STING Inhibitor

H-151 Alkyne (Compound H-151-AL) is a selective STING (Stimulator of interferon genes) inhibitor. H-151 Alkyne is promising for research of autoimmune diseases such as systemic lupus erythematosus, scleroderma, and autoinflammatory diseases.

CCCP (Standard) is the analytical standard of CCCP. This product is intended for research and analytical applications. CCCP is an oxidative phosphorylation (OXPHOS) uncoupler. CCCP induces activation of PINK1 leading to Parkin Ser65 phosphorylation.

SN-008, a less active SN-011 analog, can be used as a negative control.

STING-IN-11 (Compound 42) is an orally active STING inhibitor with an IC₅₀ of 37.8 nM. STING-IN-11 can block the palmitoylation of the STING protein and STING downstream signaling, and inhibit STING-mediated inflammation. STING-IN-11 has good in vivo safety and can be used for the research of STING-related inflammatory and autoimmune diseases.

UM-259 hydrochloride is a STING inhibitor with activity against both murine and human STING (including the STING^R232 mutant). UM-259 hydrochloride inhibits STING-dependent signaling pathways, blocks STING oligomerization, and acts on human primary CD14⁺ monocytes. UM-259 hydrochloride can be used for research on amyotrophic lateral sclerosis, lupus erythematosus, Aicardi-Goutières syndrome, and infant-onset STING-associated vasculopathy.

UM-259 is a STING inhibitor, with an EC₅₀ of 1.50 μM in THP1-Dual cells expressing wild-type STING. UM-259 blocks STING oligomerization and inhibits diABZI-induced phosphorylation of TBK1 and IRF3, thereby suppressing the transcription of IFNβ and IL6 and reducing IFNβ secretion. UM-259 can be used for the study of STING-dependent inflammatory and neurological diseases.

STING-IN-5 is a potent STING inhibitor, inhibiting LPS-induced NO synthesis in macrophages with an IC₅₀ value of 1.15 μM. STING-IN-5 inhibits the inflammatory response. STING-IN-5 can be used to research anti-inflammatory diseases and sepsis.

Jujuboside B (Standard) is the analytical standard of Jujuboside B. This product is intended for research and analytical applications. Jujuboside B is a bioactive saponin component isolated from Ziziphi Spinosae Semen (sour jujube seed), with oral efficacy and blood-brain barrier permeability. Jujuboside B induces acute leukemia cell death and drives necroptosis apoptosis by activating the RIPK1/RIPK3/MLKL pathway. Jujuboside B upregulates the expression of NOXA, PARP and caspase-3, activates AMPK, inhibits the proliferation of breast cancer cells, and induces cell apoptosis and autophagy. Jujuboside B inhibits angiogenesis and tumor growth by blocking the VEGFR-2 signaling pathway. Jujuboside B alleviates liver injury in mice by regulating the Nrf2-STING signaling pathway. Jujuboside B alleviates liver injury by regulating anti-inflammatory responses and downregulating the expression of 11β-HSD2. Jujuboside B induces ferroptosis and overcomes radioresistance in non-small cell lung cancer via the PPARγ-ATF3-Gpx4 signaling pathway. Jujuboside B exerts inhibitory effects on platelet aggregation. Jujuboside B inhibits febrile seizures by suppressing the activity of AMPA receptors. Jujuboside B reverses chronic unpredictable mild stress-promoted tumor progression by blocking the PI3K/Akt and MAPK/ERK pathways and dephosphorylating CREB signaling. Jujuboside B is applicable to related studies on acute leukemia, breast cancer, PM_2.5-induced lung injury, hepatotoxicity, liver injury, colorectal cancer, non-small cell lung cancer, thromboembolic diseases, cardiovascular diseases associated with high platelet aggregation, febrile seizures, and depressive-like phenotypes.

C-di-IMP (Cyclic-di-IMP) is a STING agonist. C-di-IMP can be used for the research of tumor.

