Figure 6. Flowchart for the mechanism of action of C6G25S.

SARS‐CoV‐2 binds to ACE2 receptors on the host cell and induces endocytosis. Cleavage of the viral spike protein by TMPRSS2 triggers membrane fusion and subsequent release of the viral sense (+) RNA genome. After hijacking the host’s ribosome, viral RNA‐dependent RNA polymerase is generated to facilitate further virus replication. Meanwhile, subgenomic transcription and translation generate large amounts of viral structural proteins, such as the nucleocapsid, spike, membrane, and envelope. The progeny virus is assembled and the mature virions are released by exocytosis. C6G25S can interact with the RNA‐induced silencing complex to digest the viral genome’s RNA and polymerase mRNA through the RNAi effect. By reducing the copy number of the viral genome and polymerase mRNA, the virus replication cycle are inhibited, the productive SARS‐CoV‐2 infection is interrupted.