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Chemical Compound Review

Tranpro     2-[3-(3,4- dimethoxyphenyl)prop-2...

Synonyms: SureCN29876, AG-F-85791, SPBio_000163, AC1L1KJK, CTK1H1807, ...
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Disease relevance of tranilast


Psychiatry related information on tranilast

  • Twenty patients fulfilled the criteria, of whom 10 were selected at random and commenced on tranilast [100 mg, 3 times daily; T(+) group] [5].

High impact information on tranilast

  • Flow cytometry analysis of isolated human and rabbit peripheral blood mononuclear cells showed that an increase in expression both of MHC class II antigen on monocytes by incubation with interferon-gamma and of IL-2 receptor on T cells by IL-2 was suppressed by the combined incubation with tranilast [6].
  • CONCLUSIONS: The results indicate that tranilast suppresses atherosclerotic development partly through direct inhibition of immunological activation of monocytes/macrophages and T cells in the atheromatous plaque [6].
  • Tranilast [N-(3,4-dimethoxycinnamoyl) anthranillic acid] inhibits release of cytokines and chemical mediators from various cells, including macrophages, leading to suppression of inflammatory and immunological responses [6].
  • Immunohistochemical staining demonstrated that, in tranilast-treated rats, p21 was already present in the neointima at day 7 and strongly expressed throughout the neointima at day 14 [2].
  • Tranilast suppressed their activities by >80% without reduction of CDK2/cyclin E and CDK4/cyclin D1 protein levels [2].

Chemical compound and disease context of tranilast


Biological context of tranilast

  • Tranilast (100 mg x kg(-1) x d(-1) p.o.) significantly (P<0.05) reduced smooth muscle cell proliferation in the neointima and media 7 days after injury and neointimal formation 21 days after injury in treated mice compared with vehicle-treated mice [11].
  • Tranilast inhibited the proliferation of cultured leiomyoma cells in a dose-dependent manner without any cytotoxic effect or induction of apoptosis [12].
  • In addition, PDGF-induced calcium influx in the late G1 phase, as assessed by measuring the initial uptake of 45Ca, was inhibited by tranilast in a concentration-dependent manner [13].
  • Therefore, in therapeutically relevant concentrations (50 microg/ml), tranilast inhibits NF-kappaB-dependent transcriptional activation by interfering with the NF-kappaB/CBP association [14].
  • Expression of the transcriptional coactivator cAMP response element binding protein binding protein (CBP) was inhibited by tranilast, resulting in a loss of interaction between NF-kappaB and CBP [14].

Anatomical context of tranilast


Associations of tranilast with other chemical compounds


Gene context of tranilast


Analytical, diagnostic and therapeutic context of tranilast

  • BACKGROUND: Tranilast, which has antikeloid and antiallergic properties and therefore may modulate the fibrotic and inflammatory tissue responses to angioplasty and stenting, has been shown to inhibit angiographic restenosis in small clinical trials [15].
  • Inhibition of neointima formation by tranilast in pig coronary arteries after balloon angioplasty and stent implantation [15].
  • METHODS: Following initial pharmacokinetic studies in two pigs to determine desirable plasma levels of orally administered tranilast, 36 crossbred juvenile pigs were randomized to placebo or tranilast before undergoing balloon angioplasty in both the left anterior descending and left circumflex plus stent implantation in the right coronary artery [15].
  • After a recession of the superior rectus muscle (SRM), a PTFE/PLGA laminate containing tranilast, PTFE alone, or balanced salt solution was applied beneath and over the SRM in the PTFE/PLGA-tranilast group (group P-T), the PTFE group (group P), and the control group, respectively [24].
  • OBJECTIVE: Recent studies suggest that tranilast inhibits a variety of agents implicated in neointimal growth and restenosis in experimental animal models and humans [25].


