Overview

Drug-carrying therapeutic exosomes can be prepared by loading therapeutic small molecules into the lumen of exosomes using membrane perforation technology. However, such engineered exosomes still cannot avoid some of them being cleared by the body's immune system. Therefore, it is necessary to modify some functional proteins that can resist immune system clearance on the surface of exosomes. Fortunately, researchers found that modifying such anti-phagocytic proteins on the surface of exosomes can increase the half-life of exosomes in circulation and improve the therapeutic potential of exosomes. Creative Biolabs provides customers with anti-phagocytic protein modified exosomes to enhance the delivery efficiency of exosomes.

Antiphagocytic Protein Introduction

Normally, immune cells called macrophages detect cancer cells, engulf them and destroy them. However, the researchers found that cancer cells can evade clearance by macrophages by overexpressing a class of antiphagocytic proteins, the best known of which is CD47. CD47 is widely expressed on the surface of normal cells and releases a signal of refusal to be phagocytized by binding to the signal regulatory protein α (SIRPα) on the surface of macrophages, thereby protecting healthy cells from being cleared by macrophages. Unfortunately, cancer cells also express abundant CD47 on the surface, allowing macrophages to treat them as normal cells and avoid being eliminated. Based on the understanding of the immune escape mechanism of cancer cells, scientists have discovered that CD47 can be modified on exosomes to inhibit the removal of exosomes in the circulatory system and enhance the delivery of exosomes to target tissues or cells. However, not only CD47, but cancer cells also have other anti-phagocytic proteins. These findings suggest that engineered exosomes modified by anti-phagocytic proteins have great therapeutic potential.

Fig.1 Immunofluorescence analysis of the phagocytosis of EXOsCD47.^1,2

Services

Anti-Phagocytosis Modified Exosomes Services at Creative Biolabs

Creative Biolabs has a professional technical team that can construct engineered exosomes that can enhance the ability to escape phagocytosis for customers according to their specific requirements and relevant literature. Specific anti-phagocytosis modification methods are divided into the endogenous modification and exogenous modification.

• For endogenous anti-phagocytosis modification, we can construct the highest quality plasmids in the genetic engineering of donor cells to improve transfection efficiency, thereby increasing the yield of engineered exosomes.
• For exogenous anti-phagocytic modification, we can choose the best binding method to provide engineered exosomes that efficiently bind anti-phagocytic proteins.

The specific anti-phagocytic protein modified exosome services are as follows.

• App1-Expressed Exosome Modification
• β2M-Expressed Exosome Modification
• CD24-Expressed Exosome Modification
• CD31-Expressed Exosome Modification
• CD44-Expressed Exosome Modification
• CD47-Expressed Exosome Modification
• DHMEQ-Expressed Exosome Modification
• PD-L1-Expressed Exosome Modification

Features

• Prolonged In Vivo Study Stability
• Enhanced Research Delivery Efficiency
• Reduced Off-Target Effects in Research
• Broad Research Application Potential
• Advanced Technical Support

Creative Biolabs is a supplier that provides a full range of exosome technology services and has been supporting the research and discovery of exosome drugs. From exosome isolation, identification, and engineering to content analysis and in vivo and in vitro functional research, our professional team can provide you with efficient services. If you want to improve the accumulation and targeting efficiency of exosomes in the body, please contact us. Our professional sales team will respond to your special needs as soon as possible.

FAQs

References

1. Ben, XY.; et al. Construction of exosomes that overexpress CD47 and evaluation of their immune escape. Frontiers in Bioengineering and Biotechnology. 2022, 10:936951.
2. Distributed under Open Access license CC BY 4.0, without modification.

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