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Table 3 Direct chemical modification of extracellular vesicles (EVs) (post-isolation modification)

From: Application of engineered extracellular vesicles for targeted tumor therapy

Modification method

Source of EVs

Strategy

Drug delivery

Application

References

Electrostatic interactions

HeLa cells

A complex formed by a cationic lipid and a pH-sensitive fusion peptide binds EVs through electrostatic interactions

Dextran, saponin

Targeting the cell membrane receptor to enhance cell uptake and release of EVs

[209]

Ligand–receptor interaction

Embryonic stem cells

The DSPE-PEG2000-cRGDyK targeting peptide is prepared by chemical reaction; subsequently, the ligand is inserted into the extracellular lipid bilayer through hydrophobic interaction

PTX

Penetration of the blood–brain barrier and the targeting of glioblastoma to inhibit tumor cell activity

[210]

Chemical reaction

Not mentioned

The coupling of EV azide lipids to target peptides using copper-free catalytic click chemistry

PTX, TPZ

Increasing the targeting of tumor tissues by EVs

[76]

Loading peptide for EVs

Tu-EVs

Covalently linking the functional N-terminal domain of HMGN1 (N1ND) to CP05

NA

Enhancement of the antitumor effect by increasing the ability of dendritic cells to stimulate T cells

[108]

Loading nucleotide sequences

Liver cancer cells (HepG2 cells)

Combination of molecular recognition between aptamer nucleotide sequences and their molecular targets with aptamer-chimeric trigger

NA

EV modification and functionalization, holds promise for a wide range of biomedical and bioanalytical applications

[211]

  1. HMGN1 high-mobility group nucleosome binding domain 1, NA not applicable, TPZ tirapazamine