New Preclinical Research Presented at AACR 2019 Reveals Unique Anti-Cancer Mechanism of Action Underscoring IMV’s Immunotherapy Program

IMV Inc. (Nasdaq: IMV; TSX: IMV), a clinical stage immuno-oncology corporation, today announced that preclinical research presented at the American Association for Cancer Research (AACR) Annual Meeting 2019 demonstrated how the mechanism of action (MOA) of IMV’s proprietary DPX technology can enhance a broad spectrum of immune cell infiltration into tumors, which included T cells, Natural Killer (NK) cells, and macrophages. Analyses also revealed the differentiated characteristics of the immune cell responses and the potential implications for enhanced anti-tumor efficacy.

“The new preclinical data shared at this year’s AACR Annual Meeting provides greater insight into the unique mechanism of our immunotherapy programs,” said Marianne Stanford, Vice President, Research at IMV. “These data demonstrate our commitment to fully understanding how our platform impacts our product candidates, which in turn informs our clinical program designs and ability to identify patient needs that are more likely to benefit from our approach.”

In the poster titled, T-distributed stochastic neighbor embedding (t-SNE) analysis of tumor infiltrating lymphocytes after treatment with a T cell activating therapy identifies a unique population of recruited CD8+ T cells and novel options for combination immunotherapy, IMV researchers used specialized data analytics to examine how DPX-based agents, when combined with cyclophosphamide (CPA), induced T cells to infiltrate tumors and attack cancerous cells. The study closely examined the types of immune cell responses and how and why they were able to affect disease.

The data indicated that this approach stimulated the infiltration of a broad base of immune cells into tumors, including T cells, NK cells, and macrophages. The specific T cell population that moved into tumors could be grouped based on the co-expression of different checkpoint molecules such as PD-1 and Tim-3. However, those stimulated to infiltrate tumors generally did not express CTLA-4 (a protein found on T cells that inhibits the immune response).

Researchers also found that combining DPX/CPA treatments with a CTLA-4-blocking antibody increased efficacy in controlling tumor growth in the animal models. The data suggested that this result was due to the antibodies acting on T cells present in the tumors, rather than those induced by treatment. This finding contrasts previously published studies with anti-PD-1 combinations in which treatment directly enhanced DPX-induced T cell responses.