Harnessing the innate immune system to combat infectious disease, inflammation, and cancer.


NEWS: STINGINN LLC. receives FDA approval to initiate Phase I Clinical Trial to treat Leukemia.


About Us

STINGINN focuses on harnessing the innate immune system to combat infectious disease, inflammation and cancer. The company was formed around the discoveries of Glen N. Barber and the STING-controlled innate immune pathway. STING is key cellular protein that regulates the production of cytokines required to fight microbial infection and to generate effective anti-tumor immunity. The STING signaling pathway also controls inflammatory responses that can cause many types of autoimmune disease. Controlling STING has enormous potential to help alleviate infectious disease, inflammation and cancer. STINGINN has developed a variety of immunotherapeutic strategies to help achieve these goals. For these discoveries, in 2020 Glen N. Barber received the William B. Coley Award for Distinguished Research in Basic and Tumor Immunology and in 2021 was elected a Fellow of the Royal Society, London.



STINGINN LLC has developed a portfolio of therapeutics to regulate innate immune signaling controlled by STING. STING signaling plays a major role in generating anti-microbial and anti-tumor activity and is implicated in modulating inflammatory responses. STINGINN LLC has played key roles in unraveling the importance of STING in these processes. STINGINN LLC’s pipeline of technologies include:



Nucleic acid-based STING activators

Tumor cells are notoriously non-immunogenic. This is because phagocytes have evolved the ability to remove millions of dying (apoptotic) cells per day without invoking an inflammatory response. Nucleases in the dying cell start to degrade genomic DNA that could otherwise inadvertently trigger innate immune sensors in the engulfing phagocyte. DNases in the phagocyte complete the process.  STAV technology takes advantage of this knowledge and modifies tumor cells with nucleic acid based activators (STAVs) that are resistant to host DNases. Irradiated tumor cells containing STAVs are phagocytosed by antigen presenting cells (APC’s). Engulfed STAVs activate STING signaling in the phagocyte which potently primes T-cells to tumor antigen.   STAV technology (STAV-1) is aimed at stimulating the immune system to fight cancer. Alone, or in synergy with checkpoints, radiation and/or established chemotherapy, STAV strategies offered a new immunoncological approaches for the treatment of cancer.


Novel small molecules

The activation of STING in tumor cells or in tumor infiltrating antigen presenting cells (APCs) potently stimulates anti-tumor T cell activity. STINGINN LLC has developed novel assays to screen for compounds that trigger STING activity. Lead compounds (SA-001) are being evaluated as anti-tumor and anti-viral agents.


STING activity is commonly defective in tumors cells. Loss of STING signaling may enable transformed cells to escape the anti-tumor immunosurveillance system. STINGINN LLC has developed a new generation of oncolytic viruses (V-1, HV-1) that target tumor cells and reconstitute STING signaling, making them highly immunogenic, especially when used in combination with checkpoint inhibitors.


STINGINN LLC has significant expertise in studying the mechanisms of STING function. Live cell-based screens have been developed to isolate new activators or inhibitors of STING signaling for use in the anti-microbial, anti-tumor or inflammatory arenas.


STING signaling is essential for anti-microbial and anti-tumor activity. But chronic stimulation of innate immune pathways may cause autoinflammatory disease including severe systemic lupus erythematosus (SLE), Aicardi Goutieres Syndrome (SLE), graft versus host disease (GVHD), inflammatory bowel disease (IBD) and SAVI (STING associated vasculopathy with onset in infancy). STINGINN LLC has developed novel compounds that target chronic innate immune signaling responsible for a growing catalogue of inflammatory disorders. Lead molecules (SI-001) are being evaluated as a new generation of powerful anti-inflammatory treatments.



