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Chemical Compound Review

Camostat     [4- (dimethylcarbamoylmethoxycarbo nylmethyl...

Synonyms: camostate, Camostatum, foypan, FOY-305, Camostat (INN), ...
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Disease relevance of Camostat

  • Administration of 0.1% FOY-305 in the diet suppressed the incidence of carcinomas induced by repeated local application of the carcinogen 3-methylcholanthrene (MCA) (P less than .05) in mouse skin and delayed the time of appearance of the skin tumors (P less than .001) [1].
  • The favorable effect on survival time and rate in the early phase of these two severe experimental forms of pancreatitis may justify an evaluation of FOY-305 in a clinically controlled study [2].
  • Prevention of rat hepatic fibrosis by the protease inhibitor, camostat mesilate, via reduced generation of active TGF-beta [3].
  • Feedback-mediated hyperplasia of the rat exocrine pancreas induced by oral treatment of rats with the protease inhibitor camostate (FOY-305) was preceded by a 15-fold transient elevation of PRG1 mRNA levels [4].
  • In mice fed camostat for 7 days, the ratio of pancreatic to body weight increased by 143%, but when rapamycin was administered daily this was reduced to a 22% increase [5].

High impact information on Camostat

  • We explored this idea using camostat mesilate, a serine protease inhibitor, to determine its effects and mechanisms of action in vivo [3].
  • Camostat treatment markedly increased the phosphorylation of both PHAS-I and eIF4E and the formation of eIF4E-eIF4G complex [6].
  • We also evaluated the effect of endogenous CCK by administering a synthetic trypsin inhibitor, camostat (100 mg/kg) [6].
  • BACKGROUND & AIMS: Feedback regulation of pancreatic enzyme secretion is well established in animals, and their pancreases are able to adapt to intraduodenal inhibition of pancreatic enzymes by proteinase inhibitors such as Camostate (FOY-305; Schwarz GmbH, Monheim, Germany) [7].
  • Intraduodenal administration of a synthetic trypsin inhibitor, camostat, resulted in significant increases in plasma concentration of both secretin and cholecystokinin in a dose-related manner that paralleled a significant increase in exocrine pancreatic secretion [8].

Chemical compound and disease context of Camostat


Biological context of Camostat

  • Intraduodenal infusion of beta-conglycinin peptone inhibited food intake in a dose-dependent manner, but that of whole soy peptone or camostat did not [14].
  • Camostat, at a high dose of 10 mg, caused significant increases in the secretory rate, bicarbonate concentration and output of pancreatic juice over their basal levels, but had little influence on the protein concentration [15].
  • The intestinal absorption of insulin and (Asu(1,7))eel-calcitonin after oral administration of the azopolymer-coated pellets containing these peptides with camostat mesilate was evaluated by measuring the hypoglycemic and hypocalcemic effects, respectively [16].
  • The cell proliferation stimulated by PDGF was inhibited by the application of FOY-007 dose dependently (1-100 microM) and FOY-305 at 100 microM [17].
  • The effects of proteolytic enzyme inhibitors, aprotinin, soybean trypsin inhibitor and camostat mesilate as absorption enhancers on the transdermal iontophoretic delivery of salmon calcitonin (SCT) have been examined in rats [18].

Anatomical context of Camostat

  • By using nonabsorbable markers, cumulative trypsin, chymotrypsin, lipase, and amylase activities were measured as delivered to duodenum, midjejunum, and distal ileum, with or without simultaneous duodenal perfusion of the protease inhibitor camostat at graded doses [19].
  • Histologic examination revealed widespread repopulation of the pancreas with acinar cells in the bombesin- and FOY-305-treated groups [20].
  • For camostat mesilate, the ED50 (required to improve the survival rate of influenza virus-infected chick embryos by 50%) was 0.80 micrograms/g, and its selectivity index, based on the ratio of the 50% toxic dose (required to reduce the viability of chick embryos by 50%) to ED50, was 280 [21].
  • Effects of camostat, a synthetic protease inhibitor, on endocrine and exocrine pancreas of the rat [22].
  • Camostat mesilate attenuates pancreatic fibrosis via inhibition of monocytes and pancreatic stellate cells activity [23].

Associations of Camostat with other chemical compounds

  • A cholecystokinin receptor antagonist, MK-329, also inhibited significantly the camostat-induced increase in pancreatic secretion; volume and bicarbonate output were reduced by 35% each and amylase output by 73% [8].
  • Stimulation of the growth of azaserine-induced nodules in the rat pancreas by dietary camostate (FOY-305) [24].
  • Gabexate and camostat, synthetic proteinase inhibitors, as direct inducing factors of water and bicarbonate secretion in the isolated and blood-perfused dog pancreas [15].
  • The increase in plasma CCK induced by camostat was not blocked by CsA or FK506 [25].
  • Intraduodenal administration of camostat or intravenous infusion of CCK-8 stimulated pancreatic secretion in control rats but not in capsaicin-treated rats [26].

