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MediciNova Announces Positive Preclinical Results Regarding MN-166 (ibudilast) in Glioblastoma (GBM) Published in Frontiers in Immunology
LA JOLLA, Calif., June 25, 2020 (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., June 25, 2020 (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 positive preclinical findings published in Frontiers in Immunology regarding the prospect of MN-166 (ibudilast) as an adjunct treatment for glioblastoma.\n The publication, entitled “Glioblastoma myeloid-derived suppressor cell subsets express differential macrophage migration inhibitory factor receptor profiles that can be targeted to reduce immune suppression”, was a collaborative effort between MediciNova and the Cleveland Clinic, led by Tyler Alban (doctoral candidate) and Dr. Justin Lathia, Co-Director of the Brain Tumor Research and Therapeutic Development Center of Excellence at the Lerner Research Institute, Cleveland Clinic, and Associate Professor, Department of Molecular Medicine at Case Western Reserve University. Dr. Lathia, Dr. Michael Vogelbaum (previously at the Cleveland Clinic, now at Moffitt Cancer Center in Tampa, FL) and colleagues previously reported on findings that GBM patients had higher levels of immune suppressive myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment and they tended to be resistant to and dependent on macrophage migration inhibitory factor (MIF). In this research publication, in collaboration with Dr. Richard Bucala (Yale University), they report the monocytic subset of MDSCs (M-MDSCs) expressed high levels of the MIF cognate receptor CD74 in the tumor microenvironment. This finding is meaningful in that targeting M-MDSCs with ibudilast, a brain penetrant MIF-CD74 interaction inhibitor, resulted in decreased MDSC function and enhanced CD8 T cell activity in the tumor microenvironment. They note that clinical trial results to date suggest that treatment with an immune stimulatory therapy alone is not effective in treating GBM and hypothesized that better clinical outcomes will be seen when an immune stimulatory therapy is combined with ibudilast, which has been shown to reverse tumor-induced immune suppression. Dr. Justin Lathia commented, “We found that the receptor CD74 may play a greater role in GBM MDSC biology because the subset of MDSCs primarily found in the tumor microenvironment were M-MDSCs, which predominantly express CD74 as a M...