This purified ABfinity™ recombinant rabbit anti-amyloid beta (Abeta) [1-42] monoclonal antibody reacts with human and mouse Abeta [1-42]. Alzheimer’s Disease (AD) is characterized by the presence of extracellular plaques and intracellular neurofibrillary tangles (NFTs) in the brain. The major component of these plaques is Aβ peptide (β-amyloid), a 40 to 43 amino acid peptide cleaved from amyloid precursor protein (APP) by β-secretase (e.g., BACE) and a putative γ secretase. This ABfinity™ recombinant rabbit anti-amyloid beta (Abeta) [1-42] monoclonal antibody is validated for use in immunohistochemistry, and immunoassay (ELISA).

Antibody Specifications:

• Applications: Validated applications for ABfinity™ recombinant rabbit anti-amyloid beta (Abeta) [1-42] monoclonal antibody are immunohistochemistry, and immunoassay (ELISA).
• Host Species and Isotype: The host species and isotype of the anti-amyloid beta (Abeta) [1-42] monoclonal antibody is rabbit IgG.
• Clone ID of Oligoclonal Antibody (pAb): The ABfinity™ recombinant rabbit anti- amyloid beta (Abeta) [1-42] monoclonal antibody clone is H31L21.
• Reactivity: Reacts with human and mouse Abeta [1-42]
• Product Size: ABfinity™ recombinant rabbit anti-amyloid beta (Abeta) [1-42] monoclonal antibody is available in a 100 µg size.

ABfinity™ recombinant rabbit monoclonal antibody validated to mouse, human and expected reactivity with human, mouse, rat, primate, canine, bovine, equine, swine, hamster, and numerous other species. This antibody is validated for use in immunohistochemistry and immunoassay (ELISA). Aβ [1-42] is encoded by the 351 gene, also known as amyloid beta (A4) precursor protein, AAA, AD1, PN2, ABPP, APPI, CVAP, ABETA, CTF-gamma.

Alzheimer’s Disease (AD) is characterized by the presence of extracellular plaques and intracellular neurofibrillary tangles (NFTs) in the brain. The major component of these plaques is Aβ peptide (β-amyloid), a 40 to 43 amino acid peptide cleaved from amyloid precursor protein (APP) by β-secretase (e.g., BACE) and a putative γ secretase. Increased release of the "longer forms" of Aβ peptide, Aβ42 or Aβ43, which have a greater tendency to aggregate than Aβ40, occurs in individuals expressing certain genetic mutations, expressing certain ApoE alleles, or may involve other, still undiscovered, factors. Many researchers theorize that this increased release of Aβ42/Aβ43 leads to the abnormal deposition of Aβ and the associated neurotoxicity in the brains of affected individuals.