amyloid β peptide

Amyloid β Peptide (42-1)(human) acetate is the inactive form of Amyloid β Peptide (1-42). Amyloid β Peptide (42-1)(human) acetate is a 42-amino acid peptide which plays a key role in the pathogenesis of Alzheimer disease.

β-Amyloid (42-1), human, is the inactive form of Amyloid β Peptide (1-42), which plays a pivotal role in the pathogenesis of Alzheimer's disease.

Amyloid-β (25-35) (Aβ (25-35)) is an 11-residue fragment of the Aβ protein that retains the physical and biological characteristics of the full length peptide. It forms fibrils that react to thioflavin T and Congo red and are organized in a cross-β arrangement of β-strands similar to Aβ (1-40) and Aβ (1-42) fibrils. Aggregated Aβ (25-35) decreases the viability of rat adrenal PC12 cells. It also decreases the viability of primary rat cortical neurons at concentrations ranging from 1 nM to 30 μM. In vivo, intracerebral injection of Aβ (25-35) (20 nmol) in rats induces lesions of neuronal and tissue loss. Aggregated Aβ (25-35) administered intracerebroventricularly to rats induces learning and memory impairments in the Y-maze, novel object recognition, and contextual fear conditioning tests.

β-Amyloid peptide(16-20), with the amino acid sequence (KLVFF) derived from Amyloid-β (Abeta), functions as an efficient inhibitor of Abeta fibril formation. This compound is modified with RG- -GR-NH2 residues at both its N- and C-terminal ends to enhance solubility [1].

Colivelin is a neuroprotective peptide and activator of STAT3. Colivelin is a hybrid peptide synthesized to enhance the neuroprotective effects of humanin (HN).

Biotin-β-Amyloid (1-42), human TFA, also known as Biotin-Amyloid β-Peptide (1-42) (human) TFA, is a biotin-labeled 42-amino acid peptide implicated in the pathogenesis of Alzheimer's disease.

β-Amyloid (1-42), human, is a 42-amino acid peptide integral to the pathogenesis of Alzheimer disease.

β-Amyloid (31-35) (β-Amyloid 31-35) is the shortest sequence of native Amyloid-β peptide.

β-Amyloid 15-21 acetate (Beta-Amyloid (15-21) acetate) is a fragment of Amyloid-β peptide, maybe used in the research of neurological disease. This fragment is involved in beta sheet formation.

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

β-Amyloid (1-16) is an amyloidogenic protein fragment derived from the β-amyloid sequence, known for its ability to bind metal ions, indicating its role in metal-binding processes. β-Amyloid, a peptide, is responsible for forming amyloid plaques in the brains of people with Alzheimer's disease (AD).

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 (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.

Amyloid β-Protein (10-20) is a fragment of Amyloid-β peptide, maybe used in the research of neurological disease.Amyloid β protein fragment containing the α-secretase processing site (Lys16-Leu17 bond). It also contains the HHQK domain (residues 13-16) re

RAGE antagonist peptide acetate is an advanced antagonist of glycation end products (RAGE). RAGE antagonist peptide acetate possesses anti-tumor and anti-inflammatory activities. RAGE antagonist peptide acetate prevents RAGE from binding with several of its most important ligands, including HMGB-1, S100P, and S100A4.

Cys-Gly-Lys-Arg-Amyloid β-Protein (1-42), a peptide fragment derived from amyloid β-protein (Aβ), is crucial in Alzheimer's disease research [1].

(Nle35)-Amyloid β-Protein (1-42) ammonium is a peptide.

β-Amyloid (1-16) rat is a fragment of the amyloid beta (Abeta) peptide's metal-binding domain, containing three amino acid substitutions compared to its human counterpart, which confer reduced susceptibility to Alzheimer's disease-like neurodegeneration in rats and mice [1].

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

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.

Exendin (5-39) is a potent antagonist of the glucagon-like peptide 1 (GLP-1) receptor that can ameliorate memory impairment in rats treated with β-amyloid protein.

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.

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 (1-42), rat TFA is a 42-aa peptide, shows the effects of cytotoxicity on acute hippocampal slices, and has been used in studies of alzheimer's disease.