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.
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- 화학식: C64H70AuF6N4O12P
- 분자량:1429.19
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- 순도&문서
- References
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Help & FAQs
Biological Activity
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STAT1 |
GPX4 |
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 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.
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Animal Model:C57BL/6 (male, 3-5 weeks old)[1]
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Dosage:2.5 mg/kg
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Administration:i.p.; every two days
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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.
Chemical Information
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분자량 1429.19
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화학식 C64H70AuF6N4O12P
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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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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Fa-Au Related Classifications
HY-183554 Related Classifications
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