Gene context of Camostat


Analytical, diagnostic and therapeutic context of Camostat


  1. Effect of the synthetic protease inhibitor [N,N-dimethylcarbamoyl-methyl 4-(4-guanidinobenzoyloxy)-phenylacetate] methanesulfate on carcinogenesis by 3-methylcholanthrene in mouse skin. Ohkoshi, M., Fujii, S. J. Natl. Cancer Inst. (1983) [Pubmed]
  2. Effect of FOY-305 (camostate) on severe acute pancreatitis in two experimental animal models. Lankisch, P.G., Pohl, U., Göke, B., Otto, J., Wereszczynska-Siemiatkowska, U., Gröne, H.J., Rahlf, G. Gastroenterology (1989) [Pubmed]
  3. Prevention of rat hepatic fibrosis by the protease inhibitor, camostat mesilate, via reduced generation of active TGF-beta. Okuno, M., Akita, K., Moriwaki, H., Kawada, N., Ikeda, K., Kaneda, K., Suzuki, Y., Kojima, S. Gastroenterology (2001) [Pubmed]
  4. PRG1: a novel early-response gene transcriptionally induced by pituitary adenylate cyclase activating polypeptide in a pancreatic carcinoma cell line. Schäfer, H., Trauzold, A., Siegel, E.G., Fölsch, U.R., Schmidt, W.E. Cancer Res. (1996) [Pubmed]
  5. Activation of the mTOR signalling pathway is required for pancreatic growth in protease-inhibitor-fed mice. Crozier, S.J., Sans, M.D., Guo, L., D'Alecy, L.G., Williams, J.A. J. Physiol. (Lond.) (2006) [Pubmed]
  6. Regulation of the initiation of pancreatic digestive enzyme protein synthesis by cholecystokinin in rat pancreas in vivo. Bragado, M.J., Tashiro, M., Williams, J.A. Gastroenterology (2000) [Pubmed]
  7. Adaptation of the human pancreas to inhibition of luminal proteolytic activity. Friess, H., Kleeff, J., Isenmann, R., Malfertheiner, P., Büchler, M.W. Gastroenterology (1998) [Pubmed]
  8. Mediation of trypsin inhibitor-induced pancreatic hypersecretion by secretin and cholecystokinin in rats. Watanabe, S., Takeuchi, T., Chey, W.Y. Gastroenterology (1992) [Pubmed]
  9. Camostate (FOY-305) improves the therapeutic effect of peritoneal lavage on taurocholate induced pancreatitis. Leonhardt, U., Seidensticker, F., Fussek, M., Stöckmann, F., Creutzfeldt, W. Gut (1990) [Pubmed]
  10. Efficacy of camostat mesilate compared with famotidine for treatment of functional dyspepsia: Is camostat mesilate effective? Ashizawa, N., Hashimoto, T., Miyake, T., Shizuku, T., Imaoka, T., Kinoshita, Y. J. Gastroenterol. Hepatol. (2006) [Pubmed]
  11. Evaluation of anti-influenza effects of camostat in mice infected with non-adapted human influenza viruses. Lee, M.G., Kim, K.H., Park, K.Y., Kim, J.S. Arch. Virol. (1996) [Pubmed]
  12. Effects of serine protease inhibitor FOY-305 and heparin on the growth of squamous cell carcinoma. Ohkoshi, M., Akagawa, T., Nakajima, M. Anticancer Res. (1993) [Pubmed]
  13. General and selective inhibition of pancreatic enzyme discharge using a proteinase inhibitor (FOY-305). Adler, G., Rausch, U., Weidenbach, F., Arnold, R., Kern, H.F. Klin. Wochenschr. (1984) [Pubmed]
  14. Soybean beta-conglycinin peptone suppresses food intake and gastric emptying by increasing plasma cholecystokinin levels in rats. Nishi, T., Hara, H., Tomita, F. J. Nutr. (2003) [Pubmed]
  15. Gabexate and camostat, synthetic proteinase inhibitors, as direct inducing factors of water and bicarbonate secretion in the isolated and blood-perfused dog pancreas. Horiuchi, A., Iwatsuki, K., Yonekura, H., Ren, L.M., Chiba, S. J. Pharmacol. Exp. Ther. (1990) [Pubmed]
  16. Enhanced absorption of insulin and (Asu(1,7))eel-calcitonin using novel azopolymer-coated pellets for colon-specific drug delivery. Tozaki, H., Nishioka, J., Komoike, J., Okada, N., Fujita, T., Muranishi, S., Kim, S.I., Terashima, H., Yamamoto, A. Journal of pharmaceutical sciences. (2001) [Pubmed]
  17. Effects of synthetic serine protease inhibitors on proliferation and collagen synthesis of human pancreatic periacinar fibroblast-like cells. Nakamura, F., Shintani, Y., Saotome, T., Fujiyama, Y., Bamba, T. Pancreas (2001) [Pubmed]
