On November 7, 2016 Aduro Biotech, Inc. (Nasdaq:ADRO) reported an oral presentation given by the company’s chief scientific officer, Thomas Dubensky Jr., Ph.D., at the 4th European Society of Medical Oncology (ESMO) (Free ESMO Whitepaper) Symposium on Immuno-Oncology held last week in Lausanne, Switzerland (Press release, Aduro BioTech, NOV 7, 2016, View Source [SID1234516350]). The data, generated from multiple preclinical models, demonstrated important changes in the tumor microenvironment and the activation of acute and systemic tumor-specific immune cell responses following intratumoral administration of ADU-S100 (also known as MIW815), an investigational STING (Stimulator of Interferon Genes) Pathway Activator immunotherapy. Importantly, these preclinical data underscore the ability for ADU-S100 to induce tumor-specific memory mediated by immune cells (e.g. T-cells and NK-cells) whereby the immune system is able to eliminate specific cancerous cells upon their reintroduction without further therapy. Additionally, the anti-tumor efficacy achieved with ADU-S100 was enhanced by combination with an anti-PD-1 immune checkpoint inhibitor, and resulted in the complete eradication of local and distal tumors. Schedule your 30 min Free 1stOncology Demo! "We are pleased to have further validated, through multiple preclinical models, our previous discoveries regarding the potential mechanism of action of the STING Pathway and the role it serves in stimulating a robust and systemic T-cell immune response," stated Dr. Dubensky. "We look forward to working in partnership with Novartis on translating our preclinical findings to a clinical experience as we continue to make progress with our ongoing Phase 1 study of ADU-S100."
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Presentation Title: Activation of the STING pathway to induce tumor immunity
In the oral presentation which was given on Saturday, November 5, Dr. Dubensky presented data from preclinical studies using multiple models that demonstrate intratumoral injection of ADU-S100 activates the STING Pathway and induces a durable local and systemic anti-tumor immune response as evidenced by induction of type I interferons (IFNs) and a CD8+ T-cell response. Additionally, preclinical data show the combination of STING activation in the tumor microenvironment and PD-1 blockade enhances antitumor efficacy. There is an ongoing Phase 1 first-in-human dose escalation clinical study to evaluate the safety, tolerability and possible anti-tumor activity of ADU-S100 in patients with cutaneously-accessible advanced metastatic solid tumors or lymphomas. To learn more about this trial, visit www.clinicaltrials.gov.
About the Tumor Microenvironment
The tumor microenvironment is the cellular environment in which the tumor exists, and, along with cancerous cells, includes support cells, immune cells, surrounding blood vessels, and the extracellular matrix. The tumor cells and the surrounding microenvironment are closely related and interact constantly. Tumors influence the microenvironment by releasing signals that promote tumor growth, immune tolerance and immune suppression. When tumors initially form, the body’s immune system recruits and activates a host of immune cells to fight the invading tumor. However, in cases where cancer develops, tumors are eventually able to evade the immune system by changing their microenvironment to inhibit the ability of the immune system to recognize and destroy the tumor thus allowing for tumor outgrowth and formation of metastasis.
About STING Pathway Activator Platform
The Aduro-proprietary STING Pathway Activator product candidates, including ADU-S100 (MIW815), are synthetic small molecule immune modulators that are designed to target and activate human STING. STING is generally expressed at high levels in immune cells, including dendritic cells. Once activated, the STING receptor initiates a profound innate immune response through multiple pathways, inducing the expression of a broad profile of cytokines, including interferons and chemokines. This subsequently leads to the development of a systemic tumor antigen-specific T cell adaptive immune response.