Lipid-soluble ethoxzolamide is metabolized in vivo into a water-soluble metabolite, maintaining high activity against its target enzyme. At the minimal effective dose of 4 mg/kg intravenously administered at 45 minutes, the intraocular pressure (IOP) reduction is 4.2 mmHg, with a concentration of 2.5 pmol/kg in the anterior uvea, and near-complete enzyme inhibition (fractional inhibition, i = 0.9995). The effect decreases quickly, largely due to the drug's very short half-life in plasma, which results in a rapid decline of free drug availability in the anterior uvea and other tissues^[1].

In mouse lungs, ETZ treatment substantially downregulates GFP reporter fluorescence, achieving a 3-fold reduction in GFP signal compared to mock-treated controls. There is also a notable decrease in bacterial survival in the lungs of mice treated with ETZ compared to those receiving mock treatment^[2].

Ethoxzolamide (ETZ) leads to more than 90% inhibition of GFP reporter fluorescence in macrophages infected with M. tuberculosis. Additionally, in a 9-day macrophage survival assay, ETZ significantly curtails the intracellular growth of M. tuberculosis^[2].