Dilazep dihydrochloride is an adenosine uptake inhibitor. It also inhibits ischemic damage, membrane transport of nucleosides, and platelet aggregation. It has cerebral and coronary vasodilating action through the enhancement of the effect of adenosine.

Dilazep, NBI and Dipyridamole have been reported to inhibit the uptake of adenosine into different cells. The uptake mechanism has been studied extensively in vitro. In these compounds, Dilazep and NBI are almost 10 times more effective than Dipyridamole. Only Dilazep is water soluble and no solubility aiding organic solvent is needed for preparing an aqueous solution[1].

Dilazep acts by inhibiting phospholipase activation in reperfused heart mitochondria and preventing lipid peroxidation in cerebral ischemia and reperfusion, potentially reducing ischemic cerebral injury through increased cerebral blood flow and protection of vascular endothelial cell membranes. Importantly, low doses (0.04-0.1 mg/kg/min) amplify the effects of adenosine, significantly enhancing superior mesenteric arterial conductance (SMAC) and raising arterial plasma adenosine levels, with a clear correlation observed between adenosine levels and SMAC changes, showing a 193.4% change in SMAC and an EC50 value of 2.8 μM. However, the vasodilatory potentiation by Dilazep is nullified by 8-phenyltheophylline, though this does not interfere with isoproterenol-induced relaxation.