DeracoxibCAS# 169590-41-4 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 169590-41-4 | SDF | Download SDF |
| PubChem ID | 3058754 | Appearance | Powder |
| Formula | C17H14F3N3O3S | M.Wt | 397.37 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | SC 046; SC 46; SC 59046 | ||
| Solubility | DMSO : 50 mg/mL (125.83 mM; Need ultrasonic) | ||
| Chemical Name | 4-[3-(difluoromethyl)-5-(3-fluoro-4-methoxyphenyl)pyrazol-1-yl]benzenesulfonamide | ||
| SMILES | COC1=C(C=C(C=C1)C2=CC(=NN2C3=CC=C(C=C3)S(=O)(=O)N)C(F)F)F | ||
| Standard InChIKey | WAZQAZKAZLXFMK-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C17H14F3N3O3S/c1-26-16-7-2-10(8-13(16)18)15-9-14(17(19)20)22-23(15)11-3-5-12(6-4-11)27(21,24)25/h2-9,17H,1H3,(H2,21,24,25) | ||
| 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 | Deracoxib, a selective cyclooxygenase-2 inhibitor, is a non-narcotic, non-steroidal anti-inflammatory drug (NSAID).
IC50 Value: 70 to 150 uM(inhibition of 3 osteosarcoma cell lines) [1]
Target: COX
in vitro: Concentration of deracoxib required for 50% inhibition of cell viability (IC50) was reached in all 3 osteosarcoma cell lines and ranged from 70 to 150 microM, whereas the IC50 for piroxicam was only reached in the POS cell line at 500 microM. Neither deracoxib nor piroxicam induced sufficient toxicity in fibroblasts to reach an IC50. Exposure of osteosarcoma cells to cytotoxic concentrations of deracoxib and piroxicam did not result in DNA fragmentation [1]. Concomitant treatment of cells with piroxicam and deracoxib resulted in significant induction of apoptosis at lower concentrations and accumulation of cells in the G?/G? phase. Significant cytotoxic effects exhibited by the combination of piroxicam and deracoxib against canine mammary carcinoma cells in vitro suggest an attractive approach for the treatment of canine mammary carcinoma [2].
in vivo: Perioperative administration of deracoxib to dogs at 1-2 mg/kg/day for 3 days significantly improves analgesia in the postoperative surgical period after soft tissue surgery [3]. Dogs were treated PO with deracoxib at a dosage of 3 mg/kg/d (1.36 mg/lb/d) as a single-agent treatment for TCC. Tumor response was assessed via radiography, abdominal ultrasonography, and ultrasonographic mapping of urinary bladder masses. Toxic effects of deracoxib administration in dogs were assessed through clinical observations and hematologic and biochemical analyses. 24 dogs for which tumor response was assessed, 4 (17%) had partial remission, 17 (71%) had stable disease, and 3 (13%) had progressive disease; initial response could not be assessed in 2 of 26 dogs. The median survival time was 323 days. Median time to progressive disease was 133 days. Renal, hepatic, and gastrointestinal abnormalities attributed to deracoxib administration were noted in 4% (1/26), 4% (1/26), and 19% (5/26) of dogs, respectively [4]. References: | |||||
Deracoxib Dilution Calculator
Deracoxib Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.5165 mL | 12.5827 mL | 25.1655 mL | 50.3309 mL | 62.9137 mL |
| 5 mM | 0.5033 mL | 2.5165 mL | 5.0331 mL | 10.0662 mL | 12.5827 mL |
| 10 mM | 0.2517 mL | 1.2583 mL | 2.5165 mL | 5.0331 mL | 6.2914 mL |
| 50 mM | 0.0503 mL | 0.2517 mL | 0.5033 mL | 1.0066 mL | 1.2583 mL |
| 100 mM | 0.0252 mL | 0.1258 mL | 0.2517 mL | 0.5033 mL | 0.6291 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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Deracoxib, a selective cyclooxygenase-2 inhibitor, is a non-narcotic, non-steroidal anti-inflammatory drug (NSAID).
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The effects of piroxicam and deracoxib on canine mammary tumour cell line.[Pubmed:23251109]
ScientificWorldJournal. 2012;2012:976740.
Cyclooxygenase (COX) inhibitors, already widely used for the treatment of pain and inflammation, are considered as promising compounds for the prevention and treatment of neoplasia. The aim of our study was to determine the direct antiproliferative effects of nonsteroidal anti-inflammatory drugs (NSAIDs), piroxicam and Deracoxib, at a variety of concentrations as both single and combined treatments on canine mammary carcinoma cell line CMT-U27 and to understand the mechanisms of cell death. MTT assay was performed to determine cell viability, and flow cytometric analyses were performed to evaluate apoptosis and cell cycle alterations. Significant decrease in cell viability was observed at high concentrations of piroxicam and Deracoxib in both single and combined treatments after 72 h incubation. Combined treatment produced a significantly greater inhibition than that caused by either agent alone. Also apoptotic cell number was increased by both drugs at the cytotoxic concentrations. However, concomitant treatment of cells with piroxicam and Deracoxib resulted in significant induction of apoptosis at lower concentrations and accumulation of cells in the G(0)/G(1) phase. Significant cytotoxic effects exhibited by the combination of piroxicam and Deracoxib against canine mammary carcinoma cells in vitro suggest an attractive approach for the treatment of canine mammary carcinoma.
