On April 14, 2016 Trillium Therapeutics Inc. (Nasdaq:TRIL; TSX: TR) an immuno-oncology company developing innovative therapies for the treatment of cancer, reported it will be providing an update on its SIRPaFc immune checkpoint inhibitor program, targeting the CD47 protein, at the 107th Annual Meeting of the American Association for Cancer Research (AACR) (Free AACR Whitepaper) (Filing, 6-K, Trillium Therapeutics, APR 14, 2016, View Source [SID:1234510766]). The meeting will be held April 16-20, 2016 in New Orleans, LA. Details of the poster presentation, entitled "SIRPαFc, a CD47-Blocking Cancer Immunotherapeutic, Triggers Phagocytosis of Lymphoma Cells by Both Classically (M1) and Alternatively (M2) Activated Macrophages", are listed below:
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Date: Monday April 18, 2016
Time: 1:00 pm – 5:00 pm (CT)
Session Category: Immunology
Session Title: Immune Checkpoints 1
Abstract #: 2345
Presenter: Dr. Natasja Nielsen Viller
Location: Section 26
The company will present data demonstrating that its SIRPaFc fusion protein, which targets the CD47 "do not eat" signal, promotes the phagocytosis of lymphoma cells by diverse types of macrophages. The studies also assess the impact of macrophage polarizing agents on drug activity and delineate the role of different Fc gamma receptors in promoting tumor cell killing by SIRPaFc.
"Macrophages are heterogeneous and certain types, notably M2s, are often implicated in tumor progression," commented Trillium’s Chief Scientific Officer, Dr. Robert Uger. "Our data indicate that TTI-621, our CD47-blocking decoy receptor, enables all macrophage subsets tested, including M2s, to kill tumor cells. These results suggest that TTI-621 is able to convert otherwise pro-tumor macrophages into efficient anti-tumor effector cells. Rather than ablating M2 macrophages in the tumor microenvironment, these data support using TTI-621 to unleash their tumoricidal function."