β amyloid

β-Amyloid (25-35) is a fragment of the Alzheimer’s amyloid beta peptide Aβ(25-35), exhibiting neurotoxic effects and commonly used to establish both cellular and animal models of Alzheimer’s disease.

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

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

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.

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.

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

GRGDSPK acetate shows inhibitory activity against integrin-fibronectin binding and can be used in research on integrins in bone formation and resorption.

Davunetide acetate is derived from activity-dependent neuroprotective protein existing in the mammalian CNS. Davunetide acetate is a microtubule-stabilizing peptide and inhibits Aβ aggregation and Aβ-induced neurotoxicity. Davunetide acetate possesses neuroprotective, neurotrophic, and cognitive protective properties.

(Rac)-Z-Phe-Phe-FMK (Cathepsin L-IN-2) is a cathepsin L inhibitor that inhibits the tendency of β-amyloid to induce apoptotic changes .

[Ala28]-β Amyloid(25-35) (β(25-35)KA), an electrically neutral mutant variant of Aβ(25-35), facilitates the accelerated aggregation of Firefly Luciferase [1].

β-Amyloid(28-35) human is a neurotoxic β-amyloid peptide fragment that contributes to Alzheimer's disease pathogenesis by interacting with neuronal membranes, modulating its secondary structure and toxicity. It also exhibits anisotropic effects on the acidic phospholipid DPH, thereby increasing the internal fluidity within lipid membrane bilayers [1].

β-Amyloid(17-28) human is a fragment of the β-amyloid peptide (Abeta) associated with Alzheimer's disease (AD), promoting the aggregation of the full-length β-Amyloid40 into toxic aggregates [1]. This lipid-induced amyloid core segment is implicated in AD pathogenesis.

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].

Acetyl-β Amyloid (15-20), Amide is a peptide fragment that inhibits β-sheet formation and stabilizes the structure of the Aβ (1–40) peptide, making it a useful tool in Alzheimer's disease research [1].

V-9-M Cholecystokinin nonapeptide (Prepro CCK Fragment V-9-M) is a precursor compound of cholecystokinin (CCK). Cholecystokinin (CCK) is a brain-intestinal peptide that stimulates gallbladder contraction and pancreatic exocrine. It can be extracted from the small intestine of dogs and cats and can cause gallbladder contraction.

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), rat/mouse TFA is a 42-amino-acid polypeptide fragment that exhibits neurotoxicity to hippocampal slices and is commonly used to establish Alzheimer's disease models for related research.

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 (1-37) (human) is potentially associated with mental status in Alzheimer's disease.

The amyloid β-protein is a 39- to 43-amino acid polypeptide that is the primary constituent of senile plaques and cerebrovascular deposits in Alzheimer's disease and Down's syndrome. Additionally it acts as an inhibitor of the ubiquitin-dependent protein degradation in vitro.

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.

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

β-Amyloid (1-38), derived from mice and rats, is a chemical compound comprising 38 amino acids, specifically residues 1-38 of the Aβ peptide. Notably, it serves as the primary constituent of amyloid plaques associated with Alzheimer's disease.

β-Amyloid (1-40) TFA is a major protein fragment found in the brain plaques of Alzheimer's disease patients and is commonly used to establish Alzheimer's disease models.