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Fenofibrate (GMP)

CAS: 49562-28-9 F: C20H21ClO4 W: 360.83

Fenofibrate (GMP) is Fenofibrate (HY-17356) produced by using GMP guidelines. GMP small molecules work appropriately as
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Bioactivity 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.
Invitro 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]。 0 --> Fenofibrate (GMP) 相关抗体:
In Vivo 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]。
Name Fenofibrate (GMP)
CAS 49562-28-9
Formula C20H21ClO4
Molar Mass 360.83
Transport Room temperature in continental US; may vary elsewhere.
Storage

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

Reference [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. [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. [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./ [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. [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.