Need Assistance?

US & Canada:
+
UK: +

Our Highlights

GMP Grade Efficient workshop for GMP production.
Optimal Prices Buying products on this site guarantees the best price!
Commercial Batches Independent GMP manufacturing suites that handle commercial batches
Prompt Delivery Warehouses in multiple cities to ensure timely delivery
Flexible Quantity Quantities available from milligrams to ton

Amyloid β-peptide (1-42) (rat)

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

Amyloid β-peptide (1-42) (rat) is the rat form of the predominant amyloid β-peptide found in plaques associated with Alzheimer's disease. It could lead to a large shift in the bax/bcl-2 ratio in favour of pro-apoptotic bax. It is neurotoxic.

Category

Peptide Inhibitors

Catalog number

BAT-010671

CAS number

166090-74-0

Molecular Formula

C199H307N53O59S

Molecular Weight

4418.02

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-[[(2R)-1-[[(2R)-1-[[(2R)-1-[[2-[[(2R)-1-[[(2R)-4-amino-1-[[(2R)-6-amino-1-[[2-[[(2R)-1-[[(2R)-1-[[(2R)-1-[[2-[[(2R)-1-[[(2R)-1-[[(2R)-1-[[2-[[2-[[(2R)-1-[[(2R)-1-[[(2R)-1-[[(1R)-1-carboxyethyl]amino]-3-methyl-1-oxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]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-[(2-amino-3-carboxypropanoyl)amino]propanoyl]amino]-5-oxopentanoic acid

Synonyms

Amyloid β-Protein (1-42) (mouse, rat); beta-Amyloid Peptide (1-42) (rat/mouse)

Sequence

DAEFGHDSGFEVRHQKLVFFAEDVGSNKGAXXGLMVGGVVXA

Storage

Store at -20°C

Solubility

Soluble to 1 mg/ml in 0.1% Ammonia

InChI

InChI=1S/C199H307N53O59S/c1-28-105(20)161(191(303)216-91-146(261)223-127(72-97(4)5)179(291)233-126(67-71-312-27)177(289)245-155(99(8)9)189(301)214-86-142(257)210-87-148(263)244-157(101(12)13)194(306)249-160(104(18)19)195(307)252-162(106(21)29-2)196(308)222-111(26)198(310)311)251-197(309)163(107(22)30-3)250-166(278)108(23)219-143(258)88-211-168(280)119(56-43-45-68-200)229-184(296)135(81-141(204)256)239-188(300)139(94-254)226-147(262)92-215-190(302)156(100(10)11)246-187(299)137(83-154(274)275)240-175(287)124(61-65-150(266)267)228-165(277)110(25)221-178(290)131(76-114-52-39-33-40-53-114)237-181(293)132(77-115-54-41-34-42-55-115)242-193(305)159(103(16)17)248-186(298)128(73-98(6)7)235-171(283)120(57-44-46-69-201)230-173(285)122(59-63-140(203)255)231-183(295)134(79-117-85-208-96-218-117)238-172(284)121(58-47-70-209-199(205)206)234-192(304)158(102(14)15)247-176(288)125(62-66-151(268)269)232-180(292)130(75-113-50-37-32-38-51-113)224-144(259)90-213-170(282)138(93-253)243-185(297)136(82-153(272)273)241-182(294)133(78-116-84-207-95-217-116)225-145(260)89-212-169(281)129(74-112-48-35-31-36-49-112)236-174(286)123(60-64-149(264)265)227-164(276)109(24)220-167(279)118(202)80-152(270)271/h31-42,48-55,84-85,95-111,118-139,155-163,253-254H,28-30,43-47,56-83,86-94,200-202H2,1-27H3,(H2,203,255)(H2,204,256)(H,207,217)(H,208,218)(H,210,257)(H,211,280)(H,212,281)(H,213,282)(H,214,301)(H,215,302)(H,216,303)(H,219,258)(H,220,279)(H,221,290)(H,222,308)(H,223,261)(H,224,259)(H,225,260)(H,226,262)(H,227,276)(H,228,277)(H,229,296)(H,230,285)(H,231,295)(H,232,292)(H,233,291)(H,234,304)(H,235,283)(H,236,286)(H,237,293)(H,238,284)(H,239,300)(H,240,287)(H,241,294)(H,242,305)(H,243,297)(H,244,263)(H,245,289)(H,246,299)(H,247,288)(H,248,298)(H,249,306)(H,250,278)(H,251,309)(H,252,307)(H,264,265)(H,266,267)(H,268,269)(H,270,271)(H,272,273)(H,274,275)(H,310,311)(H4,205,206,209)

InChI Key

HAWSUONKNKRLRH-UHFFFAOYSA-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)NC(C(C)CC)C(=O)NC(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. An Animal Model of Alzheimer Disease Based on the Intrahippocampal Injection of Amyloid β-Peptide (1-42)

Roberta Facchinetti, Maria Rosanna Bronzuoli, Caterina Scuderi Methods Mol Biol. 2018;1727:343-352. doi: 10.1007/978-1-4939-7571-6_25.

