Nrf2-IN-4
Nrf2-IN-4 is a Nrf2 inhibitor. Nrf2-IN-4 induces ferroptosis via NRF2 inhibition. Nrf2-IN-4 disrupts cellular iron homeostasis, facilitates ferritin degradation, and ultimately triggers ferroptosis. Nrf2-IN-4 induces lysosome activation by promoting iron-dependent ROS production and lysosomal acidification. Nrf2-IN-4 demonstrates significant antitumor efficacy. Nrf2-IN-4 can be used for the study of breast cancer.
For research use only. We do not sell to patients.
- CAS No.: 2417486-06-5
- Formula: C20H13Cl2N5S
- Molecular Weight:426.32
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Nrf2-IN-4 (Compound PhcY) (0.01-10 μM, 72 h) exhibits inhibitory effect on the cancer cell lines, with IC50s of 80 nM (MCF-7 cells), 3.26 μM (HepG2 cells), 0.90 μM (T24 cells), 2.89 μM (HCT116 cells), 3.27 μM (L929 fibroblasts) and 5.36 μM (HEK293 human embryonic kidney cells)[1]. Nrf2-IN-4 (40-160 nM) causes MCF-7 cells to exhibit ‘ballooning’ and rounded cell morphology with vacuolated cytosol[1]. Nrf2-IN-4 (40-80 nM, 14 days) inhibits colony formation of MCF-7 cells in a dose-dependent manner[1]. Nrf2-IN-4 (80-160 nM, 24-48 h) increases labile iron pool (LIP) and ferroptosis via inhibition of Nrf2 in MCF-7 cells[1]. Nrf2-IN-4 (80-320 nM, 24 h) induces lysosome activation by promoting iron-dependent ROS production and lysosomal acidification in MCF-7 cells[1]. Nrf2-IN-4 (40-320 nM, 0-12 h) induces ferritin degradation via ferritinophagy in MCF-7 cells[1]. Nrf2-IN-4 (80-320 nM) induces oxidative stress, resulting in a significant decrease in mitochondrial membrane potential, an effect that can be reduced by the Acetylcysteine (N-acetylcysteine) (NAC) (HY-B0215) in MCF-7 cells[1]. Nrf2-IN-4 (0.1-0.2 μM) demonstrates a potent inhibitory effect on organoid growth, surpassing the efficacy of ML385(HY-100523)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:MCF-7 cells
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Concentration:80 nM
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Incubation Time:24 h
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Result:Increased LIP and reversed the effect and the the effect was reversed by Nrf2 knockdown.
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Cell Line:MCF-7 cells
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Concentration:80, 160 nM
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Incubation Time:48 h
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Result:Increased cytotoxicity upon Nrf2 overexpression. Induced dose-dependent cytotoxicity, which was inhibited by both 1,8-Diazafluoren-9-one (DFO) (HY-D0903) and Ferrostatin-1 (Fer-1) (HY-100579).
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Cell Line:MCF-7 cells
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Concentration:80, 160, 320 nM
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Incubation Time:24 h
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Result:Increased cathepsin B activity in a dose-dependent manner, which was inhibited by Chloroquine (CQ)(HY-17589A) or DFO.
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Cell Line:MCF-7 cells
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Concentration:0, 3, 6, 9, 12 h
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Incubation Time:24 h
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Result:Showed a dose-dependent increase in Beclin-1, LC3-II, and ATG5 protein levels. Reduced intracellular FTH and FTL levels, and this reduction was reversed by autophagy inhibitors(Bafilomycin A1(HY-100558) ,CQ) and the iron chelator DFO.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:MCF-7 cells (5 × 106) were injected subcutaneously into each female adult athymic nude mouse [1]
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Dosage:10 mg/kg
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Administration:i.p. daily for 21 days
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Result:Led to the degradation of FTH and FTL, as well as the upregulation of P53 and LC3-II. Did not cause notable body weight loss or other observable adverse effects in mice.
Chemical Information
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CAS No. 2417486-06-5
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Molecular Weight 426.32
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Formula C20H13Cl2N5S
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SMILES
ClC1=C(Cl)C=C(C2=CSC(N/N=C(C3=CC=CC=N3)/C4=NC=CC=C4)=N2)C=C1
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)