OGA inhibitors offer multimodal mechanism of action with potential for multiple approaches to clinical development in Alzheimer’s and Parkinson’s disease
Lausanne, SWITZERLAND and San Francisco, CA, USA, 30 September 2021 - Asceneuron SA, a clinical stage company dedicated to targeting the root causes of neurodegenerative diseases such as the intracellular aggregation of the microtubule-associated protein tau, is pleased to announce that the Company will be presenting novel data on its O-GlcNAcase (OGA) inhibitor pipeline at the following upcoming conferences.
22nd International Conference on Alzheimer's Drug Discovery
Date: 4-5 October 2021, New York. Virtual Conference.
Session: Clinical trials and novel approaches for Dementia
Presentation: OGA inhibitors as multimodal drugs for intracellular proteinopathies on Monday, 4 October, 16:45 CET/10:45 US ET.
146th Annual Meeting of the American Neurological Association
Date: 17-19 October 2021, New Jersey. Virtual Conference.
Presentation: Efficacy of ASN51, an Orally Bioavailable Small-Molecule O-GlcNAcase Inhibitor, in Models of Parkinson's Disease and Epilepsy, on Monday, 18 October, 23:30 CET/ 18:30 US ET.
Date: 25-26 October, 2021. Lille, France.
Presentation: OGA inhibitors as multimodal drug candidates for tau- and alpha-synucleinopathies on Tuesday, 26 October, 14:55 CET.
Dirk Beher, Chief Executive Officer and Co-Founder of Asceneuron, stated: “We are delighted to have been invited to present at three leading conferences to discuss and share the latest insights on our proprietary pipeline of O-GlcNAcase inhibitors. The data generated so far are an important development in addressing the challenges seen in Alzheimer’s and Parkinson’s diseases drug development and demonstrate our continuing commitment to bring urgently needed treatments to patients with tau-related neurodegenerative diseases.”
O-GlcNAcase is an emerging drug target in central nervous system (CNS) drug development since deficient glycosylation patterns of intracellular proteins have been associated with diseases of aging and neuronal dysfunction. O-GlcNAcase inhibitors prevent the elimination of intracellular protein glycosylation, thereby halting the decline of the steady-state levels of this post-translational modification. O-GlcNAcase inhibitors have initially been pursued exclusively for tau-related diseases. Preclinical data suggest a wider application to intracellular proteinopathies such as Alzheimer’s disease and related disorders, and diseases of disturbed neuronal network function in general, with the potential to provide both disease-modifying and symptomatic benefits at the same time as multimodal drugs.
If you would like to meet with Asceneuron at any of these conferences, please contact us at the details provided below.