βamyloid (2240)

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.

This is an N-terminal fragment of beta amyloid. It consists of amino acid residues 1 to 9. Truncated beta amyloid peptide (10-40) still forms amyloid fibrils and shows fibril polymorphism.

This is a fragment of beta-amyloid peptide. It has amino acids 1 through 34.

β-Amyloid (13-27) is a synthetic peptide comprising amino acids 26 to 40 of the beta amyloid protein. It is utilized to study the kinetics of beta amyloid formation.

β-Amyloid (1-15) (Amyloid β-Protein (1-15)) 是 β-淀粉样蛋白片段，可用于研究阿尔茨海默病。

β-Amyloid (35-42) is a peptide consisting of amino acid of 35 to 42 of beta amyloid protein.

β-Amyloid 15-21 acetate (Beta-Amyloid(15-21) acetate) 是 Amyloid-β 肽的片段，可用于神经系统疾病的研究。该片段参与β折叠形成。

β-Amyloid (1-16) is an amyloidogenic protein fragment with a sequence derived from β-amyloid. It exhibits the ability to bind to metal ions, indicating its involvement in metal-binding processes. β-Amyloid, a peptide, is responsible for the formation of amyloid plaques in the brains of individuals affected by Alzheimer's disease (AD).

β-Amyloid (1-28), a fragment of the β-Amyloid protein, is involved in metal binding.

This synthetic peptide consists of amino acids 1 to 17 of beta amyloid protein. This peptide can be employed in beta amyloid solubility studies.

β-Amyloid (25-35) (Aβ25-35) 是一种阿尔茨海默氏淀粉样蛋白β肽的Aβ(25-35) 片段，在培养细胞中显示出神经毒性作用。

β-Amyloid (1-37) (human) 与阿尔茨海默病的精神状态有潜在关联。

Antibodies corresponding to beta-amyloid (4-10) are effective in vivo inhibitors of cytotoxicity, amyloid plaque formation and special memory disturbances in mice. This peptide does not elicit an inflammatory response.

Amyloid β-peptide fragment; minimum section required to bind to brain proteins. Binds with high affinity to α7-nicotinic ACh receptors, and impairs memory retention following central administration in mice in vivo.

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 (31-35) (β-Amyloid 31-35) 是一种天然 Amyloid-β 肽的最短序列，具有神经毒性。

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

β-Amyloid (11-22) is a peptide fragment of β-Amyloid. Beta-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 disorder.

β-Amyloid (12-20) is a peptide fragment of β-Amyloid containing the amino acid residues VFF at positions (18-20), suggesting amnestic effects for this triad.

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

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

β-Amyloid (33-40) is a peptide consisting of amino acid of 33 to 40 of beta amyloid protein.

β-Amyloid (29-40), a fragment of the Amyloid-β peptide, possesses physical and chemical properties similar to those of viral protein fusion peptides. The C-terminal fragments (29-40/42) of Alzheimer's beta amyloid peptide can induce the fusion of liposomes.

Intracerebroventricular administration of synthetic peptides Beta-amyloid (12-20), (12-28), and (18-28) causes amnesia in mice. These peptides have only amino acid residues VFF at position 18 to 20 in common, suggesting the amnestic effect of the triad.

Anionic interaction of Beta-amyloid (1-11) with Factor XII is suspected to cause massive activation of the C4 (complement 4) system in the cerebrospinal fluid of Alzheimer's disease patients.

This synthetic peptide consists of amino acids 1 to 20 of beta amyloid protein.

β-amyloid (12-28) TFA, a peptide fragment of β-amyloid protein (β1-42), is the major component of senile plaque cores. β-amyloid (12-28) has aggregation properties and the potential for Alzheimer's disease research.

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