| Description |
KRN2 is a selective inhibitor of nuclear factor of activated T cells (NFAT5), with an IC50 of 0.1 μM.
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| Related Catalog |
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| Target |
IC50: 0.1 μM (NFAT5)[1]
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| In Vitro |
KRN2 shows much stronger inhibition of NFAT5-dependent reporter activity in RAW 264.7 macrophages than does BBR; the IC50 value is 0.1 μM for KRN2 and 4 μM for BBR. In parallel, 0.5 μM of KRN2 significantly suppresses the LPS-stimulated increase in NFAT5 protein expression in RAW 264.7 macrophages. It is confirmed that LPS-induced NFAT5 mRNA and protein expression is nearly completely blocked by KRN2. Similarly, KRN2 inhibits the translocation of NFAT5 into the nucleus of RAW264.7 cells stimulated with LPS. KRN2 specifically represses LPS-induced NFAT5 promoter activity, whereas it fails to reduce high salt-induced NFAT5 activity in the same cells, which is consistent with the selective inhibition of TLR4-activated NFAT5, but not hypertonicity-induced NFAT5, by KRN2[1].
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| Cell Assay |
ROS production by RAW 264.7 cells stimulates with LPS (1 µg/mL) in the presence or absence of KRN2 (0.8 µM). ROS expression is determined by flow cytometry using a ROS probe. KRN2 (0.8 µM) is added to RAW 264.7 cells, which are then stimulated with LPS (1 µg/mL) in a time-dependent manner. Activity (%) of p38 isoform is measured in stable cell lines (CHO) in the presence of KRN2 or BBR, using a promoter reporter assay. Cells are treated with KRN2 in various doses (0.5, 1, 2, 5 μM) before stimulation with LPS (1 µg/mL) for 5 minutes and then fractionated into cytosolic extracts (upper panel) and nuclear extracts (lower panel)[1].
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| References |
[1]. Han EJ, et al. Suppression of NFAT5-mediated Inflammation and Chronic Arthritis by Novel κB-binding Inhibitors. EBioMedicine. 2017 Apr;18:261-273.
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