  1. Evidence for a role of mast cells in the evolution to congestive heart failure. Hara, M., Ono, K., Hwang, M.W., Iwasaki, A., Okada, M., Nakatani, K., Sasayama, S., Matsumori, A. J. Exp. Med. (2002) [Pubmed]
  2. Tranilast inhibits vascular smooth muscle cell growth and intimal hyperplasia by induction of p21(waf1/cip1/sdi1) and p53. Takahashi, A., Taniguchi, T., Ishikawa, Y., Yokoyama, M. Circ. Res. (1999) [Pubmed]
  3. Tranilast attenuates structural and functional aspects of renal injury in the remnant kidney model. Kelly, D.J., Zhang, Y., Gow, R., Gilbert, R.E. J. Am. Soc. Nephrol. (2004) [Pubmed]
  4. Long-term prospective pilot study with tranilast for the prevention of stricture progression in patients with Crohn's disease. Oshitani, N., Yamagami, H., Watanabe, K., Higuchi, K., Arakawa, T. Gut (2007) [Pubmed]
  5. Effect of tranilast in early-stage diabetic nephropathy. Soma, J., Sato, K., Saito, H., Tsuchiya, Y. Nephrol. Dial. Transplant. (2006) [Pubmed]
  6. Suppression of atherosclerotic development in Watanabe heritable hyperlipidemic rabbits treated with an oral antiallergic drug, tranilast. Matsumura, T., Kugiyama, K., Sugiyama, S., Ota, Y., Doi, H., Ogata, N., Oka, H., Yasue, H. Circulation (1999) [Pubmed]
  7. Combination therapy with tranilast and angiotensin-converting enzyme inhibition provides additional renoprotection in the remnant kidney model. Kelly, D.J., Zhang, Y., Cox, A.J., Gilbert, R.E. Kidney Int. (2006) [Pubmed]
  8. Inhibition of left ventricular fibrosis by tranilast in rats with renovascular hypertension. Hocher, B., Godes, M., Olivier, J., Weil, J., Eschenhagen, T., Slowinski, T., Neumayer, H.H., Bauer, C., Paul, M., Pinto, Y.M. J. Hypertens. (2002) [Pubmed]
  9. Tranilast prevents the progression of experimental diabetic nephropathy through suppression of enhanced extracellular matrix gene expression. Akahori, H., Ota, T., Torita, M., Ando, H., Kaneko, S., Takamura, T. J. Pharmacol. Exp. Ther. (2005) [Pubmed]
  10. Inhibition of proliferative responses of lymphocytes to food antigens by an anti-allergic drug, N(3',4'-dimethoxycinnamoyl) anthranilic acid (Tranilast) in children with atopic dermatitis. Kondo, N., Fukutomi, O., Kameyama, T., Orii, T. Clin. Exp. Allergy (1992) [Pubmed]
  11. Photochemically induced endothelial injury in the mouse as a screening model for inhibitors of vascular intimal thickening. Kikuchi, S., Umemura, K., Kondo, K., Saniabadi, A.R., Nakashima, M. Arterioscler. Thromb. Vasc. Biol. (1998) [Pubmed]
  12. Tranilast inhibits the proliferation of uterine leiomyoma cells in vitro through G1 arrest associated with the induction of p21(waf1) and p53. Shime, H., Kariya, M., Orii, A., Momma, C., Kanamori, T., Fukuhara, K., Kusakari, T., Tsuruta, Y., Takakura, K., Nikaido, T., Fujii, S. J. Clin. Endocrinol. Metab. (2002) [Pubmed]
  13. Blockade of DNA synthesis induced by platelet-derived growth factor by tranilast, an inhibitor of calcium entry, in vascular smooth muscle cells. Nie, L., Mogami, H., Kanzaki, M., Shibata, H., Kojima, I. Mol. Pharmacol. (1996) [Pubmed]
  14. Tranilast inhibits cytokine-induced nuclear factor kappaB activation in vascular endothelial cells. Spiecker, M., Lorenz, I., Marx, N., Darius, H. Mol. Pharmacol. (2002) [Pubmed]
  15. Inhibition of neointima formation by tranilast in pig coronary arteries after balloon angioplasty and stent implantation. Ishiwata, S., Verheye, S., Robinson, K.A., Salame, M.Y., de Leon, H., King, S.B., Chronos, N.A. J. Am. Coll. Cardiol. (2000) [Pubmed]
  16. Tranilast attenuates myocardial fibrosis in association with suppression of monocyte/macrophage infiltration in DOCA/salt hypertensive rats. Kagitani, S., Ueno, H., Hirade, S., Takahashi, T., Takata, M., Inoue, H. J. Hypertens. (2004) [Pubmed]
  17. Tranilast antagonizes angiotensin II and inhibits its biological effects in vascular smooth muscle cells. Miyazawa, K., Fukuyama, J., Misawa, K., Hamano, S., Ujiie, A. Atherosclerosis (1996) [Pubmed]
  18. Tranilast inhibits contraction and Ca2+ movement of porcine coronary arteries. Ishibashi, S., Ikeda, U., Ihara, T., Shimada, K. Atherosclerosis (1997) [Pubmed]
  19. Inhibitory effect of tranilast on prostaglandin D synthetase. Ikai, K., Ujihara, M., Fujii, K., Urade, Y. Biochem. Pharmacol. (1989) [Pubmed]
  20. Effects of anti-allergic drugs on human neutrophil superoxide-generating NADPH oxidase. Umeki, S. Biochem. Pharmacol. (1992) [Pubmed]
  21. N-[3,4-dimethoxycinnamoyl]-anthranilic acid (tranilast) inhibits transforming growth factor-beta relesase and reduces migration and invasiveness of human malignant glioma cells. Platten, M., Wild-Bode, C., Wick, W., Leitlein, J., Dichgans, J., Weller, M. Int. J. Cancer (2001) [Pubmed]
  22. Tranilast attenuates connective tissue growth factor-induced extracellular matrix accumulation in renal cells. Qi, W., Chen, X., Twigg, S., Polhill, T.S., Gilbert, R.E., Pollock, C.A. Kidney Int. (2006) [Pubmed]
  23. Effect of tranilast on matrix metalloproteinase production from neutrophils in-vitro. Shimizu, T., Kanai, K., Kyo, Y., Asano, K., Hisamitsu, T., Suzaki, H. J. Pharm. Pharmacol. (2006) [Pubmed]
  24. Slow-Releasing Tranilast in Polytetrafluoroethylene/Polylactide-co-glycolide Laminate Delays Adjustment after Strabismus Surgery in Rabbit Model. Lee, M.J., Jin, S.E., Kim, C.K., Choung, H.K., Jeoung, J.W., Kim, H.J., Choe, G., Hwang, J.M. Invest. Ophthalmol. Vis. Sci. (2007) [Pubmed]
  25. Application of in vivo and ex vivo magnetic resonance imaging for evaluation of tranilast on neointima formation following balloon angioplasty of the rat carotid artery. Ohlstein, E.H., Romanic, A.M., Clark, L.V., Kapadia, R.D., Sarkar, S.K., Gagnon, R., Chandra, S. Cardiovasc. Res. (2000) [Pubmed]
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