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PubMed1992

Use of Tranilast [N-(3,4-dimethoxycinnamoyl) anthranilic acid] in secretory otitis media.

Treatment with Tranilast of 45 patients (87 ears) with secretory otitis media was studied. Tranilast was administered orally for at least 1 month. The evaluation of its effectiveness was based on changes in subjective symptoms, tympanic membrane findings, hearing level, and tympanometry. Subjects were divided into three groups: allergy group (group I), nonallergy group (group II) and deformity-disorder group (group III). The respective percentages of Tranilast efficacy for these three groups were 46.2%, 42.1%, and 10.0%, respectively. Equivalent effectiveness was demonstrated whether or not allergies were present. After Tranilast administration, the drug and its metabolites were found in MEE samples from all the patients. Anaphylatoxin (C3a, C5a) activities in the MEE were shown to decrease gradually after Tranilast administration. Tranilast may be effective for treating secretory otitis media because it directly suppresses anaphylatoxin present in middle ear effusion.

Administration, Oral↗
PubMedDate not supplied

Tranilast (N-3,4-dimethoxycinamoyl anthranilic acid): a novel inhibitor of invasion-stimulating interaction between gastric cancer cells and orthotopic fibroblasts.

BACKGROUND: Fibroblasts produce various cytokines that affect the invasion ability of cancer cells. We have previously reported that gastric fibroblasts play an important role in the metastatic process of gastric cancer. Tranilast is a clinical drug for inhibition of fibroblast growth. To develop a drug for cancer invasion, the effect of Tranilast on the invasion-stimulating interaction was examined. MATERIALS AND METHODS: The human gastric carcinoma cell line, OCUM-2D, and the gastric fibroblast cell line, NF-10, were used. The effect of Tranilast on the invasion ability of OCUM-2D cells with NF-10 cells was examined by invasion assay. RESULTS: The invasion ability of OCUM-2D cells was significantly increased by co-culturing with NF-10 cells (p < 0.01). Tranilast, at concentrations of more than 0.01 mM, significantly suppressed the invasion ability of OCUM-2D cells co-cultured with NF-10 cells. Tranilast decreased matrix metalloproteinase-2 (MMP-2) and transforming growth factor-beta 1 (TGF-beta 1) production from fibroblasts. TGF-beta 1 enhanced the MMP-2 production from fibroblasts. The invasion ability of gastric cancer cells was increased by MMP-2 and TGF-beta 1 from fibroblasts and this effect was inhibited by Tranilast, which decreased the MMP-2 and TGF-beta 1 production from fibroblasts. CONCLUSION: Tranilast may be a promising new drug for preventing the metastasis of gastric cancer.

Cell Communication↗