1. Neuronal Signaling
  2. Amyloid-β
  3. β-Amyloid (25-35)

β-Amyloid (25-35) (Synonyms: Amyloid beta-peptide (25-35); Aβ25-35; β-Amyloid peptide (25-35))

Cat. No.: HY-P0128 Purity: 96.49%
Handling Instructions

β-Amyloid (25-35) (Amyloid beta-peptide (25-35)) is the fragment Aβ(25-35) of the Alzheimer's amyloid β-peptide, has shown neurotoxic activities in cultured cells.

For research use only. We do not sell to patients.

β-Amyloid (25-35) Chemical Structure

β-Amyloid (25-35) Chemical Structure

CAS No. : 131602-53-4

Size Price Stock Quantity
1 mg USD 96 In-stock
Estimated Time of Arrival: December 31
5 mg USD 288 In-stock
Estimated Time of Arrival: December 31
10 mg USD 456 In-stock
Estimated Time of Arrival: December 31
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Customer Review

Based on 4 publication(s) in Google Scholar

Top Publications Citing Use of Products
  • Biological Activity

  • Protocol

  • Purity & Documentation

  • References

  • Customer Review


β-Amyloid (25-35) (Amyloid beta-peptide (25-35)) is the fragment Aβ(25-35) of the Alzheimer's amyloid β-peptide, has shown neurotoxic activities in cultured cells[1].

In Vitro

The amino acid sequence of Aβ(25-35) peptide is NH2-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-COOH, where the first Gly represents the amino acid 25 and the last Met represents the amino acid 35. Amyloid beta-peptide(25-35) is also investigated in gel state for the first time. Comparative studies are also carried out using vibrational absorption and ECD. The conformational preference of Aβ(25-35) peptide film is also investigated using vibrational absorption and VCD spectroscopy[1]. Amyloid beta-peptide(25-35) induces apoptotic effects on isolated brain mitochondria and the redox state of methionine-35, plays a key role in the induction of programmed cellular death pathways and toxic events[2].
β-Amyloid Aggregation Guidelines (Following is our recommended protocol. This protocol only provides a guideline, and should be modified according to your specific needs).
1. Solid Aβ peptide was dissolved in cold hexafluoro-2-propanol (HFIP). The peptide was incubated at room temperature for at least 1h to establish monomerization and randomization of structure.
2. The HFIP was removed by evaporation, and the resulting peptide was stored as a film at -20 or -80 ℃.
3. The resulting film was dissolved in anhydrous DMSO at 5 mM and then diluted into the appropriate concentration and buffer (serum- and phenol red-free culture medium) with vortexing.
4. Next, the solution was age 48h at 4-8 ℃. The sample was then centrifuged at 14000g for 10 min at 4-8 ℃; the soluble oligomers were in the supernatant. The supernatant was diluted 10-200-fold for experiments.
Methods vary depends on the downstream applications.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Rats are injected with Aβ25–35 peptide intracerebroventricularly and compound Danshen (CDS) are subsequently administered once daily for 23 days. Rats’ behavior is monitored using Morris water maze and passive avoidance. Real time PCR and Western blotting are used in determining amyloid precursor protein (APP), β-site APP cleaved enzyme-1(BACE1), Presenilin-1 (PS1), Insulin-degrading enzyme (IDE) and neprilysin (NEP) in hippocampus. The Alzheimer' s disease (AD) model group present with spatial learning and memory impairments. CDS and donepezil administration significantly ameliorate the Aβ25–35 peptide-induced memory impairment in both Morris water maze (P < 0.05) and passive avoidance task (P < 0.01) compared to the AD model group[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Molecular Weight




Sequence Shortening





Room temperature in continental US; may vary elsewhere.

Powder -80°C 2 years
-20°C 1 year
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 100 mg/mL (94.32 mM; Need ultrasonic)

H2O : 3.33 mg/mL (3.14 mM; Need ultrasonic)

Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 0.9432 mL 4.7158 mL 9.4316 mL
5 mM 0.1886 mL 0.9432 mL 1.8863 mL
10 mM 0.0943 mL 0.4716 mL 0.9432 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (2.36 mM); Clear solution

*All of the co-solvents are provided by MCE.
Cell Assay

Cell viability is determined by a modified MTS assay, which is based on the conversion of Tetrazolium salt by mitochondrial dehydrogenase to a formazan product spectrophotometrically measurable at 490 nm. PC12 cells are plated in 96-well plates at a density of 10 000 cells/well and maintained for 16 h in complete medium. Cells are then incubated in the absence (control) and presence of 40 μM Aβ(31-35) and Aβ(25-35) with reduced, oxidized and norleucine-substituted methionine-35 staurosporine 10 μM is used as positive control of 100% of cellular death. After 48 h of peptide-incubation, 20 μL of MTS reagent (2.0 mg/mL) is added to each well. The cells are then incubated for 30-45 min at 37 °C in a 5% CO2 incubator. The reaction is stopped by adding 25 μL of 10% SDS. The plates are read with a microplate reader at 490 nm. Each data point is obtained using a triplet-well assay[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Administration

Fifty-four Male Sprague-Dawley rats (2 months old, 300-350 g) are used. Amyloid beta-peptide(25-35) is dissolved in sterile distilled water at a concentration of 1 mg/mL as a stocking solution. Animals are infused with 5 μL/side of sterile distilled water (control), aggregated Aβ25-35 (2 μg/μL), into bilateral cerebral lateral ventricles at a rate of 1 μL/min; the needle is left in place for 5 min. Then the needles are removed and rats are kept on a warm pad until they are awakened. To determine the neuroprotective effect on AD rats, the Aβ25-35 treated rats are treated with CDS of different doses and Donepezil once daily for 23 days (including duration of behavior test). Experiment is performed to test the effect of CDS on Aβ25-35-induced memory impairment using Morris water-maze and step-through passive avoidance tasks. Specifically, all of the rats are randomly divided into 6 groups for the experiment: (a) Vehicle 1 (for Aβ25-35)+vehicle 2 (for CDS and Donepezil), (b) Aβ25-35+vehicle 2, (c) Aβ25-35+CDS (130 mg/kg), (d) Aβ25-35+CDS (260 mg/kg), (e) Aβ25-35+CDS (520 mg/kg), (f) Aβ25-35+Donepezil (0.5 mg/kg). One day after cerebroventricular microinfusions of Aβ25-35 (10 μg/side) or its vehicle, rats are treated (i.g.) with CDS or Donepezil or vehicle 2, once daily for 14 days prior to the beginning of Morris water maze, followed by passive avoidance task.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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