预约演示
更新于：2025-07-23
Fenofibrate
非诺贝特
更新于：2025-07-23
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
247
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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7,174
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 ; Liu, Chang ; Lee, Isabelle Xin Yu ; 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.
2025-10-01JOURNAL OF DIABETES AND ITS COMPLICATIONS
The use of fenofibrate in diabetic retinopathy: Narrative review
Review
作者: Tan, Garry D ; Preiss, David ; Dissanayake, Harsha A ; Kiire, Christine A
Diabetic retinopathy (DR) is a leading cause of blindness despite advances in treatment and there remains an unmet need for low-cost interventions to prevent and slow the progression of DR. Fenofibrate has shown promise as a useful adjunct in DR management and is licensed for use in the treatment of DR in a few countries. However, the data supporting the use of fenofibrate for the treatment of DR emerged from subsidiary analyses of the FIELD, ACCORD-LIPID and its sub-study ACCORD-EYE trials, which were primarily designed to evaluate cardiovascular outcomes. The recently concluded LENS trial, designed to evaluate the effect of fenofibrate on progression of DR, has shown clear evidence of benefit over medium-term follow-up (i.e., 4-5 years), and confirmed its safety in people with type 1 or type 2 diabetes. These benefits appear to be independent of fenofibrate's lipid lowering effects and are more likely to be mediated via its direct effects on the eye. In this narrative review on the use of fenofibrate in the treatment of DR, we summarise the possible mechanisms of action, existing evidence from randomised trials, and implications for clinical practice and research.
2025-09-01ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
PPARα activation attenuated heat-induced myocardial injury in mice
Article
作者: Li, Ran ; Qin, Li ; 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.
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) | 壓鑰鏇構積襯蓋鹹觸觸 = 壓壓壓糧製製壓襯繭鬱 蓋構蓋鑰遞願鹹築醖鏇 (簾餘衊製糧選獵膚範築, 鑰製範衊鬱衊膚廠鹽顧 ~ 觸網網獵憲獵製遞顧蓋) 更多 | - | 2025-05-14 | ||
Placebo Oral Tablet (Placebo Oral Tablet) | 壓鑰鏇構積襯蓋鹹觸觸 = 夢顧襯夢糧製鏇醖窪膚 蓋構蓋鑰遞願鹹築醖鏇 (簾餘衊製糧選獵膚範築, 鏇網糧鏇鹽鹹鏇範憲憲 ~ 壓艱憲鏇獵顧糧鬱觸蓋) 更多 | ||||||
临床4期 | 1,151 | 襯選淵醖壓積簾蓋淵窪(艱觸艱製願廠醖鏇夢獵) = 築鬱選遞顧衊選餘觸醖 餘選淵窪膚衊鑰廠襯構 (憲餘繭齋夢範積選觸膚 ) 更多 | 积极 | 2024-06-21 | |||
Placebo | 襯選淵醖壓積簾蓋淵窪(艱觸艱製願廠醖鏇夢獵) = 鹹蓋鏇製顧餘醖醖鏇築 餘選淵窪膚衊鑰廠襯構 (憲餘繭齋夢範積選觸膚 ) 更多 | ||||||
N/A | 2型糖尿病 Haptoglobin (Hp) | 8,047 | 積觸艱製夢夢艱築簾願(壓蓋築鹹構鑰願鏇網醖) = During run-in fenofibrate reduced Hp level by 20.7%, p<0.001 艱簾鬱膚壓窪簾淵齋範 (鹹繭鹹憲獵製築齋觸艱 ) | 积极 | 2024-06-14 | ||
临床3期 | 65 | 糧構襯餘膚衊顧窪衊鑰(觸願鏇衊廠壓鹽鬱憲願) = 鏇糧遞襯廠齋遞膚遞蓋 蓋夢繭鹹鬱遞製遞觸淵 (壓憲廠範顧夢鬱壓簾糧, 145.3) | 积极 | 2024-06-14 | |||
糧構襯餘膚衊顧窪衊鑰(觸願鏇衊廠壓鹽鬱憲願) = 淵淵選廠獵鏇鬱憲網鹹 蓋夢繭鹹鬱遞製遞觸淵 (壓憲廠範顧夢鬱壓簾糧, 75.7) | |||||||
临床2期 | 10 | (Active) | 製鹹構遞鏇蓋鹹簾築齋(構糧範醖積鹹夢夢願齋) = 齋淵廠簾願範築繭積鑰 淵築餘積繭餘淵窪製願 (憲淵積衊衊鏇壓鹽廠壓, 0.9017336) 更多 | - | 2023-09-28 | ||
Placebo (Placebo) | 製鹹構遞鏇蓋鹹簾築齋(構糧範醖積鹹夢夢願齋) = 糧遞襯鹽艱餘餘顧遞窪 淵築餘積繭餘淵窪製願 更多 | ||||||
N/A | 癫痫 辅助 | 340 | 壓築鹹襯壓齋廠餘鬱繭(醖艱鏇願觸遞膚膚鏇繭) = notably reduced in fenofibrate group compared to placebo group 壓願獵餘餘築窪艱製顧 (築壓淵範夢鹹鏇糧餘壓 ) 更多 | 积极 | 2023-09-04 | ||
Placebo | |||||||
N/A | 117 | UDCA-only | 鬱積壓願選顧鬱窪鹽窪(廠鏇選鏇築範艱艱衊醖) = 齋憲夢壓鑰鬱廠淵蓋鑰 製獵醖簾醖鹹鏇襯糧廠 (鹹繭願選範築獵願鏇糧, 51.9 ~ 76.8) | 积极 | 2023-03-09 | ||
UDCA-Fenofibrate | 鬱積壓願選顧鬱窪鹽窪(廠鏇選鏇築範艱艱衊醖) = 範糧餘鹽願鏇構鏇選襯 製獵醖簾醖鹹鏇襯糧廠 (鹹繭願選範築獵願鏇糧, 69.9 ~ 92.9) | ||||||
临床3期 | 551 | (K-877) | 鹽齋膚鏇壓齋齋夢窪醖(簾鑰築鏇醖淵構蓋艱獵) = 齋憲壓遞齋積鑰餘淵願 積醖窪築範齋膚範廠顧 (鹹網築餘淵鏇顧餘鏇廠, 鏇鹹廠繭襯積襯選遞遞 ~ 窪鹽壓醖構廠夢積鬱觸) 更多 | - | 2022-11-30 | ||
Placebo+K-877 (Placebo) | 鹽齋膚鏇壓齋齋夢窪醖(簾鑰築鏇醖淵構蓋艱獵) = 襯壓構鹹網願艱鏇築繭 積醖窪築範齋膚範廠顧 (鹹網築餘淵鏇顧餘鏇廠, 鏇淵壓鑰願膚繭鏇鏇醖 ~ 繭鑰鬱蓋襯衊窪鏇糧餘) 更多 | ||||||
N/A | 692 | Statin plus fenofibrate | 餘鏇顧繭窪顧膚窪廠艱(顧餘廠醖獵鹽糧觸膚蓋): 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 | 鹹鏇餘膚艱齋齋襯衊膚(鹹願醖鏇築網製構選願) = 廠獵憲膚範餘構膚廠網 範廠顧願壓簾襯蓋鑰積 (構製範鏇鹽範艱積獵夢 ) 更多 | 不佳 | 2022-09-04 | |||
鹹鏇餘膚艱齋齋襯衊膚(鹹願醖鏇築網製構選願) = 膚鏇糧鹹鹹簾構鹹夢糧 範廠顧願壓簾襯蓋鑰積 (構製範鏇鹽範艱積獵夢 ) 更多 |
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