Chloramphenicol

Chloramphenicol is an orally active, potent and broad-spectrum antibiotic. Chloramphenicol shows antibacterial activity. Chloramphenicol represses the oxygen-labile transcription factor and hypoxia inducible factor-1 alpha (HIF-1α) in hypoxic A549 and H1299 cells. Chloramphenicol suppresses the mRNA levels of vascular endothelial growth factor (VEGF) and glucose transporter 1, eventually decreasing VEGF release. Chloramphenicol can be used for anaerobic infections and lung cancer research^[1][2][3]. In Vitro: Chloramphenicol (1-100 μg/mL, 18-24 h) inhibits the HIF-1α pathway in NSCLC cells in a concentration-dependent manner^[1].
Chloramphenicol (100 μg/mL, 0-24 h) induces autophagy in NSCLC cells, substantially increases the levels of autophagic biomarkers (beclin-1, Atg12-Atg5 conjugates, and LC3-II)^[1].
Chloramphenicol induces abnormal differentiation and inhibits apoptosis in activated T cells^[2].
Chloramphenicol can inhibit both bacterial and mitochondrial protein synthesis, causing mitochondrial stress and decreased ATP biosynthesis^[3].
chloramphenicol (1-100 μg/mL) can induce matrix metalloproteinase (MMP)-13 expression and increase MMP-13 protein^[3].
chloramphenicol (1-100 μg/mL) can activate c-Jun N-terminal kinases (JNK) and phosphatidylinositol 3-kinase (PI-3K)/Akt signaling, leading to c-Jun protein phosphorylation^[3].
Chloramphenicol acts primarily on the 50S subunit of bacterial 70S rihosomes and inhibits peptide bond formation by suppressing peptidyl transferase activity^[5]. In Vivo: Chloramphenicol (0-3500 mg/kg, Gavage, daily, for 5 days) decreases erythrocytes and erythrocyte precursors and reduces marrow erythroid cells were at day 1 post-dosing, and returns to normal by 14 days post-dosing^[4].