venezuelan

EIDD-1931 (Beta-d-N4-hydroxycytidine) is a ribonucleoside analog with antiviral activity that inhibits the replication of severe acute respiratory syndrome coronavirus [SARS-CoV] in Vero 76 cells, Middle East respiratory syndrome coronavirus [MERS-CoV] in Calu-3 2B4 cells, and SARS-CoV-2 in Vero cells (IC50s = 0.1, 0.15, and 0.3 μM, respectively).

ML-336 is an inhibitor of of the Venezuelan equine encephalitis virus (VEEV) strain TC-83.

Encephalitic alphavirus-IN-1 inhibited the activity of Venezuelan equine encephalitis virus (VEEV) (EC50: 0.24 μM) and eastern equine encephalitis virus (EEEV) (EC50: 0.16 μM). encephalitic alphavirus-IN-1 was not significantly cytotoxic and exhibited strong plasma stability in mice.

nsP2 Protease-IN-1 is a potent irreversible covalent inhibitor of the nsP2 cysteine protease of the Chikungunya (CHIKV) virus, exhibiting an IC50 of 60 nM. This compound demonstrates strong antiviral activity by inhibiting the replication of CHIKV and Venezuelan equine encephalitis virus (VEEV), with EC50 values of 0.01 µM and 0.3 µM, respectively.

STING agonist C11 is an agonist of the stimulator of interferon genes (STING) pathway.1 It induces secretion of type I IFN from THF and MM6 cells when used at a concentration of 50 μM. STING agonist C11 induces phosphorylation of IFN regulatory factor 3 (IRF3) and increases expression of IFIT1 and viperin, but not IL-1β, IL-6, or IL-8 in THF cells in a STING-dependent manner. It reduces viral titers of chikungunya, Venezuelan equine encephalitis, o'nyong-nyong, Mayaro, and Ross River viruses grown in THF cells (EC90s = 16.44, 16.7, 18.84, 25.19, and 22.57 μM, respectively), an effect that is dependent on the presence of STING and the IFN-α/β receptor (IFNAR).References1. Gall, B., Pryke, K., Abraham, J., et al. Emerging alphaviruses are sensitive to cellular states induced by a novel small-molecule agonist of the STING pathway. J. Virol. 92(6), e01913-01917 (2018). STING agonist C11 is an agonist of the stimulator of interferon genes (STING) pathway.1 It induces secretion of type I IFN from THF and MM6 cells when used at a concentration of 50 μM. STING agonist C11 induces phosphorylation of IFN regulatory factor 3 (IRF3) and increases expression of IFIT1 and viperin, but not IL-1β, IL-6, or IL-8 in THF cells in a STING-dependent manner. It reduces viral titers of chikungunya, Venezuelan equine encephalitis, o'nyong-nyong, Mayaro, and Ross River viruses grown in THF cells (EC90s = 16.44, 16.7, 18.84, 25.19, and 22.57 μM, respectively), an effect that is dependent on the presence of STING and the IFN-α/β receptor (IFNAR). References1. Gall, B., Pryke, K., Abraham, J., et al. Emerging alphaviruses are sensitive to cellular states induced by a novel small-molecule agonist of the STING pathway. J. Virol. 92(6), e01913-01917 (2018).

NHC-diphosphate, a phosphorylated intracellular metabolite of β-d-N4-Hydroxycytidine (NHC) in its diphosphate form[1], serves as a potent antiviral agent. As a pyrimidine ribonucleoside, NHC effectively counters the replication of Venezuelan equine encephalitis virus (VEEV), Chikungunya virus (CHIKV), and hepatitis C virus (HCV)[1].

AAK1-IN-6 is an inhibitor of AP-2 associated protein kinase 1 (AAK1, IC50 = 12 nM) and exhibits antiviral activity against Dengue virus (DNEV2, EC50 = 0.24 μM) and Venezuelan equine encephalitis virus (VEEV, EC50 = 0.30 μM). AAK1-IN-6 is applicable in antiviral research.