KetorolacCAS# 74103-06-3 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 74103-06-3 | SDF | Download SDF |
| PubChem ID | 3826 | Appearance | Powder |
| Formula | C15H13NO3 | M.Wt | 255.27 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | RS37619 | ||
| Solubility | Soluble in DMSO | ||
| Chemical Name | 5-benzoyl-2,3-dihydro-1H-pyrrolizine-1-carboxylic acid | ||
| SMILES | C1CN2C(=CC=C2C(=O)C3=CC=CC=C3)C1C(=O)O | ||
| Standard InChIKey | OZWKMVRBQXNZKK-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C15H13NO3/c17-14(10-4-2-1-3-5-10)13-7-6-12-11(15(18)19)8-9-16(12)13/h1-7,11H,8-9H2,(H,18,19) | ||
| 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 | Ketorolac(RS37619), a non-selective COX inhibitor, is a non-steroidal anti-inflammatory drug.
Target: COX
Ketorolac is a non-selective COX inhibitor. (R, S)-, (S)-, and (R)-Ketorolac inhibit both isoforms of COX in recombinant rat and human enzyme systems, and similar as inhibitors of rat COX (rCOX) and human COX (hCOX) under the conditions used. (R, S)-Ketorolac inhibits rat COX-1, rat COX-2, human COX-1 and human COX-2 with IC50 of 0.27 μM, 2.06 μM, 1.23 μM and 3.50 μM, respectively. The (S) enantiomer of Ketorolac with IC50 of 0.10 μM for rat COX-1 is approximately twice as potent as the racemate, whereas the (R)-enantiomer with IC50 of > 100 μM is virtually without activity. (R, S)-Ketorolac is significantly more potent than indomethacin or diclofenac sodium in tests of acetic acid-induced writhing, carrageenan-induced paw hyperalgesia, and carrageenan-induced edema formation in rats, with ID50 of 0.24, 0.29 and 0.08 mg/kg, respectively [1]. Ketorolac shows inhibition of eicosanoid formation in HEL cells (COX-1) and LPS-stimulated Mono Mac 6 cells (COX-2) with IC50 of 0.025 μM and 0.039 μM, respectively, but does not significantly inhibit NO accumulation in supernatants of LPS-stimulated RAW 264.7 cells up to 300 μM [2]. Ketorolac significantly inhibits thymidine incorporation of human osteoblasts (hOBs) upon 24 hours treatment in a dose-dependent manner, and inhibits proliferation and arrests cell cycle at G0/G1 phase in hOBs [3]. References: | |||||
Ketorolac Dilution Calculator
Ketorolac Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.9174 mL | 19.5871 mL | 39.1742 mL | 78.3484 mL | 97.9355 mL |
| 5 mM | 0.7835 mL | 3.9174 mL | 7.8348 mL | 15.6697 mL | 19.5871 mL |
| 10 mM | 0.3917 mL | 1.9587 mL | 3.9174 mL | 7.8348 mL | 9.7936 mL |
| 50 mM | 0.0783 mL | 0.3917 mL | 0.7835 mL | 1.567 mL | 1.9587 mL |
| 100 mM | 0.0392 mL | 0.1959 mL | 0.3917 mL | 0.7835 mL | 0.9794 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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Ketorolac(RS37619), a non-selective COX inhibitor, is a non-steroidal anti-inflammatory drug.
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Low doses of tizanidine synergize the anti-nociceptive and anti-inflammatory effects of ketorolac or naproxen while reducing of side effects.[Pubmed:28315341]
Eur J Pharmacol. 2017 Jun 15;805:51-57.
The aim of the present study was to determine whether tizanidine, an alpha2-adrenoceptor agonist, is able to increase the anti-inflammatory and anti-nociceptive effects of naproxen and Ketorolac with a low incidence of gastric injury and spontaneous activity in rats. The anti-inflammatory effect was assayed in a carrageenan test, and oral administration of tizanidine (ED40 =0.94+/-0.2mg/kg), naproxen (ED40=3.18+/-0.4mg/kg), and Ketorolac (ED40=16.4+/-1.9mg/kg) showed a dose-dependent effect on inflammation. The anti-nociceptive effect was assayed in the formalin test, and administration of tizanidine (ED40=0.39+/-0.06mg/kg, p.o.), naproxen (ED40=33.9+/-3.9mg/kg, p.o.) or Ketorolac (ED40=6.49+/-1mg/kg, p.o.) each showed a dose-dependent anti-nociceptive effect. The effects of combinations of tizanidine/naproxen and tizanidine/Ketorolac were determined considering their ED40 at a rate of 1:1. Additionally, the tizanidine/naproxen and tizanidine/Ketorolac combinations showed anti-inflammatory and anti-nociceptive effects. The tizanidine/Ketorolac combination was more potent than tizanidine/naproxen, in both inflammatory (interaction index=0.03 tizanidine/Ketorolac and 0.07 tizanidine/naproxen) and nociceptive (interaction index=0.005 tizanidine/Ketorolac and 0.01 tizanidine/naproxen) processes. In both cases, tizanidine improved naproxen and Ketorolac gastrointestinal tolerability by 50%. Furthermore, co-administration of tizanidine with naproxen or Ketorolac did not modify the spontaneous activity in the same way as individual tizanidine administration. Considering that tizanidine increases the anti-inflammatory and anti-nociceptive effects of naproxen or Ketorolac, with an increase in gastric tolerability, tizanidine could provide therapeutic advantages in the clinical treatment of inflammation and pain.
