H-151 is a highly potent and selective STING antagonist. H-151 covalently binds to Cys91 of STING and inhibits palmitoylation of Cys91, thereby inhibiting STING activity. H-151 can be used in the study of autoinflammatory diseases in vivo and ex vivo.

BMDMs:109.6 nM, HFF cells:134.4 nM, MEF cells:138 nM

METHODS: Mouse monocyte macrophage RAW264.7 was treated with H-151 (0.25-2 μM) for 1 h, and then stimulated with rmCIRP (1 μg/mL) for 24 h. The level of IFN-β was measured by ELISA.
RESULTS: IFN-β was dose-dependently reduced in the culture supernatant of cells pretreated with H-151, which inhibited eCIRP-induced activation of STING in vitro. [1]
METHODS: Human monocytes THP-1 were treated with H-151 (0.5 μM) for 2 h, and the expression levels of target proteins were measured by Western Blot.
RESULTS: H-151 inhibited the phosphorylation of TBK1, and H-151 effectively inhibited the activation of hsSTING. [2]

METHODS: To assay in vivo activity, H-151 (750 nmol, 200 μL) was administered intraperitoneally to Trex1-/- Ifnb1Δβ-luc/Δβ-luc reporter mice once daily for seven days.
RESULTS: When administered for one week, H-151 showed significant efficacy in Trex1-/- mice expressing a bioluminescent IFNβ reporter gene. [2]
METHODS: To test the role in cisplatin-induced acute kidney injury (AKI), H-151 (7 mg/kg) was administered intraperitoneally to C57BL/6J mice with cisplatin-induced AKI three times a day.
RESULTS: H-151 treatment significantly ameliorated cisplatin-induced renal injury, as evidenced by improvement in renal function, renal morphology, and renal inflammation.H-151 may be a potential therapeutic agent for the treatment of AKI, possibly by inhibiting STING-mediated inflammation and mitochondrial damage. [3]

Ethanol: 14.08 mg/mL (50.4 mM), Sonication is recommended.

DMSO: 100 mg/mL (357.99 mM), Sonication is recommended.

10% DMSO+40% PEG300+5% Tween 80+45% Saline: 12.5 mg/mL (44.75 mM), Suspension.

5% DMSO+40% PEG300+5% Tween 80+50% Saline: 5 mg/mL (17.9 mM)