ETMTC

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.