Camostat MesilateTrypsin-like protease inhibitor CAS# 59721-29-8 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 59721-29-8 | SDF | Download SDF |
PubChem ID | 5284360 | Appearance | Powder |
Formula | C21H26N4O8S | M.Wt | 494.52 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | Camostat mesilate; FOY305; FOY-S980 | ||
Solubility | DMSO : 125 mg/mL (252.77 mM; Need ultrasonic) H2O : ≥ 50 mg/mL (101.11 mM) Ethanol : 2 mg/mL (4.04 mM; Need ultrasonic) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | 4-[[4-[(Aminoiminomethyl)amino]benz | ||
SMILES | CN(C)C(=O)COC(=O)CC1=CC=C(C=C1)OC(=O)C2=CC=C(C=C2)N=C(N)N.CS(=O)(=O)O | ||
Standard InChIKey | FSEKIHNIDBATFG-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C20H22N4O5.CH4O3S/c1-24(2)17(25)12-28-18(26)11-13-3-9-16(10-4-13)29-19(27)14-5-7-15(8-6-14)23-20(21)22;1-5(2,3)4/h3-10H,11-12H2,1-2H3,(H4,21,22,23);1H3,(H,2,3,4) | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Orally active protease inhibitor. Known to inhibit trypsin and various inflammatory proteases including plasmin, kallikrein and thrombin. Suppresses pancreatitis-induced pain in rats following oral administration. |
Camostat Mesilate Dilution Calculator
Camostat Mesilate Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.0222 mL | 10.1108 mL | 20.2216 mL | 40.4433 mL | 50.5541 mL |
5 mM | 0.4044 mL | 2.0222 mL | 4.0443 mL | 8.0887 mL | 10.1108 mL |
10 mM | 0.2022 mL | 1.0111 mL | 2.0222 mL | 4.0443 mL | 5.0554 mL |
50 mM | 0.0404 mL | 0.2022 mL | 0.4044 mL | 0.8089 mL | 1.0111 mL |
100 mM | 0.0202 mL | 0.1011 mL | 0.2022 mL | 0.4044 mL | 0.5055 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Camostat is a trypsin-like protease inhibitor, inhibits airway epithelial sodium channel (ENaC) function with IC50 of 50 nM, less potent to trpsin, prostasin and matriptase.
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The serine protease inhibitor camostat mesilate attenuates the progression of chronic kidney disease through its antioxidant effects.[Pubmed:25766432]
Nephron. 2015;129(3):223-32.
BACKGROUND/AIMS: We have so far demonstrated the renoprotective effect of Camostat Mesilate (CM) in 5/6 nephrectomized rats at least partly through its antioxidant effect. However, precise mechanisms were not fully clarified. Therefore, we now examined the renoprotective and antioxidant mechanisms of CM by using the adenine-induced chronic kidney disease (CKD) rat model. METHODS: In protocol 1, we analyzed the effect of CM on CKD. Rats were fed on a 0.75% adenine diet for 3 weeks to induce CKD followed by the experimental period with vehicle, CM, or hydralazine (HYD) treatment for 5 weeks. In protocol 2, we examined the safety of CM and HYD on the normal rats. In addition, we explored free radical scavenging activities of CM and its metabolites in vitro using electron paramagnetic resonance (EPR) spectroscopy. RESULTS: CM, but not HYD, significantly reduced the serum creatinine levels, although both treatments showed similar reduction in the blood pressure. CM decreased mRNA expression and protein levels of fibrotic markers, the severity of renal fibrosis, the accumulation of oxidative stress, and the expression of NADPH oxidase components in the kidney. In the protocol 2, there were no statistically significant differences in general parameters except for the systolic blood pressure in HYD group. EPR study revealed that CM and its metabolites have potent hydroxyl radical scavenging activities in vitro. CONCLUSION: Our findings indicate that CM significantly ameliorates the progression of CKD partly through its antioxidant effect independently from its blood pressure-lowering effect. Our results suggest the possibility that CM could be a new therapeutic agent that could arrest the progression of CKD.
Combination therapy with renin-angiotensin-aldosterone system inhibitor telmisartan and serine protease inhibitor camostat mesilate provides further renoprotection in a rat chronic kidney disease model.[Pubmed:26887332]
J Pharmacol Sci. 2016 Feb;130(2):110-6.
We previously reported that Camostat Mesilate (CM) had renoprotective and antihypertensive effects in rat CKD models. In this study, we examined if CM has a distinct renoprotective effect from telmisartan (TE), a renin-angiotensin-aldosterone system (RAS) inhibitor, on the progression of CKD. We evaluated the effect of CM (400 mg/kg/day) and/or TE (10 mg/kg/day) on renal function, oxidative stress, renal fibrosis, and RAS components in the adenine-induced rat CKD model following 5-weeks treatment period. The combination therapy with CM and TE significantly decreased the adenine-induced increase in serum creatinine levels compared with each monotherapy, although all treatment groups showed similar reduction in blood pressure. Similarly, adenine-induced elevation in oxidative stress markers and renal fibrosis markers were significantly reduced by the combination therapy relative to each monotherapy. Furthermore, the effect of the combination therapy on plasma renin activity (PRA) and plasma aldosterone concentration (PAC) was similar to that of TE monotherapy, and CM had no effect on both PRA and PAC, suggesting that CM has a distinct pharmacological property from RAS inhibition. Our findings indicate that CM could be a candidate drug for an add-on therapy for CKD patients who had been treated with RAS inhibitors.
