prasinezumab   Click here for help

GtoPdb Ligand ID: 13330

Synonyms: PRX002 | RG-7935 | RG7935 | RO-7046015 | RO7046015
Compound class: Antibody
Comment: Prasinezumab (RO7046015) is a monoclonal antibody that binds the C-terminus of neurotoxic (aggregated) forms of α-synuclein. It was designed to reduce the cell-to-cell spread of toxic α-synuclein aggregates in the brains of people with Parkinson's disease, as a disease-modifying therapeutic approach to slow the rate of neuronal damage and disease progression.
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Ligand Activity Visualisation Charts

These are box plot that provide a unique visualisation, summarising all the activity data for a ligand taken from ChEMBL and GtoPdb across multiple targets and species. Click on a plot to see the median, interquartile range, low and high data points. A value of zero indicates that no data are available. A separate chart is created for each target, and where possible the algorithm tries to merge ChEMBL and GtoPdb targets by matching them on name and UniProt accession, for each available species. However, please note that inconsistency in naming of targets may lead to data for the same target being reported across multiple charts.

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View interactive charts of activity data across species
Bioactivity Comments
Binding avidity for α-synuclein aggregates is substantially higher than for monomeric α-synuclein [3].
Selectivity at other protein targets
Key to terms and symbols Click column headers to sort
Target Sp. Type Action Value Parameter Concentration range (M) Reference
synuclein alpha Hs Antibody Binding 7.7 – 10.3 pKd - 3
⤷ pKd 10.3 (Kd 4.8x10-11 M) [3]
Description: Affinity for aggregated α-synuclein
pKd 7.7 (Kd 2x10-8 M) [3]
Description: Affinity for monomeric α-synuclein
Targets where the ligand is described in the comment field
Target Comment
synuclein alpha The formation of abnormal and toxic synuclein alpha oligomers and larger fibrilar aggregates underlies neurodegeneration in Parkinson's disease and other neurodegenerative diseases. There has therefore been much interest in developing therapeutics that are able to prevent formation or functionally block these aggregates as potential disease-modifying options to slow disease progression. As of early 2024, clinical evidence was beginning to demonstrate two pharmaceutical mechanisms that offered disease-modifying efficacy (in patients in the early stages of Parkinson's disease): anti-diabetes GLP-1 agonist drugs (lixisenatide and exenatide/exendin-4 for example) [1-2,4] and the monoclonal antibody prasinezumab that selectively targets aggregated forms synuclein alpha [5]. It remains to be determined if these mechanisms hold in larger clinical studies.