JAK2-IN-20

JAK2-IN-20 (compound 4B) potently protects MDCK cells against damage induced by H1N1 influenza virus (EC₅₀=14.71 nM) and inhibits the cap-binding activity of influenza A PB2 protein (IC₅₀=3.337 nM)^[1].
JAK2-IN-20 exhibits low cytotoxicity in multiple cell lines, with a CC₅₀ of >100 μM (48 h) in MDCK cells^[1].
JAK2-IN-20 (1 μM; 60 min; 37°C) exhibits excellent metabolic stability in mouse liver microsomes, with a half-life of 47.8 min and an intrinsic clearance (CL_int) of 29.0 μL/min/mg^[1].
JAK2-IN-20 (250-2000 nM) binds directly to the cap-binding domain of influenza A virus PB2, with a K_d value of 2.82 μM^[1].
JAK2-IN-20 (5-10 μM; 30 min; 6 h) dose-dependently inhibits LPS (1 μg/mL)-induced expression of pro-inflammatory cytokines (IL-6, IL-1β) and IFN-β in RAW 264.7 macrophages, and exhibits potent activity at 10 μM^[1].
JAK2-IN-20 (5-10 μM; 30 min; 6 h) potently inhibits the expression of poly (I:C)-induced proinflammatory cytokines (IL-6, TNF-α) and type I interferons (IFN-α, IFN-β) in RAW 264.7 macrophages at a concentration of 10 μM^[1].
JAK2-IN-20 (250-500 nM; 24 h) inhibits the expression of H1N1 virus PB2 mRNA and reduces the levels of virus-induced proinflammatory cytokines (IL-6, TNF-α) in A549 cells at a concentration of 500 nM^[1].
JAK2-IN-20 inhibits the JAK/STAT signaling pathway in both H1N1-infected A549 cells and IFN-β-stimulated THP-1 cells by reducing the phosphorylation levels of STAT1 and STAT3^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.