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Verdinexor inhibits the viability of Jurkat, OCI-Ly3, OCI-Ly10, and CLBL1 cells with IC50 of 0.3 nM, 2.1 nM, 41.8 nM, and 8.5 nM, respectively. KPT-335 also induces apoptosis in CLBL1 cells and primary canine DLBCL cells that express XPO1 and SINE. Verdinexor potently and selectively inhibits vRNP export and effectively inhibits the replication of various influenza virus A and B strains, including pandemic H1N1 virus, highly pathogenic H5N1 avian influenza virus, and the recently emerged H7N9 strain. Verdinexor (25 mg/kg twice daily, p.o.) reduces proinflammatory cytokine expression in the lung, produces in vivo antiviral activity by reducing lung virus titers, and thus reduces pulmonary disease pathogenesis and death associated with lethal influenza A virus challenge. In autosomal-dominant polycystic kidney disease model, Verdinexor (5 mg/kg, i.p.) attenuates cyst growth via inhibition of XPO1. For the detailed information of Verdinexor (KPT-335), the solubility of Verdinexor (KPT-335) in water, the solubility of Verdinexor (KPT-335) in DMSO, the solubility of Verdinexor (KPT-335) in PBS buffer, the animal experiment (test) of Verdinexor (KPT-335), the cell expriment (test) of Verdinexor (KPT-335), the in vivo, in vitro and clinical trial test of Verdinexor (KPT-335), the EC50, IC50,and affinity,of Verdinexor (KPT-335), For the detailed information of Verdinexor (KPT-335), the solubility of Verdinexor (KPT-335) in water, the solubility of Verdinexor (KPT-335) in DMSO, the solubility of Verdinexor (KPT-335) in PBS buffer, the animal experiment (test) of Verdinexor (KPT-335), the cell expriment (test) of Verdinexor (KPT-335), the in vivo, in vitro and clinical trial test of Verdinexor (KPT-335), the EC50, IC50,and affinity,of Verdinexor (KPT-335), Please contact DC Chemicals. |
