Amyloid-β (25-35) Peptide (human) (trifluoroacetate salt)

Amyloid-β (25-35) Peptide (human) (trifluoroacetate salt) Suppliers list
Company Name: TargetMol Chemicals Inc.  
Tel: +1-781-999-5354; +1-00000000000
Email: marketing@targetmol.com
Company Name: ChemeGen(Shanghai) Biotechnology Co.,Ltd.  
Tel: 18818260767
Email: sales@chemegen.com

Amyloid-β (25-35) Peptide (human) (trifluoroacetate salt) manufacturers

Amyloid-β (25-35) Peptide (human) (trifluoroacetate salt) Basic information
Product Name:Amyloid-β (25-35) Peptide (human) (trifluoroacetate salt)
Synonyms:Amyloid-β (25-35) Peptide (human) (trifluoroacetate salt)
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MW:0
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Amyloid-β (25-35) Peptide (human) (trifluoroacetate salt) Structure
Amyloid-β (25-35) Peptide (human) (trifluoroacetate salt) Chemical Properties
solubility Water: 1 mg/ml
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MSDS Information
Amyloid-β (25-35) Peptide (human) (trifluoroacetate salt) Usage And Synthesis
DescriptionAmyloid-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.1 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) (Item No. 21617) and Aβ (1-42) (Item No. 20574) fibrils.2,3 Aggregated Aβ (25-35) decreases the viability of rat adrenal PC12 cells.2 It also decreases the viability of primary rat cortical neurons at concentrations ranging from 1 nM to 30 μM.4 In vivo, intracerebral injection of Aβ (25-35) (20 nmol) in rats induces lesions of neuronal and tissue loss.5 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.6WARNING This product is not for human or veterinary use.
References[1] YURY G. KAMINSKY . Subcellular and metabolic examination of amyloid-β peptides in Alzheimer disease pathogenesis: Evidence for Aβ25–35[J]. Experimental Neurology, 2010, 221 1: Pages 26-37. DOI: 10.1016/j.expneurol.2009.09.005
[2] E. HUGHES A D R Burke. Inhibition of Toxicity in the Alzheimer’s Disease Peptide Fragment β(25–35) Using N-Methylated Derivatives[J]. Biochemical Society transactions, 2000, 28 1. DOI: 10.1042/bst028a072b
[3] WEI G, JEWETT A I, SHEA J E. Structural diversity of dimers of the Alzheimer amyloid-β(25–35) peptide and polymorphism of the resulting fibrils†[J]. Physical Chemistry Chemical Physics, 2010, 14: 3622-3629. DOI: 10.1039/c000755m
[4] YONG WANG . Mechanism of soluble beta-amyloid 25–35 neurotoxicity in primary cultured rat cortical neurons[J]. Neuroscience Letters, 2016, 618: Pages 72-76. DOI: 10.1016/j.neulet.2016.02.050
[5] DOUGLAS K. RUSH  Michael C M  Suzann Aschmies. Intracerebral /sB-amyloid(25–35) produces tissue damage: Is it neurotoxic[J]. Neurobiology of Aging, 1992, 13 5: Pages 591-594. DOI: 10.1016/0197-4580(92)90061-2
[6] HIROKO TSUNEKAWA . Synergistic effects of selegiline and donepezil on cognitive impairment induced by amyloid beta (25–35)[J]. Behavioural Brain Research, 2008, 190 2: Pages 224-232. DOI: 10.1016/j.bbr.2008.03.002
Amyloid-β (25-35) Peptide (human) (trifluoroacetate salt) Preparation Products And Raw materials
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