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Amyloid β-peptide (1-40) rat

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

Amyloid β-peptide (1-40) (rat) is the rat form of the amyloid β-peptide found in plaques, which is the major constituent observed in the brain of Alzheimer's disease. It is the prone-to-aggregation product of amyloid precursor protein proteolytic cleavage. It is shown to have both neurotrophic and neurotoxic effects.

Category

Peptide Inhibitors

Catalog number

BAT-010440

CAS number

144409-98-3

Molecular Formula

C190H291N51O57S

Molecular Weight

4233.76

Specification
Reference Reading

IUPAC Name

(4S)-5-[[(2S)-1-[[2-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[2-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-amino-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[2-[[(2S)-1-[[(2S)-4-amino-1-[[(2S)-6-amino-1-[[2-[[(2S)-1-[[(2S,3S)-1-[[(2S,3S)-1-[[2-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[2-[[2-[[(2S)-1-[[(1S)-1-carboxy-2-methylpropyl]amino]-3-methyl-1-oxobutan-2-yl]amino]-2-oxoethyl]amino]-2-oxoethyl]amino]-3-methyl-1-oxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-2-oxoethyl]amino]-3-methyl-1-oxopentan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-1-oxohexan-2-yl]amino]-1,4-dioxobutan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-3-methyl-1-oxobutan-2-yl]amino]-3-carboxy-1-oxopropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-1-oxopropan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-3-(1H-imidazol-4-yl)-1-oxopropan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-2-oxoethyl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-3-carboxy-1-oxopropan-2-yl]amino]-3-(1H-imidazol-4-yl)-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-[[(2S)-2-[[(2S)-2-amino-3-carboxypropanoyl]amino]propanoyl]amino]-5-oxopentanoic acid

Synonyms

β-Amyloid (1-40), rat; H-Asp-Ala-Glu-Phe-Gly-His-Asp-Ser-Gly-Phe-Glu-Val-Arg-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-OH; L-alpha-aspartyl-L-alanyl-L-alpha-glutamyl-L-phenylalanyl-glycyl-L-histidyl-L-alpha-aspartyl-L-seryl-glycyl-L-phenylalanyl-L-alpha-glutamyl-L-valyl-L-arginyl-L-histidyl-L-glutaminyl-L-lysyl-L-leucyl-L-valyl-L-phenylalanyl-L-phenylalanyl-L-alanyl-L-alpha-glutamyl-L-alpha-aspartyl-L-valyl-glycyl-L-seryl-L-asparagyl-L-lysyl-glycyl-L-alanyl-L-isoleucyl-L-isoleucyl-glycyl-L-leucyl-L-methionyl-L-valyl-glycyl-glycyl-L-valyl-L-valine; Rat amyloid-beta peptide 1-40; Rat amyloid-β peptide 1-40; Amyloid b-Protein (1-40) (Mouse, rat)

