FK 3311Selective COX-2 inhibitor CAS# 116686-15-8 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 116686-15-8 | SDF | Download SDF |
PubChem ID | 164009 | Appearance | Powder |
Formula | C15H13F2NO4S | M.Wt | 341.33 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | DMSO : ≥ 100 mg/mL (292.97 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | N-[4-acetyl-2-(2,4-difluorophenoxy)phenyl]methanesulfonamide | ||
SMILES | CC(=O)C1=CC(=C(C=C1)NS(=O)(=O)C)OC2=C(C=C(C=C2)F)F | ||
Standard InChIKey | DIIYLGZNZGPXRR-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C15H13F2NO4S/c1-9(19)10-3-5-13(18-23(2,20)21)15(7-10)22-14-6-4-11(16)8-12(14)17/h3-8,18H,1-2H3 | ||
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 | Cyclooxygenase-2 (COX-2) inhibitor. Inhibits zymosan-induced prostaglandin E2 production by rat peritoneal neutrophils in vitro and adjuvant-induced arthritis in vivo. Anti-inflammatory. |
FK 3311 Dilution Calculator
FK 3311 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.9297 mL | 14.6486 mL | 29.2972 mL | 58.5943 mL | 73.2429 mL |
5 mM | 0.5859 mL | 2.9297 mL | 5.8594 mL | 11.7189 mL | 14.6486 mL |
10 mM | 0.293 mL | 1.4649 mL | 2.9297 mL | 5.8594 mL | 7.3243 mL |
50 mM | 0.0586 mL | 0.293 mL | 0.5859 mL | 1.1719 mL | 1.4649 mL |
100 mM | 0.0293 mL | 0.1465 mL | 0.293 mL | 0.5859 mL | 0.7324 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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FK 3311, a cell-permeable and orally available sulfonanilide, is a highly selective inhibitor of cyclooxygenase (COX)-2 with IC 50 value of 1.6 μM.
Cyclooxygenase-2 (COX-2) is a membrane bound enzyme that transfers the electrons from cytochrome c to the catalytic subunit 1. The expression of COX-2 is tightly regulated and induced by different mediators such as cytokine, growth factor, and endotoxin.
FK3311 was shown to selectively inhibit consititutive and inducible COX-2 activity in human platelets and mononuclear cells [1].
The component has also been used extensively in various animal models to study the role of COX-2. In ischemia-reperfusion rat model, administration of FK 3311 via the penile vein can significantly reduce the serum levels of aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alanine aminotransferase (ALT) and thromboxane (Tx) B2. However, FK 3311 treatment did not reduce the 6-keto-PG F1a levels in these rats[2]. In addition, liver tissue blood flow was remarkably better in the FK3311 treated rat compared with their control group. Histological examination of the livers revealed that FK3311 treatment reduced the hepatic tissue damage and improved the liver graft function [3]. In the canine lung transplantation model, treatment of FK3311 reduced lung damage, neutrophil infiltration into lung, technetium-99m-albumin accumulation and thromboxane B2 level. The lung with FK3311 treatment had better pulmonary gas exchange and hemodynamics [4].
References:
1.Grossman CJ, Wiseman J, Lucas FS, Trevethick MA, Birch PJ. Inhibition of constitutive and inducible cyclooxygenase activity in human platelets and mononuclear cells by NSAIDs and Cox 2 inhibitors. Inflamm Res 1995,44:253-257.
2.Kobayashi M, Takeyoshi I, Kurabayashi M, Matsumoto K, Morishita Y. The effects of a cyclooxygenase-2 inhibitor, FK3311, on total hepatic ischemia-reperfusion injury of the rat. Hepatogastroenterology 2007,54:522-526.
3.Oshima K, Yabata Y, Yoshinari D, Takeyoshi I. The effect of cyclooxygenase (COX)-2 inhibition on ischemia-reperfusion injury in liver transplantation. J Invest Surg 2009,22:239-245.
4.Sunose Y, Takeyoshi I, Tsutsumi H, Ohwada S, Oriuchi N, Matsumoto K, et al. Effect of a cyclooxygenase-2 inhibitor, FK3311, in a canine lung transplantation model. Ann Thorac Surg 2001,72:1165-1171; discussion 1171-1162.
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Effects of the COX-2 inhibitor FK3311 on ischemia - reperfusion injury in the rat lung.[Pubmed:17613692]
J Invest Surg. 2007 May-Jun;20(3):175-80.
