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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- CAS. Nr.: 117666-86-1
- Formel: C14H18O4S
- Molecular Weight:282.36
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
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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.
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Cell Line:primary human umbilical cord endothelial cells
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Concentration:70 μM
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Incubation Time:1, 2, 4, 6 h (pre-treatment); 1, 2 h (post-treatment); 16 h (total incubation)
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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.
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Cell Line:primary human umbilical cord endothelial cells
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Concentration:70 μM
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Incubation Time:2 h pre-treatment; 4 h TNF-α induction
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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.
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Cell Line:primary human umbilical cord endothelial cells
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Concentration:70 μM
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Incubation Time:2 h pre-treatment; 30 min TNF-α induction
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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.
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Cell Line:Beas-2B human bronchial epithelial cells
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Concentration:0.01, 0.1, 1, 5, 10, 20 μM
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Incubation Time:16 h
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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.
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Cell Line:Beas-2B human bronchial epithelial cells
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Concentration:5, 10 μM
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Incubation Time:16 h
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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.
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Cell Line:Beas-2B human bronchial epithelial cells
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Concentration:10 μM (alone or with 10 mM NAC)
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Incubation Time:24 h
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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.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (8-10 week old male; ovalbumin-sensitized and challenged asthma model)[4]
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Dosage:0.1 mg/kg; 1 mg/kg; 10 mg/kg; 15 mg/kg
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Administration:p.o.; twice daily; 12 days
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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.
Chemical Information
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CAS. Nr. 117666-86-1
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Molecular Weight 282.36
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Formel C14H18O4S
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SMILES
S=C(/C=C/C1=CC(OC)=C(C(OC)=C1)OC)OCC
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[1]. Kumar S, et al. Novel natural product-based cinnamates and their thio and thiono analogs as potent inhibitors of cell adhesion molecules on human endothelial cells. European journal of medicinal chemistry. 2011 Nov;46(11):5498-511. [Content Brief]
[2]. Kumar S, et al. Ethyl 3',4',5'-trimethoxythionocinnamate modulates NF-κB and Nrf2 transcription factors. European journal of pharmacology. 2013 Jan 30;700(1-3):32-41. [Content Brief]
[3]. Kumar S, et al. Anti-inflammatory and antioxidant properties of Piper species: a perspective from screening to molecular mechanisms. Current topics in medicinal chemistry. 2015;15(9):886-93. [Content Brief]
[4]. Kumar S, et al. A novel cinnamate derivative attenuates asthma features and reduces bronchial epithelial injury in mouse model. International immunopharmacology. 2013 Jan;15(1):150-9. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
ETMTC Related Classifications
HY-183448 Related Classifications
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