Appearance

White Lyophilized Powder

Purity

≥95%

Sequence

DAEFGHDSGFEVRHQKLVFFAEDVGSNKGAIIGLMVGGVV

Storage

Store at -20°C

Solubility

Soluble in Water

InChI

InChI=1S/C190H291N51O57S/c1-25-101(19)155(184(292)207-87-140(250)213-121(68-93(3)4)172(280)223-120(63-67-299-24)170(278)235-149(95(7)8)182(290)205-82-136(246)201-83-142(252)234-151(97(11)12)187(295)239-154(100(17)18)189(297)298)241-188(296)156(102(20)26-2)240-159(267)103(21)210-137(247)84-202-161(269)113(52-39-41-64-191)219-177(285)129(77-135(195)245)229-181(289)133(90-243)216-141(251)88-206-183(291)150(96(9)10)236-180(288)131(79-148(263)264)230-168(276)118(57-61-144(255)256)218-158(266)105(23)212-171(279)125(72-108-48-35-29-36-49-108)227-174(282)126(73-109-50-37-30-38-51-109)232-186(294)153(99(15)16)238-179(287)122(69-94(5)6)225-164(272)114(53-40-42-65-192)220-166(274)116(55-59-134(194)244)221-176(284)128(75-111-81-199-92-209-111)228-165(273)115(54-43-66-200-190(196)197)224-185(293)152(98(13)14)237-169(277)119(58-62-145(257)258)222-173(281)124(71-107-46-33-28-34-47-107)214-138(248)86-204-163(271)132(89-242)233-178(286)130(78-147(261)262)231-175(283)127(74-110-80-198-91-208-110)215-139(249)85-203-162(270)123(70-106-44-31-27-32-45-106)226-167(275)117(56-60-143(253)254)217-157(265)104(22)211-160(268)112(193)76-146(259)260/h27-38,44-51,80-81,91-105,112-133,149-156,242-243H,25-26,39-43,52-79,82-90,191-193H2,1-24H3,(H2,194,244)(H2,195,245)(H,198,208)(H,199,209)(H,201,246)(H,202,269)(H,203,270)(H,204,271)(H,205,290)(H,206,291)(H,207,292)(H,210,247)(H,211,268)(H,212,279)(H,213,250)(H,214,248)(H,215,249)(H,216,251)(H,217,265)(H,218,266)(H,219,285)(H,220,274)(H,221,284)(H,222,281)(H,223,280)(H,224,293)(H,225,272)(H,226,275)(H,227,282)(H,228,273)(H,229,289)(H,230,276)(H,231,283)(H,232,294)(H,233,286)(H,234,252)(H,235,278)(H,236,288)(H,237,277)(H,238,287)(H,239,295)(H,240,267)(H,241,296)(H,253,254)(H,255,256)(H,257,258)(H,259,260)(H,261,262)(H,263,264)(H,297,298)(H4,196,197,200)/t101-,102-,103-,104-,105-,112-,113-,114-,115-,116-,117-,118-,119-,120-,121-,122-,123-,124-,125-,126-,127-,128-,129-,130-,131-,132-,133-,149-,150-,151-,152-,153-,154-,155-,156-/m0/s1

InChI Key

KBNPAOMRSZGNFV-XBBCIFKHSA-N

Canonical SMILES

CCC(C)C(C(=O)NC(C(C)CC)C(=O)NCC(=O)NC(CC(C)C)C(=O)NC(CCSC)C(=O)NC(C(C)C)C(=O)NCC(=O)NCC(=O)NC(C(C)C)C(=O)NC(C(C)C)C(=O)O)NC(=O)C(C)NC(=O)CNC(=O)C(CCCCN)NC(=O)C(CC(=O)N)NC(=O)C(CO)NC(=O)CNC(=O)C(C(C)C)NC(=O)C(CC(=O)O)NC(=O)C(CCC(=O)O)NC(=O)C(C)NC(=O)C(CC1=CC=CC=C1)NC(=O)C(CC2=CC=CC=C2)NC(=O)C(C(C)C)NC(=O)C(CC(C)C)NC(=O)C(CCCCN)NC(=O)C(CCC(=O)N)NC(=O)C(CC3=CNC=N3)NC(=O)C(CCCNC(=N)N)NC(=O)C(C(C)C)NC(=O)C(CCC(=O)O)NC(=O)C(CC4=CC=CC=C4)NC(=O)CNC(=O)C(CO)NC(=O)C(CC(=O)O)NC(=O)C(CC5=CNC=N5)NC(=O)CNC(=O)C(CC6=CC=CC=C6)NC(=O)C(CCC(=O)O)NC(=O)C(C)NC(=O)C(CC(=O)O)N

1. Potentiation of NMDA-Mediated Responses by Amyloid-β Peptide 1-40 in Rat Sympathetic Preganglionic Neurons

Chih-Chia Lai, Hsuan Lo, Hong-Guo Lin, Hsun-Hsun Lin J Alzheimers Dis. 2019;67(4):1291-1303. doi: 10.3233/JAD-180886.