Ischemia-reperfusion injury is induced by activation of the arachidonic acid cascade following the induction of cyclooxygenase-2. This study evaluated the effects of a selective cyclooxygenase-2 inhibitor, FK3311, on warm ischemia-reperfusion injury in the lung. Male Wistar rats were divided into two groups. In the FK3311 group (n = 27), FK3311 (4 mg/kg) was administered intravenously 5 min before ischemia, while in the control group (n = 27) only vehicle was injected. Warm ischemia was induced for 1 h by clamping the left hilus. The arterial oxygen pressure (PaO(2)) and saturation (SaO(2)) were measured 30 and 120 min after reperfusion. Serum thromboxane B(2) and 6-keto-prostaglandin F(1alpha) were also measured 30 min after reperfusion. Lung specimens were harvested 120 min after reperfusion for histologic examination and polymorphonuclear counts, and immunostained with cyclooxygenase-2. The 1-week survival rate in the two groups was compared. PaO(2) and SaO(2) 30 and 120 min after reperfusion were significantly (p < .05) better in the FK3311 group. Serum thromboxane B(2) levels were significantly (p < .05) lower in the FK3311 group. However, there was no significant difference in 6-keto-prostaglandin F(1alpha). Histologically, tissue damage was mild and polymorphonuclear infiltration was reduced in the FK3311 group compared to the control group. The expression of cyclooxygenase-2 in the alveolar epithelium based on immunostaining was suppressed in the FK3311 group. The 1-week survival rate was significantly (p < .05) higher in the FK3311 group. We conclude that FK3311 has protective effects on pulmonary ischemia-reperfusion injury, and results in improvement in the 1-week survival rate.
The effects of a selective cyclooxygenase-2 inhibitor on small bowel ischemia-reperfusion injury.[Pubmed:14696445]
Hepatogastroenterology. 2003 Nov-Dec;50(54):1970-4.
BACKGROUND/AIMS: The purpose of this study was to investigate the effects of a selective COX-2 inhibitor, FK3311, on warm ischemia-reperfusion injury of the canine small intestine. METHODOLOGY: Ten adult mongrel dogs were used. FK (1 mg/kg) was administered intravenously 15 minutes prior to ischemia and 15 minutes prior to reperfusion in the FK group (n = 5), and only an inert vehicle was injected in the control group (n = 5). The superior mesenteric artery and vein were clamped closed for 2 hours and then unclamped for 12 hours of reperfusion. Arterial and intramucosal pH were measured, and samples were taken for histological examination at 1, 3, 6, and 12 hours after the start of reperfusion. Serum thromboxane B2 and 6-keto-prostaglandin F1 alpha (stable metabolites of TxA2 and PGI2) were measured 30 minutes after reperfusion began. RESULTS: Arterial and intramucosal pH changes were significantly (p < 0.05) smaller in the FK group than in the control group. Histological ischemia-reperfusion injury was significantly (p < 0.05) more severe in the control group than in the FK group. Serum thromboxane B2 and 6-keto-prostaglandin F1 alpha levels were significantly (p < 0.05) lower in the FK group compared to the control group. CONCLUSIONS: FK protects the small bowel from ischemia-reperfusion injury by suppression of prostanoid production.
Inhibition of cyclooxygenase-2 improves cardiac function following long-term preservation.[Pubmed:16713604]
J Surg Res. 2006 Oct;135(2):380-4.
BACKGROUND: Cyclooxygenase (COX) is an intracellular enzyme that converts arachidonic acid to prostaglandin endoperoxide (PGG(2)). There are two isoforms of COX, namely constitutive COX-1 and inducible COX-2. It has been reported that COX-2 plays an important role in ischemia-reperfusion injury and that COX-2 mRNA and protein expression were up-regulated during cardiac allograft rejection. FK3311 is a suppressor of COX-2 activation. The purpose of this study was to evaluate the effectiveness of inhibiting COX-2 with FK3311 for the minimization of ischemia-reperfusion injury and for the improvement of donor heart function following transplantation in a canine model. MATERIALS AND METHODS: Adult mongrel dogs were used. After the measurement of hemodynamic parameters [cardiac output (CO), left ventricular pressure (LVP), and the maximum rates of increase and decrease in LVP (+/-LVdp/dt)], coronary vascular beds were washed out with a hypothermic (4 degrees C) University of Wisconsin (UW) solution following cardiac arrest in response to cold (4 degrees C) glucose-insulin-potassium solution. The heart was then excised and preserved in hypothermic (4 degrees C) UW solution for 12 h. FK3311 (3 mg/kg) was administered intravenously to five dogs prior to reperfusion, while vehicle was administered intravenously to a control group (n = 5). After 3 h of orthotopic transplantation using cardiopulmonary bypass, the hemodynamic parameters were compared with preoperative values of the donor animals under the condition of 10 mm Hg right atrial pressure and 5 mug/kg/min dopamine support. RESULTS: The recovery rates of CO and +/-LVdP/dt were significantly (P < 0.05) higher in the FK-treated dogs than in the controls (CO: 93 +/- 6 versus 66% +/- 4%; +LVdp/dt: 125 +/- 8 versus 77 +/- 10%; and -LVdp/dt: 81 +/- 7 versus 52 +/- 6%; for FK-treated versus control dogs, respectively). The recovery rate of LVP was higher in the FK-treated dogs than in the controls (90 +/- 5 versus 72 +/- 5%), but this difference was not statistically significant. Immunohistochemical staining revealed that COX-2 expression was reduced significantly in the myocardium of FK-treated dogs compared with controls. CONCLUSION: Hemodynamic parameters following transplantation were improved significantly in dogs treated with FK3311. Therefore, the inhibition of COX-2 improves transplanted cardiac function following long-term preservation.
