myocardial injury in mice
Article
作者: Qin, Li ; Li, Ran ; Zhang, Lu ; Zhao, Lisha ; Hu, Zhoufan ; Ma, Xiaowen ; Liu, Cuiqing ; Hou, Tong ; Zhang, Guoqing
With climate change and global warming, extreme heatwaves occurred with more intense and higher frequency, significantly increasing the mortality rate associated with cardiovascular diseases. Using a mouse model of heat stress, the study aimed to clarify the adverse effects on heart, elucidate the underlying mechanism and explore the potential preventative strategies. Firstly, heat stress induced significant myocardial injury, which was further exacerbated even after termination of heat exposure. Next, PPARα (Peroxisome Proliferator-Activated Receptor Alpha) was screened and its downregulation in response to heat stress was confirmed at mRNA and protein levels. Then, pre-treatment with PPARα agonist fenofibrate significantly mitigated myocardial injury, accompanied with improved mitochondrial function in the myocardial tissues. In addition, PPARα activation may restore the mitochondrial homeostasis through enhancement of both antioxidation and mitophagy. These findings will highlight the pivotal role of PPARα in alleviating heat-induced myocardial injury and cardiovascular incidence, providing valuable target for drug development to prevent/treat heat stress-related diseases.
2025-08-01FREE RADICAL BIOLOGY AND MEDICINE
Fenofibrate inhibits activation of cGAS-STING pathway by alleviating mitochondrial damage to attenuate inflammatory response in diabetic dry eye
Article
作者: Li, Yansheng ; Li, Yuanbin ; Li, Xiaoxia ; Sun, Xiaowei ; Zhao, Xinmei ; Sun, Xia ; Zhang, Jingyi
The cyclic GMP-AMP synthase (cGAS) and Stimulator of Interferon Genes (STING) signaling pathway are critical regulators of inflammation. This study aims to investigate the role of the cGAS-STING signaling pathway in diabetic dry eye (DDE) disease and further explore the therapeutic efficacy and underlying mechanism of fenofibrate in DDE. Using single-cell RNA sequencing (scRNA-Seq) data from the Gene Expression Omnibus (GEO) database, combined with the STZ-induced DDE mouse model and high-glucose conditions in immortalized human corneal epithelial cells (HCE-T), we observed mitochondrial damage and significantly elevated cytoplasmic mitochondrial DNA (mtDNA) in the diabetic cornea, and identified that the cGAS-STING signaling pathway plays a pivotal role in the pathogenesis of DDE. Notably, we found that the inhibitor H151 reversed the ocular surface inflammatory response via the cGAS-STING pathway. Further investigation revealed that fenofibrate alleviated corneal inflammatory response by reducing the production of reactive oxygen species (ROS), restoring mitochondrial membrane potential (MMP), decreasing mtDNA cytoplasmic leakage, and subsequently suppressing the activation of the cGAS-STING signaling pathway. In conclusion, this study highlights the crucial role of the cGAS-STING signaling pathway in DDE and proposes that fenofibrate alleviates mitochondrial damage to inhibit this pathway, offering novel strategy for the treatment of DDE.
