Cancer immunotherapy aims to harness the immune system of patients to target and eliminate cancer cells. In particular, immune checkpoint blockade (ICB) therapy using antibodies to target ligands and receptors involved in the immune checkpoint, such as programmed cell death protein 1 (PD-1), programmed cell death ligand 1 (PD-L1), and cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4), has made a clinical impact in the treatment of patients with advanced-stage cancers, including lung cancer and melanoma 1, 2. However, the proportion of patients responding to ICB therapy is still limited to < 30% [2].

A promising approach to improve cancer immunotherapy is to augment the innate immune system’s capacity to recognize and mount an immune attack against cancer cells by immune adjuvants. One of the prominent candidates is the agonists of the cyclic guanosine monophosphate (GMP)–adenosine monophosphate (AMP) synthase (cGAS)-Stimulator of Interferon Genes (STING) pathway, which plays a critical role in the body's defense mechanisms against viruses, bacteria, and malignant cells [3]. The STING protein (DNA sensor) is located in the cellular cytosol and activated by foreign and abnormal DNA of the invaders. Its activation initiates a series of intricate signaling cascades, leading to the production of type-I interferons (IFNs) and other proinflammatory cytokines, such as tumor necrosis factor (TNF)-α [3]. Those secreted cytokines activate immune cells such as T cells and natural killer cells (NK cells) to recognize and eliminate cancer cells. Owing to the strong immunostimulatory effect of the STING pathway, its agonists have emerged as promising candidates for standalone therapeutics or adjuvant drugs in cancer immunotherapy [4].