hk-2

MDK-3046 is a YycG histidine kinase (HK) inhibitor with potent antibiofim activity against Staphylococcus epidermidis.

L-Ornithine hydrochloride ((S)-2,5-Diaminopentanoic acid) has an antifatigue effect by increasing the efficiency of energy consumption and promoting the excretion of ammonia. It is one of the key reactants in the urea cycle.

Fenoldopam mesylate (Corlopam mesylate) is a selective dopamine-1 receptor (DA1) agonist with natriuretic diuretic properties. It lowers blood pressure through arteriolar vasodilation.

SP4f, an activator of PPAR-γ, exhibits an EC50 value of 826 nM in HK-2 cells. In Swiss albino mice, it diminishes blood glucose levels and lipid peroxidation while enhancing glutathione levels and catalase activity [1].

p-nitro-Pifithrin-α is a cell-permeable analog of pifithrin-α, a potent p53 inhibitor. It suppresses p53-mediated TGF-β1 expression in HK-2 cells and inhibits the activation of caspase-3 by Zika virus (ZIKV) strains. Moreover, p-nitro-Pifithrin-α attenuates steatosis and liver injury in mice subjected to a high-fat diet, mitigating the effects of non-alcoholic fatty liver disease [1] [2] [3] [4].

2a,3a,23-Trihydroxyurs-12,20(30)-dien-28-oic acid (compound 3), a triterpenoid, markedly reduces fibronectin levels by 27.66% at a 10 μM concentration in HK-2 cells subjected to high-glucose and TGF-b1 induction [1].

GSK-3β Inhibitor 17 (compound 5 n) reduces the expression of p-p65 and KIM-1 proteins in a dose-dependent manner (16, 32, 64 µM) induced by cisplatin. Additionally, at a concentration of 32 µM, it decreases the levels of TNF-α, IL-1β, IL-6, and MCP-1 mRNA in an acute kidney injury (AKI) model of HK-2 cells triggered by cisplatin.

SP4e, a PPAR-γ activator, exhibits an EC50 of 739 nM in HK-2 cells. In Swiss albino mice, it diminishes blood glucose and lipid peroxidation while enhancing glutathione levels and catalase activity [1].

RIPK3-IN-4 (Compound 42) is a RIPK3 inhibitor that mitigates necroptosis, inflammatory responses, and HK-2 cell damage. It alleviates acute kidney injury by attenuating Cisplatin- and I R-induced kidney damage, along with associated inflammatory responses and necroptosis [1].