MSA-2 is an orally available non-nucleotide STING agonist. The non-covalent dimer of MSA-2 binds to STING with nanomolar affinity. It shows anti-tumor activity in syngeneic mouse tumor models, synergizes with anti-PD-1, stimulates tumor secretion of interferon-β, induces tumor regression, and has long-lasting anti-tumor immunity. [3]

human STING isoforms HAQ:24 μM, human STING isoforms WT:8.3 μM

METHODS: PK-15 cells were treated with MSA-2 at concentrations of 20, 30, 40 and 50 μM for 24 hours and then infected with SVV at 10 MOI. SVV RNA levels in treated cells were detected by RT-qPCR at 24 h post-infection (hpi).
RESULTS Viral RNA levels in MSA-2-treated cells were significantly reduced in a dose-dependent manner. [2]

METHODS: The EMT-6 mouse model was treated with MSA-2 (50 mg/kg, orally), and the changes in intratumoral cytokines and chemokines after MSA-2 treatment in vivo were explored.
RESULTS IFN-β, IL-6, TNF-α, IFN-γ, and classical activation-associated chemokines including CCL2, CCL3, CCL4, CCL5, CXCL1, CXCL9, and CXCL10 were significantly upregulated in EMT-6 tissues. [1]
METHODS: MSA-2 was orally administered at a single dose of 50 mg/kg to mice bearing U14 and TC-1 cervical tumor models. Mice were treated with 5 mg/kg of anti-PD-1 every other day for a total of 3 treatments. Tumor volume was assessed every other day.
RESULTS The tumor volume of mice was significantly reduced. [2]

Animal Model was MC38 tumor-bearing C57BL6 mice,and The dosage was 60 mg/kg.Administration was P.o.;s.c (50 mg/kg);single dose[1]