Torbafylline is a xanthine derivative. Torbafylline significantly ameliorated the decreased skeletal muscle blood flow, red cell flux and surface pO2 after acute occlusion of the femoral artery, with more pronounced effects on the microcirculatory parameters, the laser-Doppler flux and pO2. Torbafylline treatment caused an increased lactate dehydrogenase activity in intact fast muscles and decreased it in soleus. Torbafylline decreased the activity of citrate synthase but increased activity of 3-hydroxyacyl-CoA dehydrogenase in soleus. Torbafylline is a powerful inhibitor of muscle wasting that blocks enhanced Ub-proteasome-dependent proteolysis in situations where TNF production rises, including cancer and sepsis. Torbafylline suppresses malaria antigen or LPS-induced secretion of TNF-a and IL-1a secretion, but not of IL-6 from human mononuclear cells in vitro. Torbafylline also blocks TNF-a and IL-1a secretion by malaria parasite preparations indicating that it may be useful in the treatment of malaria. Torbafylline has a protective effect on antigen-induced bronchoconstriction in guinea pigs and may be a useful agent in the therapy of bronchial asthma. Torbafylline had been in phase II clinical trial for the treatment of peripheral arterial occlusive disorders. However, this development was discontinued.