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GT Biopharma and Fate Therapeutics Present Preclinical Data Highlighting Novel Dual Antigen Targeting Approach For The Treatment of AML at ASH 2022
Presentation shows the therapeutic potential of combining iPSC-derived CAR NK cells and NK cell engagers to overcome the clinical heterogeneity of AML
About this update from Fate Therapeutics, Inc.
[{"type":"text","content":"Presentation shows the therapeutic potential of combining iPSC-derived CAR NK cells and NK cell engagers to overcome the clinical heterogeneity of AML BRISBANE, CALIFORNIA, Dec. 12, 2022 (GLOBE NEWSWIRE) -- GT Biopharma, Inc. (NASDAQ: GTBP) today announced the presentation of new preclinical data at the American Society of Hematology's 64th Annual Meeting (ASH 2022). The presentation highlights the potential of a novel dual antigen targeting approach for the treatment of acute myeloid leukemia (AML) by combining GT Biopharma’s Tri-specific Killer Engager (TriKE) with the induced pluripotent stem cell (iPSC) product platform of Fate Therapeutics, Inc. (NASDAQ:FATE). The poster presentation titled, “A Novel Dual-Antigen Targeting Approach Enables Off-the-Shelf CAR NK Cells to Effectively Recognize and Eliminate the Heterogeneous Population Associated with AML,” showcases the phenotypic and functional properties of multiplexed-engineered, iPSC-derived NK cells (α3 MICA/B iNK cells) incorporating four functional modalities: a chimeric antigen receptor (CAR) targeting the α3 domain of MICA/B; a high-affinity, non-cleavable CD16 Fc receptor; an IL-15 fusion receptor; and a knock-out of CD38. In preclinical models, α3 MICA/B iNK cells demonstrated potent anti-leukemic activity against AML cell lines, and the kinetics of cytotoxicity were enhanced in combination with an anti-CD33 TriKE (GTB-3650). Jeffrey Miller*, MD, Deputy Director of the University of Minnesota's** Masonic Cancer Center and Consulting Chief Scientific Officer of GT Biopharma noted, “The preclinical data suggest that dual-antigen targeting strategies using iPSC-derived CAR NK cells in combination with antigen-specific TriKE targeting CD33 are a promising approach to address the clinical heterogeneity of AML and enhance outcomes for patients with advanced disease.” Conclusions α3 MICA/B iNK cells exhibited antigen-specific activation in vitro as measured by interferon-gamma production and CD107a degranulation across a broad range of solid tumor cell lines.α3 MICA/B iNK cells demonstrated robust cytotoxicity in vitro against an array of AML cell lines, including those with proteolytic cleavage of the α1 and α2 domains of MICA/B, which is a known mechanism of tumor escape from NK cell cytotoxicity. The kinetics of cytotoxicity were enhanced in combination with GTB-3650, ...