Fenofibrate 

Fenofibrate (GMP) is Fenofibrate (HY-17356) produced by using GMP guidelines. GMP small molecules work appropriately as an auxiliary reagent for cell therapy manufacture. Fenofibrate is a selective PPARα agonist with an EC₅₀ of 30 μM. Fenofibrate also inhibits human cytochrome P450 isoforms, with IC₅₀s of 0.2, 0.7, 9.7, 4.8 and 142.1 μM for CYP2C19, CYP2B6, CYP2C9, CYP2C8, and CYP3A4, respectively.

Fenofibrate 是一种相对有效的 CYP2B6 (IC₅₀=0.7±0.2 μM) 和 CYP2C19 (IC₅₀=0.2±0.1 μM) 抑制剂。Fenofibrate 也是 CYP2C8 (IC₅₀=4.8±1.7 μM) 和 CYP2C9 (IC₅₀=9.7 μM) 的中度抑制剂^[1]。
Fenofibrate 以比 PPARα 更高的亲和力结合并抑制细胞色素 P450 环氧化酶 (CYP)2C。Fenofibrate 是一种众所周知的 PPARα 激动剂，但对 209 种常用处方药和相关异生素的体外评估表明，Fenofibrate 也是细胞色素 P450 环氧化酶 (CYP)2C 的有效抑制剂。Fenofibrate 对 CYP2C 的亲和力 (EC₅₀=2.39±0.4 μM) 比对 PPARα (EC₅₀=30 μM) 高 10 倍以上。
低剂量的 Fenofibrate 可抑制 CYP2C8 活性，而不激活 PPARα^[2]。 Fenofibrate (25 μM, 24小时) 降低 GSC 侵袭和 GSC 干细胞标记物 (CD133, Oct4) 的表达^[3]。
Fenofibrate (5 μM, 7 天) 能抑制线粒体诱导的 DMD hiPSC 衍生心肌细胞凋亡^[4]。
Fenofibrate (25 μM, 72 小时) 不能提高患者 iPSC 衍生神经祖细胞中 TPP1 的活性^[5]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

每日摄入如此低剂量（10 μg/g/天）的 Fenofibrate 可抑制 CYP2C8 过表达诱导的视网膜和脉络膜新生血管形成，抑制率分别为 29% (P=0.021) 和 36% (P=1.2×10^-9)^[2]。

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

360.83

C₂₀H₂₁ClO₄

49562-28-9

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Schelleman H, et al. Pharmacoepidemiologic and in vitro evaluation of potential drug-drug interactions of sulfonylureas with fibrates and statins. Br J Clin Pharmacol. 2014 Sep;78(3):639-48.  [Content Brief]

  [2]. Gong Y, et al. Fenofibrate Inhibits Cytochrome P450 Epoxygenase 2C Activity to Suppress Pathological Ocular Angiogenesis. EBioMedicine. 2016 Sep 30. pii: S2352-3964(16)30448-0.  [Content Brief]

  [3]. Binello E, et al. Characterization of fenofibrate-mediated anti-proliferative pro-apoptotic effects on high-grade gliomas and anti-invasive effects on glioma stem cells. J Neurooncol. 2014 Apr;117(2):225-34./  [Content Brief]

  [4]. Sun C, et al. Duchenne muscular dystrophy hiPSC-derived myoblast drug screen identifies compounds that ameliorate disease in mdx mice. JCI Insight. 2020 Jun 4;5(11):e134287.  [Content Brief]

  [5]. Lojewski X, et al. Human iPSC models of neuronal ceroid lipofuscinosis capture distinct effects of TPP1 and CLN3 mutations on the endocytic pathway. Hum Mol Genet. 2014 Apr 15;23(8):2005-22.  [Content Brief]