Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D02027 (Tranilast)
 205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Restenosis after percutaneous intervention remains a significant clinical problem. Although stent implantation has significantly reduced the rate of restenosis by approximately 25% to 33%, intimal hyperplasia within stents still limits long-term vessel patency. The clinical sequelea of this neointimal proliferation is more pronounced in certain patient subgroups, eg, patients with diatbetes mellitus, diffuse disease, smaller vessels, chronic total occlusions, and lesions located in saphenous vein bypass grafts. Pharmacologic agents studied to date have failed to prevent restenosis. Tranilast, a novel anti-inflammatory agent, interferes with the proliferation and migration of vascular smooth muscle cells (VSMCs) induced by platelet-derived growth factor and transforming growth factor beta-1. Basic and preliminary clinical studies conducted with tranilast in Japan have shown encouraging results in terms of reducing restenosis. The Prevention of Restenosis with Tranilast and its Outcomes study (PRESTO), a double-blind, placebo-controlled study (n = 11,500), will test the efficacy of two doses (300 and 450 mg twice a day) of tranilast administered for 1 and 3 months compared with placebo. The primary objective is to compare the composite clinical event rate (death, myocardial infarction, or the need for ischemia-driven target vessel revascularization) after 9 months in patients treated with tranilast or placebo. Angiographic and intravascular ultrasound studies will be peformed in order to assess the effects of tranilast on angiographic restenosis and the volume of intimal hyperplastic tissue. If successful, tranilast will be the first drug to reduce angiographic and clinical restenosis.
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PMID:Tranilast in the Therapy of Coronary Artery Disease. 1109 62

Tranilast is an antiallergic drug that interferes with proliferation and migration of vascular smooth muscle cell induced by platelet-derived growth factor (PDGF) and transforming growth factor-beta1 (TGF-beta1). We investigated the local effect of tranilast on neointimal hyperplasia using tranilast-coated prosthetic grafts. The inner sides of the thin-walled polytetrafluoroethylene (PTFE) grafts were coated with chitosan and tranilast containing chitosan solution. Wistar albino rats (32) were used in the study. Patches (1 x 2 mm) for vascular grafts were prepared. Three groups were tested: group 1 (n = 12; tranilast coated), group 2 (n = 10; adhesive-only film-layer-coated), and group 3 (n = 10; normal ePTFE patch grafts sutured to the carotid arteries of the rats). Recipient sites of the carotid arteries were excised 4 weeks after surgery. All sections were examined histologically for graft patency, thrombus formation, and neointimal thickness. Expression of PDGF, fibroblast growth factor, and TGF-beta1 on cross-sections of the neointima were evaluated by immunohistochemistry. No significant differences were found regarding mean neointimal thicknesses. PDGF and TGF-beta-1 expressions were significantly lower in group 1. Although a decrease in local effect of tranilast was observed for growth factor expressions at a drug concentration of 0.05 mg/cm(2), a significant reduction in neointimal hyperplasia was not achieved. The coating concentration of 0.05 mg/cm(2) may have been too low to produce an antiproliferative effect. Given our promising results, further studies are recommended and planned using different drug concentrations and time intervals.
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PMID:Evaluation of neointimal hyperplasia on tranilast-coated synthetic vascular grafts: an experimental study. 1761 91


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