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STING agonists and inhibitors act on an adaptor protein of the cytosolic DNA sensing pathway. Stimulator of interferon genes (STING) was described in 2008 as an endoplasmic reticulum adaptor needed for innate immune signaling and type I interferon induction. STING binds cyclic dinucleotides directly, both bacterial molecules such as cyclic di-GMP and the mammalian second messenger made by cyclic GMP-AMP synthase (cGAS) once it detects cytosolic DNA. Agonists listed here include 2',3'-cGAMP, Cyclic-di-GMP, ADU-S100 disodium salt (MIW815 disodium salt) and numbered compounds such as STING agonist-1. Inhibitors include H-151 and the mouse-directed C-176 and C-178, which belong to a class of covalent compounds that modify a cysteine of the transmembrane region.
H-151 is a highly potent, selective and covalent antagonist of STING, reduces TBK1 phosphorylation and suppresses human STING palmitoylation.
STING antagonist-1 is a selective antagonist of the Stimulator of Interferon Genes (STING) pathway, exhibiting an IC50 of 3.8 nM. This compound is valuable for research applications related to autoimmune and inflammatory diseases, allowing for the investigation of STING-mediated cellular responses and therapeutic interventions.
STING antagonist-3 is a highly effective antagonist of the stimulator of interferon genes (STING) with an IC50 of 2.3 nM against human wild-type STING, as well as against the gain-of-function mutants N154S and V155M. This compound has been shown to inhibit the production of IFN-α2a in stimulated human whole blood and to reduce IP-10 levels in activated human dermal microvascular endothelial cells (HMVEC-d). STING antagonist-3 is valuable for research in autoimmune diseases, autoinflammatory diseases, interferonopathies, and fibrotic disorders.
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