Actym to Present Preclinical Data on Clinical Candidate ACTM-838 at 38th SITC Annual Meeting

03 Nov 2023
ImmunotherapyAACRClinical Study
BERKELEY, Calif., Nov. 3, 2023 /PRNewswire/ -- Actym Therapeutics, pioneering a new drug modality to treat solid tumors, announced today that it will present preclinical data of its lead asset, ACTM-838, in a poster presentation at the 2023 38th Society for Immunotherapy of Cancer (SITC) Annual Meeting in San Diego, California. The presentation will feature data examining the tumor-specific enrichment and payload delivery of ACTM-838 in multiple tumor models.
"Utilizing genetically modified bacteria to elicit a potent and comprehensive immune response has the potential to bring a new level of therapeutic impact to cancer patients across multiple solid tumor types," said Dr. Christopher D. Thanos, President, CEO, and Co-founder of Actym. "The data presented at this year's SITC Meeting highlights ACTM-838's ability to specifically accumulate in the tumor microenvironment and deliver two potent engineered payloads. We believe that these results further validate our scientific approach and provide a strong rationale to advance our candidate into the clinic."
ACTM-838 is a novel immunotherapy designed to locally deliver engineered IL-15 (IL-15plex) and engineered STING (eSTING) payloads to phagocytic tumor-resident myeloid cells to induce a durable anti-tumor immune response, following intravenous administration. The data that will be presented demonstrates specific uptake by tumor-resident myeloid cells in a mouse model of breast cancer, leading to the expression of IL-15plex and eSTING in the tumor microenvironment (TME), with no evidence of payload expression in other tissues. TME-specific payload delivery and efficacy was also observed in a mouse breast cancer model of metastatic disease. Actym will also show that treatment with ACTM-838 induces tumor-antigen-specific cytolytic T cells and effector T cells. Furthermore, Actym will show that in healthy human donor cells, ACTM-838 treatment results in significantly lowered inflammatory cytokines than a control strain lacking ACTM-838's genetic modifications. Patient tumor database analysis revealed numerous tumor types that have both an adenosine pathway signature for tumor-specific enrichment, and a tumor-associated myeloid cell signature for payload delivery, by ACTM-838. In addition to demonstrating compelling efficacy characteristics, intravenously administered ACTM-838 exhibits a strong safety profile in mice and non-human primates with a first-in-human clinical trial planned in Australian cancer patients in early 2024.
SITC Poster Presentation details:
Abstract Title: PK/PD biomarker analysis to assess tumor-specific enrichment and payload delivery of ACTM-838, a microbial-based immunotherapy
Abstract number: 408
Presenter: Dr. Akshata Udyavar
Location: Ground Level - Exhibit Halls A and B1 - San Diego Convention Center
Date/Time: Saturday, November 4, 11:55 AM – 1:25 PM and 7:00 PM – 8:30 PM (PST)
About Actym
Actym Therapeutics has engineered a new drug modality harnessing the power of a genetically modified bacterial vehicle that safely introduces therapeutic payloads to activate the immune response in the tumor microenvironment. To achieve targeted anti-tumor effects, we have developed a systemically administered treatment that exploits intrinsic TME-specific metabolites, enabling selective enrichment of the bacterial vehicle in tumors. After cell-specific entry, our lead candidate, ACTM-838, positively activates tumor-resident myeloid cells and delivers two synergistic payloads, optimized IL-15 and STING, unlocking a comprehensive and durable innate and adaptive anti-tumor immune response. With the ability to tailor our platform utilizing a range of payload combinations, we aim to achieve a new level of therapeutic impact for cancer patients across multiple tumor types.
Contacts
Christopher Thanos, CEO
E-Mail: [email protected]
Media Requests for Actym
Dr. Alison Opalko or Sara Ortiz
Trophic Communications
Phone: +49 151 54041130 or +49 170 3222493
E-Mail: [email protected]
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