β-Amyloid (31-35)

β-Amyloid (31-35) is the shortest sequence of native Amyloid-β peptide that retains neurotoxic activity.

Product information

CAS Number: 149385-65-9

Molecular Weight: 545.74

Formula: C25H47N5O6S

Chemical Name: (2S)-2-[[(2S)-2-[[2-[[(2S, 3S)-2-[[(2S, 3S)-2-amino-3-methylpentanoyl]amino]-3-methylpentanoyl]amino]acetyl]amino]-4-methylpentanoyl]amino]-4-methylsulfanylbutanoic acid

Smiles: CC(C)CC(NC(=O)CNC(=O)C(NC(=O)C(N)C(C)CC)C(C)CC)C(=O)NC(CCSC)C(O)=O

InChiKey: ZMDGLWRNBGRYQB-UHFFFAOYSA-N

InChi: InChI=1S/C25H47N5O6S/c1-8-15(5)20(26)23(33)30-21(16(6)9-2)24(34)27-13-19(31)28-18(12-14(3)4)22(32)29-17(25(35)36)10-11-37-7/h14-18,20-21H,8-13,26H2,1-7H3,(H,27,34)(H,28,31)(H,29,32)(H,30,33)(H,35,36)

Technical Data

Appearance: Solid Power

Purity: ≥98% (or refer to the Certificate of Analysis)

Solubility: DMSO : 5 mg/mL (9.16 mM; ultrasonic and adjust pH to 7 with HCl).

Shipping Condition: Shipped under ambient temperature as non-hazardous chemical or refer to Certificate of Analysis

Storage Condition: Dry, dark and -20 ^oC for 1 year or refer to the Certificate of Analysis.

Shelf Life: ≥12 months if stored properly.

Stock Solution Storage: 0 - 4 ^oC for 1 month or refer to the Certificate of Analysis.

Drug Formulation: To be determined

HS Tariff Code: 382200

How to use

In Vitro:

β-Amyloid (31-35) is a functional cytotoxic domain of Aβ peptide. β-Amyloid (31-35) increases the phosphorylation of biotinylated Aβ(1-40), enhances CDK-1 activity, and also inhibits binding of Aβ to cyclin B1. β-Amyloid (31-35) is cytotoxic, and such an effect can be inhibited by olomoucine in differentiated human teratocarcinoma cell line, Ntera 2/cl-D1 (NT-2) neurons. 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 °C. 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 °C. The sample was then centrifuged at 14000g for 10 min at 4-8 °C; the soluble oligomers were in the supernatant. The supernatant was diluted 10-200-fold for experiments. Methods vary depends on the downstream applications.

References:

1. Milton NG, et al. The amyloid-beta peptide binds to cyclin B1 and increases human cyclin-dependent kinase-1 activity. Neurosci Lett. 2002 Apr 5;322(2):131-3.
2. Misiti F, et al. Fragment 31-35 of beta-amyloid peptide induces neurodegeneration in rat cerebellar granule cells via bax gene expression and caspase-3 activation. A crucial role for the redox state of methionine-35 residue. Neurochem Int. 2006 Oct;49(5):525-32.
3. M Jess Perez de Vega, et al. Synthesis and biological properties of beta-turned Abeta(31-35) constrained analogues. Bioorg Med Chem Lett. 2008 Mar 15;18(6):2078-82.

Products are for research use only. Not for human use.