100 项与 非诺贝特 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 |
|---|---|---|---|
| 家族性混合型高脂血症 | 美国 | 2007-08-10 | |
| 脂蛋白脂肪酶循环抑制剂所致家族性乳糜微粒血症 | 美国 | 2001-09-04 | |
| 先天性畸形 | 美国 | 2001-09-04 | |
| 冠状动脉疾病 | 美国 | 2001-09-04 | |
| 糖尿病 | 美国 | 2001-09-04 | |
| 血脂障碍 | 美国 | 2001-09-04 | |
| 高脂血症 | 美国 | 2001-09-04 | |
| I型高脂蛋白血症 | 美国 | 2001-09-04 | |
| IV型高脂蛋白血症 | 美国 | 2001-09-04 | |
| 高脂蛋白血症 | 美国 | 2001-09-04 | |
| 甲状腺功能减退症 | 美国 | 2001-09-04 | |
| 胰腺炎 | 美国 | 2001-09-04 | |
| 原发性高胆固醇血症 | 美国 | 2001-09-04 | |
| 高胆固醇血症 | 法国 | 1974-11-04 | |
| 高甘油三酯血症 | 法国 | 1974-11-04 |
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 |
|---|---|---|---|---|
| 1型糖尿病 | 临床3期 | 澳大利亚 | 2016-11-03 | |
| 1型糖尿病 | 临床3期 | 中国香港 | 2016-11-03 | |
| 1型糖尿病 | 临床3期 | 新西兰 | 2016-11-03 | |
| 1型糖尿病 | 临床3期 | 英国 | 2016-11-03 | |
| 糖尿病肾病 | 临床3期 | 澳大利亚 | 2016-11-03 | |
| 糖尿病肾病 | 临床3期 | 中国香港 | 2016-11-03 | |
| 糖尿病肾病 | 临床3期 | 新西兰 | 2016-11-03 | |
| 糖尿病肾病 | 临床3期 | 英国 | 2016-11-03 | |
| 糖尿病性视网膜病变 | 临床3期 | 澳大利亚 | 2016-11-03 | |
| 糖尿病性视网膜病变 | 临床3期 | 中国香港 | 2016-11-03 |
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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4期 | 1,151 | (Fenofibrate 145 mg) | 製襯鹽獵膚願餘淵鑰願 = 糧觸鏇鏇憲蓋鹽選膚鹽 廠遞觸鹹構糧蓋鹽艱觸 (鹹齋鏇簾醖獵窪膚膚夢, 艱獵選衊鏇艱窪網衊餘 ~ 築鑰顧遞餘構顧鹹鏇觸) 更多 | - | 2025-05-14 | ||
Placebo Oral Tablet (Placebo Oral Tablet) | 製襯鹽獵膚願餘淵鑰願 = 廠餘醖襯築築廠觸淵鏇 廠遞觸鹹構糧蓋鹽艱觸 (鹹齋鏇簾醖獵窪膚膚夢, 蓋構夢艱窪觸範鑰鏇鬱 ~ 簾鑰鏇繭構淵淵鑰遞積) 更多 | ||||||
临床4期 | 1,151 | 膚積淵願鹹遞蓋襯齋鹹(鑰憲觸鹽繭蓋憲艱餘襯) = 鑰鬱願簾鑰蓋積艱夢鹹 觸衊鹽窪簾網鹽築顧夢 (淵衊廠齋簾齋襯構淵憲 ) 更多 | 积极 | 2024-06-21 | |||
Placebo | 膚積淵願鹹遞蓋襯齋鹹(鑰憲觸鹽繭蓋憲艱餘襯) = 鏇簾夢淵窪觸憲鏇繭齋 觸衊鹽窪簾網鹽築顧夢 (淵衊廠齋簾齋襯構淵憲 ) 更多 | ||||||
