2. NF-κB Apoptosis Metabolic Enzyme/Protease Immunology/Inflammation
  3. NF-κB Keap1-Nrf2 Caspase Heme Oxygenase (HO) Reactive Oxygen Species (ROS)
  4. ETMTC

ETMTC is an orally active anti-inflammatory and antioxidant agent. ETMTC inhibits IKK-mediated phosphorylation and degradation of IkBα, blocks nuclear translocation and activation of NF-κB, and reduces the expression of ICAM-1, VCAM-1, E-selectin, Th2 cytokines and eosinophil chemokines. ETMTC abrogates neutrophil adhesion to endothelial monolayers and inhibits TNF-α-induced ROS production. ETMTC activates Nrf2, and enhances the activities of mitochondrial complex I and IV. ETMTC reduces lipid peroxidation levels, oxidative DNA damage, cytochrome c and caspase 9 activity, and decreases goblet cell metaplasia and subepithelial fibrosis. ETMTC can be used for the research of inflammatory diseases and asthma.

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ETMTC

ETMTC Chemical Structure

CAS No. : 117666-86-1

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ETMTC Related Antibodies

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HO-1 HO-2

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Description

ETMTC is an orally active anti-inflammatory and antioxidant agent. ETMTC inhibits IKK-mediated phosphorylation and degradation of IkBα, blocks nuclear translocation and activation of NF-κB, and reduces the expression of ICAM-1, VCAM-1, E-selectin, Th2 cytokines and eosinophil chemokines. ETMTC abrogates neutrophil adhesion to endothelial monolayers and inhibits TNF-α-induced ROS production. ETMTC activates Nrf2, and enhances the activities of mitochondrial complex I and IV. ETMTC reduces lipid peroxidation levels, oxidative DNA damage, cytochrome c and caspase 9 activity, and decreases goblet cell metaplasia and subepithelial fibrosis. ETMTC can be used for the research of inflammatory diseases and asthma[1][2][3][4].

IC50 & Target[2][4]

NF-κB

 

Caspase-9

 

In Vitro

ETMTC (2.5-20 μg/mL; 2 h pre-incubation) potently inhibits TNF-α-induced expression of ICAM-1, VCAM-1 and E-selectin in primary human umbilical vein endothelial cells, with an IC50 of 10 μg/mL for the inhibition of ICAM-1[1].
Pre-incubation with ETMTC (20 μg/mL) for 2 h inhibits the TNF-α-induced expression of ICAM-1, VCAM-1 and E-selectin on human primary umbilical vein endothelial cells by over 95%, as detected by flow cytometry[1].
ETMTC (2.5-20 μg/mL; 2 h pre-incubation) potently inhibits TNF-α-induced adhesion of neutrophils to primary human umbilical vein endothelial cells in a concentration-dependent manner[1].
ETMTC (compound 54) (70 μM; 1-6 h pre-treatment, 1-2 h post-treatment, 16 h total incubation) potently inhibits TNF-α-induced ICAM-1 expression in primary human umbilical vein endothelial cells. However, it exerts this effect only when administered before or concurrently with TNF-α treatment, and shows no such effect when administered after TNF-α induction[2].
ETMTC (70 μM; 2 h pre-treatment, 4 h TNF-α induction) significantly inhibits TNF-α-induced transcription of ICAM-1, VCAM-1 and E-selectin genes in primary human umbilical vein endothelial cells; it suppresses TNF-α-induced nuclear translocation of the NF-κB p65 subunit in primary human umbilical vein endothelial cells; and it inhibits TNF-α-induced activation of NF-κB in primary human umbilical vein endothelial cells and A549 lung epithelial cells[2].
ETMTC (70 μM; 2-4 h pre-treatment, 5-60 min TNF-α induction) inhibits TNF-α-induced phosphorylation and degradation of IkBα, as well as suppresses IKK kinase activity, in human primary umbilical vein endothelial cells[2].
ETMTC (70 μM; 2 h pre-treatment, 30 min TNF-α induction) completely inhibits TNF-α-induced reactive oxygen species production in primary human umbilical vein endothelial cells[2].
ETMTC (0.01-20 μM; 16 h) induces concentration-dependent expression of Nrf2-regulated antioxidant genes GCLM, HO1, and NQO1 in human bronchial epithelial cells Beas-2B[2].
ETMTC (5-10 μM; 16 h) upregulates the expression levels of Nrf2-regulated antioxidant proteins NQO1 and HO1, downregulates the level of Nrf2 inhibitor Keap1, and upregulates the level of Nrf2 activator DJ-1 in human bronchial epithelial cells Beas-2B[2].
ETMTC (0.01-10 μM; 16 h) induces concentration-dependent activation of Nrf2-mediated transcription in human bronchial epithelial cells Beas-2B[2].
ETMTC (10 μM; 24 h) activates the expression of Nrf2-regulated antioxidant genes in Beas-2B human bronchial epithelial cells in a reactive oxygen species-dependent manner[2].
ETMTC (0.01-20 μM) inhibits TNF-α-induced reactive oxygen species production in human endothelial cells and induces concentration-dependent expression of Nrf2-regulated antioxidant genes in human bronchial epithelial cells[3].