The effects of a cyclooxygenase-2 inhibitor, FK3311, on total hepatic ischemia-reperfusion injury of the rat.[Pubmed:17523312]
Hepatogastroenterology. 2007 Mar;54(74):522-6.
BACKGROUND/AIMS: This study was designed to investigate the effects of a selective cyclooxygenase-2 inhibitor, FK3311, on warm ischemia-reperfusion injury of the rat liver. METHODOLOGY: Male Sprague-Dawley rats were used in this experimental study. Total hepatic ischemia was induced with a clamping portal triad. The animals were divided into two groups: the control group and the FK group, in which FK3311 (FK, 1.0 mg/kg) was administered via the penile vein. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were measured 2 h after reperfusion, while those of thromboxane (Tx) B2 and 6-ketoprostaglandin (PG) F1alpha (stable metabolites of TxA2 and PGI2) were measured 30 min after reperfusion. The liver tissue blood flow was measured at preischemia, end-ischemia, and 30, 60, 90, and 120 min after reperfusion. The liver tissues obtained from animals at 2h after reperfusion were excised for histopathology. RESULTS: The serum levels of AST, ALT, and LDH were significantly lower in the FK group than in the control group. Similarly, in the FK group, the serum levels of TxB2 were significantly lower than in the control group. By contrast, the 6-keto-PG F1a levels were not significantly reduced. The liver tissue blood flow at 120 min after reperfusion was significantly higher in the FK group than in the control group. The histopathological study showed that hepatic tissue damage was milder in the FK group than in the control group. CONCLUSIONS: FK has protective effects on hepatic ischemia-reperfusion injury stemming from the marked inhibition of TxA2.
The effects of cyclooxygenase (COX)-2 inhibition on ischemia-reperfusion injury in liver transplantation.[Pubmed:19842898]
J Invest Surg. 2009 Jul-Aug;22(4):239-45.
PURPOSE: Our objective was to evaluate whether COX-2 inhibition with FK3311, a selective cyclooxygenase (COX)-2 inhibitor, improves transplanted liver function. METHODS: Inbred male Lewis rats weighing 200-260 g were used. The donor liver was perfused with cold University of Wisconsin (UW) solution and then stored in the same solution at 4 degrees C for 18 hr. After the preservation period, orthotopic liver transplantation was performed. Animals were divided into three groups: the control group; the FK low-dose group (1 mg/kg FK3311 i.v. 20 min before reperfusion); and the FK high-dose group (3 mg/kg FK3311 i.v. 20 min before reperfusion). Survival rate, serum GOT and GPT levels, liver tissue blood flow, and serum thromboxane B(2) (TxB(2)) levels were compared among groups. RESULTS: Survival rate was significantly better (p <. 05) and serum GOT levels 30 min after reperfusion were significantly lower (p <. 05) in the FK high-dose group compared to the other two groups. Four hours after reperfusion, GPT levels and liver tissue flow were significantly (p <. 05) better in the FK high-dose group compared to the control. Both 30 min and 4 hr after reperfusion, serum TxB(2) levels were significantly lower in the FK high-dose group compared to the control (p <. 05). CONCLUSION: COX-2 activity results in deteriorated liver function after I/R injury associated with transplantation, and selective COX-2 inhibition improved liver graft function.
Studies on antiinflammatory agents. I. Synthesis and pharmacological properties of 2'-phenoxymethanesulfonanilide derivatives.[Pubmed:1446362]
Chem Pharm Bull (Tokyo). 1992 Sep;40(9):2399-409.
Various 2'-phenoxymethanesulfonanilide derivatives were synthesized and evaluated for antiinflammatory and analgesic activities. Some compounds bearing an electron-attracting substituent at the 4'-position strongly inhibited adjuvant-induced arthritis in rats and acetic acid-induced writhing syndrome in mice without causing gastro-intestinal irritation. Among them, 4'-cyano-(FK867) and 4'-acetyl-(FK3311) 2'-(2,4-difluorophenoxy)methanesulfonanilides were selected as the candidates for further development.