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2021 11.10 Repairing damaged neural tissues in patient’s brain is a plausible therapeutic approach for Alzheimer’s disease (AD) and other neurodegenerative diseases. In this study, we report that inhibition of Mitogen-activated protein kinase (Extracellular Receptor Kinase) signaling by trametinib induces generation of new neurons from endogenous neural stem cells in the brain regions affected by the disease and recovers cognitive functions of AD model animals. We propose that trametinib is a promising therapeutic candidate for Alzheimer’s disease. |
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2021 11.10 Administration of trametinib, a MEK1/2 specific inhibitor, is shown to improve survival and motor functions of the Amyotrophic lateral sclerosis (ALS) model animals. Enhancement of neuroprotective autophagy is the mechanism of trametinib’s therapeutic effects for ALS. Trametinib is currently in clinical trial (Phase I/IIa) for the indication of ALS in Korea (NCT04326283). |
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2021 06.10 Genuv presented three posters at the Keystone Virtual Symposium “Neurodegenerative Disease: Genes, Mechanisms and Therapeutics,” that show promising preclinical results for our new drug candidate, SNR1611. In mouse models of amyotrophic lateral sclerosis (Lou Gehrig’s Disease), SNR1611 showed positive neurogenesis and neuroprotective effects. The studies are an important validation of our ATRIVIEW® platform, which screens for compounds that induce differentiation of neurons without neuronal cell death in simulated disease conditions. |
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2021 06.10 MEK1/2 Inhibition Rescues Neurodegeneration in Alzheimer’s Disease Models by Enhancing Autophagy Genuv presented three posters at the Keystone Virtual Symposium “Neurodegenerative Disease: Genes, Mechanisms and Therapeutics,” that show promising preclinical results for our new drug candidate, SNR1611. In mouse models of Alzheimer’s Disease, SNR1611 showed positive neurogenesis and neuroprotective effects. In one of the studies of a mouse model of Alzheimer’s, orally administered drug led to reduced beta amyloid plaque deposits and recovery of impaired neuronal structures and cognitive functions. The studies are an important validation of our ATRIVIEW® platform, which screens for compounds that induce differentiation of neurons without neuronal cell death in simulated disease conditions. |
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2021 06.10 Genuv presented three posters at the Keystone Virtual Symposium “Neurodegenerative Disease: Genes, Mechanisms and Therapeutics,” that show promising preclinical results for our new drug candidate, SNR1611. In mouse models of Alzheimer’s Disease, SNR1611 showed positive neurogenesis and neuroprotective effects. In one of the studies of a mouse model of Alzheimer’s, orally administered drug led to reduced beta amyloid plaque deposits and recovery of impaired neuronal structures and cognitive functions. The studies are an important validation of our ATRIVIEW® platform, which screens for compounds that induce differentiation of neurons without neuronal cell death in simulated disease conditions. |
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2021 05.22 Mechanisms That Activate 26S Proteasomes and Enhance Protein Degradation Hyoung Tae Kim, Chief Science Officer and head of GENUV’s Neuroscience Research Center, co-authored a paper showing the mechanisms that activate 26S proteasomes and enhance protein regulation in Biomolecules. |
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2021 05.17 Chae Gyu Park, Managing Director of the Antibody Research Center, co-authored a paper in Frontiers which shows that the global gene expression of T Cells is differentially regulated by peritoneal Dendritic Cell subsets in an IL-2 dependent manner. |