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#11115 Anti-Human Amyloidβ (38-42) (44A3) Mouse IgG MoAb

  • IHC Human Alzheimer’s Disease Brain
  • WB / IP
Intended Use:
Research reagents
Package Size1:
50 μg
Package Size2:
5 μg
Note on Application Abbreviations
WB:Western Blotting

※ The product indicated as "Research reagents" in the column Intended Use cannot be used
  for diagnostic nor any medical purpose.
※ The datasheet listed on this page is sample only. Please refer to the datasheet
  enclosed in the product purchased before use.

Product Overview

Product Code 11115
Product Name Anti-Human Amyloidβ (38-42) (44A3) Mouse IgG MoAb
Maker Name Immuno-Biological Laboratories Co., Ltd.
Intended Use Research reagents
Application WB, IP, IHC
Species Human
Immunizing antigen Synthetic peptide of human Amyloidβ(38-42) (GVVIA)
Source Mouse-Mouse hybridoma (X63 – Ag 8.653 × BALB/c mouse spleen cells, supernatant)
Clone Name 44A3
Subclass IgG2b
Purification Method Affinity purified with antigen peptide
Specificity Human Amyloidβ (1-42) specific.
Not detect Human Amyloidβ (1-40) or Amyloidβ (1-43) at the same level in western blotting.
Reacts with Mouse and Rat.
Package Form Lyophilized product in PBS containing 1 % BSA and 0.05 % NaN3
Storage Condition 2 ~ 8 ℃
Poisonous and Deleterious Substances Applicable
Cartagena Not Applicable
Package Size 1 50 μg
Package Size 2 5 μg
Remarks1 The commercial use of products without our permission is prohibited. Please make sure to contact us and obtain permission.

Product Description

Alzheimer's disease (AD) is characterized by the presence of extracellular plaques and intracellular neurofibrillary tangles (NFTs) in the brain. The major protein component of these plaques is beta amyloid (Aβ) peptide, a 40 to 43 amino acid peptide cleaved from amyloid precursor protein by β-secretase and γ-secretase. Increased release of Aβ42 or Aβ43, both of which exibit a greater tendency to aggregate than Aβ40, occurs in individuals expressing certain genetic mutations, ApoE alleles or may involve other undiscovered factors. Many researchers theorize that it is this increased release of Aβ42/Aβ43 which leads to the abnormal deposition of Aβ and the associated neurotoxicity in the brains of affected individuals. It is also reported that a distinct Aβpeptide, AβN3pE, is deposited in senile plaques in a dominant and differential manner as compared with the standard Aβpeptide.

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Note: This product is for research use only. It cannot be used as a diagnostic tool or drug.