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View ProductsSize | 100ug, 1MG |
---|---|
Isotype | IgG1, kappa |
Brand | ProteoGenix |
Product type | Primary Antibodies |
Clonality | Monoclonal Antibody |
Expression system | Mammalian cells |
Applications | Elisa, WB |
Product name | Donanemab Biosimilar - Anti-APP mAb - Research Grade |
---|---|
Source | CAS 1931944-80-7 |
Species | Humanized |
Expression system | Mammalian |
Purity | >85% |
Buffer | PBS buffer PH7.5 |
Delivery condition | Blue ice (+4°C) |
Delivery lead time in business days | 3-5 days if in stock; 3-5 weeks if production needed |
Delivery Time | 3-5 days if in stock; 3-5 weeks if production needed |
Storage condition | store at -80°C |
Brand | ProteoGenix |
Aliases /Synonyms | Donanemab ,LY3002813,APP,anti-APP |
Reference | PX-TA1549 |
Note | For research use only. Not suitable for human use. |
Isotype | IgG1-kappa |
Clonality | Monoclonal Antibody |
Donanemab is a humanized monoclonal antibody (IgG1) derived from mouse mE8-IgG2a specifically for the treatment of Alzheimer’s disease (AD). It has a unique mechanism of action that targets and clears a protein called amyloid-beta (Aβ). The latter is responsible for the build-up of plaques in the brains of Alzheimer’s patients, causing neuronal damage and dementia.
Donanemab is a plaque-binding antibody, that provides a unique approach to treating the disease. It is designed to specifically target the N-truncated pyroglutamate amyloid beta peptide at position 3 (pGlu3-Aβ, AβpE3), which is a specific form of pyroglutamate of the amyloid beta protein. By binding to these plaques, donanemab promotes their clearance, potentially reducing the burden on neurons and slowing disease progression.
Donanemab facilitates their clearance from the brain by selectively binding to these plaques, addressing a key feature of Alzheimer’s disease pathology. This targeted approach distinguishes Donanemab from other treatments that focus solely on preventing plaque deposition or growth. Because it acts directly to clear existing amyloid plaques by specifically binding to them, it has a high affinity for deposited plaques. This mechanism of action offers a novel therapeutic strategy in the fight against Alzheimer’s disease.
Donanemab represents an innovative approach to the treatment of Alzheimer’s disease. Its mechanism of action, which focuses on clearing Aβ plaques, offers an alternative strategy to previously approved treatments. Donanemab has the potential to offer Alzheimer’s patients a more specialized and effective treatment option by directly targeting the underlying disease.
Clinical trials of Donanemab have shown encouraging results for AD patients in terms of cognitive development and functional outcomes. In a study of 1,736 people, Donanemab showed a significant 35% reduction in mental decline over 18 months compared to the placebo group.
Participants also experienced a significant 40% reduction in loss of ability to perform daily activities. These encouraging clinical results demonstrate the potential efficacy of donanemab in improving cognitive function and maintaining independence in patients with Alzheimer’s disease.
As any therapeutic intervention must take safety into account. Throughout its development, Donanemab has undergone rigorous safety evaluations. Because of its humanized antibody structure, it reduces the possibility of negative side effects, making it well tolerated by patients. This improved safety profile is critical to the commercialization and future use of Donanemab as a therapeutic option for Alzheimer’s disease.
Donanemab represents a significant advancement in the treatment of Alzheimer’s disease. Through its targeted approach of selectively binding and clearing amyloid-beta plaques, Donanemab holds promise for slowing disease progression and improving cognitive function in Alzheimer’s disease patients.
Publication
Epitope Sequence and Modification Fingerprints of Anti-Aβ Antibodies, Ivan Talucci, Timon Leske, Hans-Wolfgang Klafki, Mohammed Mehedi Hassan, Annik Steiert, Barbara Morgado, Sebastian Bothe, Lars van Werven, Thomas Liepold, Jochen Walter, Hermann Schindelin, Jens Wiltfang, Oliver Wirths, Olaf Jahn, Hans-Michael Maric, bioRxiv 2025.02.26.640323; doi: https://doi.org/10.1101/2025.02.26.640323
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