In 2008, the laboratory of Glen N. Barber reported the discovery of STING (for stimulator of interferon genes) that controlled a new innate immune signaling pathway. This research lead to elucidating how DNA based microbes trigger host defense countermeasures (Ishikawa and Barber, Nature 2008; Ishikawa, Ma and Barber Nature 2009). The cytosol is supposed to be devoid of DNA species. If DNA species are present, then it likely comes from an invading microbe, from damaged mitochondria or from the nucleus of a DNA-damaged cell. In such circumstances, STING signaling activates cytokine production, likely to attract the immune system to the problematic region. STING is a cytosolic sensor for cyclic dinucleotides (CDN’s; such as GMP-GMP, GMP-AMP). CDN’s are generated by intracellular bacteria or via a cellular synthase referred to as cGAS, which manufactures CDN’s following interaction with cytosolic microbial or self-dsDNA species. Research indicates that that transient STING activity is essential for host defense countermeasures following infection by DNA viruses, bacteria and parasites (Ishikawa and Barber, Nature 2008; Ishikawa et al., Nature 2009; Barber G.N., Nature Immunology Reviews, 2015).

STING Signaling and Cancer

Research has indicated that DNA from dying tumor cells plays an important role in triggering extrinsic STING signaling in engulfing phagocytes (antigen presenting cells; APC’s) Extrinsic STING-dependent cytokine production in APC’s is essential for the efficient cross presentation of tumor cell antigens and the generation of anti-tumor T cell responses. STING-deficient mice do not efficiently generate anti-tumor T cell responses (Woo et al., Immunity 2014). However, tumor cells are notoriously non-immunogenic since their genomic DNA inefficiently actives STING in APC’s. Indeed, tumor cells mimic normal apoptotic cells following phagocytic engulfment and do not generate a robust immune response. This is because DNases in apoptotic cells (DNase III) and phagocytes (DNase II) ensure that all the dead cell’s DNA is degraded to avoid STING-dependent inflammation (Ahn et al., PNAS 2012). Subsequently, this knowledge has enabled STINGINN develop new therapeutic approaches to overcome these obstacle and to make non-immunogenic tumor cells (cold) highly immunogenic (hot) using STING agonists [referred to as STAVs- STING activators] [Ahn et al., Cancer Cell, 2018]. The use of STING agonists are also being evaluated as immunotherapeutic anti-cancer agents, in the clinic.

Autoinflammatory Disease and STING

Research indicates that chronic STING signaling can be a cause inflammatory disease (Ahn et al., PNAS, 2012). In large part, these events arise due to genetic defects in DNAses that normally ensure that any genomic DNA that leaks into the cytoplasm is rapidly degraded prior to activating STING signaling. For example, patients suffering from (Aicardi-Goutieres Syndrome AGS), a severe form of SLE, exhibit defects in DNase III which causes chronic STING signaling manifested by undigested cytosolic self-DNA (Gall et al., Immunity 2012; Ahn et al., J. Immunol, 2014). These observations subsequently raised the possibility that STING-signaling could conceivably be involved in a wide variety of alternate inflammatory malaise. Indeed, it has now been reported that inflammation can be caused by mutations in the STING gene itself, which causes the molecule to be permanently active (STING-associated vasculopathy with onset in infancy- SAVI) (Konno et al., CELL Reports 2018). Evidence also suggests that STING in macrophages interacts with commensal bacteria to maintain gut immune homeostasis (Ahn et al., Cell Reports 2017). Thus, disruption of STING signaling could play a key role in facilitating inflammatory bowel disease (IBD). STING signaling also plays a role in manifesting graft v host disease. Aside from providing significant new mechanistic insight into self-DNA manifested diseases, such research has opened up the notion that drugs that could suppress STING signaling may be beneficial for the treatment of a wide variety of inflammatory disorders.

