DDO-6513

DDO‑6513 (0.39‑50 μM; 12 h) inhibits cGAMP-stimulated STING-dependent IRF reporter gene activity in THP‑1‑Dual cells with an IC₅₀ of 1.93 μM^[1].
DDO‑6513 (3.13‑50 μM; 12‑24 h) does not exhibit significant cytotoxicity in THP‑1 and WI‑38 cells^[1].
DDO‑6513 (5-20 μM; 24 h) blocks the recruitment of TBK1 to STING in cGAMP-stimulated THP-1 and HFF cells, reduces the phosphorylation levels of TBK1 and IRF3, and inhibits IRF3 dimerization and nuclear translocation^[1].
DDO‑6513 induces the formation of high-order abnormal oligomers in purified human STING-CTD protein in vitro^[1].
DDO‑6513 (20 μM; 12-24 h) induces the formation of STING punctate aggregates and blocks the trafficking of STING from the endoplasmic reticulum to the Golgi apparatus in HeLa and WI‑38 cells overexpressing GFP‑STING^[1].
DDO‑6513 (10 μM; 24 h) reduces the elevated expression levels of ISG-related genes in PBMCs derived from AGS, DM, and SLE donors^[1].
DDO‑6513 (10 μM; 18-24 h) inhibits the mRNA expression of IFNB1, CXCL10, and IL6 induced by multiple STING agonists including cGAMP, dsDNA, c‑di‑GMP, and HT‑DNA in THP‑1 cells; it also suppresses the mRNA expression of IFNB1, CXCL10, and ISG56 in HEK293T cells transfected with SAVI-associated gain-of-function STING mutants ^[1].

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