High impact information on ONO3708

• In monkey and dog cerebral artery strips, angiotensin (ANG) II (10(-7) M) produced a transient contraction, which was abolished or suppressed by treatment with indomethacin, aspirin, ONO3708, diphloretin phosphate, antagonists of prostaglandins (PGs) and OKY046, a thromboxane A2 synthesis inhibitor, and by endothelium denudation [1].
• Binding of S-145 to the platelet membranes was enhanced by divalent cations (Mg2+ and Ca2+), and the binding affinity in the presence of 20 mM MgCl2 was 0.75 nM, a value which was smaller than those of SQ29,548 (8.7 nM) and ONO3708 (3.7 nM) [2].
• The Ki values of TXA2 antagonists for the inhibition of phosphoinositide hydrolysis (nM) were 0.10 for ONO NT-126, 3.31 for S-145, 8.31 for SQ29548 and 19.49 for ONO3708 all of which were similar to those for receptor binding [3].
• The STA2-induced accumulation of IPs was inhibited concentration dependently by ONO3708, a TXA2 receptor antagonist, with an inhibition constant (Ki) of about 10 nM [4].
• Relaxations induced by PGE2 and beraprost, a PGI2 analogue, were augmented by cyclooxygenase inhibitors and tranylcypromine but were not affected by ONO3708, an antagonist of vasoconstrictor prostanoids, and endothelium denudation [5].

Anatomical context of ONO3708

• Interactions of ONO3708, a thromboxane (TX) A2 analog, and epithio-methano-TXA2 (sTXA2) or prostaglandins (PGs) were investigated in helical strips of dog cerebral, coronary, renal, and mesenteric arteries [6].

References