Dilazep dihydrochloride 是一种腺苷摄取的抑制剂。它可抑制缺血性损伤，血小板聚集和核苷的膜转运。它能够增强腺苷的作用，进而具有脑和冠状血管舒张作用。

Dilazep dihydrochloride is an adenosine uptake inhibitor. Dilazep dihydrochloride also inhibits the ischemic damage, membrane transport of nucleosides and platelet aggregation. Dilazep dihydrochloride has cerebral and coronary vasodilating action through enhancement of 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 inhibits the phospholipase activation in reperfused heart mitochondria and also inhibits the lipid peroxidation caused by cerebral ischemia and reperfusion. Dilazep may prevent ischemic cerebral injury due to an increase in cerebral blood flow and/or its protective effects on vascular endothelial cell membrane. After administration of Dilazep, even low doses (0.04-0.1 mg/kg/min) of exogenous adenosine significantly increases superior mesenteric arterial conductance (SMAC) and elevates arterial plasma adenosine concentration. The increased adenosine levels were highly correlated with the increased percentage of change of SMAC and values for Rmax and EC50 were 193.4% change of SMAC and 2.8 μM, respectively. Administration of bolus doses of 8-phenyltheophylline abolishes the ability of Dilazep to potentiate vasodilation. However, it did not affect isoproterenol-induced relaxation[1].

20153-98-4

C31H45ClN2O10

641.15

DMSO:60 mg/mL (88.55 mM),Need ultrasonic
H2O:80 mg/mL (118.06 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years