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Amyloid β-Protein (4-42)

* Please kindly note that our products are not to be used for therapeutic purposes and cannot be sold to patients.

Amyloid β-Protein (4-42) is one of the earliest and most prominent Aβ species deposited in AD brain. In familial AD patients with V261I PS1 mutation, it was found to be a component of cotton boll plaques. It has also been found in amyloid deposits in vascular dementia and familial Danish dementia patients. These results suggest that Aβ 4-42 May be involved in the development of various CNS diseases.

Category

Functional Peptides

Catalog number

BAT-014667

CAS number

157884-72-5

Molecular Formula

C191H294N52O53S

Molecular Weight

4198.82

Specification
Reference Reading

IUPAC Name

(4S)-4-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-6-amino-2-[[(2S)-5-amino-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-amino-3-phenyl-propanoyl]amino]-5-guanidino-pentanoyl]amino]-3-(1H-imidazol-4-yl)propanoyl]amino]-3-carboxy-propanoyl]amino]-3-hydroxy-propanoyl]amino]acetyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-carboxy-butanoyl]amino]-3-methyl-butanoyl]amino]-3-(1H-imidazol-4-yl)propanoyl]amino]-3-(1H-imidazol-4-yl)propanoyl]amino]-5-oxo-pentanoyl]amino]hexanoyl]amino]-4-methyl-pentanoyl]amino]-3-methyl-butanoyl]amino]-3-phenyl-propanoyl]amino]-3-phenyl-propanoyl]amino]propanoyl]amino]-5-[[(1S)-2-[[(1S)-1-[[2-[[(1S)-2-[[(1S)-3-amino-1-[[(1S)-5-amino-1-[[2-[[(1S)-2-[[(1S,2S)-1-[[(1S,2S)-1-[[2-[[(1S)-1-[[(1S)-1-[[(1S)-1-[[2-[[2-[[(1S)-1-[[(1S)-1-[[(1S,2S)-1-[[(1S)-1-carboxyethyl]carbamoyl]-2-methyl-butyl]carbamoyl]-2-methyl-propyl]carbamoyl]-2-methyl-propyl]amino]-2-oxo-ethyl]amino]-2-oxo-ethyl]carbamoyl]-2-methyl-propyl]carbamoyl]-3-methylsulfanyl-propyl]carbamoyl]-3-methyl-butyl]amino]-2-oxo-ethyl]carbamoyl]-2-methyl-butyl]carbamoyl]-2-methyl-butyl]amino]-1-methyl-2-oxo-ethyl]amino]-2-oxo-ethyl]carbamoyl]pentyl]carbamoyl]-3-oxo-propyl]amino]-1-(hydroxymethyl)-2-oxo-ethyl]amino]-2-oxo-ethyl]carbamoyl]-2-methyl-propyl]amino]-1-(carboxymethyl)-2-oxo-ethyl]amino]-5-oxo-pentanoic acid

Synonyms

Aβ (4-42); H-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-Lys-Leu-Val-Phe-Phe-Ala-Glu-Asp-Val-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-Val-Gly-Gly-Val-Val-Ile-Ala-OH

Appearance

White Powder

Purity

≥95%

Sequence

FRHDSGYEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA

Storage

Store at -20°C

Solubility

Soluble in Acetic Acid, DMSO; Insoluble in DMF, Water

InChI

InChI=1S/C191H294N52O53S/c1-27-102(20)155(183(288)208-87-142(252)215-124(68-94(4)5)170(275)224-123(63-67-297-26)168(273)236-149(96(8)9)181(286)206-83-139(249)203-84-144(254)235-151(98(12)13)186(291)240-154(101(18)19)187(292)243-156(103(21)28-2)188(293)214-107(25)190(295)296)242-189(294)157(104(22)29-3)241-159(264)105(23)212-140(250)85-204-161(266)117(50-39-41-64-192)220-176(281)132(77-138(196)248)229-180(285)136(90-245)217-143(253)88-207-182(287)150(97(10)11)237-179(284)134(79-148(261)262)230-166(271)121(58-61-145(255)256)218-158(263)106(24)213-169(274)127(71-109-46-35-31-36-47-109)226-172(277)128(72-110-48-37-32-38-49-110)232-184(289)153(100(16)17)239-178(283)125(69-95(6)7)225-163(268)118(51-40-42-65-193)221-165(270)120(57-60-137(195)247)222-173(278)129(74-112-80-199-91-209-112)228-175(280)131(76-114-82-201-93-211-114)233-185(290)152(99(14)15)238-167(272)122(59-62-146(257)258)223-171(276)126(73-111-53-55-115(246)56-54-111)216-141(251)86-205-162(267)135(89-244)234-177(282)133(78-147(259)260)231-174(279)130(75-113-81-200-92-210-113)227-164(269)119(52-43-66-202-191(197)198)219-160(265)116(194)70-108-44-33-30-34-45-108/h30-38,44-49,53-56,80-82,91-107,116-136,149-157,244-246H,27-29,39-43,50-52,57-79,83-90,192-194H2,1-26H3,(H2,195,247)(H2,196,248)(H,199,209)(H,200,210)(H,201,211)(H,203,249)(H,204,266)(H,205,267)(H,206,286)(H,207,287)(H,208,288)(H,212,250)(H,213,274)(H,214,293)(H,215,252)(H,216,251)(H,217,253)(H,218,263)(H,219,265)(H,220,281)(H,221,270)(H,222,278)(H,223,276)(H,224,275)(H,225,268)(H,226,277)(H,227,269)(H,228,280)(H,229,285)(H,230,271)(H,231,279)(H,232,289)(H,233,290)(H,234,282)(H,235,254)(H,236,273)(H,237,284)(H,238,272)(H,239,283)(H,240,291)(H,241,264)(H,242,294)(H,243,292)(H,255,256)(H,257,258)(H,259,260)(H,261,262)(H,295,296)(H4,197,198,202)/t102-,103-,104-,105-,106-,107-,116-,117-,118-,119-,120-,121-,122-,123-,124-,125-,126-,127-,128-,129-,130-,131-,132-,133-,134-,135-,136-,149-,150-,151-,152-,153-,154-,155-,156-,157-/m0/s1

