Amyloid β-peptide (25-35) (human)
Fragment of human amyloid β-peptide, functionally required for the neurotrophic and neurotoxic effects associated with Alzheimer's disease.
|Storage||Desiccate at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solubility||Soluble to 0.50 mg/ml in water|
Preparing Stock Solutions
The following data is based on the product molecular weight 1060.27. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||0.94 mL||4.72 mL||9.43 mL|
|5 mM||0.19 mL||0.94 mL||1.89 mL|
|10 mM||0.09 mL||0.47 mL||0.94 mL|
|50 mM||0.02 mL||0.09 mL||0.19 mL|
References are publications that support the products' biological activity.
Rush et al (1992) Intracerebral β-amyloid(25-35) produces tissue damage: is it neurotoxic? Neurobiol.Aging 13 591 PMID: 1281289
Schenk et al (1995) Therapeutic approaches related to amyloid-β peptide and Alzheimer's Disease J.Med.Chem. 38 4141 PMID: 7473539
Yankner et al (1990) Neurotrophic and neurotoxic effects of amyoid β protein: reversal by tachykinin neuropeptides. Science 250 279 PMID: 2218531
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1 Citation for Amyloid β-peptide (25-35) (human)
Citations are publications that use Tocris products. Selected citations for Amyloid β-peptide (25-35) (human) include:
Ostrovskaya et al (2014) Neuroprotective effect of novel cognitive enhancer noopept on AD-related cellular model involves the attenuation of apoptosis and tau hyperphosphorylation. J.Biomed.Sci. 21 74 PMID: 25096780
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Literature in this Area
Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.