Phio Pharmaceuticals Corp. (NASDAQ:PHIO), a biotechnology company developing the next generation of immuno-oncology therapeutics based on its proprietary self-delivering RNAi (INTASYL™) therapeutic platform, today announced a poster presentation at the American Association for Cancer Research (AACR) 2020 Virtual Annual Meeting which further details data demonstrating the potential of a TIGIT targeting INTASYL compound as an immuno-oncology therapeutic through the suppression of TIGIT in the tumor microenvironment (TME). The Phio poster presentation will also be available under the "Investors – Events and Presentations" section of the Company's website (click here).
"In our poster presentation at the AACR 2020 Virtual Annual Meeting, we announced detailed data supporting the potential for PH-804, our TIGIT targeting INTASYL compound, as an immuno-oncology therapeutic and a viable alternative to anti-TIGIT antibodies. This data provides insight around the mechanisms of action of the tumor growth suppression with PH-804, as previously announced from a study in a validated animal model, namely through increases in immune cell count and immune cell activation in the tumor micro-environment," said Dr. Simon Fricker, Phio's VP of Research. "These preclinical results build upon the recent data we announced at the ASCO 2020 Annual Meeting that show the ability and safety of INTASYL RNAi technology to reprogram immune cells, such as T cells or NK cells, to improve their efficacy."
In an in vivo study, tumor growth inhibition was determined for both PH-804 and an anti-TIGIT antibody in colorectal carcinoma tumor bearing mice. Results from the study demonstrated that our INTASYL compound was efficiently delivered intratumorally to immune cells, resulting in a dose dependent inhibition of tumor growth, reaching statistical significance levels for PH-804 and anti-TIGIT antibody treatment arms. More detailed data from the study provides evidence of an "on-target" effect of PH-804 as shown by silencing of TIGIT mRNA expression in tumor infiltrating lymphocytes isolated from the treated tumors. In addition, analysis of the TME of the PH-804 treated mice showed a dose dependent increase in cytotoxic effector T cells, and a dose dependent activation of such T cells as shown by the expression of activation makers such as CD25 and CD69.
These data demonstrate the potential of a TIGIT targeting INTASYL compound for the suppression of TIGIT in the TME and support the hypothesis that local TIGIT silencing with INTASYL is a promising therapeutic approach.