InChI Key

MEZUZHZSAILDSS-JSBQEKMMSA-N

1. Synaptic Alterations in Mouse Models for Alzheimer Disease-A Special Focus on N-Truncated Abeta 4-42

Katharina Dietrich, Yvonne Bouter, Michael Müller, Thomas A Bayer Molecules. 2018 Mar 21;23(4):718. doi: 10.3390/molecules23040718.

This commentary reviews the role of the Alzheimer amyloid peptide Aβ on basal synaptic transmission, synaptic short-term plasticity, as well as short- and long-term potentiation in transgenic mice, with a special focus on N-terminal truncated Aβ4-42. Aβ4-42 is highly abundant in the brain of Alzheimer's disease (AD) patients. It demonstrates increased neurotoxicity compared to full length Aβ, suggesting an important role in the pathogenesis of AD. Transgenic Tg4-42 mice, a model for sporadic AD, express human Aβ4-42 in Cornu Ammonis (CA1) neurons, and develop age-dependent hippocampal neuron loss and neurological deficits. In contrast to other transgenic AD mouse models, the Tg4-42 model exhibits synaptic hyperexcitability, altered synaptic short-term plasticity with no alterations in short- and long-term potentiation. The outcomes of this study are discussed in comparison with controversial results from other AD mouse models.

2. Ion channel formation by N-terminally truncated Aβ (4-42): relevance for the pathogenesis of Alzheimer's disease

Abhijith G Karkisaval, Agueda Rostagno, Rustam Azimov, Deependra K Ban, Jorge Ghiso, Bruce L Kagan, Ratnesh Lal Nanomedicine. 2020 Oct;29:102235. doi: 10.1016/j.nano.2020.102235. Epub 2020 Jun 10.

Aβ deposition is a pathological hallmark of Alzheimer's disease (AD). Besides the full-length amyloid forming peptides (Aβ1-40 and Aβ1-42), biochemical analyses of brain deposits have identified a variety of N- and C-terminally truncated Aβ variants in sporadic and familial AD patients. However, their relevance for AD pathogenesis remains largely understudied. We demonstrate that Aβ4-42 exhibits a high tendency to form β-sheet structures leading to fast self-aggregation and formation of oligomeric assemblies. Atomic force microscopy and electrophysiological studies reveal that Aβ4-42 forms highly stable ion channels in lipid membranes. These channels that are blocked by monoclonal antibodies specifically recognizing the N-terminus of Aβ4-42. An Aβ variant with a double truncation at phenylalanine-4 and leucine 34, (Aβ4-34), exhibits unstable channel formation capability. Taken together the results presented herein highlight the potential benefit of C-terminal proteolytic cleavage and further support an important pathogenic role for N-truncated Aβ species in AD pathophysiology.

3. N-truncated amyloid β (Aβ) 4-42 forms stable aggregates and induces acute and long-lasting behavioral deficits

Yvonne Bouter, et al. Acta Neuropathol. 2013 Aug;126(2):189-205. doi: 10.1007/s00401-013-1129-2. Epub 2013 May 18.

N-truncated Aβ4-42 is highly abundant in Alzheimer disease (AD) brain and was the first Aβ peptide discovered in AD plaques. However, a possible role in AD aetiology has largely been neglected. In the present report, we demonstrate that Aβ4-42 rapidly forms aggregates possessing a high aggregation propensity in terms of monomer consumption and oligomer formation. Short-term treatment of primary cortical neurons indicated that Aβ4-42 is as toxic as pyroglutamate Aβ3-42 and Aβ1-42. In line with these findings, treatment of wildtype mice using intraventricular Aβ injection induced significant working memory deficits with Aβ4-42, pyroglutamate Aβ3-42 and Aβ1-42. Transgenic mice expressing Aβ4-42 (Tg4-42 transgenic line) developed a massive CA1 pyramidal neuron loss in the hippocampus. The hippocampus-specific expression of Aβ4-42 correlates well with age-dependent spatial reference memory deficits assessed by the Morris water maze test. Our findings indicate that N-truncated Aβ4-42 triggers acute and long-lasting behavioral deficits comparable to AD typical memory dysfunction.