STING Signaling and Viral Oncolytic Agents

STING SIGNALING AND VIRAL ONCOLYTIC AGENTS: It has been noted that normal cells exhibit resistance to virus infection compared to cancer cells. During the transformation process, cancer cells may have acquired defects in their intrinsic innate immune signaling pathways, which render them susceptible to infection (Balachandran and Barber, Cancer Cell, 2004; Xia et al, Cancer Research 2016). These studies have led to using viruses such as vesicular stomatitis virus (VSV) as therapeutics for the treatment of cancer. Such studies has enabled the initiation of Phase I and soon Phase II trials using recombinant VSV, an RNA virus, as an oncolytic agent (Obuchi et al.Journal of Virology, 2003). Recombinant herpes simplex virus (HSV) a DNA virus, is also being used as an oncolytic virotherapy. The STING pathway and subsequent studies related to STING signaling in cancer cells (or lack of) has shed considerable light into why certain tumors may be susceptible or not to HSV-mediated oncolysis. For example, our investigations indicate that during the transformation process, STING signaling is suppressed (typically by epigenetic silencing of cGAS or STING; Xia et al Cell Reports, 2016). Evidence indicates that carcinogens induce DNA damage and cause the leakage of genomic DNA into the cytosol, which activates STING signaling and cytokine production (Ahn et al., Nature Communications 2014). This alerts the immunosurveillance system which attempts to eliminate the damaged cells, by phagocytosis. This procedure generates anti-tumor T cell activity (Ahn et al., Cancer Cell, 2018). Thus, suppression of STING signaling, while helping to avoid anti-tumor immune responses, inadvertently leaves such cells susceptible to viral oncolytics. STINGINN LLC portfolio includes developing novel viral oncolytics that are designed to reconstitute STING signaling, for use as potent immunotherapeutic agents to treat cancer.



STINGINN, LLC has acquired a wide range of intellectual property (IP) based on the discoveries of Glen N. Barber and the STING controlled cytosolic DNA signaling pathway, first found by his laboratory. STINGINN LLC's IP portfolio thus includes the first patent describing the discovery and use of STING and the STING signaling pathway. STINGINN’s IP collection also comprises activators of STING signaling (STAVs) for use in anti-tumor activity. STINGINN has IP on the generation of oncolytic viruses which reconstitute STING signaling in tumor cells to enhance anti-tumor T cell activity. STINGINN has identified new small molecular compounds that activate or inhibit STING signaling to stimulate anti-microbial/anti-tumor activity or prevent inflammatory disease, respectively. STINGINN has proprietary novel high throughput screening assays to identify compounds that regulate innate immune signaling (activators and inhibitors).


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  • Founder and CEO, Glen N. Barber receives the William B. Coley Award for Distinguished Research in Basic and Tumor Immunology 2020.


Contact Us


Glen N. Barber, PhD. FRS


STINGINN, LLC - Headquarters

Life Sciences & Technology Park

Converge Laboratories, CIC Miami

1951 N.W. 7th Avenue, Suite 600

Miami, Florida 33136




Ahn J, Xia T, Rabasa Capote A, Betancourt D, Barber GN. Extrinsic Phagocyte-Dependent STING Signaling Dictates the Immunogenicity of Dying Cells. Cancer Cell. 2018 May 14;33(5):862-873.e5. doi: 10.1016/j.ccell.2018.03.027. Epub 2018 Apr 26. PMID: 29706455

Russell SJ, Barber GN. Oncolytic Viruses as Antigen-Agnostic Cancer Vaccines. Cancer Cell. 2018 Apr 9;33(4):599-605. doi: 10.1016/j.ccell.2018.03.011. Review. PMID: 29634947

Ahn J, Son S, Oliveira SC, Barber GN. STING-Dependent Signaling Underlies IL-10 Controlled Inflammatory Colitis. Cell Reports. 2017 Dec 26;21(13):3873-3884. doi: 10.1016/ j.celrep.2017.11.101. PMID: 29281834

Swanson KV, Junkins RD, Kurkjian CJ, Holley-Guthrie E, Pendse AA, El Morabiti R, Petrucelli A, Barber GN, Benedict CA, Ting JP. A noncanonical function of cGAMP in inflammasome priming and activation. Journal of Experimental Medicine. 2017 Dec 4;214(12):3611-3626. doi: 10.1084/jem.20171749. Epub 2017Oct 13. PMID: 29030458

Dou Z, Ghosh K, Vizioli MG, Zhu J, Sen P, Wangensteen KJ, Simithy J, Lan Y, Lin Y, Zhou Z, Capell BC, Xu C, Xu M, Kieckhaefer JE, Jiang T, Shoshkes-Carmel M, Tanim KMAA, Barber GN, Seykora JT, Millar SE, Kaestner KH, Garcia BA, Adams PD, Berger SL. Cytoplasmic chromatin triggers inflammation in senescence and cancer. Nature. 2017 Oct 4. doi: 10.1038/nature24050 PMID: 28976970

