High-affinity peptide for tumor necrosis factor alpha and application of high-affinity peptide

Abstract

The invention belongs to the technical field of biology, and particularly relates to a high-affinity peptide for a tumor necrosis factor alpha and an application of the high-affinity peptide. An amino acid sequence of the peptide is as shown in SEQ. ID. NO.1 and SEQ. ID. NO.3 or single or multi-repeated tandem or branched peptide molecular sequences in the SEQ. ID. NO.1 and the SEQ. ID. NO.3 and the amino acid sequence is as shown in SEQ. ID. NO.4; and the peptide can be combined with the tumor necrosis factor alpha at high affinity and is capable of antagonizing the function. An animal is directly injected with the peptide, so that the occurrence degree of inflammation of an animal body can be significantly reduced and the resistivity of the animal body on an inflammatory injury can be improved. The peptide can be used for developing an antagonist drug for the tumor necrosis factor alpha and treating body damages caused by various acute and chronic inflammations, such as autoimmune and stress damages caused by various physical, chemical and biological factors, and has an extremely wide application prospect, small in molecular weight, low in immunogenicity and easy to synthesize, and the side effect and the disadvantages of a traditional monoclonal antibody drug antagonist are avoided.

Description

technical field [0001] The invention belongs to the field of biotechnology, and specifically relates to a high-affinity peptide (TNFα antagonistic peptide) of tumor necrosis factor alpha (TNFα) and its application. Background technique [0002] Tumor necrosis factor was initially induced by endotoxin injection in 1975, and was identified as a serum active factor that can induce apoptosis of tumors transplanted into mice, so it was named tumor necrosis factor. With the deepening of research, it is found that TNFα is a very important inflammatory factor. In inflammatory diseases induced by immune responses, the expression of TNFα in tissues increases, and at the same time induces a series of pathogenic responses and the expression of related inflammatory factors, eventually leading to tissue damage, such as bone destruction, cartilage degradation, fibroblast proliferation , keratinocyte proliferation, etc., making TNFα an important target for the treatment of various inflamma...

AI Technical Summary

Problems solved by technology

[0003] The existing antagonists of TNFα mainly focus on monoclonal antibodies and monoclonal antibody-derived molecules, but monoclonal antibody drugs have strong immunogenicity and can induce the production of anti-drug antibodies in the body, that is, the production of anti-antibodies, without any Doubt will affect the efficacy of drugs, on the other hand, it may also induce antibody-dependent cell-mediated cytotoxicity and antibody-mediated complement-dependent cytotoxicity, which is likely to cause damage to the body and side effects. Decreased efficacy

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