NS-3-008 (5 mg/kg; oral administration; daily; for 4 weeks; wild-type 5/6Nx mice) treatment results in decreased levels of G0s2 and Ccl2 mRNA in the kidneys. The phosphorylation of Stat5 and p65 protein is decreased, and SUN concentrations and renal caspase 3/7 activity decreased in 5/6Nx mice treated with NS-03-08. The F4/80-positive area and F4/80 protein levels are decreased in 5/6Nx mice treated with NS-3-008[1].
In Vitro
NS-3-008 binds to Hsd17b4; knockdown of Hsd17b4 decreased G0s2 mRNA levels, whereas overexpression of Hsd17b4 induced G0s2 mRNA expression. The inhibitory effects of NS-3-008 are blocked by knockdown of Hsd17b4 or deletion of the Stat5 binding site in the G0s2 promoter. NS-3-008 decreases the nuclear phosphorylation of Stat5[1].
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Matsunaga N, et al. Inhibition of G0/G1 Switch 2 Ameliorates Renal Inflammation in Chronic Kidney Disease. EBioMedicine. 2016 Nov;13:262-273.
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