2. Metabolic Enzyme/Protease Apoptosis NF-κB Immunology/Inflammation Stem Cell/Wnt JAK/STAT Signaling
  3. TrxR Glutathione Peroxidase Ferroptosis Reactive Oxygen Species (ROS) IFNAR STAT
  4. Fa-Au

Fa-Au is a TrxR inhibitor. Fa-Au downregulates GPX4, induces oxidative stress, mitochondria-associated ferroptosis (ferroptosis) and immunogenic cell death. Fa-Au induces ROS production in hepatoma cells. Fa-Au remodels the tumor immune microenvironment via M1 macrophage polarization, dendritic cell maturation, CD8+ T cell activation and reduction of regulatory T cells. Fa-Au induces an anti-tumor immune feedback loop through the IFNγ/STAT1/SLC7A11 axis. Fa-Au inhibits tumor growth. Fa-Au is applicable to hepatocellular carcinoma-related research.

For research use only. We do not sell to patients.

Fa-Au

Fa-Au Chemical Structure

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Fa-Au Related Antibodies

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TrxR1 TrxR2

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GPX1 GPX4

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STAT3 STAT5 STAT6 STAT1

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Description

Fa-Au is a TrxR inhibitor. Fa-Au downregulates GPX4, induces oxidative stress, mitochondria-associated ferroptosis (ferroptosis) and immunogenic cell death. Fa-Au induces ROS production in hepatoma cells. Fa-Au remodels the tumor immune microenvironment via M1 macrophage polarization, dendritic cell maturation, CD8+ T cell activation and reduction of regulatory T cells. Fa-Au induces an anti-tumor immune feedback loop through the IFNγ/STAT1/SLC7A11 axis. Fa-Au inhibits tumor growth. Fa-Au is applicable to hepatocellular carcinoma-related research[1].

IC50 & Target[1]

STAT1

 

GPX4

 

In Vitro

Fa-Au (Compound 8) (72 h) potently inhibits the proliferation of HepG2 and Hepa 1-6 hepatocellular carcinoma cells, with IC50 values of 0.48 μM and 0.69 μM respectively after 72 h of incubation[1].
Fa-Au (0.5-2 μM; 24 h) inhibits TrxR activity in HepG2 hepatocellular carcinoma cells in a concentration-dependent manner in vitro[1].
Fa-Au (2 μM; 6 h) induces ROS production in HepG2 hepatocellular carcinoma cells, and this effect is reversed by 6 h pretreatment with the ROS scavenger NAC (HY-B0215)[1].
Fa-Au (0.5-2 μM) induces ROS-mediated endoplasmic reticulum stress in HepG2 hepatocellular carcinoma cells, which is evidenced by concentration-dependent Ca2+ release and upregulation of key ERS markers, and this effect is reversed by pretreatment with NAC[1].
Fa-Au (0-10 μM) induces ferroptosis in HepG2 hepatocellular carcinoma cells via lipid peroxide accumulation, mitochondrial damage, and downregulation of GPX4 and SLC7A11[1].
Fa-Au (2 μM) induces immunogenic cell death in HepG2 hepatocellular carcinoma cells, which is characterized by CRT exposure, HMGB1 release, reduced intracellular ATP levels, and altered expression of ICD-related proteins[1].
Treatment of HepG2 hepatocellular carcinoma cells with Fa-Au (2 μM; 24 h) induces significant changes in the expression of genes associated with oxidative stress and immune response pathways[1].
IFN-γ enhances Fa-Au-induced ferroptosis in HepG2 hepatocellular carcinoma cells via the IFN-γ/STAT1/SLC7A11 axis[1].

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

Fa-Au Related Antibodies

Immunofluorescence[1]

Cell Line: HepG2 liver cancer cells
Concentration: 2 μM
Incubation Time: 6 h
Result: Induced ROS generation.

RT-PCR[1]

Cell Line: HepG2 liver cancer cells
Concentration: 2 μM
Incubation Time: 24 h
Result: Upregulated DDIT3 and IL18, downregulated GPX1, SELK and TXNRD2.
In Vivo

Fa-Au (2.5 mg/kg; i.p.; every two days) potently suppresses liver tumor growth in male C57BL/6 mice, reduces tumor weight and volume, enhances antitumor immune infiltration, and exhibits favorable biosafety[1].
Fa-Au inhibits the proliferation and migration of HepG2 liver cancer cells in an implantable zebrafish tumor model[1].

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

Animal Model: C57BL/6 (male, 3-5 weeks old)[1]
Dosage: 2.5 mg/kg
Administration: i.p.; every two days
Result: Significantly suppressed tumor growth, with lower tumor weight and smaller tumor volume than both the model group and oxaliplatin group.
Caused no significant body weight changes, and histopathological examination of major organs showed no obvious toxicity.
Increased apoptosis, elevated ROS levels, upregulated ATF-4 expression, downregulated GPX4 expression, increased CRT exposure, and increased HMGB1 release in tumors.
Significantly increased tumor infiltration of CD4+ T cells, CD8+ T cells, and CD86+ immune cells.
Markedly reduced the proportion of immunosuppressive Tregs (CD4+ and Foxp3+) in tumor tissues.
Molecular Weight

1429.19

Formula

C64H70AuF6N4O12P
SMILES

COC1=CC=C(C2=C(C3=CC=C(OC)C=C3)N(CCCOC(/C=C/C4=CC=C(O)C(OC)=C4)=O)C([Au+]C5N(CCCOC(/C=C/C6=CC=C(O)C(OC)=C6)=O)C(C7=CC=C(OC)C=C7)=C(C8=CC=C(OC)C=C8)N5CC)N2CC)C=C1.F[P-](F)(F)(F)(F)F
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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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Fa-Au Related Classifications

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Help & FAQs
  • 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:

Fa-AuTrxRGlutathione PeroxidaseFerroptosisReactive Oxygen Species (ROS)IFNARSTATThioredoxin ReductaseInterferon-α/β receptorInterferon-alpha/beta receptordendritic cell maturationGPX4immunogenic cell deathCD8+ T cell activationthioredoxin reductaseIFN-γ/STAT1/SLC7A11 axisHepG2oxidative stressferroptosisM1 macrophage polarizationInhibitorinhibitorinhibit

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