Various Products / Alzheimer's Disease
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Various Products / Alzheimer's Disease

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Cat. # Product Name Price
10-101-317Galanin, humanInquiry
A13004Amyloid Toxicity Inhibitor Peptide 110Inquiry
A13119Beta-Amyloid/A4 Protein Precursor (APP) (96-110)Inquiry
A13180Humanin, humanInquiry
A13208Non-beta-Amyloid Component of Alzheimer.s Disease (NAC)Inquiry
A13355Serum Amyloid P-ComponentInquiry
A13365Amyloid Toxicity Inhibitor Peptide 13Inquiry
A13374Amyloid Toxicity Inhibitor Peptide 11Inquiry
A13376Amyloid Toxicity Inhibitor Peptide 111Inquiry
C07001Acetyl-Calpastatin (184-210) (human)Inquiry
C29004CRF (6-33) (human, rat)Inquiry
CAD-076Amyloid Bri Protein Precursor₂₇₇ (244-266)Inquiry
CAD-077Amyloid Bri Protein Precursor₂₇₇ (244-277) (reduced)Inquiry
CAD-078Amyloid Dan Protein Precursor₂₇₇ (244-277)Inquiry
CAD-079Amyloid P Component (27-38) amideInquiry
CAD-080Tyr-Amyloid P Component (27-38) amideInquiry
CAD-081Amyloid P Component (33-38) amideInquiry
CAD-082(Asp(4-aminobutylamide)¹·⁷·²³,Glu(4-aminobutylamide)³·¹¹·²²)-Amyloid β-Protein (1-40)Inquiry


Alzheimer’s disease (AD) is the most common fatal neurodegenerative disease (ND),) characterized by loss of neuronal structure and function. Over the past few decades, AD and its associated risk factors have become a major health care problem in most developed countries. In addition, Alzheimer's disease is reported to be the fifth leading cause of death among people over 65 years of age, with an incidence of more than 5 million cases per year in the United States (Alzheimer’s Association, 2017). The World Health Organization (WHO) estimates that the prevalence of Alzheimer’s disease worldwide will quadruple to about 114 million people by 2050 (Alzheimer’s Association, 2017).


The pathological features of AD include extracellular plaques (extracellular amyloid plaques) and neurofibrillary tangles within neurons (hyperphosphorylated tau protein accumulation; Vanitallie, 2015). These pathological changes gradually lead to loss of neurons, and ultimately lead to neuron death. Although the etiology and pathogenesis of AD is still unclear, the amyloid cascade theory has been widely accepted and supported by some studies (Drachman, 2014; Herrup, 2015). A protective mutation of amyloid precursor protein (APP) (APP) was found near the β -cleavage site of amyloid precursor protein (APP), which could prevent the development of late-onset dementia (Jonsson et al., 2012). This assumption is further reinforced.

Application of Peptide in Alzheimer’s disease

In the past few years, the applicability of several Aβ aggregation peptide inhibitors as new therapeutic lead compounds has been studied. In conclusion, very few IA β5, Aβ 12-28P, LPYF Da, Trp-Aib, D-4F and D3 are effective in rodent models. It is not clear whether peptide inhibitors should target Aβ, oligomeric Aβ or Aβ fibrils deposited in plaques. It is not clear whether Aβ 1-40 or Aβ 1-42 should be treated, and weather compounds need to pass through BBB to be effective. More work needs to be done to elucidate the properties of the most synaptotoxic Aβ species in the genesis and development of AD. The ongoing studies on the peptides of different Aβ species and their effects on the aggregation and toxicity of Aβ will provide a basis for further understanding the molecular mechanism of AD.

1. Hilbich, C., Kisters-Woike, B., Reed, J., Masters, C. L., & Beyreuther, K. (1991). Aggregation and secondary structure of synthetic amyloid βA4 peptides of Alzheimer’s disease. Journal of molecular biology, 218(1), 149-163.
2. Roberts, B. R., Ryan, T. M., Bush, A. I., Masters, C. L., & Duce, J. A. (2012). The role of metallobiology and amyloid‐β peptides in Alzheimer’s disease. Journal of neurochemistry, 120, 149-166.

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