March 4, 2021 Syngle Therapeutics and Hirosaki University announce their collaboration to evaluate Syngle’s anti-alphasynuclein antibody 26F1 in the adult onset Multiple System Atrophy (MSA) animal model developed by the Department of Neuropathology at Hirosaki University Graduate School of Medicine. The 26F1 antibody has been developed with support by the Michael J. Fox Foundation (Grant 11877).
Multiple System Atrophy is a form of atypical parkinsonism affecting 4-5 per 100,000 people. MSA usually occurs in adults with signs and symptoms appearing around age 55. Typically, patients with MSA decease within 7–9 years of disease onset. There is no cure for this rare neurodegenerative disease.
MSA is characterized by progressive loss of cells in various regions of the central nervous system caused by clumps – also referred to as aggregates – of abnormal alpha-synuclein protein that for unknown reasons build up inside cells.
The 26F1 antibody of Syngle has been developed specifically for binding such abnormal aggregates and not the monomeric form of alpha-synuclein. In other words: to target the pathological species and to avoid binding the alpha-synuclein with a physiological function. This aggregate-specificity is considered to be key for an effective treatment while reducing the risk of unacceptable side-effects.
The adult-onset MSA animal model developed by Hirosaki University is particularly relevant, because it enables to study the effect of an early stage treatment of the disease. Other MSA models develop accumulation of α-synuclein immediately after fertilization. The Hirosaki University model allows to induce the pathology at adulthood and thus provides a more realistic model of the disease.
For further information, please contact:
Guus Scheefhals
CEO Syngle Therapeutics
