2. Others NF-κB MAPK/ERK Pathway Stem Cell/Wnt TGF-beta/Smad
  3. Isotope-Labeled Compounds NF-κB ERK TGF-beta/Smad
  4. Fluorofenidone-d3

Fluorofenidone-d3  (Synonyms: AKF-PD-d3)

目录号: HY-121246S
产品使用指南 技术支持

Fluorofenidone-d3 (AKF-PD-d3) 是 Fluorofenidone (AKF-PD) (HY-121246) 氘代物。Fluorofenidone 是一种具有口服活性的化合物，具有抗纤维化、抗氧化和抗炎的药理作用。Fluorofenidone 下调 ACSL4 的表达，上调 GPX4 的表达，并抑制 NF-κB 信号通路以减轻炎症和纤维化。Fluorofenidone 通过抑制小鼠肝脏的 Erk/-Egr-1 信号通路和 Tgfβ1/Smad 通路改善胆汁淤积和纤维化。Fluorofenidone 在小鼠中对慢性肺损伤表现出保护作用。Fluorofenidone 可用于慢性阻塞性肺疾病 (COPD)，肺间质纤维化 (PIF) 和非小细胞肺癌 (NSCLC) 的研究。

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Fluorofenidone-d<sub>3</sub>

Fluorofenidone-d3 Chemical Structure

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Other Forms of Fluorofenidone-d3:

Fluorofenidone-d3 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Fluorofenidone-d3 (AKF-PD-d3) is deuterium labeled Fluorofenidone (AKF-PD) (HY-121246). Fluorofenidone is an orally active compound with anti-fibrotic, antioxidant, and anti-inflammatory pharmacological effects. Fluorofenidone downregulates the expression of ACSL4, upregulates GPX4 expression and inhibits the NF-κB signaling pathway to alleviate inflammation and fibrosis. Fluorofenidone ameliorates cholestasis and fibrosis by inhibiting hepatic Erk/-Egr-1 signaling and Tgfβ1/Smad pathway in mice. Fluorofenidone demonstrates protective effects against chronic lung injury in mice. Fluorofenidone can be used for the study of chronic obstructive pulmonary disease (COPD), pulmonary interstitial fibrosis (PIF) and non-small cell lung cancer (NSCLC)[1][2][3].

体外研究
(In Vitro)

Fluorofenidone (24 h) 在 BEAS-2B 细胞中部分逆转香烟烟雾提取物 (CSE) 诱导的细胞活力抑制，并降低培养上清液中炎症因子 IL-1β、IL-6 和 TNF-α 的水平[1]。
Fluorofenidone (24 h) 部分逆转 CSE 引起的 BEAS-2B 细胞上清液中 MDA 水平升高和 GSH 水平降低[1]。
Fluorofenidone (24 h) 改善 CSE 诱导的线粒体损伤，下调 ACSL4 的表达并上调 GPX4 的表达[1]。
Fluorofenidone (200-800 μg/mL，24 小时) 以剂量依赖方式抑制 A549 和 H1299 细胞的增殖，其 EC50 值分别为 1030 μg/mL (A549) 和 1118 μg/mL (H1299)[3]。
Fluorofenidone (400-800 μg/mL，3 小时) 显著降低 EdU 阳性增殖细胞的百分比[3]。
Fluorofenidone (200-800 μg/mL，12-24 小时) 以抑制 A549 和 H1299 细胞的迁移，并减少侵袭细胞的数量[3]。
Fluorofenidone (200-800 μg/mL) 上调上皮标志物 E-cadherin 的表达，下调 A549 和 H1299 细胞中介质标志物 MMP9、vimentin 和 SNAIL 的表达[3]。
Fluorofenidone (200-800 μg/mL) 抑制 A549 和 H1299 细胞中 JNK、ERK、P38 (MAPK 通路) 以及 p-PI3K、p-AKT、p-mTOR (PI3K/AKT/mTOR 通路) 的磷酸化[3]。

