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Chemical Compound Review

SQ-28053     (Z)-7-[(1R,4S,5S,6R)-5-[(2...

Synonyms: SQ-29548, SQ29548, SQ 28053, SQ 29548, [3H]SQ-28053, ...
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Disease relevance of SQ 28053

  • TxB2 and 6-keto-PGF1 alpha, measured in blood samples obtained from the coronary artery distal to the thrombus, were significantly increased at reperfusion and at reocclusion in control animals and in dogs receiving SQ 29548 [1].
  • Infusion of papaverine to maintain stable pulmonary artery (PA) pressures, incubation of G-6-PD-inhibited platelets with acetylsalicylate, or infusion of a thromboxane-prostaglandin endoperoxide receptor site antagonist, SQ 29548, into the lung perfusate prevented augmentation of lung edema and the PA pressor response by G-6-PD-inhibited platelets [2].
  • The recovery of force generation of IMA, but not RA, upon reoxygenation after 30 min of hypoxia was significantly reduced in the initial phase of reoxygenation by indomethacin and SQ-29548 and by endothelin receptor blocker BQ-123 [cyclo(l-Leu-d-Trp-d-Asp-l-Pro-d-Val)] [3].
  • GBS-induced pulmonary hypertension could be reversed by SQ 29548; SRI 63072 did not affect PPA when administered to pigs with GBS-induced elevation in PPA [4].
  • The response was receptor specific since arrhythmias were absent after pretreatment with a specific TxA(2) receptor antagonist (SQ-29548) and did not occur in response to another prostaglandin, PGF(2alpha) [5].

High impact information on SQ 28053


Chemical compound and disease context of SQ 28053


Biological context of SQ 28053


Anatomical context of SQ 28053


Associations of SQ 28053 with other chemical compounds

  • Indomethacin and SQ 29548 had identical actions, preventing the decrease of GFR and antinatriuresis evoked by hyperchloremia, e.g., sodium excretion rate in the SQ 29548 and indomethacin groups increased to 7.2 +/- 1.3 and 7.1 +/- 1.2 microEq/min, respectively, compared with 2.6 +/- 0.7 microEq/min in the control group [23].
  • In contrast to control tissue, indomethacin (10 microm), the COX-2 inhibitor NS 398 (10 microm), the TXA2/PGH2 receptor antagonist SQ 29548 (1 microm) and the TXA2 synthase inhibitor furegrelate (1 microm) reduced 5-HT contraction of LPS-treated arteries from hour one [24].
  • Both TXA2 synthase inhibitor furegrelate (Fureg) and TXA2 receptor antagonist SQ-29548 (SQ) substantially blocked enhanced increase of PP in the LPS group (4.9 +/- 0.4 vs. 3.6 +/- 0.5 vs. 2.6 +/- 0.6 mmHg for LPS alone, LPS + Fureg, and LPS + SQ, respectively; P < 0.05) while having no significant effect on controls [25].
  • Dazoxiben (a pure TX synthase inhibitor) and SQ 29548 (a pure TXA2 receptor antagonist) did not affect cyclic AMP levels in AA-treated platelets.(ABSTRACT TRUNCATED AT 250 WORDS)[26]
  • We found that the IL-1-induced increase in contraction in response to ANG II was completely inhibited by 10(-5) M of the cyclooxygenase inhibitor indomethacin and also by 10(-5) M of the prostaglandin H2/thromboxane A2-receptor antagonist SQ-29548 [27].

Gene context of SQ 28053


Analytical, diagnostic and therapeutic context of SQ 28053

  • The effects of a thromboxane A2 (TxA2)-endoperoxide receptor antagonist, SQ 29548, on jejunal blood flow, oxygen uptake, and capillary filtration coefficient (Kfc) were determined in anesthetized dogs under resting conditions and during the presence of predigested food in the jejunal lumen in three series of experiments [33].
  • The stable TX mimetic U-46619 caused a dose-dependent increase in perfusion pressure that was inhibited by the TX receptor antagonist SQ 29548 [34].
  • In series 1, 2.0 micrograms intra-arterial administration of SQ 29548 was found to abolish completely the vasoconstrictor action of graded doses (0.05-2.0 micrograms) of intra-arterial injection of a TxA2-endoperoxide analogue, U44069 [33].


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  15. Protein kinase C-zeta modulates thromboxane A(2)-mediated apoptosis in adult ventricular myocytes via Akt. Shizukuda, Y., Buttrick, P.M. Am. J. Physiol. Heart Circ. Physiol. (2002) [Pubmed]
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  17. Cyclooxygenase inhibition prevents PMA-induced increases in lung vascular permeability. Zanaboni, P.B., Bradley, J.D., Baudendistel, L.J., Webster, R.O., Dahms, T.E. J. Appl. Physiol. (1990) [Pubmed]
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  19. Protective actions of a thromboxane receptor antagonist, SQ 29548 on the ischemic myocardium: morphologic and hemodynamic effects. Singh, J., Seth, S.D., Manchanda, S.C., Seth, S. Prostaglandins Leukot. Essent. Fatty Acids (1997) [Pubmed]
  20. Time-dependent hyperreactivity to phenylephrine in aorta from untreated diabetic rats: role of prostanoids and calcium mobilization. Xavier, F.E., Davel, A.P., Rossoni, L.V., Vassallo, D.V. Vascul. Pharmacol. (2003) [Pubmed]
  21. Stimulation of rat mesangial cell thromboxane A2 receptors inhibits particulate but not soluble guanylyl cyclase. Paul, R.V., Saxenhofer, H., Wackym, P.S., Halushka, P.V. Am. J. Physiol. (1996) [Pubmed]
  22. Role of superoxide anion and endothelium in vasoconstrictor action of prostaglandin endoperoxide. Tesfamariam, B., Cohen, R.A. Am. J. Physiol. (1992) [Pubmed]
  23. Analysis of eicosanoid mediation of the renal functional effects of hyperchloremia. Askari, B., Bell-Quilley, C.P., Fulton, D., Quilley, J., McGiff, J.C. J. Pharmacol. Exp. Ther. (1997) [Pubmed]
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  29. Different effects of endothelin-3 on the Ca2+ discharge induced by agonists and Ca(2+)-ATPase inhibitors in human platelets. Astarie-Dequeker, C., Korichneva, I., Devynck, M.A. Br. J. Pharmacol. (1995) [Pubmed]
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