10-Butyl EtherMinocycline is a derivative of Minocycline and acts as an inhibitor of MMP-8 and MMP-9, with IC50 values of 69.4 µM and 47.0 µM, respectively. It exhibits negligible antibacterial activity against E. coli, S. typhi, and C. albicans. Additionally, 10-Butyl EtherMinocycline inhibits LPS-induced microglial activation and VEGF-induced endothelial cell migration, as well as L-Glutamine-induced ROS levels. This compound significantly reduces alcohol consumption in a chronic intermittent ethanol (CIE) mouse model and is utilized in studies related to neuroinflammation and alcohol use disorder (AUD).

10-Butyl Ether Minocycline exhibits negligible antibacterial activity against E. coli, S. typhi, and C. albicans at concentrations of 1.56-100 µg/mL. It induces a dose-dependent reduction in the viability of neuroblastoma (NB) cells, with an IC50 of 102.1 µM, when used at 0.1-500 µM for 24 hours. At a concentration of 25 µM for 12 hours, it inhibits LPS-mediated activation of microglial cells in N9 microglia. In HUVECs cells, 10-Butyl Ether Minocycline at 100 µM for 12 hours suppresses VEGF-induced endothelial cell migration. Furthermore, it diminishes L-Glutamine-induced ROS generation in N9 microglia in a dose-dependent manner at 30-120 µM. Additionally, it inhibits 15-LOX with an IC50 of 92.6 µM. In HCT 116 cells, 10-Butyl Ether Minocycline at 30-120 µM does not exhibit significant mitochondrial toxicity compared to sodium azide.

A single intraperitoneal injection of 10-Butyl Ether Minocycline (60 mg/kg) significantly reduces alcohol consumption in a chronic intermittent ethanol (CIE) mouse model of alcohol dependence.