The intrahippocampal injection of amyloid beta peptide (1-42) (Aβ(1-42)) represents one of the most useful animal models of Alzheimer disease. Since none of these available models fully represents the main pathological hallmarks of Alzheimer disease, stereotaxic Aβ(1-42) infusion provides researchers with an in vivo alternative paradigm. When performed by well-trained individuals, this model is the best-suited one for short-term studies focusing on the effects of Aβ(1-42) on a specific brain region or circuitry. Here, we describe all methodological phases of such a model.

2. Extracellular Zn2+-Dependent Amyloid-β1-42 Neurotoxicity in Alzheimer's Disease Pathogenesis

Yuichi Sato, Mako Takiguchi, Haruna Tamano, Atsushi Takeda Biol Trace Elem Res. 2021 Jan;199(1):53-61. doi: 10.1007/s12011-020-02131-w. Epub 2020 Apr 13.

The basal level of extracellular Zn2+ is in the range of low nanomolar (~ 10 nM) in the hippocampus. However, extracellular Zn2+ dynamics plays a key role for not only cognitive activity but also cognitive decline. Extracellular Zn2+ dynamics is modified by glutamatergic synapse excitation and the presence of amyloid-β1-42 (Aβ1-42), a causative peptide in Alzheimer's disease (AD). When human Aβ1-42 reaches high picomolar (> 100 pM) in the extracellular compartment of the rat dentate gyrus, Zn-Aβ1-42 complexes are readily formed and taken up into dentate granule cells, followed by Aβ1-42-induced cognitive decline that is linked with Zn2+ released from intracellular Zn-Aβ1-42 complexes. Aβ1-42-induced intracellular Zn2+ toxicity is accelerated with aging because of age-related increase in extracellular Zn2+. The recent findings suggest that Aβ1-42 secreted continuously from neuron terminals causes age-related cognitive decline and neurodegeneration via intracellular Zn2+ dysregulation. On the other hand, metallothioneins (MTs), zinc-binding proteins, quickly serve for intracellular Zn2+-buffering under acute intracellular Zn2+ dysregulation. On the basis of the idea that the defense strategy against Aβ1-42-induced pathogenesis leads to preventing the AD development, this review deals with extracellular Zn2+-dependent Aβ1-42 neurotoxicity, which is accelerated with aging.

3. Amyloid-β (1-42) peptide induces rapid NMDA receptor-dependent alterations at glutamatergic synapses in the entorhinal cortex

Olayemi Joseph Olajide, Clifton Andrew Chapman Neurobiol Aging. 2021 Sep;105:296-309. doi: 10.1016/j.neurobiolaging.2021.05.006. Epub 2021 May 24.

The hippocampus and entorhinal cortex (EC) accumulate amyloid beta peptides (Aβ) that promote neuropathology in Alzheimer's disease, but the early effects of Aβ on excitatory synaptic transmission in the EC have not been well characterized. To assess the acute effects of Aβ1-42 on glutamatergic synapses, acute brain slices from wildtype rats were exposed to Aβ1-42 or control solution for 3 hours, and tissue was analyzed using protein immunoblotting and quantitative PCR. Presynaptically, Aβ1-42 induced marked reductions in synaptophysin, synapsin-2a mRNA, and mGluR3 mRNA, and increased both VGluT2 protein and Ca2+-activated channel KCa2.2 mRNA levels. Postsynaptically, Aβ1-42 reduced PSD95 and GluN2B protein, and also downregulated GluN2B and GluN2A mRNA, without affecting scaffolding elements SAP97 and PICK1. mGluR5 mRNA was strongly increased, while mGluR1 mRNA was unaffected. Blocking either GluN2A- or GluN2B-containing NMDA receptors did not significantly prevent synaptic changes induced by Aβ1-42, but combined blockade did prevent synaptic alterations. These findings demonstrate that Aβ1-42 rapidly disrupts glutamatergic transmission in the EC through mechanisms involving concurrent activation of GluN2A- and GluN2B-containing NMDA receptors.