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Actuate Announces Scientific Reports Publication on Elraglusib’s Novel Immunomodulatory Mechanism of Action as a GSK-3β Inhibitor
New Mechanistic Insights Underscore Multiple Potential Roles for Elraglusib as an Immune Modulator in the treatment of NeuroblastomaStudy Illustrates
About this update from Actuate Therapeutics, Inc.
[{"type":"text","content":"New Mechanistic Insights Underscore Multiple Potential Roles for Elraglusib as an Immune Modulator in the treatment of NeuroblastomaStudy Illustrates Potential to Activate the Immune System Even in Cancers That Have Not Previously Responded to Checkpoint Inhibitors CHICAGO and FORT WORTH, Texas, Sept. 23, 2024 (GLOBE NEWSWIRE) -- Actuate Therapeutics, Inc. (NASDAQ: ACTU) (“Actuate” or the “Company”), a clinical-stage biopharmaceutical company, focused on developing therapies for the treatment of high-impact, difficult-to-treat cancers through the inhibition of glycogen synthase kinase-3 beta (GSK-3β), announced the Scientific Reports publication of novel mechanistic data for its development candidate, elraglusib. The article, entitled, “Targeted inhibition of glycogen synthase kinase‑3 using 9‑ING‑41 (elraglusib) enhances CD8 T‑cell‑reactivity against neuroblastoma cells” is available online. “The mechanistic data published in Scientific Reports provides crucial evidence of elraglusib’s ability to enhance activation of the immune system by tumor cells,” said Daniel Schmitt, President & Chief Executive Officer of Actuate. “By improving antigen presentation and enhancing the activation of CD8+ cytotoxic T cells, we are paving the way for more effective immunotherapeutic strategies including combinations of elraglusib with checkpoint inhibitors.” Using neuroblastoma, which is typically refractory to checkpoint inhibitors, as a model system, these findings illustrate the potential to activate the immune system even in cancers that have not previously responded to checkpoint inhibitors and underscore elraglusib’s potential as a highly innovative treatment for challenging cancers. The summary of key mechanistic findings: Elraglusib significantly enhances MHC-I molecule surface expression of neuroblastoma cells, improving their recognition by cytotoxic T lymphocytes (CTLs)Treatment with elraglusib leads to the disruption of NK-κB signaling, a key contributor to tumor cell survival, promoting cancer cell apoptosis and reducing treatment resistanceElraglusib boosts IFNγ signaling through the JAK/STAT pathway, particularly STAT1, which further supports improved antigen presentation and immune responseWhen combined with an anti-PD-1 treatment, elraglusib boosted CD8+ T cell proliferation and activation by neuroblastoma cells, showing poten...