ifn a-ifnar-in-1

IFN alpha-IFNAR-IN-1 hydrochloride is an inhibitor of the interaction between IFN-α and IFNAR. IFN alpha-IFNAR-IN-1 hydrochloride inhibits MVA-induced IFN-α responses by BM-pDCs with IC50 of 2-8 μM.

IFN alpha-IFNAR-IN-1 is a nonpeptidic, low-molecular-weight inhibitor of the interaction between IFN-α and IFNAR. It inhibits MVA-induced IFN-α responses by BM-pDCs (IC50: 2-8 μM).

StA-IFN-1 is an inhibitor of the interferon (IFN) induction pathway with an IC50 value of 4.1 μM in a GFP reporter assay for IFN induction similar to TPCA-1 , which specifically inhibits the IKKβ component of the IFN induction pathway. It does not show inhibitory activity in a GFP reporter assay for IFN signaling in which ruxolitinib , which is specific for the IFN signaling component JAK1, is active. StA-IFN-1 reduces the levels of IFN-β, but not ISG MxA, mRNA, suggesting that it is selective for the IFN induction pathway and not the IFN signaling pathway.

IFN-γ Antagonist 1 (AYCRDGKIGPPKLDIRKEEKQI), an interferon γ (IFN γ) antagonist, effectively inhibits IFN-γ induced HLR/DR antigen expression in Colon 205 cells, demonstrating an IC50 of approximately 35 μM. This compound shows promise for applications in immune regulation [1].

IFN-γ Antagonist 1 (AYCRDGKIGPPKLDIRKEEKQI) acetate, an interferon γ (IFN γ) antagonist, effectively inhibits the expression of HLR/DR antigen in Colon 205 cells induced by IFN-γ, with an inhibition concentration (IC 50) of approximately 35 μM. This compound holds promise for applications in immune regulation [1].

IFN-α Receptor Recognition Peptide 1, associated with receptor interactions, is a peptide of IFN-α.

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).