cGAMP disodium is a cyclic dinucleotide (CDN) found in bacteria that acts as an endogenous second messenger affecting interferon production in response to cytoplasmic DNA. cGAMP disodium cascades signals from type I interferons and other immune mediators by activating interferon gene stimulator (STING). cGAMP disodium is a potent sublingual immune adjuvant that enables better immune function (serum anti-PA neutralization and airway secretions anti-PA SIgA response).

cGAMP disodium directly activates mouse and human dendritic cells in in vitro experiments [1]. It promotes the antigen-specific proliferative capacity of mouse spleen cells [2]. Furthermore, cGAMP disodium induces the induction of antiviral state and the secretion of type I IFNs through activation of the endoplasmic reticulum (ER)-resident receptor STING [3]. cGAMP disodium causes fibroblasts from patients to exhibit increased transcription of IFNB1, which encodes interleukin-1 (IL1), interleukin-6 (IL6) or tumor necrosis factor (TNF) genes did not show a transcriptional increase [4].

The titers of OVA specific IgA, total IgG, IgG1 and IgG2c in the serum of female C57BL/6 (H-2b) mice were higher than those of OVA immunized mice after the injection of 5μg at 6-8 weeks of age.