Polypeptide compound with aza-containing heterocyclic modification and its application

Abstract

The present invention discloses one kind of nitrogen heterocycle modified polypeptide compound and its application in preparing medicine for preventing and treating Alzheimerdis, Parkinson's disease and other degenerative nerve system diseases and medicine for preventing and treating type II diabetes. Research shows that the nitrogen heterocycle modified polypeptide compound can inhibit Abeta aggregation, disaggregate Abeta, hydrolyze to eliminate Abeta protein and inhibit and eliminate Abeta toxicity, and possesses wide application foreground in pharmaceutical field.

Description

technical field The present invention relates to polypeptide compounds and applications thereof, in particular to polypeptide compounds modified with nitrogen-containing heterocycles and their use in the preparation of drugs for the treatment and prevention of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and type 2 diabetes in the application. Background technique Neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease and type 2 diabetes are protein conformation diseases. Among them, Alzheimer's disease (AD), also known as Alzheimer's disease, is a degenerative disease of the central nervous system, clinically manifested as cognitive impairment, memory loss, and eventually loss of thinking ability, movement disorders, and life. Can not take care of themselves. The pathological features are mainly senile plaque (SP), neurofibrillary tangles (neurofibrillary tangles, NFT) and selective loss of neurons and synapses. As ...

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Problems solved by technology

For many years, the main drug for clinical treatment of this disease is cholinesterase inhibitor, which acts on the cholinergic nervous system and has a relieving effect on the disease, but it cannot prevent the occurrence and development of the disease

At present, the pathogenesis of Alzheimer's disease is not very clear, but it is generally believed that the key cause of the disease is the aggregate (SP) formed by misfolding of excess β-amyloid peptide (Aβ). main component) damages cell membranes, synapses and axons, and causes neurofibrillary tangles

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