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

ETMTC Related Antibodies

ELISA Assay[2]

Cell Line: primary human umbilical cord endothelial cells
Concentration: 70 μM
Incubation Time: 1, 2, 4, 6 h (pre-treatment); 1, 2 h (post-treatment); 16 h (total incubation)
Result: Significantly inhibited TNF-α-induced ICAM-1 expression when added prior to or simultaneously with TNF-α, with pre-treatment showing time-dependent efficacy.
Did not significantly inhibit TNF-α-induced ICAM-1 expression when added after TNF-α induction.

RT-PCR[2]

Cell Line: primary human umbilical cord endothelial cells
Concentration: 70 μM
Incubation Time: 2 h pre-treatment; 4 h TNF-α induction
Result: Significantly reduced TNF-α-induced transcript levels of ICAM-1, VCAM-1, and E-selectin.
Had no effect on basal transcript levels of ICAM-1, VCAM-1, and E-selectin.
Did not alter β-actin transcript levels.

Western Blot Analysis[2]

Cell Line: primary human umbilical cord endothelial cells
Concentration: 70 μM
Incubation Time: 2 h pre-treatment; 30 min TNF-α induction
Result: Prevented TNF-α-induced decrease in cytoplasmic NF-κB p65 levels.
Prevented TNF-α-induced increase in nuclear NF-κB p65 levels.
Had no effect on basal NF-κB p65 localization.

Real Time qPCR[2]

Cell Line: Beas-2B human bronchial epithelial cells
Concentration: 0.01, 0.1, 1, 5, 10, 20 μM
Incubation Time: 16 h
Result: Caused concentration-dependent increase in GCLM, HO1, and NQO1 transcript levels.
Induced initial increases in GCLM, HO1, and NQO1 transcript levels at 1 μM, with robust induction at 20 μM.
Induced significantly higher levels of GCLM, HO1, and NQO1 genes at 10 μM compared to sulforaphane at the same concentration.

Western Blot Analysis[2]

Cell Line: Beas-2B human bronchial epithelial cells
Concentration: 5, 10 μM
Incubation Time: 16 h
Result: Significantly increased protein levels of NQO1 and HO1 in a concentration-dependent manner.
Significantly decreased protein levels of the Nrf2 inhibitor Keap1.
Significantly increased protein levels of the Nrf2 activator DJ-1.

Real Time qPCR[2]

Cell Line: Beas-2B human bronchial epithelial cells
Concentration: 10 μM (alone or with 10 mM NAC)
Incubation Time: 24 h
Result: Significantly increased GCLM, HO1, and NQO1 transcript levels when applied alone.
Had its induced increase in GCLM, HO1, and NQO1 transcript levels completely abolished by co-treatment with NAC.
In Vivo

ETMTC (0.1-15 mg/kg; p.o.; twice daily; 12 days), at an optimal dose of 10 mg/kg, reduces airway hyperresponsiveness, inflammation, epithelial injury, and airway remodeling features in ovalbumin-induced asthmatic BALB/c mice by inhibiting NF-κB activation, restoring mitochondrial function, and modulating Th2 cytokine and adhesion molecule expression[4].

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

Animal Model: BALB/c (8-10 week old male; ovalbumin-sensitized and challenged asthma model)[4]
Dosage: 0.1 mg/kg; 1 mg/kg; 10 mg/kg; 15 mg/kg
Administration: p.o.; twice daily; 12 days
Result: Boosted MCh PC200 Penh vs OVA vehicle; 10 mg/kg served as optimal dose.
Cut airway resistance, inflammation scores, lung ICAM-1/VCAM-1/E-selectin/IL-4/IL-5/eotaxin/8-isoprostane.
Suppressed lung NF-κB, serum OVA-IgE/IgG1; restored mitochondrial I/IV; lowered cytochrome c/caspase 9.
Lessened BALF 8-OHdG, epithelial TUNEL, goblet metaplasia/collagen buildup; recovered 15-(S)-HETE.
Molecular Weight

282.36

Formula

C14H18O4S
CAS No.
SMILES

S=C(/C=C/C1=CC(OC)=C(C(OC)=C1)OC)OCC
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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ETMTC 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:

ETMTC117666-86-1NF-κBKeap1-Nrf2CaspaseHeme Oxygenase (HO)Reactive Oxygen Species (ROS)Nuclear factor-κBNuclear factor-kappaBHeme OxygenaseICAM-1E-selectinNrf2primary human umbilical cord vein endothelial cellsKeap1IKKIkBαVCAM-1DJ-1Inhibitorinhibitorinhibit

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