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

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).

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Fluorofenidone-d<sub>3</sub>

Fluorofenidone-d3 Chemical Structure

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Fluorofenidone-d3 Related Antibodies

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Description

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].

Application

1. This compound can be used as a tracer.
2. This compound can be used as an internal standard for quantitative analysis by NMR, GC-MS, or LC-MS.

In Vitro

Fluorofenidone (24 h) partially reverses the inhibition of cell viability and reduces the levels of inflammatory factors IL-1β, IL-6, and TNF-α in the culture supernatant induced by cigarette smoke extract (CSE) in BEAS-2B cells[1].
Fluorofenidone (24 h) partially reverses the increase in MDA level and decrease in GSH level in BEAS-2B cell supernatant caused by CSE[1].
Fluorofenidone (24 h) improves CSE-induced mitochondrial damage, downregulates the expression of ACSL4 and upregulates the expression of GPX4 in BEAS-2B cells[1].
Fluorofenidone (200-800 μg/mL, 24 h) inhibits proliferation of A549 and H1299 cells in a dose-dependent manner, with EC50 of 1030 μg/mL (A549) and 1118 μg/mL (H1299)[3].
Fluorofenidone (400-800 μg/mL, 3 h) significantly reduces the percentage of EdU-positive proliferating cells[3].
Fluorofenidone (200-800 μg/mL, 12-24 h) dose- and time-dependently inhibits cell migration and reduces the number of invasive cells in A549 and H1299 cells[3].
Fluorofenidone (200-800 μg/mL) upregulates the expression of epithelial marker E-cadherin and downregulates mesenchymal markers MMP9, vimentin, and SNAIL in A549 and H1299 cells[3].
Fluorofenidone (200-800 μg/mL) suppresses phosphorylation of JNK, ERK, P38 (MAPK pathway) and p-PI3K, p-AKT, p-mTOR (PI3K/AKT/mTOR pathway) in A549 and H1299 cells[3].

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

Fluorofenidone-d3 Related Antibodies
In Vivo

Fluorofenidone (5 mg/kg, i.p., once daily, 7 weeks) alleviates cigarette smoke (CS)/LPS (HY-D1056)-induced lung tissue morphological damage in mice[1].
Fluorofenidone (0.45% in diet, p.o., 14 days) markedly alleviates hepatic inflammation in 3,5-diethoxycarbonyl-1,4-dihydroxychollidine (DDC)-induced cholestasis model of mice[2].
Fluorofenidone (400 mg/kg, p.o., daily, 3 weeks) combined with Cisplatin (HY-17394) significantly reduces the size, weight and volume of subcutaneous tumors in C57 mice bearing Lewis lung cancer cells[3].

MedChemExpress (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.
Molecular Weight

206.23

Formula

C12H7D3FNO
Unlabeled CAS
SMILES

O=C1C=CC(C)=CN1C2=C([2H])C=C([2H])C(F)=C2[2H]
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Fluorofenidone-d3 Related Classifications

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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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