Disease relevance of Ditazol

• The activity of ditazole in reducing thrombus weight was comparable to that of aspirin [1].
• We postulate that ditazol may prevent or reduce diabetic retinopathy [2].
• Ditazole and platelets III. Effect of ditazole on tumor-cell induced thrombocytopenia and on bleeding time in mice [3].
• Ditazole (4,5-diphenyl-2-bis-(2-hydroxyethyl)-aminoxazol) inhibits in vivo platelet aggregation induced in mice by intravenous injection of cells derived from an experimental tumor, the Lewis lung carcinoma [3].

High impact information on Ditazol

• Effect of ditazole, an inhibitor of platelet aggregation, on a metastasizing tumour in mice [4].
• Ditazole (4,5-diphenyl-2-bis-(2-hydroxyethyl)-aminoxazol) is a weak anti-inflammatory drug and has been shown to inhibit thrombus formation following electrically stimulated vascular damage in the microcirculation of the hamster cheek pouch [5].
• In addition, ditazole does not prolong the bleeding time in rats, but even tends to shorten it [6].
• The present study indicates that ditazole, at doses similar to those inhibiting prostaglandin formation in rat, inhibits in vivo collagen--but not ADP-induced rat platelet aggregation [6].
• The effect of ditazole, a new antiaggregant oxazole derivative as well as its possible interaction with urokinase on the formation of electrically induced thrombus, was assayed in rabbits [1].

Biological context of Ditazol

• 4,5-Diphenyl-2-bis(2-hydroxyethyl)aminoxazole (ditazole) 200 mg/kg administered orally for 3 days significantly reduced the one-stage prothrombin time in rats treated concomitantly with bishydroxycoumarin (BHC) or warfarin, orally or i.p., as compared with rats given only BHC or warfarin [7].

Gene context of Ditazol

• This study was performed by the photometric method (Born) on platelet rich plasma (PRP), preincubated with ditazole at final concentrations of 1, 2.5, 4 and 40 micrograms/ml [8].

Analytical, diagnostic and therapeutic context of Ditazol

• Ditazole, after intravenous injection in rats (20 mg/kg), entered preferentially into the brain, the liver, and the heart in decreasing order [9].
• Ditazole also inhibited ADP-reptilase clot retraction and modified thrombin-induced clot formation [10].
• The inhibition of platelet aggregation exerted by ditazole in plasma could be removed following gel filtration of platelets on Sepharose 2-B gel [10].
• The in vitro activity of the non-steroidal anti-inflammatory agent Ditazole was investigated in a group of 20 male patients at thrombotic risk in comparison with placebo in a completely randomized cross-over design [11].

References