beta-amyloid 22-40

Beta-MSH (1-22) (human) acetate (Beta-MSH (1-22) (human) acetate (17908-57-5 Free base)) , is an endogenous melanocortin-4 receptor (MC4-R) agonist.

Amyloid beta-protein(1-40) Arctic variant (Ab40ARC (E22G)), featuring a glycine at position 22 (Gly22), is a peptide utilized in Alzheimer's disease research [1].

This synthetic peptide consists of amino acids 22 to 40 of beta amyloid protein. This peptide sequence is often used in beta amyloid structure and aggregation studies.

Rat form of the beta-Amyloid (1-40) peptide

β-Amyloid (29-40) is a fragment of Amyloid-β peptide. Alzheimer's beta amyloid peptide (29-40 42) C-terminal fragments exhibit physical and chemical properties similar to fusion peptides of viral proteins, inducing liposome fusion in vitro.

β-Amyloid (22-35) is a 14-aa peptide, shows aggregates and induces neurotoxicity in the hippocampal cells. Beta amyloid (22-35) is a synthetic truncated fragment of beta-amyloid peptide.

β-Amyloid (1-40), England mutation, is a biologically active peptide with a histidine (His) to arginine (Arg) substitution at position 6, known to enhance oligomerization kinetics that serve as fibril seeds and increase neurotoxicity in cultured neurons. This alteration is one of several mutations in the beta-amyloid precursor gene implicated in autosomal dominant Alzheimer's Disease across multiple kindreds.

(Gln22,Asn23)-Amyloid β-Protein (1-40) is a peptide used to study Cerebral Amyloid Angiopathy Mutations [1].

Beta-Amyloid(1-14),mouse,rat is a 1 to 14 fragment of Amyloid-β peptide. This peptide is amino acids 1 to 14 fragment of Beta-Amyloid peptide.

β-Amyloid 22-35 (Amyloid β-Protein 22-35) TFA, a fragment comprising residues 22-35 of the β-amyloid protein, exhibits cytotoxicity towards cultured rat hippocampal neurons in serum-free media. It aggregates and forms typical amyloid fibrils in neutral buffer solution, mirroring those observed with the full-length β-amyloid protein [1].

β-Amyloid (1-40) TFA, a principal protein in plaques observed in the brains of Alzheimer's disease patients [1], is pivotal in research focused on this neurodegenerative disorder.

β-Amyloid (1-40), FAM-labeled, is a β-Amyloid (1-40) peptide tagged with a FAM fluorescent label, exhibiting an excitation wavelength (λ ex) of 492 nm and an emission wavelength (λ em) of 518 nm.

β-Amyloid (1-40), FAM-labeled TFA, is a FAM fluorescently-labeled β-Amyloid (1-40) peptide (λ ex = 492 nm and λ em = 518 nm) [1].

(Pyr11)-Amyloid β-Protein (11-40) (Aβ11pE-40), a peptide, is utilized in Alzheimer's disease research [1].

β-Melanocyte Stimulating Hormone (MSH), human (Synonyms: Beta-MSH (1-22) (human)) β-Melanocyte Stimulating Hormone (MSH), human, a 22-residue peptide, acts as an endogenous melanocortin-4 receptor (MC4-R) agonist.

β-Amyloid (33-40) is a peptide composed of amino acids 33 to 40 from the beta-amyloid protein.

β-Amyloid (11-22) is a peptide fragment of β-Amyloid. β-Amyloid peptide (Abeta), the primary component of amyloid plaques in the brains of Alzheimer’s patients, is believed to be the cause of Alzheimer’s Disease (AD), the most common neurodegenerative disease, affecting approximately 10% of the population over 60.

Biotin-β-Amyloid (1-40) is an amyloid-β-(1-40) peptide with an N-terminal biotinylation.

Biotin-β-Amyloid (17-40) is a biotinylated amyloid-ß-(1-40) peptide labeled at the N-terminal, comprising a 24-residue fragment from the post-translational processing of amyloid precursor protein (APP) [1].

Amyloid β1-40 is one of the fragments generated after cleavage of the amyloid peptide precursor protein by β and γ secretases.

[Asn23] β-Amyloid (1-40), Iowa mutation, is a biologically active peptide linked to autosomal dominant Alzheimer's Disease in multiple families. This involves the substitution of Asp 23 with Asn, causing severe cerebral amyloid beta-protein angiopathy (CAA). Individuals with this mutation exhibit a missense alteration in the APP gene at position 694, resulting in the mutated β-amyloid peptide aggregating more quickly and forming toxic fibrils.

[Asn23]-beta-Amyloid (1-42), Iowa mutation, is a biologically active peptide with increased aggregation propensity and fibril toxicity. This mutation involves the substitution of Aspartic acid (Asp) at position 23 with Asparagine (Asn), contributing to autosomal dominant Alzheimer's Disease and associated with severe cerebral amyloid beta-protein angiopathy (CAA) due to a missense alteration at position 694 of the amyloid precursor protein (APP) gene.