Disease relevance of furegrelate

• Furegrelate treatment starting in an established stage of nephritis had no effect [1].
• Finally, development of lung metastasis in C57Bl/6J mice intravenously injected with Lewis lung carcinoma or B16a cells was significantly inhibited by thromboxane synthase inhibitors, CI or furegrelate sodium [2].
• RESULTS: In this study, we demonstrate that the treatment of human glioma cells with the specific thromboxane synthase inhibitor furegrelate leads first to caspase activation (detectable 6 h after treatment), then to DNA fragmentation (24-48 h after treatment) and subsequent cell death [3].
• Furegrelate or SQ-29548 partially inhibited the pressor effect and bradycardia elicited by melittin [4].

Psychiatry related information on furegrelate

• In endothelium-denuded arteries, the dilation to furegrelate was attenuated in both the ORX and ORX + T groups, and the difference between the groups was abolished [5].

High impact information on furegrelate

• RESULTS: Preincubation of isolated glomeruli with either the cyclooxygenase inhibitor indomethacin or the thromboxane synthase inhibitor furegrelate protected glomeruli from the increase in Palb caused by FSGS serum [6].
• Finally, concentration-response curves for PPP and the corresponding production of eicosanoids in response to anandamide (1.44 x 10(-10)-1.44 x 10(-3) M) after indomethacin (COX inhibitor), piriprost (5-LOX inhibitor), or furegrelate (thromboxane A(2) synthase inhibitor) preincubation were obtained [7].
• Neither daltroban nor another receptor antagonist, ifetroban, or the thromboxane synthase inhibitor furegrelate enhanced prostanoid release from Kupffer cells [8].
• Inhibition of prostaglandin D2 clearance in rat hepatocytes by the thromboxane receptor antagonists daltroban and ifetroban and the thromboxane synthase inhibitor furegrelate [8].
• Furthermore, the inhibition of thromboxane synthase by furegrelate increases cells' susceptibility to the induction of DNA fragmentation by camptothecin, etoposide, N,N'-bis(2-chloroethyl)-N-nitrosourea, and anti-CD95 antibodies [3].

Biological context of furegrelate

• With a single 8 mg/kg dose of U-63,557A (furegrelate) administered prior to coronary ligation, platelet aggregation and serum TXA2 formation declined significantly (p less than 0.02) for up to 48 hours [9].
• Pharmacokinetics of furegrelate after oral administration to normal humans [10].
• We conclude that furegrelate attenuates the renal vasoconstriction of angiotensin II, presumably by enhancing the formation of vasodilator prostaglandins [11].
• Because TXA2 synthesis inhibition may be incomplete and unmetabolized PGH2 may cause vasoconstriction, we reasoned that adding a PGH2/TXA2 receptor antagonist (BMS 180,290, formerly SQ 29548 (SQ)) to furegrelate should cause further renal vasodilation in the presence of AII [12].
• Furegrelate administration (100, 250 and 500 microg, i.c.v.) attenuated the fall in arterial pressure evoked by acute haemorrhage and caused significant increases in heart rate at all doses injected [13].

Anatomical context of furegrelate

• Pretreatment with the Tx synthase inhibitor, Furegrelate, or the arachidonate 12-LO inhibitor, Baicalein, had no effect, indicating that eicosanoids of arachidonate 5-LO but not those of 12-LO or Tx modulate mesangial cell proliferation following immune injury [14].
• Pretreatment of animals with the thromboxane synthase inhibitor, Furegrelate, or the thromboxane receptor antagonist SQ-29,548 ameliorated or completely abolished the decrements in GFR and RBF without reducing glomerular leukocyte infiltration [15].

Associations of furegrelate with other chemical compounds

• Effect of furegrelate on renal plasma flow after angiotensin II infusion [11].
• Urine excretion of the prostacyclin hydrolysis product 6-ketoprostaglandin F1 alpha was increased by furosemide in the presence of furegrelate [16].
• The effects of furegrelate (a thromboxane synthase inhibitor), indomethacin, and the combination on urine volume (V), para-aminohippurate clearance (CPAH), and mean arterial pressure (MAP) before and after intravenous furosemide were examined in Sprague-Dawley rats [16].
• ACh-induced renal vasodilatation was significantly weaker in STZ-induced diabetic rats than in age-matched controls, and it was not affected by treatment with 10 muM furegrelate (TXA(2)-synthase inhibitor) or 1 muM SQ29548 (TXA(2)- receptor antagonist) in either group [17].
• Thromboxane synthase inhibition (furegrelate) did not affect U-46619-induced contraction, but it was reduced by cytosolic phospholipase A2 inhibition [18].

Gene context of furegrelate

• In comparison, neither the selective thromboxane A2 synthetase inhibitor furegrelate sodium, the stable epoprostenol (PGI2) analog ciprostene calcium, nor the selective 5-lipoxygenase inhibitor piriprost potassium caused any therapeutic effect [19].
• Inhibition of TXA(2) synthesis with furegrelate or CI reduced HUVEC migration stimulated by VEGF or bFGF [2].

Analytical, diagnostic and therapeutic context of furegrelate

• Effects of Furegrelate (Upjohn 63557A) on patency and platelet deposition after canine carotid endarterectomy [20].

References