Additionally, Clarithromycin at a dose of 200 mg/kg exhibits efficacy against four in vivo tested pathogens[5], further highlighting its broad-spectrum antimicrobial activity^[4].

In various cell lines, especially HCT116 cells, Clarithromycin prompts the formation of numerous intracytoplasmic vacuoles after 24 hours. Extended treatment with Clarithromycin at concentrations of 40, 80, and 160 µM not only affects cell proliferation but also induces apoptotic cell death in colorectal cancer (CRC) cells. The inhibition of cell proliferation is enhanced when Clarithromycin is reapplied to the cells after initial treatment. For instance, reapplication of 160 µM Clarithromycin following a 48-hour incubation period leads to a halt in cell proliferation at 72 hours, with similar outcomes observed in LS174T cells^[3].

Moreover, Clarithromycin significantly elevates the LC3-II/LC3-I ratio in a dose- and time-dependent fashion, reaching a peak at 24 hours of treatment. This increase in autophagic markers is also marked by a reduction in p62/SQSTM1 levels, indicating autophagy activation^[3].