STING-IN-19 is a STING inhibitor with a K_d value of 2.31 μM for human STING. STING-IN-19 inhibits the activation of TBK1 and IRF3 by binding to STING, thereby suppressing the activation of downstream signaling pathways. STING-IN-19 reduces the levels of key inflammatory cytokines IL-1β, IL-6 and TNF-α in colonic tissues and serum of mice with ulcerative colitis. STING-IN-19 can be used in studies related to ulcerative colitis.

diABZI-i is an orthogonal STING inhibitor. diABZI-i significantly inhibits cGAMP-induced IFNβ in PBMCs. diABZI-i also activates constitutive signaling of V155M SAVI and exerts potent agonistic effects in the STING V155M THP-1 cell model. diABZI-i can be used for research on monogenic autoinflammatory diseases such as SAVI.

STING-IN-14 is an inhibitor of STING (IC₅₀: 0.6 nM). STING-IN-14 inhibits the activation of the IRF pathway in THP1-Dual^TM cells. STING-IN-14 can be used in autoimmune diseases research.

PPARα agonist 4 (compound BH400) is a PPARα agonist (EC₅₀= 1.2 μM). PPARα agonist 4 also inhibits STING (IC₅₀: 8.1 μM). PPARα agonist 4 reduces the CoCl₂-induced production of ROS and LPS-induced secretion of IL-6. The PPARα agonist 4 restores the decreased expression of PCG1α induced by LPS.

UM-242 is a STING inhibitor, with an EC₅₀ of 1.70 μM in THP1-Dual cells expressing wild-type STING. UM-242 blocks STING oligomerization and inhibits diABZI-induced phosphorylation of TBK1 and IRF3, thereby suppressing the transcription of IFNβ and IL6 and reducing IFNβ secretion. UM-242 can be used for the study of STING-dependent inflammatory and neurological diseases.

STING-IN-17 (compound 10a) is an orally active STING (human STING IC₅₀ = 29 nM, mouse STING IC₅₀ = 15 nM) inhibitor. STING-IN-17 can inhibit the phosphorylation of STING, TBK1 and IRF3. STING-IN-17 dose dependently inhibits the mRNA expression of IP10, IFNB1 and ISG56. STING-IN-17 can reduce ROS and inhibit the expression of cleaved-PARP/caspase-3. STING-IN-17 can improve kidney function. STING-IN-17 can be used for research on inflammatory conditions such as acute kidney injury.

DDO-88109 is a STING inhibitor with a K_d value of 317 nM for hSTING and 0.625 μM for mSTING. DDO-88109 competitively occupies the CDN-binding pocket of STING, thereby maintaining STING in an inactive state. It inhibits cGAS-STING signaling—including STING translocation from the endoplasmic reticulum to the Golgi apparatus, STING oligomerization, and the phosphorylation of IRF3, p65, TBK1, and STING—and attenuates the production of inflammatory cytokines and tissue inflammation in mouse models of TREX1-deficiency-driven autoinflammation and cisplatin (HY-17394)-induced acute kidney injury. DDO-88109 is suitable for research on inflammatory diseases, autoimmune disorders, and acute kidney injury driven by the cGAS-STING pathway.

STING ligand-4 (Compound 2) is a nitro-free covalent STING inhibitor with an IC₅₀ < 0.2 μM. STING ligand-4 can be used for synthesis of PROTAC STING degrader-4 (HY-176180).

STING modulator-3 is a STING inhibitor. STING modulator-3 inhibits R232 STING with an K_i value of 43.1 nM in scintillation proximity assay. STING modulator-3 has no effect on IRF-3 activation or TNF-β induction in THP-1 cells.

STING-IN-18 is an orally active STING inhibitor. STING-IN-18 exhibits an IC₅₀ of 86 nM against STING in murine RAW-Lucia^TM ISG cells. STING-IN-18 inhibits STING activation and blocks downstream signaling pathways. STING-IN-18 suppresses kidney injury and inflammation. STING-IN-18 can be used for the research of autoimmune and inflammatory diseases.

STING-IN-12 (compound Y2) is an inhibitor of STING. STING-IN-12 inhibits IFNβ gene expression (IC₅₀=0.75μM) induced by SR717. STING-IN-12 inhibits STING pathway activation induced by the STING agonist SR717 in THP1 cells and MSA-2-induced STING pathway activation in vivo in mice.