Disease relevance of Suplatast tosylate

• Suplatast tosilate inhibits goblet-cell metaplasia of airway epithelium in sensitized mice [1].
• Successful treatment of eosinophilic gastroenteritis with suplatast tosilate [2].
• Improvement of interstitial cystitis symptoms and problems that developed during treatment with oral IPD-1151T [3].
• Effects of suplatast tosilate, a new type of anti-allergic agent, on airway cough hypersensitivity induced by airway allergy in guinea-pigs [4].
• Among the drugs tested, only suplatast tosilate remarkably inhibited blood and tissue eosinophilia and the ear swelling responses [5].

High impact information on Suplatast tosylate

• METHODS: 85 patients with moderate to severe asthma taking high doses (> or = 1500 microg per day) of inhaled beclometasone dipropionate, were assigned suplatast tosilate (100 mg three times daily) or placebo for 8 weeks in a double-blind, randomised, parallel-group, multicentre trial [6].
• OBJECTIVE: We sought to determine the suppressive effects of suplatast tosilate, an inhibitor of T(H)2-type cytokines, on eosinophilic inflammation of the bronchial mucosa in patients with mild asthma [7].
• Pretreatment with suplatast tosilate also prevented OVA-induced increase in IL-4 and IL-13 levels and decreased the number of lymphocytes and eosinophils in bronchoalveolar lavage fluid (P <.05 compared with values of mice given OVA alone) [1].
• CONCLUSION: These results indicate that suplatast tosilate prevents allergen-induced goblet-cell metaplasia and the recruitment of eosinophils and lymphocytes into the airways [1].
• Suplatast tosilate inhibited OVA-induced goblet-cell metaplasia in airway epithelium in a dose-dependent fashion; 50 mg.kg(-1).d(-1) decreased the AB/PAS area to 22.7% +/- 2.7% (P <.05 compared with OVA sensitization alone) [1].

Chemical compound and disease context of Suplatast tosylate

• METHODS: The effect of the orally active Th2 cytokine inhibitor suplatast tosilate on cough response to inhaled capsaicin was examined in eleven patients with stable atopic asthma and compared with patients having non-atopic asthma and chronic bronchitis (the latter of which is not related to Th2 cytokines) [8].
• CONCLUSIONS: Dimethyl sulfide metabolized from suplatast tosilate may be a potential cause of halitosis [9].

Biological context of Suplatast tosylate

• The effect of suplatast tosilate, which has been proven to inhibit T-cell synthesis of IL-4 and IL-5, on the response to antigen inhalation challenge was investigated in sensitized guinea pigs [10].
• Among them (+/-)-2-[N-[4-(3-ethoxy-2-hydroxypropoxy)phenyl]carbamoyl]ethyldimeth ylsulfonium p-toluenesulfonate (1a, IPD-1151T) was found to possess considerable activity in the PCA test, and it was launched as Suplatast tosilate in Japan [11].
• CONCLUSION: Through inhibition of chemotaxis, IPD-1151T might limit the number of eosinophils at the inflammation site [12].
• The oral administration of IPD-1151T to immunized BALB/c mice suppressed the primary IgE antibody response and depressed the elevation of serum IgE levels, whereas the same treatment did not affect the IgG antibody response [13].
• IPD-1151T inhibited both antigen- and MCh-mediated bronchoconstriction in actively sensitized mice [14].

Anatomical context of Suplatast tosylate

• BACKGROUND: Suplatast tosilate is an anti-allergic agent that suppresses cytokine production by human Th2 cells [15].
• PURPOSE: We examined the efficacy of Suplatast Tosilatedouble dagger (IPD-1151T), a new immunoregulator that suppresses helper T cell mediated allergic responses, including IgE production and eosinophilic inflammation for treating patients with interstitial cystitis [3].
• Suplatast tosilate (IPD-1151T), a new anti-allergic agent, has shown beneficial effect in the treatment of asthma, associated with reduced bronchoalveolar lavage eosinophil infiltration and eosinophilic cationic protein (ECP) release in serum and sputum [12].
• However, the growth of mast cells from the splenocyte culture was dose dependently inhibited by IPD-1151T [16].
• Furthermore, IPD-1151T inhibited the proliferation of mast cell progenitor cells, IC-2, but not that of splenocytes or mature mast cells [16].

Associations of Suplatast tosylate with other chemical compounds

• One group (the control group, n = 15) was treated with a non-steroid anti-inflammatory ointment (bufexamac ointment), while the other group (the suplatast tosilate group, n = 17) was treated with the anti-allergic medications, suplatast tosilate and bufexamac ointment [17].
• Effect of suplatast tosilate (IPD-1151T) on cytokine production by allergen-specific human Th1 and Th2 cell lines [18].
• The inhibitory effect of anti-allergic agent suplatast tosilate (IPD-1151T) on methacholine- and allergen-induced bronchoconstriction in sensitized mice. asakazu@med.showa-u.dc.jp [14].
• Interestingly, suplatast tosilate (IPD-1151T), known to be antiallergic agent capable of suppressing IgE synthesis and chemical mediator release, but not disodium cromoglycate, selectively suppressed eosinophil accumulation [19].

Gene context of Suplatast tosylate

• RESULTS: The chemotactic response to fMLP, IL-5 and eotaxin was significantly inhibited by IPD-1151T [12].
• Upon activation by anti-CD28, only IL-13 production was inhibited by IPD-1151T, whereas release of IL-2 and IFN-gamma was not affected [12].
• IL-10 release induced by sIgA was also inhibited by IPD-1151T [12].
• Activation by sIgA and CD28 ligation resulted in the release of ECP and EDN, which was inhibited by IPD-1151T [12].
• Interestingly, IPD-1151T concentration-dependently inhibited the production of interleukin 4 (IL-4) by D10G4.1, known to be a typical Th2 clone [13].

Analytical, diagnostic and therapeutic context of Suplatast tosylate

• METHODS: Airway hyperresponsiveness tests, pulmonary function tests, eosinophil measurements in induced sputum, and bronchial mucosa biopsies were performed before and after treatment with suplatast tosilate for 6 weeks in 15 patients with mild asthma and in 13 control patients with mild asthma not receiving suplatast tosilate [7].
• The influence of IPD-1151T (suplatast-tosilate) on murine mast cell induction was examined by in vitro cell culture [16].
• These results strongly suggest that oral administration of suplatast tosilate suppresses airway hyperresponsiveness in asthma patients by reducing eosinophilic inflammation in the airways [20].
• It was further demonstrated from the adoptive transfer experiment that IPD-1151T, administered to hapten-primed B cell donors, but not to carrier-primed T cell donors, exerted its suppressive influence on the hapten-specific secondary IgE antibody response in irradiated syngeneic recipients [13].
• The use of suplatast tosilate together with immunotherapy may blunt the initial rise in specific IgE and decrease serum levels of specific IgE more quickly [21].

References