1. NF-κB Apoptosis Metabolic Enzyme/Protease Immunology/Inflammation
  2. Keap1-Nrf2 Apoptosis Ferroptosis Reactive Oxygen Species (ROS)
  3. Nrf2 activator-25

Nrf2 activator-25 is a Nrf2 activator. Nrf2 activator-25 promotes the dissociation of Nrf2 from Keap1 (with a Kd of 21.3 μM for Keap1), drives Nrf2 nuclear translocation, and increases the production of downstream antioxidant enzymes. Nrf2 activator-25 inhibits apoptosis, ferroptosis and vascular fibrosis, and protects vascular endothelial cells from damage. Nrf2 activator-25 can be used in the research of diabetic vascular diseases.

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Nrf2 activator-25

Nrf2 activator-25 Chemical Structure

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Description

Nrf2 activator-25 is a Nrf2 activator. Nrf2 activator-25 promotes the dissociation of Nrf2 from Keap1 (with a Kd of 21.3 μM for Keap1), drives Nrf2 nuclear translocation, and increases the production of downstream antioxidant enzymes. Nrf2 activator-25 inhibits apoptosis, ferroptosis and vascular fibrosis, and protects vascular endothelial cells from damage. Nrf2 activator-25 can be used in the research of diabetic vascular diseases[1].

In Vitro

Nrf2 activator-25 (Compound 3h) at 20 μM maintains the survival rate of serum- and growth factor-starved human umbilical vein endothelial cells (HUVECs) at 93.61%, with extremely low cytotoxicity[1].
Nrf2 activator-25 (5-20 μM; 6-24 h) concentration-dependently inhibits apoptosis and ferroptosis of HUVECs damaged by ox-LDL, high glucose and CoCl2 after 12 h of treatment[1].
Nrf2 activator-25 (5-20 μM; 6-12 h) concentration-dependently inhibits the expression of ICAM-1 and VCAM-1 in HUVECs damaged by ox-LDL, high glucose and CoCl2[1].
Nrf2 activator-25 (20 μM; 6-24 h) protects HUVECs injured by ox-LDL, high glucose and CoCl2 against mitochondrial membrane potential loss[1].
Nrf2 activator-25 (20 μM; 6-24 h) inhibits ROS accumulation in HUVECs damaged by ox-LDL, high glucose and CoCl2[1].
Nrf2 activator-25 (5-20 μM; 6-24 h) concentration-dependently inhibits lipid peroxidation in HUVECs damaged by ox-LDL, high glucose, and CoCl2, respectively[1].

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

Apoptosis Analysis[1]

Cell Line: ox-LDL-injured human umbilical vein endothelial cells (HUVECs)
Concentration: 5, 10 and 20 μM
Incubation Time: 6 h
Result: Reduced the percentage of apoptotic HUVECs with condensed/fragmented nuclei in a concentration-dependent manner, relative to ox-LDL-only treated cells.

Apoptosis Analysis[1]

Cell Line: high glucose (HG)-injured human umbilical vein endothelial cells (HUVECs)
Concentration: 5, 10 and 20 μM
Incubation Time: 24 h
Result: Reduced the percentage of apoptotic HUVECs with condensed/fragmented nuclei in a concentration-dependent manner, relative to HG-only treated cells.

Apoptosis Analysis[1]

Cell Line: CoCl2-injured human umbilical vein endothelial cells (HUVECs)
Concentration: 5, 10 and 20 μM
Incubation Time: 12 h
Result: Reduced the percentage of apoptotic HUVECs with condensed/fragmented nuclei in a concentration-dependent manner, relative to CoCl2-only treated cells.

Western Blot Analysis[1]

Cell Line: ox-LDL-injured human umbilical vein endothelial cells (HUVECs)
Concentration: 5, 10 and 20 μM
Incubation Time: 6 h
Result: Concentration-dependently reduced the ox-LDL-induced upregulation of ICAM-1 and VCAM-1 protein levels, with greater efficacy than tBHQ.

Western Blot Analysis[1]

Cell Line: high glucose (HG)-injured human umbilical vein endothelial cells (HUVECs)
Concentration: 5, 10 and 20 μM
Incubation Time: 24 h
Result: Concentration-dependently reduced the HG-induced upregulation of ICAM-1 and VCAM-1 protein levels, with greater efficacy than tBHQ.

Western Blot Analysis[1]

Cell Line: CoCl2-injured human umbilical vein endothelial cells (HUVECs)
Concentration: 5, 10 and 20 μM
Incubation Time: 12 h
Result: Concentration-dependently reduced the CoCl2-induced upregulation of ICAM-1 and VCAM-1 protein levels, with greater efficacy than tBHQ.
In Vivo

Nrf2 activator-25 (Compound 3h) (1 mg/kg; i.p.; daily; 8 weeks) robustly attenuates endothelial damage and vascular fibrosis in STZ (HY-13753)-induced diabetic mice, while reducing apoptosis, lipid peroxidation, and restoring glutathione levels[1].

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

Animal Model: C57BL/6 (male, 6-8 weeks old, STZ-induced diabetes)[1]
Dosage: 1 mg/kg
Administration: i.p.; daily; 8 weeks
Result: Significantly alleviated intimal damage and vascular fibrosis, with lower relative fibrosis severity compared to the STZ-only group.
Reduced the proportion of apoptotic cells in the thoracic aortic endothelium compared to the STZ-only group.
Decreased aortic tissue MDA and LPO content relative to the STZ-only group.
Increased aortic tissue GSH content relative to the STZ-only group.
Molecular Weight

259.30

Formula

C15H17NO3

SMILES

O=C(N1C=CC=C1)OC2=CC=C(O)C(C(C)(C)C)=C2

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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  • 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.

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Product Name:
Nrf2 activator-25
Cat. No.:
HY-183353
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