Io Therapeutics, Inc., announces presentation of data from studies of its RAR gamma agonist compound IRX5010 in treatment of a mouse model of triple negative breast cancer, demonstrating combination treatment effects with an anti-PDL-1 monoclonal ant

SPRING, Texas, Dec. 11, 2024 (GLOBE NEWSWIRE) -- Io Therapeutics, Inc., presented results from studies done in a mouse model of triple negative breast cancer with the companys newest anti-cancer compound IRX5010, an agonist of the retinoic acid nuclear receptor gamma which was discovered in the companys oncology drug program. The presentation titled The RAR gamma nuclear receptor agonist IRX5010 has combination inhibitory effects with an anti-PDL-1 checkpoint inhibitor on the growth of EMT-6 triple negative breast cancer was delivered as a late-breaking abstract at the San Antonio Breast Cancer Symposium 2024, currently underway in San Antonio, Texas. The poster presentation was authored by Vidyasagar Vuligonda, Ph.D., Chief Scientific Officer of the company and inventor of the compound; and Martin E. Sanders, M.D., the companys Chief Executive Officer.

The presented studies showed treatment of the EMT-6 mouse model of triple negative breast cancer with IRX5010 plus a checkpoint inhibitor monoclonal anti-PDL-1 resulted in substantial 84% inhibition of tumor growth. This was a 9% increase of inhibitory effect on tumor growth of the combination over treatment with anti-PDL-1 alone. Treatment with IRX5010 increased numbers of tumor-infiltrating effector memory CD4 and CD8 phenotype T-cells (TIL), and inhibited tumor infiltration by granulocytic myeloid derived suppressor cells (gMDSC). Additive or synergistic effects on each of these outcomes were observed with the combination treatment of IRX5010 with anti-PDL-1.

Dr. Vuligonda stated These findings are the first demonstration of additive and synergistic effects of combination treatment with an RAR gamma nuclear receptor agonist and an anti-PDL-1 monoclonal antibody checkpoint inhibitor in a triple negative breast cancer mouse model. The data presented today add to our growing evidence that IRX5010 has immune-mediated mechanisms of action, including promotion of TIL and inhibition of MDSC, and that these effects are increased in combination with an anti-PDL-1 checkpoint inhibitor. We have previously reported that oral treatment with IRX5010 alone resulted in suppression of growth in mouse models of breast, lung, colon, and prostate cancers. In all four types of these highly prevalent cancers, we observed that IRX5010 induced increased numbers of TIL associated with reduction in tumor growth. With our current studies in triple negative breast cancer, we now add combination effects with anti-PDL-1 of promotion of tumor infiltration by TIL and inhibition of tumor infiltration by MDSC, to the growing list of anti-cancer mechanisms of action of IRX5010.

Dr. Sanders stated, IRX5010 has potential to be a new treatment for multiple currently inadequately treated cancers, including triple negative breast cancer, a historically difficult to treat type of cancer. This is supported by its demonstrated mechanisms of action in the immune system of increasing tumor-infiltration of anti-cancer T-cells, while also decreasing tumor infiltration of myeloid derived suppressor cells, a type of cell known to inhibit anti-cancer responses to checkpoint inhibitors. We look forward to translating IRX5010 into clinical trials in patients with triple negative breast cancer.

About Io Therapeutics: Io Therapeutics, Inc. is a privately held company headquartered in Spring, Texas. More information on Io Therapeutics and its product development programs is available on the companys web site: www.io-therapeutics.com

Forward Looking Statements: This news release contains forward-looking statements within the meaning of the safe harbor provisions of the United States Private Securities Litigation Reform Act of 1995.

info@io-therapeutics.com

A OESP nao e(sao) responsavel(is) por erros, incorrecoes, atrasos ou quaisquer decisoes tomadas por seus clientes com base nos Conteudos ora disponibilizados, bem como tais Conteudos nao representam a opiniao da OESP e sao de inteira responsabilidade da GlobeNewswire