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MediciNova Announces Publication of MN-166 (ibudilast) Data regarding Prevention of Metastasis in Uveal Melanoma in Molecular Cancer Research
LA JOLLA, Calif., April 20, 2022 (GLOBE NEWSWIRE) -- MediciNova, Inc., a biopharmaceutical company traded on the NASDAQ Global Market (NASDAQ:MNOV) and the
About this update from Medicinova, Inc.
[{"type":"text","content":"LA JOLLA, Calif., April 20, 2022 (GLOBE NEWSWIRE) -- MediciNova, Inc., a biopharmaceutical company traded on the NASDAQ Global Market (NASDAQ:MNOV) and the JASDAQ Market of the Tokyo Stock Exchange (Code Number: 4875), today announced data demonstrating that MN-166 (ibudilast) prevents metastasis in a uveal melanoma (UM) animal model was published in the journal Molecular Cancer Research. The publication entitled “Uveal Melanoma Exosomes Induce a Prometastatic Microenvironment through Macrophage Migration Inhibitory Factor,” was co-authored by MediciNova’s collaborators Dr. Grazia Ambrosini, Research Scientist at The Herbert Irving Comprehensive Cancer Center (HICCC), Columbia University Medical Center; Alex J. Rai, PhD, Associate Professor of Pathology and Cell Biology, Columbia University Irving Medical Center; Richard D. Carvajal, MD, Associate Professor of Medicine at Columbia Vagelos College of Physicians and Surgeons and co-director of the Precision Oncology and Systems Biology research program at the HICCC; and Gary Schwartz, MD, Professor of Oncology at Vagelos College of Physicians and Surgeons, Division Chief of Hematology/Oncology at Columbia University Irving Medical Center, and Deputy Director at the HICCC. The publication describes a preclinical study which characterized the proteomic content of uveal melanoma exosomes and identified the presence of markers with metastatic properties. The study included an evaluation of MN-166 (ibudilast) in a metastatic uveal melanoma model. Key take-aways in the publication include: Uveal melanoma exosomes (UM-exo) induce activation of cell signaling pathways and the release of cytokines and growth factors from hepatocytes. These exosome-stimulated liver cells could in turn induce migration of UM cells.The proinflammatory cytokine macrophage migration inhibitory factor (MIF) was over expressed in UM exosomes and was a major player in these mechanisms. MIF blockade inhibited UM cell migration in co-cultures with exosome-stimulated hepatocytes and prevented the development of metastases in vivo.Most inhibitors of hepatocyte-derived cytokines and growth factors had little or partial effects in blocking UM cell migration toward exosome-stimulated hepatocytes.The MIF inhibitor MN-166 (ibudilast) dramatically inhibited UM cell migration (p","length":3091,"tagName":"div"}]