Ni G, Konno H, Barber, GN. Ubiquitination of STING at lysine 224 controls IRF3 activation. Science Immunology. 2017 May 5;2(11). pii: eaah7119. doi: 10.1126/sciimmunol.aah7119. PMID: 28763789

Xia T, Konno H, Barber, GN. Recurrent Loss of STING Signaling in Melanoma Correlates with Susceptibility to Viral Oncolysis. Cancer Research 2016, Nov 15;76(22):6747-6759. doi: 10.1158/0008-5472.CAN-16-1404. Epub 2016 Sep 28. PMID: 27680683

Xia T, Konno H, Ahn J, Barber, GN. Deregulation of STING Signaling in Colorectal Carcinoma Constrains DNA-Damage Responses and Correlates With Tumorigenesis. Cell Reports. 2016 Jan;14(2):282-97. doi:10.2016/j.celrep.2015.12.029. PubMed PMID: 26748708.

Barber GN. STING: infection, inflammation and cancer. Nature Review Immunology. 2015 Dec;15(12):760-70. doi: 10.1038/nri3921. PubMed

PMID: 26603901

Betancourt D, Ramos JC, Barber GN. Retargeting Oncolytic Vesicular Stomatitis Virus to    Human T-Cell Lymphotropic Virus Type 1-Associated Adult T-Cell Leukemia. Journal of Virology. 2015 Dec;89(23):11786-800. doi: 10.1128/JVI.01356-15. PubMed PMID: 26378177.

Ahn J, Konno H, Barber GN. Diverse roles of STING-dependent signaling on the development of cancer. Oncogene. 2015 Oct. doi: 10.1038/onc.2014.457. PubMed PMID: 25639870.

Ma Z, Jacobs SR, West JA, Stopford C, Zhang Z, Davis Z, Barber GN, Glaunsinger BA, Dittmer DP, Damania B. Modulation of the cGAS-STING DNA sensing pathway by gammaherpesviruses. Proceedings of the National Academy of Sciences of the United States of America. 2015 Aug;112(31):E4306-15. doi: 10.1073/pnas.1503831112. PubMed PMID: 26199418; PubMed Central PMCID: PMC4534226.

Hyun J, Ramos JC, Toomey N, Balachandran S, Lavorgna A, Harhaj E, Barber GN. Oncogenic human T-cell lymphotropic virus type 1 tax suppression of primary innate immune signaling pathways. Journal of Virology. 2015 May;89(9):4880-93. doi: 10.1128/JVI.02493-14. PubMed PMID: 25694597.

Ahn J, Barber GN. Self-DNA, STING-dependent signaling and the origins of autoinflammatory disease. Current opinion in immunology. 2014 Dec.;31:121-6. doi: 10.1016/j.coi.2014.10.009. PubMed PMID: 25459004.


Ahn J, Ruiz P, Barber GN. Intrinsic Self-DNA triggers inflammatory disease dependent on STING. Journal of Immunology. 2014 Nov;193(9):4634-42. doi: 10.4049/jimmunol.1401337. PubMed PMID: 25261479.

Woo SR, Fuertes MB, Corrales L, Spranger S, Furdyna MJ, Leung MY, Duggan R, Wang Y, Barber GN, Fitzgerald KA, Alegre ML, Gajewski TF. STING-dependent cytosolic DNA sensing mediates innate immune recognition of immunogenic tumors. Immunity. 2014;41(5):830-42. doi: 10.1016/j.immuni.2014.10.017. PubMed PMID: 25517615; PubMed Central PMCID: PMC4384884.

Ahn J, Xia T, Konno H, Konno K, Ruiz P, Barber GN. Inflammation-driven carcinogenesis is mediated through STING. Nature Communications. 2014 Oct;5:5166. doi: 10.1038/ncomms6166. PubMed PMID: 25300616.

Barber GN. STING-dependent cytosolic DNA sensing pathways. Trends in Immunology. 2014 Feb.;35(2):88-93. Epub 2013/12/07. doi: 10.1016/j.it.2013.10.010. PubMed PMID: 24309426.

Konno H, Konno K, Barber GN. Cyclic Di Nucleotides Trigger ULK1 (ATG1) Phosphorylation of STING to Prevent Sustained Innate Immune Signaling. Cell. 2013 Oct. doi: 10.1016/j.cell.2013.09.049. PubMed PMID: 24119841.