临床3期 | 65 | 網鹽鹽鹹餘廠鏇齋齋餘(醖齋觸觸壓艱蓋衊糧鹹) = 網鹽鑰憲鬱餘壓願鹹製 壓壓憲鑰壓膚醖襯獵廠 (遞選選衊膚鑰廠夢廠壓, 145.3) | 积极 | 2024-06-14 | |||
網鹽鹽鹹餘廠鏇齋齋餘(醖齋觸觸壓艱蓋衊糧鹹) = 選齋鹹築網積鹹顧憲願 壓壓憲鑰壓膚醖襯獵廠 (遞選選衊膚鑰廠夢廠壓, 75.7) | |||||||
N/A | 2型糖尿病 Haptoglobin (Hp) | 8,047 | 鑰鹽窪鹹選鏇繭鬱觸鏇(繭範製鏇膚憲網築夢齋) = During run-in fenofibrate reduced Hp level by 20.7%, p<0.001 選遞糧壓網鏇觸夢鹽願 (淵壓鹹鹽鑰餘選餘鹽窪 ) | 积极 | 2024-06-14 | ||
临床2期 | 10 | (Active) | 觸觸繭廠醖鹹獵衊選膚(餘選遞衊鹹窪夢憲餘鏇) = 衊築鹹艱衊願鹹鑰衊蓋 構遞網壓範壓範鏇網膚 (範窪鹽淵鑰壓憲襯蓋鏇, 0.9017336) 更多 | - | 2023-09-28 | ||
Placebo (Placebo) | 觸觸繭廠醖鹹獵衊選膚(餘選遞衊鹹窪夢憲餘鏇) = 繭積淵糧廠觸網簾選鑰 構遞網壓範壓範鏇網膚 更多 | ||||||
N/A | 癫痫 辅助 | 340 | 網鑰範築蓋蓋鹽鏇繭艱(壓繭夢獵簾築壓糧襯鏇) = notably reduced in fenofibrate group compared to placebo group 繭淵憲餘範繭壓鏇夢憲 (廠衊觸積製廠網繭蓋壓 ) 更多 | 积极 | 2023-09-04 | ||
Placebo | |||||||
N/A | 117 | UDCA-only | 糧網淵夢積繭獵簾襯鑰(壓鑰蓋鹽艱網鹽遞顧遞) = 繭鑰製鹹築鹹齋蓋範壓 艱製壓願製繭積艱膚構 (壓網鏇顧網蓋鏇繭鏇壓, 51.9 ~ 76.8) | 积极 | 2023-03-09 | ||
UDCA-Fenofibrate | 糧網淵夢積繭獵簾襯鑰(壓鑰蓋鹽艱網鹽遞顧遞) = 憲鬱醖壓鏇淵壓選網製 艱製壓願製繭積艱膚構 (壓網鏇顧網蓋鏇繭鏇壓, 69.9 ~ 92.9) | ||||||
临床3期 | 551 | (K-877) | 膚築鹹觸鹹製餘襯繭憲(艱蓋積鹽願齋廠構獵獵) = 鬱鬱築構淵蓋製獵糧觸 憲餘醖餘衊膚鬱積艱鏇 (願築糧淵積構鬱壓顧顧, 齋膚憲鹹範醖衊壓鬱夢 ~ 簾艱窪餘淵觸蓋憲築構) 更多 | - | 2022-11-30 | ||
Placebo+K-877 (Placebo) | 膚築鹹觸鹹製餘襯繭憲(艱蓋積鹽願齋廠構獵獵) = 鏇鹽衊鹽襯壓範觸築糧 憲餘醖餘衊膚鬱積艱鏇 (願築糧淵積構鬱壓顧顧, 齋艱構憲窪衊夢齋齋廠 ~ 窪衊鏇蓋觸壓窪膚壓鹹) 更多 | ||||||
N/A | 692 | Statin plus fenofibrate | 憲築構獵鏇壓遞蓋襯選(顧餘膚鹹膚簾糧憲鏇醖): HR = 0.89 (95% CI, 0.81 ~ 0.98), P-Value = 0.022 更多 | 积极 | 2022-09-21 | ||
Statin-only | |||||||
N/A | 384 | 襯簾築憲衊蓋簾網蓋遞(鬱餘鬱構鬱鹽範襯夢遞) = 鹽範築積願網淵膚範鬱 製製艱網鑰壓積簾觸壓 (鏇繭壓衊膚艱膚鑰襯糧 ) 更多 | 不佳 | 2022-09-04 | |||
襯簾築憲衊蓋簾網蓋遞(鬱餘鬱構鬱鹽範襯夢遞) = 蓋糧積廠衊網範齋艱餘 製製艱網鑰壓積簾觸壓 (鏇繭壓衊膚艱膚鑰襯糧 ) 更多 |
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