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Merck

F6020

Sigma-Aldrich

非诺贝特

≥99% (TLC), powder, PPARα agonist

别名:

2- [4-(4-氯苯甲酰)苯氧基]-2-甲基丙酸异丙酯

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About This Item

经验公式(希尔记法):
C20H21ClO4
CAS号:
分子量:
360.83
EC號碼:
MDL號碼:
分類程式碼代碼:
12352200
PubChem物質ID:
NACRES:
NA.77

产品名称

非诺贝特, ≥99%, powder

品質等級

化驗

≥99%

形狀

powder

顏色

off-white

起源

Abbott

儲存溫度

room temp

SMILES 字串

CC(C)OC(=O)C(C)(C)Oc1ccc(cc1)C(=O)c2ccc(Cl)cc2

InChI

1S/C20H21ClO4/c1-13(2)24-19(23)20(3,4)25-17-11-7-15(8-12-17)18(22)14-5-9-16(21)10-6-14/h5-13H,1-4H3

InChI 密鑰

YMTINGFKWWXKFG-UHFFFAOYSA-N

基因資訊

human ... PPARA(5465)

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相关类别

應用

非诺贝特已被用于:
  • 研究其对血浆脂质、肝脏表型和基因表达的影响
  • 研究其对胸主动脉内皮依赖性血管舒张的影响
  • 给予 NASH 敲入小鼠以及高脂肪饮食 (HFD) 以研究其效果

生化/生理作用

非诺贝特通过减少胆固醇酯转运蛋白的表达增加高密度脂蛋白水平。用于治疗血液中胆固醇水平升高条件体内脂质水平异常以及高甘油三酯血症。非诺贝特是一种调脂药物和增殖物激活受体-α (PPARα) 介导其操作。降低血浆纤维蛋白原和 C 反应蛋白水平。非诺贝特可改善血流介导的血管扩张,降低动脉粥样硬化的风险。已知非诺贝特也可降低尿酸水平。

特點和優勢

该化合物在受体分类和信号转导手册的 核受体(PPAR) 页面上有详细描述。如需浏览其他手册页面,请点击此处
该化合物由 Abbott 开发。如需浏览其他制药公司开发的化合物和批准的药物/候选药物列表,请点击此处

象形圖

Health hazard

訊號詞

Warning

危險聲明

防範說明

危險分類

STOT RE 2 Oral

標靶器官

Liver

儲存類別代碼

11 - Combustible Solids

水污染物質分類(WGK)

WGK 1

閃點(°F)

Not applicable

閃點(°C)

Not applicable

個人防護裝備

dust mask type N95 (US), Eyeshields, Gloves


历史批次信息供参考:

分析证书(COA)

Lot/Batch Number

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访问文档库

Early diet-induced non-alcoholic steatohepatitis in APOE2 knock-in mice and its prevention by fibrates
Shiri-Sverdlov R, et al.
Journal of Hepatology, 44(4), 732-741 (2006)
Intrahepatic cholesterol influences progression, inhibition and reversal of non-alcoholic steatohepatitis in hyperlipidemic mice
Wouters K, et al.
Febs Letters, 584(5), 1001-1005 (2010)
Oshri Avraham et al.
eLife, 10 (2021-09-30)
Sensory neurons with cell bodies in dorsal root ganglia (DRG) represent a useful model to study axon regeneration. Whereas regeneration and functional recovery occurs after peripheral nerve injury, spinal cord injury or dorsal root injury is not followed by regenerative
Kristiaan Wouters et al.
FEBS letters, 584(5), 1001-1005 (2010-02-02)
Hepatic inflammation is the key factor in non-alcoholic steatohepatitis (NASH) and promotes progression to liver damage. We recently identified dietary cholesterol as the cause of hepatic inflammation in hyperlipidemic mice. We now show that hepatic transcriptome responses are strongly dependent
Fenofibrate
Keating GM and Croom KF
Drugs, 67(1), 121?153-121?153 (2012)

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