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

Fluorofenidone-d3 相关抗体:
体内研究
(In Vivo)

Fluorofenidone (5 mg/kg，腹腔注射，每日一次，连续 7 周) 可减轻香烟烟雾 (CS)/LPS (HY-D1056) 诱导的小鼠肺组织形态学损伤[1]。
Fluorofenidone (饮食中添加 0.45%，口服，14 天) 可显著减轻小鼠 3,5-diethoxycarbonyl-1,4-dihydroxychollidine (DDC) 诱导的胆汁淤积模型中的肝脏炎症[2]。
Fluorofenidone (400 mg/kg，口服，每日一次，持续 3 周) 联合 Cisplatin (HY-17394) 显著减少携带 Lewis 肺癌细胞的 C57 小鼠皮下肿瘤的大小、重量和体积[3]。

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

Animal Model: C57BL/6 J mice (4-week-old, 18-20 g) were used to construct the chronic obstructive pulmonary disease (COPD) model[1]
Dosage: 5 mg/kg
Administration: i.p., once daily, 7 weeks
Result: Alleviated CS/LPS-induced lung tissue morphological damage, including reducing interstitial inflammatory cell infiltration, alleviating lung overexpansion, thinning alveolar septa, and lowering lung injury score.
Reduced the levels of inflammatory factors IL-1β, IL-6, and TNF-α in bronchoalveolar lavage fluid (BALF) and serum.
Inhibited lung collagen deposition, decreased lung fibrosis score, downregulated mRNA and protein expressions of fibrosis markers α-SMA, FAP, and COL3A1 in lung tissue, and reduced lung hydroxyproline content.
Downregulated ACSL4 expression and upregulated GPX4 expression in lung tissue, reversed CS/LPS-induced increase in MDA level and decrease in GSH level in lung tissue and serum.
Animal Model: 3,5-diethoxycarbonyl-1,4-dihydroxychollidine (DDC)-induced cholestasis model of 7-week-old male C57BL/6J mice[2]
Dosage: 0.45% in diet
Administration: p.o., 14 days
Result: Reduced serum ALT, AST, ALP, and TBA levels, as well as hepatic BAs levels, and decreased the liver/body weight ratio.
Reduced mRNA levels of hepatic inflammatory cytokines and chemokines, lowered serum levels of these inflammatory factors, and decreased F4/80 expression to reduce macrophage infiltration.
Downregulated mRNA levels of profibrogenic markers, inhibited phosphorylation of Smad2/3, and reduced α-SMA protein level, thus mitigating hepatic fibrosis.
Downregulated expression of Cyp7a1 and Cyp27a1, upregulated expression of hepatic detoxification enzymes, and facilitated nuclear translocation.
Suppressed phosphorylation of Erk1/2, reduced Egr-1 protein level, and blocked the Tgfβ1/Smad pathway.
Animal Model: C57 mice (5-week-old, 16-18 g) were used to construct the Lewis lung cancer subcutaneous xenograft model by subcutaneously injecting 5 × 105 Lewis lung cancer cells (C7205) into the axillary region[3]
Dosage: 400 mg/kg combined with Cisplatin (5 mg/kg, i.p., weekly, 3 weeks)
Administration: p.o., daily, 3 weeks
Result: Reduced the size, weight and volume of subcutaneous tumors.
Downregulated the expression of mesenchymal marker N-cadherin.
分子量

206.23

Formula

C12H7D3FNO
非标记 CAS
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

Fluorofenidone-d3 相关分类

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Fluorofenidone-d3AKF-PD-d3Isotope-Labeled CompoundsNF-κBERKTGF-beta/SmadNuclear factor-κBNuclear factor-kappaBExtracellular signal regulated kinasesTransforming growth factor betaanti-fibroticantioxidantanti-inflammatoryErk/-Egr-1Tgfβ1/SmadInhibitorinhibitorinhibit

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