In vitro effects of doxorubicin and deracoxib on oxidative-stress-related parameters in canine mammary carcinoma cells.[Pubmed:25038953]
Acta Vet Hung. 2014 Sep;62(3):372-85.
The present study evaluated the effects of doxorubicin (DOX) and Deracoxib (DER), as single agents and in combination treatments, on antioxidant parameters in the canine mammary carcinoma cell line CMT-U27. The cells were exposed to DOX and DER for 24, 48 and 72 h. The viability and malondialdehyde (MDA), nitric oxide (NO), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSHPx) and total glutathione (GSH) activities of CMT-U27 cells were determined. The half inhibition concentration (IC50) of DOX was found to be approximately 0.9 muM in the 72-h period. IC50 and 1/10 IC50 concentrations of DOX were combined with all concentrations of DER (50-1000 muM) in the combination experiments. The results showed increased oxidative status associated with significant decreases of CAT and GSH levels in CMT-U27 cells exposed to 10-muM and higher concentrations of DOX compared to control cells. In contrast, there were no significant changes in the groups tested with any of the concentrations of DER (50-1000 muM). In combination treatments, DER attenuated DOX-induced oxidative damage by modulating the enzymatic and non-enzymatic components in CMT-U27 cells. We suggest that the combination of DOX and DER can be beneficial in the treatment of cancer cells by increasing cellular responses to oxidative stress. In conclusion, the use of COX inhibitor in conjunction with a chemotherapeutic agent may provide a basis for new concepts of cancer treatment through systematic modulation of the antioxidant defence systems in mammary cancers of animals.
Doxorubicin and deracoxib adjuvant therapy for canine splenic hemangiosarcoma: a pilot study.[Pubmed:23997259]
Can Vet J. 2013 Mar;54(3):237-42.
Canine hemangiosarcoma (HSA) is a highly malignant tumor for which standard chemotherapy has done little to substantially improve survival. Cyclooxygenase-2 (Cox-2) plays a role in the formation, growth, and metastasis of tumors and inhibitors have demonstrated therapeutic benefit with certain canine cancers. In this prospective study, 21 dogs received adjuvant therapy combining the selective Cox-2 inhibitor Deracoxib with doxorubicin, following splenectomy for HSA. The combination was well-tolerated with only low-grade gastrointestinal and hematologic toxicities noted. An overall median survival of 150 days (range; 21 to 1506 days) was noted. Although there was no significant difference in survival based upon stage of disease, dogs with stage III HSA (n = 11) had a median survival of 149 days, which appears to be longer than previously reported. Further studies are warranted to evaluate the potential benefit of Cox-2 inhibitors in the treatment of canine HSA.
Synergistic growth inhibitory effect of deracoxib with doxorubicin against a canine mammary tumor cell line, CMT-U27.[Pubmed:26822118]
J Vet Med Sci. 2016 May 3;78(4):657-68.
Cyclooxygenase (COX) inhibitors have been shown to exert anti-angiogenic and anti-tumor activities on many types of malignant tumors. These anticancer properties make it worthwhile to examine the possible benefit of combining COX inhibitors with other anti-cancer agents. In the present study, we evaluated the potential of Deracoxib (DER) in potentiating antitumor activity of doxorubicin (DOX) in canine mammary carcinoma cells (CMT-U27). DER (50-250 microM) enhanced the antiproliferative activity of DOX by reducing the IC50 (approximately 3- to 3.5 fold). Interaction analysis of the data showed that combinations of DOX at 0.9 microM with DER (100-250 microM) produced synergism in the CMT-U27 cell line, with a ratio index ranging from 1.98 to 2.33. In additional studies identifying the mechanism of observed synergistic effect, we found that DER strongly potentiated DOX-caused G0/G1 arrest in cell cycle progression. Also, DER (100-250 microM) augmented apoptosis induction with approximately 1.35- and 1.37- fold increases in apoptotic response caused by DOX in the cells. DER enhanced the antiproliferative effect of DOX in conjunction with induction of apoptosis by modulation of Bcl-2 expression and changes in the cell cycle of the CMT-U27 cell line. Although the exact molecular mechanism of the alterations in the cell cycle and apoptosis observed with DER and DOX combinations require further investigations, the results suggest that the synergistic effect of DOX and DER combinations in CMT therapy may be achieved at relatively lower doses of DOX with lesser side effects. Therefore, combining DER with DOX may prove beneficial in the clinical treatment of canine mammary cancer.
