e-6123 and Asthma

e-6123 has been researched along with Asthma* in 4 studies

Reviews

1 review(s) available for e-6123 and Asthma

ArticleYear
[PAF receptor antagonist in asthma therapy].
    Nihon rinsho. Japanese journal of clinical medicine, 1996, Volume: 54, Issue:11

    Platelet-activating factor (PAF), proposed as an important inflammatory mediator in asthma, reproduces several of the features of asthma, such as micro vascular leakage, mucus secretion, broncoconstriction, and possibly increased airway responsiveness. The recognition that PAF may be a central mediator in asthma has been a relatively recent event, so that those interested in asthma research may be unfamiliar with the chemistry, biochemistry and biology of this material. It seemed appropriate therefore to assemble a group of expert investigators to make presentations and to discuss the current status of PAF research with a specific bias toward asthma. In this way, it has been possible to focus upon PAF in asthma and to provide the necessary background for consideration of the effects of existing antiasthma drugs to suppress pulmonary responses to PAF. The capacity of existing antiasthma drugs to suppress pulmonary responses to PAF implies that this will be necessary feature of many of the newer antiasthma drugs and this knowledge allows a more balanced judgment of the prospects for PAF receptor antagonists in this disease.

    Topics: Animals; Asthma; Azepines; Humans; Platelet Activating Factor; Triazoles

1996

Other Studies

3 other study(ies) available for e-6123 and Asthma

ArticleYear
Involvement of PAF in postallergic propranolol-induced bronchoconstriction in guinea-pigs.
    The European respiratory journal, 1996, Volume: 9, Issue:10

    Administration of propranolol can provoke bronchoconstriction in asthmatic patients. Recently, we successfully developed a guinea-pig model for propranolol-induced bronchoconstriction (PIB). We hypothesized that such bronchoconstriction may result from the inflammatory mediators released by an allergic reaction. The purpose of this study was to examine the role of platelet-activating factor (PAF) in the development of PIB after allergic reaction. Propranolol, at a concentration of 10 mg.mL-1 was inhaled 20 min after antigen challenge in passively sensitized, anaesthetized and artificially-ventilated guinea-pigs. The animals were treated intravenously with PAF antagonists, E6123 (1 and 10 micrograms.kg-1) or Y-24180 (1 and 10 mg.kg-1), 10 min before or 15 min after antigen challenge. Propranolol inhaled 20 min after antigen challenge caused bronchoconstriction. E6123 and Y-24180 administered 15 min after antigen challenge as well as 10 min before antigen challenge reduced the PIB in a dose-dependent manner. We conclude that platelet-activating factor may contribute to the development of propranolol-induced bronchoconstriction after allergic reaction in our guinea-pig model.

    Topics: Administration, Inhalation; Adrenergic beta-Antagonists; Anesthesia, General; Animals; Antigens; Asthma; Azepines; Bronchoconstriction; Disease Models, Animal; Dose-Response Relationship, Drug; Guinea Pigs; Hypersensitivity; Immunization; Inflammation Mediators; Injections, Intravenous; Male; Platelet Activating Factor; Propranolol; Respiration, Artificial; Time Factors; Triazoles

1996
Pharmacological effects of oral E6123, a novel PAF antagonist, on biological changes induced by PAF inhalation in guinea pigs.
    Prostaglandins, 1991, Volume: 42, Issue:5

    The effects of a newly synthesized PAF antagonist E6123, (S)-(+)-6-(2-chlorophenyl)-3-cyclopropanecarbonyl-8,11-dimethyl-2, 3,4,5- tetrahydro-8H-pyrido[4',3':4,5]thieno[3,2-f][1,2,4]triazolo [4,3-a][1,4]diazepine, on in vivo inhaled PAF-induced pulmonary changes were investigated. E6123 inhibited PAF inhalation-induced bronchoconstriction in guinea pigs with an ED50 value (p.o.) of 1.3 micrograms/kg which was lower than those of other PAF-antagonists such as WEB2347 (ED50 = 26 micrograms/kg) and Y-24180 (ED50 = 12 micrograms/kg). E6123 significantly inhibited PAF inhalation-induced eosinophil infiltration into the bronchiole and trachea, and bronchial hyperreactivity in guinea pigs after oral administration at 1 and 10 micrograms/kg, respectively. E6123 inhibited the PAF-induced increase in intracellular free calcium ion concentration ([Ca2+]i) in guinea pig eosinophils with an IC50 value of 14 nM. The present results suggest that E6123 may be beneficial for the treatment of asthma, in which PAF is assumed to be involved.

    Topics: Administration, Oral; Analysis of Variance; Animals; Asthma; Azepines; Bronchial Hyperreactivity; Bronchoconstriction; Calcium; Eosinophils; Guinea Pigs; Lung; Male; Platelet Activating Factor; Triazoles

1991
Inhibitory effects of a novel PAF antagonist E6123 on anaphylactic responses in passively and actively sensitized guinea pigs and passively sensitized mice.
    Prostaglandins, 1991, Volume: 42, Issue:6

    The effects of the platelet-activating factor (PAF) antagonist, E6123, on anaphylactic responses in guinea pigs and mice were investigated. E6123 inhibited i.v. antigen (Ag)- or inhaled Ag-induced bronchoconstriction in passively and actively sensitized guinea pigs after oral administration at 3 and 10 micrograms/kg, respectively. E6123 inhibited Ag inhalation-induced airway hyperreactivity in guinea pigs after oral administration at 30 micrograms/kg. E6123 protected mice from anaphylactic death with an ED50 value (p.o.) of 7 micrograms/kg. The inhibitory effects of E6123 described above were very potent compared to those of the PAF-antagonists WEB2347 and Y-24180. The present results suggest that E6123 may be beneficial for the treatment of asthma, a condition in which PAF is assumed to be involved.

    Topics: Administration, Inhalation; Anaphylaxis; Animals; Antigens; Asthma; Azepines; Guinea Pigs; Male; Mice; Mice, Inbred ICR; Ovalbumin; Platelet Activating Factor; Propranolol; Pyrilamine; Triazoles

1991