High impact information on BW A 868C

• Moreover, the potent DP receptor antagonist BW A868C restores LC migration in infected mice [1].
• Furthermore, they were not shared by the selective DP receptor agonist BW245C and were not prevented by the selective DP receptor antagonist BWA868C, indicating that they were not mediated by DP receptors [2].
• Neither SQ 29,548 nor BW A868C (TP and DP(1) receptor antagonists, respectively) attenuated the enhancement of G-CSF release evoking any of the prostanoids studied [3].
• The DP(1) receptor antagonist BWA868C [3-[(2-cyclohexyl-2-hydroxyethyl)amino]-2,5-dioxo-1-(phenylmethyl)-4-imidazolidine-heptanoic acid] enhanced PGD(2)-induced CD203c expression, suggesting that interaction of PGD(2) with DP(1) receptors can limit activation of basophils by this prostaglandin [4].
• 4. DP receptor class prostanoids (e.g. ZK118182, BW245C, BWA868C, PGD(2)) exhibited high (nanomolar) affinities for [(3)H]-BWA868C binding, while prostanoids selective for EP, FP, IP and TP receptors showed a low (micromolar) affinity [5].

Biological context of BW A 868C

• 1. BW A868C, a novel compound, behaved as a simple competitive antagonist in a human washed platelet aggregation assay [6].
• Following exposure to the specific DP receptor antagonist, BW A868C ((+/-)-3-benzyl-5-(6-carboxyhexyl)-1-(2-cyclohexyl-2-hydroxyethylamin o)- hydantoin; 50 micrograms), which had no effect on intraocular pressure by itself, 572C85 (50 micrograms) did not reduce intraocular pressure in rabbits and cats [7].
• PGD2 induced increases in conjunctival microvascular permeability were inhibited by BW A868C, despite the fact that DP receptor agonists failed to evoke a plasma exudation response [8].
• The DP antagonist, BWA868C, effectively antagonized the effects of AL-6556 with a high potency (IC50 = 22.8 +/- 3.9 nM; n = 3) [9].

Anatomical context of BW A 868C

• Effects of a selective DP receptor agonist (BW 245C) and antagonist (BW A868C) on the canine colonic epithelium: an argument for a different DP receptor [10]?
• PGD(2) also increased eNOS expression on choroids of juveniles, and this effect was blocked by BW A868C [11].
• The DP receptor antagonist BWA868C competitively antagonized the PGD(2)-induced cAMP accumulation in embryonic bovine tracheal fibroblast cells (pA(2) = 7.83 +/- 0.08) [12].
• The affinity estimates of BW A868C against BW245C and prostaglandin D2 obtained from dog dorsal nasal vein, major palatine artery and saphenous vein were found to be consistent [13].
• The concentration and agonist dependence of the action of BW A868C suggests that putative DP receptor agonists relax human myometrium by more than one mechanism [14].

Associations of BW A 868C with other chemical compounds

• This binding was displaced by unlabeled ligands in the following order: PGD2 > BW 245C (a PGD agonist) > BW A868C (a PGD antagonist) > STA2 (a thromboxane A2 agonist) [15].
• The role of prostanoid TP- and DP-receptors in the bronchoconstrictor effect of inhaled PGD2 in anaesthetized guinea-pigs: effect of the DP-antagonist BW A868C [16].
• The activation of cyclic AMP production by PGD(2) and L-644,698, but not PGE(2), was inhibited by the selective DP antagonist BW A868C [17].
• TS-022, {4-[(1R, 2S, 3R, 5R)-5-Chloro-2-((S)-3-cyclohexyl-3-hydroxyprop-1-ynyl)-3-hydroxycyclopentyl] butylthio} acetic acid monohydrate, inhibits ADP-induced platelet aggregation, an effect significantly antagonized, as in the case of prostaglandin D(2) by the prostanoid DP(1) receptor antagonist (BW A868C) [18].
• The prostanoid DP receptor antagonist BW A868C (3-benzyl-5-(6-carboxyhexyl)-1-(2-cyclohexyl-2-hydroxyethylamino)h ydantoin) (50 nM) had no effect on responses to prostaglandin E2 or misoprostol [19].

Gene context of BW A 868C

• 5. The contractile effects of PGD2 in guinea-pig tracheal strips were resistant to 10 microM BW A868C indicating that they were not mediated through DP-receptors [6].
• Finally, the DP-receptor antagonist BW A868C did not block the Ca2+ transient response to PGD2, indicating an absence of DP-receptor involvement [20].
• However, BW A868C effectively antagonized only the mucin secretion mediated by PGD(2) and L-644,698 and not PGE(2) [17].
• The presence of an AH6809-sensitive, AH23848B- and BW A868C-insensitive mechanism is consistent with the hypothesis that inhibitory EP receptor agonists cause relaxation of human non-pregnant myometrium by an EP2 receptor-mediated process [19].

Analytical, diagnostic and therapeutic context of BW A 868C

• These effects were mediated via the DP prostanoid receptor; DP receptor agonists BW245C or SQ27986 induced neuronal damage, while the DP receptor antagonist BWA868C was neuroprotective in co-cultures [21].
• The dilation was converted to constriction by INDO (-54%+/-9%; P<0.05 versus non-IBD) or by BWA868C (PGD2 receptor antagonist) [22].

References