Our system is currently under heavy load due to increased usage. We're actively working on upgrades to improve performance. Thank you for your patience.
1996
DOI: 10.1016/s0014-2999(96)00810-2
|View full text |Cite
|
Sign up to set email alerts
|

Suplatast tosilate, a new type of antiallergic agent, prevents the expression of airway hyperresponsiveness in guinea pigs

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

1
10
0

Year Published

2000
2000
2007
2007

Publication Types

Select...
5
1

Relationship

0
6

Authors

Journals

citations
Cited by 19 publications
(11 citation statements)
references
References 18 publications
1
10
0
Order By: Relevance
“…1), {2-[4-(3-ethoxy-2-hydroxypropoxy)-phenylcarbamoyl]-ethyl} dimethylsulforium p-toluenesulfonate, is an anti-allergic drug (Ushio and Yamamoto, 1994). It shows effectiveness for the treatment of type I allergy-related diseases such as bronchial asthma, allergic rhinitis urticaria and similar maladies (Satoh et al, 2003;Taniguchi et al, 1996). After oral administration, suplatast tosilate is metabolized to 4-(3-ethoxy-2-hydroxypropoxy) acrylanilide (M-1) by alkaline hydrolysis, and the in vivo effect of this drug is mainly due to the action of this metabolite (Keizo and Dotai, 1992).…”
Section: Introductionmentioning
confidence: 99%
“…1), {2-[4-(3-ethoxy-2-hydroxypropoxy)-phenylcarbamoyl]-ethyl} dimethylsulforium p-toluenesulfonate, is an anti-allergic drug (Ushio and Yamamoto, 1994). It shows effectiveness for the treatment of type I allergy-related diseases such as bronchial asthma, allergic rhinitis urticaria and similar maladies (Satoh et al, 2003;Taniguchi et al, 1996). After oral administration, suplatast tosilate is metabolized to 4-(3-ethoxy-2-hydroxypropoxy) acrylanilide (M-1) by alkaline hydrolysis, and the in vivo effect of this drug is mainly due to the action of this metabolite (Keizo and Dotai, 1992).…”
Section: Introductionmentioning
confidence: 99%
“…However, the degree or nature of airway inflammation was not evaluated in the report. Taniguchi et al [15]also demonstrated that IPD could inhibit BHR to acetylcholine in a guinea pig model of asthma, in which the animal was sensitized twice and challenged once with aerosolized OVA. Although specific IgE was not detected in this model, eosinophils in BALF and in peribronchioles were significantly decreased to about half and one third, respectively, by IPD treatment of 100 mg/kg/day.…”
Section: Discussionmentioning
confidence: 99%
“…In the treated group (IPD group), IPD (100 mg/kg/100 µl) was orally given to mice once a day for 21 days (days 0–20). The dose was determined by previous reports showing obvious inhibition of IgE synthesis [14, 15]. In the positive control group (OVA control group), saline alone was used instead of the compound.…”
Section: Methodsmentioning
confidence: 99%
See 1 more Smart Citation
“…Recently, IL-5, which is derived from Th2 cells, has been shown to play an important role in the development of eosinophil infiltration [17 -20]. Suplatast has been reported to inhibit IL-5 production by Th2 cells [13] and antigeninduced eosinophil infiltration into the lung and the skin [21,22]. Thus, inhibition of the LPR by suplatast is due to the suppression of eosinophil infiltration, accompanied by its suppressive effects on IL-5 production.…”
Section: Effects Of Oral Administration Of Drugs On the Lpr In Balb/cmentioning
confidence: 99%