Disease relevance of Ono-RS-082

• This possibility was confirmed by results showing that pertussis toxin suppressed basic FGF-stimulated but not HDL-stimulated EC motility and that inhibitors of phospholipase A2, aristolochic acid and ONO-RS-082, also blocked the promigratory activity of basic FGF but had no effect on the activity of HDL.(ABSTRACT TRUNCATED AT 250 WORDS)[1]

High impact information on Ono-RS-082

• Epinephrine evokes (i) an increased turnover of ester-linked arachidonic acid in aspirin treated platelets that is inhibited by ONO-RS-082, EDTA, yohimbine, or the absence of fibrinogen and (ii) a rapid cytoplasmic alkalinization that is inhibited partially by blockage of cyclooxygenase activity and completely by A2A9 or EIPA [2].
• Inhibition of PLA(2) activity by the PLA(2) inhibitors, AACOCF(3) and ONO-RS-082, diminished DEN-2 virus-induced apoptosis [3].
• We next studied the involvement of the PLA2 inhibitor ONO-RS-082 (ONO) and the COX inhibitor INDO in IL regulation of iNOS [4].
• Endogenously generated 20-HETE significantly inhibited the EDHF-mediated relaxation of coronary arteries, which was potentiated by the phospholipase A2 inhibitors AACOCF3 and ONO-RS-082, as well as by the omega-hydroxylase inhibitors 17-octadecynoic acid and DDMS [5].
• We also obtained evidence that 2-(p-amylcinnamoyl)amino-4-chlorobenzoic acid (ONO-RS-082), a phospholipase A(2) inhibitor, potentiated alkyl-LPA-induced platelet aggregation, but inhibited highly unsaturated acyl-LPA-induced platelet aggregation [6].

Biological context of Ono-RS-082

• The minimum concentrations of lipocortin I and ONO-RS-082 required for switching the 12H5 cells to the formation of unglycosylated IgE-BF were comparable to or less than IC50 of the inhibitors for PLA2 [7].
• The phospholipase A(2) inhibitor ONO-RS-082 (5 microM) inhibited the DPB-induced Ser19 phosphorylation but only transiently decreased the tension, suggesting the involvement of arachidonic acid in the phosphorylation and the existence of a MLC(20) phosphorylation-independent mechanism [8].

Anatomical context of Ono-RS-082

• Formation of lysophospholipids in [3H]glycerol-labelled membranes and decrease in [3H]AA liberated by the phospholipase A2 inhibitors mepacrine and ONO-RS-082 suggest that [3H]AA release is mainly catalysed by phospholipase A2 [9].
• It was also found that lipocortin I and ONO-RS-082, but not neomycin, facilitated the generation of GIF-producing T cells [7].
• Phospholipase A2 inhibitors (BPB, ONO-RS-082, quinacrine and AACOCF3) and the lipoxygenase inhibitor AA861 delayed the initial outgrowth of NG108-15 cell neurites on laminin [10].
• Our study demonstrated that pertussis toxin, a specific inhibitor of PLA(2)-coupled G-protein, did not suppress human fetal skin fibroblast migration, but 2-(p-amylcinnamyl)amino-4-chlorobensoic acid (ONO-RS-082), a PLA(2) inhibitor, did [11].
• RBC known to possess AQP-1 at the plasma membrane, swell on exposure to the Galphai-agonist mastoparan, and respond similarly to ONO-RS-082 and glyburide, as ZGs [12].

Associations of Ono-RS-082 with other chemical compounds

• The cytosolic phospholipase A2 inhibitor, AACOCF3 ¿arachidonyl trifluoromethyl ketone¿, decreased responses to bradykinin by up to 90% whereas inhibitors of the secretory form of phospholipase A2 oleyloxyethyl phosphorylcholine and ONO-RS-082 ¿2-(p-amylcinnamoyl)amino-4-chlorobenzoic acid¿ were less effective than either AACOCF3 or U73122 [13].
• Simvastatin response was not altered by the phospholipase A(2) inhibitor ONO-RS-082, or the combination of superoxide dismutase plus catalase [14].
• The inhibitors of protein kinase C (PKC) (staurosporine, 10 nM), of phospholipase C (U73122, 2 microM), of phospholipase A2 (PLA2), (indomethacin 30 microM, mepacrin 50 microM, nordihydroguaiaretic acid 10 microM, ONO-RS-082 3,5 microM), none prevented it [15].
• Pretreatment with ONO-RS-082, the secretory PLA2 (sPLA2) inhibitor, at 1 to 10 micromol/l reduced IL-1beta-stimulated nitrite production and iNOS expression [16].
• At concentrations around 10 pM, CCK-8 elicited [Ca2+]i oscillations, which were blocked by elimination of extracellular Ca2+, by a phospholipase C inhibitor, U-73122, by a protein kinase C inhibitor, H7, as well as by phospholipase A2 (PLA2) inhibitors, ONO-RS-082 and aristolochic acid [17].

References