Abe T, Harashima A, Xia T, Konno H, Konno K, Morales A, Ahn J, Gutman D, Barber GN. STING recognition of cytoplasmic DNA instigates cellular defense. Molecular Cell. 2013;50(1):5-15. doi: 10.1016/j.molcel.2013 April.01.039. PubMed PMID: 23478444.

Ahn J, Gutman D, Saijo S, Barber GN. STING manifests self DNA-dependent inflammatory disease. Proceedings of the National Academy of Sciences of the United States of America. 2012 Nov;109(47):19386-91. doi: 10.1073/pnas.1215006109. PubMed PMID: 23132945; PubMed Central PMCID: PMC3511090.

Barber GN. STING-dependent signaling. Nature Immunology. 2011 Sep 20;12(10):929-30. doi: 10.1038/ni.2118. Erratum in: Nat Immunol. 2012 Feb;13(2):196. PMID: 21934672.

Gall A, Treuting P, Elkon KB, Loo YM, Gale M, Jr., Barber GN, Stetson DB. Autoimmunity initiates in non-hematopoietic cells and progresses via lymphocytes in an interferon-dependent autoimmune disease. Immunity. 2012 Jan.;36(1):120-31. doi: 10.1016/j.immuni.2011.11.018. PubMed PMID: 22284419; PubMed Central PMCID: PMC3269499.

Heiber JF, Barber GN. Vesicular stomatitis virus expressing tumor suppressor p53 is a highly attenuated, potent oncolytic agent. Journal of Virology. 2011 Oct.;85(20):10440-50. doi: 10.1128/JVI.05408-11. PubMed PMID: 21813611; PubMed Central PMCID: PMC3187518.

Barber GN. Cytoplasmic DNA innate immune pathways. Immunological Reviews. 2011 Sep;243(1):99-108. doi: 10.1111/j.1600-065X.2011.01051.x. Review. PMID: 21884170

Sharma S, DeOliveira RB, Kalantari P, Parroche P, Goutagny N, Jiang Z, Chan J, Bartholomeu DC, Lauw F, Hall JP, Barber GN, Gazzinelli RT, Fitzgerald KA, Golenbock DT. Innate immune recognition of an AT-rich stem-loop DNA motif in the Plasmodium falciparum genome.Immunity. 2011 Aug 26;35(2):194-207. doi: 10.1016/j.immuni.2011.05.016. Epub 2011 Aug 4. PMID: 21820332.


Barber GN. (2011). Innate immune DNA sensing pathways: STING, AIMII and the regulation of interferon production and inflammatory responses. Curr Opin Immunol, 2011 Feb;23(1):10-20. PMID: 21239155

Ishikawa H, Ma Z, Barber GN. STING regulates intracellular DNA-mediated, type I interferon-dependent innate immunity. Nature. 2009 Oct.;461(7265):788-92. doi: 10.1038/nature08476. PubMed PMID: 19776740.

Ishikawa H, Barber GN. STING an endoplasmic reticulum adaptor that facilitates innate immune signaling. Nature. 2008 Oct.;455(7213):674-8. doi: 10.1038/nature07317. PubMed PMID: 18724357; PubMed Central PMCID: PMC2804933.

Majid AM, Ezelle H, Shah S, Barber GN. Evaluating replication-defective vesicular stomatitis virus as a vaccine vehicle. Journal of Virology. 2006 July;80(14):6993-7008. doi: 10.1128/JVI.00365-06. PubMed PMID: 16809305; PubMed Central PMCID: PMC1489030.

Balachandran S, Thomas E, Barber GN. A FADD-dependent innate immune mechanism in mammalian cells. Nature. 2004 Nov;432(7015):401-5. doi: 10.1038/nature03124. PubMed PMID: 15549108.

Balachandran S, Barber GN. Defective translational control facilitates vesicular stomatitis virus oncolysis. Cancer Cell. 2004 Jan;5(1):51-65. PubMed

PMID: 14749126.

