Catalog No.S1439 Synonyms: SB 252218
Molecular Weight(MW): 327.33
Tranilast is an antiallergic drug by inhibiting lipid mediator and cytokine release from inflammatory cells, used for the treatment of allergic disorders such as asthma, allergic rhinitis and atopic dermatitis.
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|Description||Tranilast is an antiallergic drug by inhibiting lipid mediator and cytokine release from inflammatory cells, used for the treatment of allergic disorders such as asthma, allergic rhinitis and atopic dermatitis.|
Tranilast is an anti-allergic drug inhibiting the release of substances such as histamine and prostaglandins from mast cells, which suppresses collagen synthesis of fibroblasts derived from keloid tissues. Tranilast (3-300 mM) suppresses the collagen synthesis of fibroblasts from keloid and hypertrophic scar tissue but not healthy skin fibroblasts. Tranilast (30-300 mM) inhibits the release of transforming growth factor (TGF)-beta 1 from keloid fibroblasts, which enhances the collagen synthesis of keloid fibroblasts.  Tranilast improves keloids and hypertrophic scars which originate from the abnormal proliferation and excessive collagen accumulation of fibroblasts. Tranilast inhibits the release of TGF-beta 1, IL-1 beta and PGE2 from the human monocytes-macrophages.  Tranilast inhibits the proliferation stimulated with fetal bovine serum (FBS), TGF-beta 1 and platelet-derived growth factor-BB (PDGF-BB) as well as PDGF-BB-induced migration. Tranilast exhibits inhibitory effects on spontaneous collagen synthesis and TGF-beta 1-induced collagen and glycosaminoglycan synthesis. 
|In vivo||Tranilast results in a 58% reduction in TGF-beta1-induced 3[H]-hydroxyproline incorporation in the diabetic heart of rats. Tranilast attenuates cardiac fibrosis by 37% in association with reduction in phospho-Smad2 in the diabetic heart of rats.  Tranilast treatment completely prevents the increase in chymaselike activity, reduces the chymase mRNA levels by 43%, and decreases the carotid intima/media ratio by 63% in the carotid artery of dogs. |
-  Suzawa H, et al. Jpn J Pharmacol, 1992, 60(2), 91-96.
-  Suzawa H, et al. Jpn J Pharmacol, 1992, 60(2), 85-90.
-  Miyazawa K, et al. Atherosclerosis, 1995, 118(2), 213-221.
|In vitro||DMSO||66 mg/mL (201.63 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01052987||Completed||Gout|Hyperuricemia||Nuon Therapeutics, Inc.||January 2010||Phase 2|
|NCT00995618||Completed||Gout|Hyperuricemia||Nuon Therapeutics, Inc.||September 2009||Phase 2|
|NCT00882024||Completed||Active Rheumatoid Arthritis||Nuon Therapeutics, Inc.||March 2009||Phase 2|
|NCT01003613||Completed||Pterygium||Gildasio Castello de Almeida Junior|Hospital de Base|Sao Jose do Rio Preto University||February 2009||Phase 3|
|NCT00717808||Withdrawn||Rheumatoid Arthritis||Imperial College London|Nuon Therapeutics, Inc.||September 2008||Phase 1|
|NCT00818805||Completed||Allergic Conjunctivitis||Alcon Research||July 2008||Phase 4|
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