[Camostat mesilate, a protease inhibitor, inhibits visceral sensitivity and spinal c-fos expression in rats with acute restraint stress].[Pubmed:25345960]
Nan Fang Yi Ke Da Xue Xue Bao. 2014 Oct;34(10):1546-50.
OBJECTIVE: To observe the effect of gut protease activity on visceral hypersensitivity in rats with acute restraint stress. METHODS: Sprague-Dawley rats were given 30, 100 or 300 mg/kg Camostat Mesilate (CM), a protease inhibitor, or saline intragastrically 30 min before acute restraint stress induced by wrapping the fore shoulders, upper forelimbs and thoracic trunk for 2 h. Visceral perception of the rats was quantified as the visceral motor response with an electromyography, and the rectal mucosa and feces protease activity and spinal c-fos expression were measured. RESULTS: CM dose-dependently reduced visceral sensitization elicited by rectal distension, but these doses did not completely inhibit stress-induced visceral sensitization. In normal rats, c-fos expression was found mainly in the superal spinal cord dorsal horn, and after the administration the CM, c-fos-positive cells decreased significantly in all dose groups (P<0.05). In 30 mg/kg CM group, fecal and rectal mucosal protease activity significantly decreased as compared with that in the stress group (P<0.05), and as CM dose increased to 100 and 300 mg/kg, the protease activity decreased even further (P<0.01). CONCLUSION: The gut protease is involved in acute stress-induced visceral hypersensitivity, and CM can lower the visceral sensitivity and spinal c-fos expression in rats.
Acute eosinophilic pneumonia caused by camostat mesilate: The first case report.[Pubmed:27408783]
Respir Med Case Rep. 2016 Jun 16;19:21-3.
Camostat Mesilate is in widespread clinical use mainly to treat chronic pancreatitis, and drug-induced lung injury has not been previously reported. However, pulmonary infiltration with peripheral blood eosinophilia appeared after taking Camostat Mesilate for ten days. The histological findings showed eosinophilic infiltration into the alveolar space and interstitum, and drug lymphocyte stimulation test of peripheral blood was positive. Both peripheral blood eosinophilia and pulmonary involvements improved two weeks later with the cessation of this drug. To the best of our knowledge, this case is the first report of Camostat Mesilate-induced acute eosinophilic pneumonia.
The proteinase inhibitor camostat mesilate suppresses pancreatic pain in rodents.[Pubmed:17433371]
Life Sci. 2007 May 1;80(21):1999-2004.
Camostat Mesilate, an orally available proteinase inhibitor, is clinically used for treatment of pancreatitis. Given recent evidence that pancreatic proteinases including trypsin and/or proteinase-activated receptor-2 (PAR2) might be involved in pancreatic pain, we examined if Camostat Mesilate could suppress spinal Fos expression, a marker for neuronal activation, following specific application of trypsin to the pancreas, and pancreatitis-related referred allodynia. Trypsin, administered into the pancreatic duct, caused delayed expression of Fos proteins in the superficial layer of the bilateral T8 and T9 spinal dorsal horns in rats. The trypsin-induced spinal Fos expression was completely abolished by oral pre-administration of Camostat Mesilate at 300 mg/kg. After hourly repeated (6 times in total) administration of caerulein, mice showed typical symptoms of pancreatitis, accompanied by mechanical allodynia in the upper abdomen (i.e., referred hyperalgesia/allodynia), as assessed by use of von Frey filaments. Camostat Mesilate at 100-300 mg/kg, given orally twice before the 1st and 4th doses of caerulein, abolished the pancreatitis-related abdominal allodynia, while it partially prevented the inflammatory signs. The same doses of Camostat Mesilate, when administered once after the final dose of caerulein, also revealed significant anti-allodynic effect. These data suggest that Camostat Mesilate prevents and/or depresses pancreatitis-induced pain and/or referred hyperalgesia/allodynia, in which proteinases including trypsin would play a critical role.
Gabexate and camostat, synthetic proteinase inhibitors, as direct inducing factors of water and bicarbonate secretion in the isolated and blood-perfused dog pancreas.[Pubmed:1688943]
J Pharmacol Exp Ther. 1990 Jan;252(1):320-6.
The effects of proteinase inhibitors on the secretion of pancreatic juice were investigated in preparations of the isolated and blood-perfused dog pancreas as compared with those of secretin. Each drug tested was administered i.a. Graded doses of gabexate (1-10 mg) elicited dose-dependent biphasic responses for the secretory rates, bicarbonate concentrations and outputs of pancreatic juice, with maximum effects at approximately 5 mg, but had little effect on the protein concentrations. 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. Secretin (0.03-0.3 U) usually produced similar to gabexate-induced results (1-5 mg). Both bicarbonate and protein concentrations of the juice obtained with gabexate or camostat were almost the same as those obtained with secretin at a similar secretory rate of pancreatic juice, suggesting the secretory action of gabexate or camostat might be similar to that of secretin. In addition, gabexate (3 mg) and camostat (10 mg) elicited more than the respective additive secretory responses in the presence of i.a. infusion of a phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (12 micrograms/min) as well as secretin (0.1 U). These results indicate that gabexate and camostat induce water and bicarbonate secretion by acting directly on ductular cells of the dog pancreas, which might be mediated at least partially through cyclic AMP.