  18. Effects of proteolytic enzyme inhibitors as absorption enhancers on the transdermal iontophoretic delivery of calcitonin in rats. Morimoto, K., Iwakura, Y., Nakatani, E., Miyazaki, M., Tojima, H. J. Pharm. Pharmacol. (1992) [Pubmed]
  19. Feedback regulation of human pancreatic secretion. Effects of protease inhibition on duodenal delivery and small intestinal transit of pancreatic enzymes. Layer, P., Jansen, J.B., Cherian, L., Lamers, C.B., Goebell, H. Gastroenterology (1990) [Pubmed]
  20. The effect of endogenous cholecystokinin released by bombesin and trypsin inhibitor on the regeneration of the pancreas. Parekh, D., Ishizuka, J., Townsend, C.M., Rajaraman, S., Thompson, J.C. Ann. Surg. (1993) [Pubmed]
  21. Comparative inhibitory effects of various nucleoside and nonnucleoside analogues on replication of influenza virus types A and B in vitro and in ovo. Hosoya, M., Shigeta, S., Ishii, T., Suzuki, H., De Clercq, E. J. Infect. Dis. (1993) [Pubmed]
  22. Effects of camostat, a synthetic protease inhibitor, on endocrine and exocrine pancreas of the rat. Müller, M.K., Goebell, H., Alfen, R., Ehlers, J., Jäger, M., Plümpe, H. J. Nutr. (1988) [Pubmed]
  23. Camostat mesilate attenuates pancreatic fibrosis via inhibition of monocytes and pancreatic stellate cells activity. Gibo, J., Ito, T., Kawabe, K., Hisano, T., Inoue, M., Fujimori, N., Oono, T., Arita, Y., Nawata, H. Lab. Invest. (2005) [Pubmed]
  24. Stimulation of the growth of azaserine-induced nodules in the rat pancreas by dietary camostate (FOY-305). Lhoste, E.F., Roebuck, B.D., Longnecker, D.S. Carcinogenesis (1988) [Pubmed]
  25. Calcineurin mediates pancreatic growth in protease inhibitor-treated mice. Tashiro, M., Samuelson, L.C., Liddle, R.A., Williams, J.A. Am. J. Physiol. Gastrointest. Liver Physiol. (2004) [Pubmed]
  26. Differential mechanism and site of action of CCK on the pancreatic secretion and growth in rats. Yamamoto, M., Otani, M., Jia, D.M., Fukumitsu, K., Yoshikawa, H., Akiyama, T., Otsuki, M. Am. J. Physiol. Gastrointest. Liver Physiol. (2003) [Pubmed]
  27. Different effects of oral administration of synthetic trypsin inhibitor on the pancreas between cholecystokinin-A receptor gene knockout mice and wild type mice. Sato, N., Suzuki, S., Kanai, S., Ohta, M., Jimi, A., Noda, T., Takiguchi, S., Funakoshi, A., Miyasaka, K. Jpn. J. Pharmacol. (2002) [Pubmed]
  28. Hepatocyte growth factor stimulates the invasion of gallbladder carcinoma cell lines in vitro. Li, H., Shimura, H., Aoki, Y., Date, K., Matsumoto, K., Nakamura, T., Tanaka, M. Clin. Exp. Metastasis (1998) [Pubmed]
  29. Effects of the cholecystokinin A receptor antagonist loxiglumide on the proliferation and cell cycle time of pancreatic acinar cells in rats. Kanemitsu, D., Sakagami, J., Motoyoshi, T., Nakajima, T., Kataoka, K. Pancreas (2006) [Pubmed]
  30. Expression of c-myc, c-raf-1, and c-Ki-ras in azaserine-induced pancreatic carcinomas and growing pancreas in rats. Silverman, J.A., Kuhlmann, E.T., Zurlo, J., Yager, J.D., Longnecker, D.S. Mol. Carcinog. (1990) [Pubmed]
  31. Oral trypsin inhibitor can improve reflux esophagitis after distal gastrectomy concomitant with decreased trypsin activity. Kono, K., Takahashi, A., Sugai, H., Umekawa, T., Yano, T., Kamiyasu, K., Teramatsu, M., Fujii, H. Am. J. Surg. (2005) [Pubmed]
  32. Protease inhibitor therapy for recessive dystrophic epidermolysis bullosa. In vitro effect and clinical trial with camostat mesylate. Ikeda, S., Manabe, M., Muramatsu, T., Takamori, K., Ogawa, H. J. Am. Acad. Dermatol. (1988) [Pubmed]
  33. Preparation and characterization of biodegradable or enteric-coated microspheres containing the protease inhibitor camostat. Uchida, T., Yasuda, N., Matsuyama, K. J. Pharm. Pharmacol. (2001) [Pubmed]
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