Azathioprine acts through the metabolite 6-mercaptopurine, which competitively inhibits hypoxanthine involved in cellular DNA and RNA synthesis; it mainly acts on T and B cells in the proliferative phase and induces hypolymphocytosis. In vitro studies have found that it inhibits the expression of T and B cell surface receptors (CD2) and blocks mitogen-induced responses as well as antibody responses. aza inhibits antigen- and mitogen-induced T cell proliferative responses in vitro to a lesser extent than cyclophosphamide (CTX). It has mild anti-inflammatory effects that may be related to the inhibition of mononuclear precursor cell division. Azathioprine is commonly used in patients with frequent, hormone-dependent demyelination at an initial dose of 50 mg twice daily. The dose may be increased to 2-3 mg/kg/day in some patients. Most patients tolerate azathioprine well, but a few patients may experience side effects. Fever, nausea, vomiting, and abdominal pain occur in about 10% of patients within a few weeks of initial treatment. Approximately 10% have mutations in the azathioprine methyltransferase gene, with reduced enzyme activity, decreased azathioprine metabolism, and increased toxicity. Leukopenia and hepatic impairment are important side effects and should be monitored regularly. Azathioprine is teratogenic and is contraindicated in pregnant women.