2. NF-κB Metabolic Enzyme/Protease Immunology/Inflammation Apoptosis
  3. NF-κB Keap1-Nrf2 Heme Oxygenase (HO) Interleukin Related TNF Receptor Reactive Oxygen Species (ROS) SOD
  4. NF-κB-IN-20

NF-κB-IN-20 is an orally active NF-κB inhibitor. NF-κB-IN-20 directly binds to the Keap1 protein, activating the Keap1/Nrf2/HO-1 antioxidant pathway, and simultaneously inhibiting the NF-κB inflammatory pathway, thereby synergistically reducing oxidative stress and inflammatory responses. NF-κB-IN-20 M11 inhibits the expression of IL-6, IL-1β, and TNF-α, significantly reduces the level of ROS, and restores the mitochondrial membrane potential. NF-κB-IN-20 can be used for the study of acute lung injury (ALI).

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

NF-κB-IN-20

NF-κB-IN-20 Chemical Structure

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NF-κB-IN-20 Related Antibodies

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Description

NF-κB-IN-20 is an orally active NF-κB inhibitor. NF-κB-IN-20 directly binds to the Keap1 protein, activating the Keap1/Nrf2/HO-1 antioxidant pathway, and simultaneously inhibiting the NF-κB inflammatory pathway, thereby synergistically reducing oxidative stress and inflammatory responses. NF-κB-IN-20 M11 inhibits the expression of IL-6, IL-1β, and TNF-α, significantly reduces the level of ROS, and restores the mitochondrial membrane potential. NF-κB-IN-20 can be used for the study of acute lung injury (ALI)[1].

IC50 & Target[1]

NF-κB

 

IL-6

 

IL-1β

 

HO-1

 

In Vitro

NF-κB-IN-20 (Compound M11) (0.01‑100 μM, 5 h) exhibits good in vitro safety (CC50 > 100 μM) in LPS (HY-D1056)-induced Raw264.7 cells, attenuates the mRNA expression levels of the inflammatory and oxidative stress markers IL-6 (IC50 = 6.55 μM), IL-1β, TNF-α, and SOD in a dose-dependent manner and inhibits ROS expression, enhances mitochondrial membrane potential, therefore mitigating LPS-induced cellular damage[1].

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

NF-κB-IN-20 Related Antibodies

RT-PCR[1]

Cell Line: Raw264.7 cells
Concentration: 25, 50 and 100 μM
Incubation Time: 1 h and stimulated with LPS for 4 h.
Result: Reduced the mRNA expressions of IL-6, IL-1β, and TNF-α and increased the mRNA expression of SOD.
Parmacokinetics[1]
Species Dose Route Indicator value
Mice 5 mg/kg p.o. AUC0-t 14 ng·h/mL
Mice 1 mg/kg i.v. AUC0-t 142 ng·h/mL
Mice 1 mg/kg i.v. AUC0-∞ 144 ng·h/mL
Mice 5 mg/kg p.o. AUC0-∞ 16 ng·h/mL
Mice 5 mg/kg p.o. Cmax 35 ng/mL
Mice 1 mg/kg i.v. Cmax 184 ng/mL
Mice 5 mg/kg p.o. T1/2 0.51 h
Mice 1 mg/kg i.v. T1/2 0.33 h
Mice 5 mg/kg p.o. Tmax 0.25 h
Mice 1 mg/kg i.v. Vd 3332.24 mL/kg
Mice 5 mg/kg p.o. F 1.99 %
Mice 1 mg/kg i.v. CL 7069.13 mL/h/kg
In Vivo

NF-κB-IN-20 (Compound M11) (15-60 mg/kg, i.g., once daily for 7 days) alleviates ALI induced lung injury and oxidative stress in mice, and inhibits collagen formation and polarization of M1 macrophages[1].
NF-κB-IN-20 (15-60 mg/kg, i.g., once daily for 7 days) enhances sputum secretion and mitigated coughing in mice, thereby contributing to the management of pulmonary diseases[1].
NF-κB-IN-20 (500 mg/kg, i.g., single dose) exhibits good in vivo safety profile in SD rats during the 14-day During the 14-day observation period[1].

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

Animal Model: LPS induced ALI model established in five-to six-week-old male BALB/c mice[1]
Dosage: 15, 30 and 60 mg/kg
Administration: Oral gavage (i.g.), once daily for 7 days
Result: Significantly reduced the total number of inflammatory cells in BALF.
Enhanced the activities of SOD and GSH-Px in lung tissue, while reducing the level of ROS, effectively reversing the oxidative stress caused by LPS.
Improved the pathological phenomena such as inflammatory cell infiltration, destruction of alveolar structure, and thickening of alveolar septa.
Inhibited the expression of M1-type macrophage markers (iNOS, CD86), while promoting the expression of M2-type markers (Arg-1, CD163).
Animal Model: Cecal puncture induced ALI model established in five-to six-week-old male BALB/c mice[1]
Dosage: 15, 30 and 60 mg/kg
Administration: Oral gavage (i.g.), once daily for 7 days
Result: Alleviated lung injury caused by sepsis infection.
Ameliorated inflammatory cell infiltration, alleviated alveolar atrophy, and inhibited collagen formation and fibrosis.
Reversed the expression of inflammatory cytokine and oxidative stress related factors.
Animal Model: 5 % ammonia-induced cough assay established in five-to six-week-old male BALB/c mice[1]
Dosage: 15, 30 and 60 mg/kg
Administration: Oral gavage (i.g.), once daily for 7 days
Result: Demonstrated a significant increase in phenol red secretion in the BALF.
Led to a prolonged cough latency period and a decreased frequency of coughs.
Molecular Weight

353.41

Formula

C21H23NO4
SMILES

O=C(N(C)/C=C\C1=CC=CC=C1)/C=C/C2=CC(OC)=C(OC)C(OC)=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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NF-κB-IN-20 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:

NF-κB-IN-20NF-κBKeap1-Nrf2Heme Oxygenase (HO)Interleukin RelatedTNF ReceptorReactive Oxygen Species (ROS)SODNuclear factor-κBNuclear factor-kappaBHeme OxygenaseILTumor Necrosis Factor ReceptorTNFRSuperoxide DismutaseAcute lung injuryAnti-inflammationLansiummaide B analoguesOxidative stressInhibitorinhibitorinhibit

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