Product details
Background：Cinpanemab is a human-derived monoclonal antibody directed against α-synuclein. Genetic and pathology evidence implicate this protein in the molecular pathogenesis of Parkinson’s disease (PD) and other α-synucleinopathies such as dementia with Lewy bodies (DLB). In 2010, Biogen licensed cinpanemab from Neurimmune. The antibody was generated with reverse translational medicine technology from naturally occurring, presumably protective antibodies found in healthy aged donors, as were aducanumab and other antibodies in the Biogen-Neurimmune partnership. The antibody, previously known as BIIB054, binds to α-synuclein residues 1-10, with 800-fold higher affinity for aggregated over monomeric α-synuclein. The antibody inhibits α-synuclein spreading in cell-based assays, and slows pathology and motor symptoms in mice (Weihofen et al., 2019).
• Direct evidence for ultrastructures of the α-synuclein-associated synaptic vesicle pool in presynaptic terminals., PMID:39233262
• Progress in the pathogenesis and genetics of Parkinson’s disease., PMID:18426756
• Genetics of Parkinson disease., PMID:15717024
• [Genetic factors associated with dementia in Parkinson’s disease (PD)]., PMID:25739491
• Analysis of GWAS-linked loci in Parkinson disease reaffirms PARK16 as a susceptibility locus., PMID:20697102
• Molecular findings in familial Parkinson disease in Spain., PMID:12056932
• Are genetic and sporadic Parkinson’s disease patients equally susceptible to develop dementia?, PMID:19740488
• Caenorhabditis elegans as an experimental tool for the study of complex neurological diseases: Parkinson’s disease, Alzheimer’s disease and autism spectrum disorder., PMID:22068627
• TRAF6 promotes atypical ubiquitination of mutant DJ-1 and alpha-synuclein and is localized to Lewy bodies in sporadic Parkinson’s disease brains., PMID:20634198
• Positron emission tomography changes in PARK1 mutation., PMID:16211612
