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Direct Activation of STING in the Tumor Microenvironment Leads to Potent and Systemic Tumor Regression and Immunity

Direct Activation of STING in the Tumor Microenvironment Leads to Potent and Systemic Tumor Regression and Immunity

Leticia Corrales, Laura Hix Glickman, Sarah M McWhirter, David B Kanne, Kelsey E Sivick, George E Katibah, Seng-Ryong Woo, Edward Lemmens, Tamara Banda, Justin J Leong, Ken Metchette, Thomas W Dubensky Jr, etc.

Cell Rep. 2015 May 19;11(7):1018-30.

PMID: 25959818

Abstract:

Spontaneous tumor-initiated T cell priming is dependent on IFN-β production by tumor-resident dendritic cells. On the basis of recent observations indicating that IFN-β expression was dependent upon activation of the host STING pathway, we hypothesized that direct engagement of STING through intratumoral (IT) administration of specific agonists would result in effective anti-tumor therapy. After proof-of-principle studies using the mouse STING agonist DMXAA showed a potent therapeutic effect, we generated synthetic cyclic dinucleotide (CDN) derivatives that activated all human STING alleles as well as murine STING. IT injection of STING agonists induced profound regression of established tumors in mice and generated substantial systemic immune responses capable of rejecting distant metastases and providing long-lived immunologic memory. Synthetic CDNs have high translational potential as a cancer therapeutic.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP117570533	DMXAA		117570-53-3	Price

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