CAS 131602-53-4 β-Amyloid (25-35)

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CAS 131602-53-4 β-Amyloid (25-35)
Details
Neurotoxic core fragment GSNKGAIIGLM;
Category: Aβ25-35 toxic-core peptide / in-vitro neurotoxicity model.
Peptide Purity (HPLC) ≥95%
CAS No. 131602-53-4
Structure Linear 11-mer (Aβ25-35, GSNKGAIIGLM)
Solubility Readily soluble in water/PBS
Storage Powder, −20°C, dry, light-protected
Category
Beta-Amyloid Peptides
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Description

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Description GSNKGAIIGLM (residues 25–35), one of the shortest functional fragments retaining aggregation and neurotoxicity (oxidative stress, neuronal injury); a common short in-vitro toxicity model.

 

Product Basic Information Table

 

Standard English Name Abbreviations/Aliases Functional Tags Structural Core Molecular Formula Exact MW (Da) Average MW (Da) Salt Form Length (aa)
β-Amyloid (25-35), CAS:131602-53-4 Aβ(25-35); Amyloid-beta 25-35; Neurotoxic core fragment Alzheimer disease,Aβ neurotoxic core,aggregation,neurotoxicity,mitochondrial dysfunction,oxidative stress,calcium overload,membrane permeabilization,short tool peptide GSNKGAIIGLM C45H81N13O14S1 1059.57 1060.28 Free acid 11

 

Physicochemical Solubility & Storage Parameters

 

Product Code Appearance Long-term Storage Short-term Storage Solution Stability Solid Stability
PEP-AB2535-01 White to off-white /solid powder; relatively lipophilic. -20 °C, dry, light-protected, sealed. 2–8 °C short-term; dissolve in DMSO or water, aliquot and store at -20 °C. Slowly aggregates in water while retaining neurotoxicity; relatively lipophilic, dissolve in DMSO then dilute into aqueous buffer; prepare fresh as aggregation progresses over time. Solid powder stable ≥2 years at -20 °C dry & light-protected.

 

Functional Description

 

Product Code Short Summary (listing) Detailed Biological Function Research Areas Targets/Receptors
PEP-AB2535-01 11-aa neurotoxic core of Aβ; retains aggregation and neurotoxicity, a widely used cost-effective tool peptide for AD mechanism and drug screening. Aβ(25-35) (GSNKGAIIGLM) is the C-terminal hydrophobic core fragment of human Aβ that retains major neurotoxicity; it can be generated by proteolytic cleavage in brain. Despite only 11 residues, it recapitulates most key toxicities of full-length Aβ: it aggregates into β-sheet oligomers/fibrils in aqueous phase; inserts into neuronal membranes forming ion channels/pores causing Ca²⁺ overload; triggers mitochondrial membrane depolarization, ROS/free-radical generation and lipid peroxidation; activates caspase-3/9 apoptotic pathways; promotes microglial activation and IL-1β/TNF-α release; and induces tau hyperphosphorylation. Inexpensive, stable and directly bioactive, it is widely used for cell/animal-level AD drug primary screening and toxicity-mechanism studies. Alzheimer disease,Aβ toxicity mechanism,mitochondrial damage,oxidative stress,calcium overload,primary drug screening,neuronal apoptosis Neuronal membrane (pore/channel); mitochondria; NMDA receptor; microglial NLRP3; tau kinases (GSK-3β, CDK5)

 

 

 

 

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