Disease relevance of Skf 102922

• The slow-reacting substance of anaphylaxis antagonist, FPL 55712, and the newly reported dithioacetal LTD4 receptor antagonists (SKF 102922 and SKF 102081) did not induce synthesis and release of TxB2 and 6-keto-PGF1 alpha in concentrations that blocked the agonist-induced smooth muscle contraction [1].

High impact information on Skf 102922

• Furthermore, a specific receptor antagonist, SKF 102922, inhibited LTD4-induced [3H]IP1 formation in guinea pig lung [2].
• SK&F 102922 and FPL 55712 selectively blocked the coronary vasoconstriction produced by LTD4, but had no effect on vasoconstriction produced by the other agonists.(ABSTRACT TRUNCATED AT 250 WORDS)[3]
• Metabolism of the leukotriene receptor antagonist 5-(2-(8-phenyloctyl)phenyl)-4,6-dithianonanedioic acid (SK&F 102922) in the guinea pig. Rearrangement of the acyl glucuronide [4].
• Mediators released from mast cells in immune animals challenged with beta-lactoglobulin evoked an increase in short-circuit current that was reduced by SK&F 102922, a peptidoleukotriene antagonist [5].
• Administration of SK&F 102922, even at doses which caused marked decreases in blood pressure and heart rate, also did not significantly alter the cardiovascular changes and the mortality rate induced by left coronary artery ligation [6].

Gene context of Skf 102922

• [3H]LTD4 binding was blocked by a specific LTD4 receptor antagonist, SKF 102922 [7].
• Oxygen-induced constrictions were inhibited in a dose-dependent fashion by two structurally distinct 5-lipoxygenase inhibitors (U 60257 and SC 43251) and two different leukotriene receptor antagonists (SKF 102922 and FPL 55712) [8].

Analytical, diagnostic and therapeutic context of Skf 102922

• The efficacy of the leukotriene receptor antagonist, SKF-102922, was verified in the cremaster muscle: 10 microM SKF-102922 completely abolished constriction induced by topical application of leukotriene D4 [9].

References