Obuchi M, Fernandez M, Barber GN. Development of recombinant vesicular stomatitis viruses that exploit defects in host defense to augment specific oncolytic activity. Journal of Virology. 2003 Aug;77(16):8843-56. PubMed PMID: 12885903; PubMed Central PMCID: PMC167243.

Fernandez M, Porosnicu M, Markovic D, Barber GN. Genetically engineered vesicular stomatitis virus in gene therapy: application for treatment of malignant disease. Journal of Virology. 2002 Jan;76(2):895-904. PubMed PMID: 11752178; PubMed Central PMCID: PMC136833.

Balachandran S, Barber GN. Vesicular stomatitis virus (VSV) therapy of tumors. IUBMB Life. 2000 Aug;50(2):135-8. doi: 10.1080/713803696. PubMed PMID: 11185959.

Balachandran S, Roberts PC, Brown LE, Truong H, Pattnaik AK, Archer DR, Barber GN. Essential role for the dsRNA-dependent protein kinase PKR in innate immunity to viral infection. Immunity. 2000 July ;13(1):129-41. PubMed PMID: 10933401.

Balachandran S, Roberts PC, Kipperman T, Bhalla KN, Compans RW, Archer DR, Barber GN. Alpha/beta interferons potentiate virus-induced apoptosis through activation of the FADD/Caspase-8 death signaling pathway. Journal of Virology. Feb 2000;74(3):1513-23. PubMed PMID: 10627563; PubMed Central PMCID: PMC111487.

Barber GN, Thompson S, Lee TG, Strom T, Jagus R, Darveau A, Katze MG. The 58-kilodalton inhibitor of the interferon-induced double-stranded RNA-activated protein kinase is a tetratricopeptide repeat protein with oncogenic properties. Proceedings of the National Academy of Sciences of the United States of America. 1994;91(10):4278-82. PubMed PMID: 7514301; PubMed Central PMCID: PMC43768.

Federal Funded Projects

Project Title: STING Activators as Therapy for Cancer - 2021 

Phase I Small Business Technology Transfer (STTR) - National Cancer Institute


The ability of dying cells to activate antigen presenting cells (APCs) is carefully controlled to avoid unwarranted inflammatory responses. Thus, tumor cells avoid aggravating APCs by efficiently simulating regular dying cells which following phagocytosis do not trigger inflammatory responses required for efficient cytotoxic T lymphocyte (CTL) priming. However, dying tumor cells containing exogenous innate immune agonists such as cytosolic DNA, potently activate APCs in trans through extrinsic innate immune, STING- dependent signaling to generate potent CTL activity. In the absence of STING agonists, dying cells were ineffectual in the stimulation of APCs in trans. Indeed, cytosolic STING activators, including cytosolic DNA and cyclic dinucleotides (CDNs), constitute cellular danger associated molecular patterns (DAMPs) usually only generated by viral infection or following DNA damage events, that can render tumor cells highly immunogenic (make a ‘cold’ tumor ‘hot’). Taking advantage of our mechanistic insight and discoveries, we have now developed a new generation of innate immune activators that trigger STING signaling (referred to as STAVs: STING activators). Tumor cells transfected with STAVs activated APCs in trans and can generate potent anti-tumor T cell activity. Immunocompetent mice bearing metastatic syngeneic tumors could be ‘cured’ following inoculation with STAV ‘loaded’ tumor cells. Our strategy provides a new, simple, inexpensive therapeutic approach for the treatment of cancer. We have recently published our findings in the journal Cancer CELL and patented our intellectual property through the University of Miami’s Office of Technology Transfer (OTT). This technology has been licensed to STINGINN LLC, to acquire sufficient pre-clinical data to warrant the consideration of clinical trials. For this study, we aim to evaluate whether our STAV strategy could be useful for the treatment of leukemia (focusing on adult T cell leukemia/lymphoma [ATLL] and Acute Myeloid Leukemia [AML]). ATLL is a clonal disease, invariably lethal and there is no cure or vaccine. AML is among the most aggressive of leukemias and only 5-10% of patients over 60 survive up to 5 years using standard treatments. We have developed a murine tumor model for the study of these diseases. The objective is to procure sufficient data to consider the development of pre-clinical trials for the treatment of this and ultimately other types of leukemia and lymphoma related cancers.