InVivoMAb anti-human/mouse/rat amyloid-beta

Catalog #BE0368
Mouse, Human, Rat

$164.00 - $4,280.00

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  • 100 mg - $4,280.00
  • 50 mg - $3,024.00
  • 25 mg - $2,009.00
  • 5 mg - $600.00
  • 1 mg - $164.00
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Product Details

The MOAB-2 monoclonal antibody (epitope mapped to residues 1-5 of human Aβ) is a pan-specific antibody. Using synthetic Aβ, it recognizes unaggregated, oligomeric or fibrillar forms of Aβ42 and unaggregated Aβ40, and is selective for human Aβ42 over Aβ40. With synthetic Aβ or human or rodent brain homogenates, MOAB-2 specifically detects Aβ, but not amyloid precursor protein (APP), which is cleaved by β- and Y- secretase to release Aβ.  With immunostaining of human or rodent tissue, MOAB-2 detects intraneuronal Aβ, as well as diffuse or compact amyloid plaques.


Isotype Mouse IgG2b, λ
Recommended Isotype Control(s) InVivoMAb mouse IgG2b isotype control, unknown specificity
Recommended Dilution Buffer InVivoPure pH 7.0 Dilution Buffer
Conjugation This product is unconjugated. Conjugation is available via our Antibody Conjugation Services.
Immunogen Human Aβ42
Reported Applications Western blot
Formulation PBS, pH 7.0
Contains no stabilizers or preservatives
Endotoxin <2EU/mg (<0.002EU/μg)
Determined by LAL gel clotting assay
Purity >95%
Determined by SDS-PAGE
Sterility 0.2 µm filtration
Purification Protein A
RRID AB_2927505
Molecular Weight 150 kDa
Storage The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.
Western Blot, Immunohistochemistry, Immunofluorescence, Immunoprecipitation, ELISA
Youmans, K. L., et al. (2012). "Intraneuronal Abeta detection in 5xFAD mice by a new Abeta-specific antibody" Mol Neurodegener 7: 8. PubMed

BACKGROUND: The form(s) of amyloid-beta peptide (Abeta) associated with the pathology characteristic of Alzheimer’s disease (AD) remains unclear. In particular, the neurotoxicity of intraneuronal Abeta accumulation is an issue of considerable controversy; even the existence of Abeta deposits within neurons has recently been challenged by Winton and co-workers. These authors purport that it is actually intraneuronal APP that is being detected by antibodies thought to be specific for Abeta. To further address this issue, an anti-Abeta antibody was developed (MOAB-2) that specifically detects Abeta, but not APP. This antibody allows for the further evaluation of the early accumulation of intraneuronal Abeta in transgenic mice with increased levels of human Abeta in 5xFAD and 3xTg mice. RESULTS: MOAB-2 (mouse IgG2b) is a pan-specific, high-titer antibody to Abeta residues 1-4 as demonstrated by biochemical and immunohistochemical analyses (IHC), particularly compared to 6E10 (a commonly used commercial antibody to Abeta residues 3-8). MOAB-2 did not detect APP or APP-CTFs in cell culture media/lysates (HEK-APPSwe or HEK-APPSwe/BACE1) or in brain homogenates from transgenic mice expressing 5 familial AD (FAD) mutation (5xFAD mice). Using IHC on 5xFAD brain tissue, MOAB-2 immunoreactivity co-localized with C-terminal antibodies specific for Abeta40 and Abeta42. MOAB-2 did not co-localize with either N- or C-terminal antibodies to APP. In addition, no MOAB-2-immunoreactivity was observed in the brains of 5xFAD/BACE-/- mice, although significant amounts of APP were detected by N- and C-terminal antibodies to APP, as well as by 6E10. In both 5xFAD and 3xTg mouse brain tissue, MOAB-2 co-localized with cathepsin-D, a marker for acidic organelles, further evidence for intraneuronal Abeta, distinct from Abeta associated with the cell membrane. MOAB-2 demonstrated strong intraneuronal and extra-cellular immunoreactivity in 5xFAD and 3xTg mouse brain tissues. CONCLUSIONS: Both intraneuronal Abeta accumulation and extracellular Abeta deposition was demonstrated in 5xFAD mice and 3xTg mice with MOAB-2, an antibody that will help differentiate intracellular Abeta from APP. However, further investigation is required to determine whether a molecular mechanism links the presence of intraneuronal Abeta with neurotoxicity. As well, understanding the relevance of these observations to human AD patients is critical.