Mouse monoclonal antibody to Amyloid beta peptide (A-beta 40/42), [MOAB-2] - Biotinylated

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The amyloid beta peptide is derived from the cleavage of the Amyloid precursor protein (APP) and varies in length from 39 to 43 amino acids. However, the form(s) of amyloid-beta peptide (Aß) associated with the pathology characteristic of Alzheimer€™s disease (AD) remains unclear. In particular, the neurotoxicity of intraneuronal Aß accumulation is an area of considerable research and controversy principally because antibodies thought to be specific for Aß have been shown to actually detect intraneuronal APP and not Aß exclusively.

MOAB-2 (mouse IgG2b) is a pan-specific, high-titer antibody to Aß residues 1-4 as demonstrated by biochemical and immunohistochemical analyses (IHC), and is highly specific just to amyloid beta peptide. 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 Aß40 and Aß42. MOAB-2 did not co-localize with either N- or C-terminal antibodies to APP. In addition, no MOAB-2-immunreactivity 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 Aß, distinct from Aß associated with the cell membrane. MOAB-2 demonstrated strong intraneuronal and extra-cellular immunoreactivity in 5xFAD and 3xTg mouse brain tissues.

Biosensis now offers biotinylated MOAB-2 antibody allowing more flexibility in experimental design by using the biotin-avidin/streptavidin detection method. Biotinylated MOAB-2 antibody may also help to reduce background staining in difficult-to-stain tissues and increase detection sensitivity. The ability of biotinylated MOAB-2 antibody to detect amyloid beta has been validated by IHC.

Purified, non-biotinylated MOAB-2 antibody is available here.

Labviva Id: LV-0358-0020



More Information
Attribute Type Attribute Value
Species Reactivity HUMAN, RODENT
Antibody Isotype MONOCLONAL
Alternative Name Beta-APP42; Beta-APP40; Beta-amyloid protein 42; Beta-amyloid protein 40; ABPP; APPI; Amyloid beta A4 protein; MOAB2; MOAB-2; Alzheimer's antibody; AB40; AB42; abeta
Target Protein A4
References Count 10.0000
Uniprot Number Only P05067
Uniprot Full Accession Number & Name P05067 A4_HUMAN
Storage After reconstitution keep aliquots at -20 °C to -70 °C for a higher stability. At 2-8 °C keep up to one week; use sterile methods and pipettes. Highly purified glycerol (1:1) may be added for an additional stability. Avoid repetitive freeze/thaw cycles. K
Reconstitution Spin vial briefly before opening. Reconstitute in 50 µL of sterile water to give a concentration of 1 mg/mL. Centrifuge to remove any insoluble material. Final buffer is PBS, pH 7.4 without preservative.
Product Specificity MOAB-2 detects preparations enriched in U-, O-, F-Aß42, and U-Aß40 by dot-blot, and is thus a pan-specific Aß antibody. However, MOAB-2 is selective for the more neurotoxic Aß42 compared to Aß40. Indeed, MOAB-2 demonstrated a titration against antigen con
UNSPSC Code 41116161
Shipping Temperature 25°C (Ambient)
Expiry Date 12 months after purchase.
Conjugate Biotin
Manufacturer BIOSENSIS
Purity Antibody was purified from cell culture supernatant by Protein G chromatography, biotinylated and buffer-exchanged into PBS, pH 7.4 buffer
Clone Name MOAB-2
Related Products Purified, non-biotinylated MOAB-2 antibody, cat# M-1586-100
Oligomeric Aß ELISA Kit, cat# BEK-2215-1P/2P
Immunogen Recombinant human amyloid beta protein 42 (Aß42): DAEFRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA
Product Type Antibody
Format contains no preservative., Lyophilized from PBS buffer, pH 7.4
Product Size 50 µg

Supporting Literature

Protocols & Papers

Protocols & Papers

Sortilin inhibits amyloid pathology by regulating non-specific degradation of APP.

Ruan CS; Liu J; Yang M; Saadipour K; Zeng YQ; Liao H; Wang YJ; Bobrovskaya L; Zhou XF

Experimental neurology.; Volume 299, Issue Pt A 2018/01/01

View Reference

ER-associated degradation regulates Alzheimer's amyloid pathology and memory function by modulating ?-secretase activity.

Zhu B; Jiang L; Huang T; Zhao Y; Liu T; Zhong Y; Li X; Campos A; Pomeroy K; Masliah E; Zhang D; Xu H

Nature communications.; Volume 8, Issue 1 2017/11/13

View Reference

SORLA attenuates EphA4 signaling and amyloid ß-induced neurodegeneration.

Huang TY; Zhao Y; Jiang LL; Li X; Liu Y; Sun Y; Piña-Crespo JC; Zhu B; Masliah E; Willnow TE; Pasquale EB; Xu H

The Journal of experimental medicine.; Volume 214, Issue 12 2017/12/04

View Reference

Peripheral Inflammation, Apolipoprotein E4, and Amyloid-ß Interact to Induce Cognitive and Cerebrovascular Dysfunction.

Marottoli FM; Katsumata Y; Koster KP; Thomas R; Fardo DW; Tai LM

ASN neuro.; Volume 9, Issue 4 2017 Jul-Aug

View Reference

Epidermal growth factor prevents APOE4 and amyloid-beta-induced cognitive and cerebrovascular deficits in female mice.

Thomas R; Zuchowska P; Morris AW; Marottoli FM; Sunny S; Deaton R; Gann PH; Tai LM

Acta neuropathologica communications.; Volume 4, Issue 1 2016/10/27

View Reference

The role of APOE in cerebrovascular dysfunction.

Tai LM; Thomas R; Marottoli FM; Koster KP; Kanekiyo T; Morris AW; Bu G

Acta neuropathologica.; Volume 131, Issue 5 2016/05/01

View Reference

A 3D human neural cell culture system for modeling Alzheimer's disease.

Kim YH; Choi SH; D'Avanzo C; Hebisch M; Sliwinski C; Bylykbashi E; Washicosky KJ; Klee JB; Brüstle O; Tanzi RE; Kim DY

Nature protocols.; Volume 10, Issue 7 2015/07/01

View Reference

Microglia constitute a barrier that prevents neurotoxic protofibrillar Aß42 hotspots around plaques.

Condello C; Yuan P; Schain A; Grutzendler J

Nature communications.; Volume 6, Issue 2015/01/29

View Reference

Intracellular Aß pathology and early cognitive impairments in a transgenic rat overexpressing human amyloid precursor protein: a multidimensional study.

Iulita MF; Allard S; Richter L; Munter LM; Ducatenzeiler A; Weise C; Do Carmo S; Klein WL; Multhaup G; Cuello AC

Acta neuropathologica communications.; Volume 2, Issue 2014/06/05

View Reference

Neuronal inclusions of a-synuclein contribute to the pathogenesis of Krabbe disease.

Smith BR; Santos MB; Marshall MS; Cantuti-Castelvetri L; Lopez-Rosas A; Li G; van Breemen R; Claycomb KI; Gallea JI; Celej MS; Crocker SJ; Givogri MI; Bongarzone ER

The Journal of pathology.; Volume 232, Issue 5 2014/04/01

View Reference

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