C92 is a first-in-class allosteric small-molecule human STING agonist designed to activate antitumor immunity by targeting STING’s proton channel rather than the orthosteric cGAMP-binding site. The study shows that C92 activates human STING, drives strong type I interferon signaling, avoids key IFN-independent effects such as autophagy and inflammasome formation, and demonstrates antitumor activity across systemic, oral and intratumoral administration routes. These findings support the translational potential of systemically delivered STING agonists for advanced and/or metastatic cancer immunotherapy.
C92 generated robust antitumor immune responses as a single agent and synergized with checkpoint inhibitor treatment, while its human STING selectivity enabled the authors to show that therapeutic activity can be mediated through STING activation in either tumor cells or non-tumor host cells. The study positions proton channel-blocking allosteric STING agonism as a differentiated strategy to overcome limitations observed with orthosteric STING agonists.
Human STING Knockin C57BL/6 mouse — genOway-developed, syngeneic tumor efficacy model
Immuno-oncology, STING agonist, allosteric agonist, innate immunity, type I interferon, proton channel, tumor microenvironment, checkpoint inhibitor combination, antitumor immunity, solid tumor immunotherapy
Human STING Knockin mouse, preclinical evaluation of human STING-targeting therapeutics, systemic STING agonist activity in syngeneic tumor models
From model design to experimental results
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