The abnormal accumulation of amyloid-β peptides (Aβ) is one of the main characteristics of Alzheimer's disease (AD). Cerebro- and cardiovascular diseases may be the risk factors for developing AD. The effect of Aβ on central sympathetic control of cardiovascular function remains unclear. The present study examines the acute effects of Aβ oligomers on the function of NMDA receptors, a subtype of ionotropic glutamate receptors, in rat sympathetic preganglionic neurons (SPNs). In the in vitro electrophysiological study, Aβ1-40 but not Aβ1-42 applied by superfusion for 5 min significantly potentiated NMDA-induced depolarizations in SPNs of neonatal rat spinal cord slice preparation. Application of Aβ1-40 had little effects on AMPA-induced depolarizations or GABA-induced hyperpolarizations. Treatment with a selective protein kinase C (PKC) inhibitor applied together with Aβ1-40 blocked the augmentation by Aβ1-40 of NMDA-induced depolarizations. Western blot analysis showed an increase in the levels of phosphoserine 896, selectively regulated by PKC, without significant changes in phosphoserine 897 on GluN1 subunits in lateral horn areas of spinal cord slices following treatment with Aβ1-40. In the in vivo study, intrathecal injection of Aβ1-40 (0.2 nmol) potentiated the pressor effects induced by NMDA (2 nmol) injected intrathecally in urethane-anesthetized rats. These results suggest that different fragments of Aβ may have differential effects on the NMDA receptor function and the selective augmentation of NMDA receptor function by Aβ1-40 may involve PKC-dependent mechanisms in sympathetic preganglionic neurons.

2. Extracellular Zn2+-independently attenuated LTP by human amyloid β1-40 and rat amyloid β1-42

Haruna Tamano, Mako Takiguchi, Ryota Shimaya, Paul A Adlard, Ashley I Bush, Atsushi Takeda Biochem Biophys Res Commun. 2019 Jun 30;514(3):888-892. doi: 10.1016/j.bbrc.2019.05.037. Epub 2019 May 10.

Human amyloid-β1-40 (Aβ1-40) and rat Aβ1-42 have lower affinity for extracellular Zn2+ than human Aβ1-42. Here we report extracellular Zn2+-independent attenuation of dentate gyrus long-term potentiation (LTP) by human Aβ1-40 and rat Aβ1-42. On the basis of the data that dentate gyrus LTP is extracellular Zn2+-dependently attenuated after local injection of human Aβ1-42 (25 pmol, 1 μl) into the dentate gyrus, which increases intracellular Zn2+ in the dentate gyrus, the toxicity of human Aβ1-40 and rat Aβ1-42 was compared in the in vivo system with human Aβ1-42. Dentate gyrus LTP was attenuated after injection of human Aβ1-40 and rat Aβ1-42 (25 pmol, 1 μl) into the dentate gyrus, which did not increase intracellular Zn2+ in the dentate gyrus. The attenuated LTP was not rescued by co-injection of CaEDTA, an extracellular Zn2+ chelator. The present study suggests that human Aβ1-40 and rat Aβ1-42 affect cognitive activity via extracellular Zn2+-independent mechanism at low micromolar concentration.

3. Rat hippocampal proteomic alterations following intrahippocampal injection of amyloid beta peptide (1-40)

Xiang Shi, Xiaoguang Lu, Libin Zhan, Li Liu, Mingzhong Sun, Xiaoyang Gong, Hua Sui, Xinping Niu, Shuqing Liu, Luping Zheng, Jing Chen, Yan Zhou Neurosci Lett. 2011 Aug 15;500(2):87-91. doi: 10.1016/j.neulet.2011.06.009. Epub 2011 Jun 14.

Amyloid beta peptide 1-40 (Aβ(1-40)) is closely associated with the progressive neuronal loss and cognitive decline observed in Alzheimer's disease (AD). This study aimed to establish a proteomic strategy for the profiling of AD tissues for disease-specific changes in protein abundance. Intrahippocampal injection of Aβ(1-40) induced spatial memory and learning decline in rats. Proteomic analysis revealed the changes in protein expression in the rat hippocampus treated with Aβ(1-40). Four proteins of interest which was in abundance was significantly altered in Aβ(1-40)-treated rats were identified by peptide mass fingerprint (PMF). These proteins corresponded to synapsin Ib, protein disulfide-isomerase A3 precursor, tubulin β chain and ATP synthase β subunit. Our results provide new insights into the relationship between Aβ and the pathogenesis of AD, and suggest potential targets for the therapy of AD.