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Drugs that trigger the cell's built-in 'virus alarm' inside tumours to summon immune cells.
STING agonists are cyclic dinucleotide or non-nucleotide molecules that activate the STING to TBK1 to IRF3 axis, driving type I interferon and summoning immune cells into the tumour. In models this converts cold tumours, but intratumoural STING agonists (ADU-S100, MK-1454) disappointed in the clinic. Systemic and antibody-conjugated versions (TAK-500, XMT-2056), TLR9 agonists (vidutolimod), and CD40 agonists (sotigalimab) continue in trials as the next attempts. The cGAS-STING pathway also mediates the immune effects of radiation and ADCs, which is why the biology remains important even where the drugs have not worked. Weak clinical activity to date is the central open problem. The simple version is a drug that sets off the cell's built-in virus alarm inside the tumour.
Cyclic dinucleotide or non-nucleotide agonists activate STING → TBK1 → IRF3 → type I interferon.
ADU-S100 was the first STING agonist in the clinic. Injected directly into tumours, it produced almost no responses, alone or with checkpoint blockade.
Query for this technology: (TITLE:"STING agonist" OR ABSTRACT:"STING agonist" OR TITLE:"cGAS-STING" OR ABSTRACT:"cGAS-STING") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about STING & innate immune agonists, not a curated reading list.
Shares Cold tumours: immune deserts and exclusion and the tag frontier.
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Shares Turn one tumour into a vaccine to treat all the others, In situ vaccination, cGAS-STING innate sensing, The cancer-immunity cycle.
Shares Turn one tumour into a vaccine to treat all the others, In situ vaccination, cGAS-STING innate sensing, Cold tumours and the immunosuppressive microenvironment.