Ketorolac versus Magnesium Sulfate in Migraine Headache Pain Management; a Preliminary Study.[Pubmed:28286809]
Emerg (Tehran). 2017;5(1):e2. Epub 2017 Jan 8.
INTRODUCTION: Migraine is a common cause of emergency department (ED) visits. To date, there is no recommended drug of choice for pain management of these patients. In the present study, we aimed to evaluate the effectiveness of Ketorolac and magnesium sulfate in this regard. METHODS: This is a cross-sectional study performed on all 18 - 60 year-old patients, visiting two different EDs with complaint of moderate to severe migraine headache. Patients were treated with 30 mg Ketorolac in one hospital and 1 gram magnesium sulfate in the other. Pain scores were assessed on arrival, 1 and 2 hours after drugs administration and quality of pain management was compared between two groups using SPSS 22. RESULTS: 70 patients with the mean age of 36.4 +/- 11.4 years were enrolled (51.4% male). The two groups were similar regarding baseline characteristics (p > 0.05). The improvement in pain score in magnesium sulfate group was greater than Ketorolac group after both one hour (6 vs 3; p < 0.001) and two hours (7 vs 5; p < 0.001). CONCLUSION: It seems that both Ketorolac and magnesium sulfate are significantly effective in pain control of patients with migraine headache presenting to the emergency department. Magnesium sulfate was superior to Ketorolac both one and two hours after drug administration.
Comparative Evaluation of Premedication with Ketorolac and Prednisolone on Postendodontic Pain: A Double-blind Randomized Controlled Trial.[Pubmed:28320541]
J Endod. 2017 May;43(5):667-673.
INTRODUCTION: The present clinical trial aimed to evaluate and compare the effect of a single pretreatment dose of Ketorolac (20 mg), prednisolone (30 mg), and placebo on postendodontic pain in patients undergoing endodontic therapy for irreversible pulpitis or pulpal necrosis using a visual analog scale. METHODS: Ninety-two subjects were included in the present trial; 46 subjects had a pulpal diagnosis of irreversible pulpitis, and the other 46 had pulpal necrosis. These subjects were randomly allocated into 1 of the 3 pretreatment medication groups: Ketorolac (20 mg), prednisolone (30 mg), or a placebo. The drugs were administered 30 minutes before the procedure followed by a routine single-visit root canal treatment. Preoperative and postoperative pain was evaluated using a visual analog scale at 6 time intervals. A comparison between the different groups was performed using one-way analysis of variance followed by the Tukey post hoc test. A comparison of pain within each group at various time intervals was performed using repeated measures analysis of variance followed by the paired t test and Bonferroni correction. RESULTS: At the end of 6 hours, in irreversible pulpitis cases, the Ketorolac group showed an effective reduction in pain scores compared with the other drugs. At the end of 12 hours, the prednisolone group significantly reduced the pain scores compared with the other drugs. CONCLUSIONS: From this study, it could be concluded that a single pretreatment dose of prednisolone has a more sustained effect in reducing postendodontic pain compared with placebo or Ketorolac.
Antihyperalgesic Effects of Indomethacin, Ketorolac, and Metamizole in Rats: Effects of Metformin.[Pubmed:28294366]
Drug Dev Res. 2017 Mar;78(2):98-104.
Preclinical Research Metformin-dependent mechanisms have been implicated in the antinociceptive effect of some non-steroidal anti-inflammatory drugs (NSAIDs). In this study, the effect of local peripheral or systemic administration of metformin on the local peripheral or systemic antinociception induced by indomethacin, Ketorolac and metamizole was assessed in the rat carrageenan-induced thermal hyperalgesia model. Rats were injected with carrageenan (1%, 50 microl) into the right hindpaw which reduced paw withdrawal latency, a measure of thermal hyperalgesia. Local peripheral or systemic administration of indomethacin, Ketorolac or metamizole dose-dependently reduced carrageenan-induced thermal hyperalgesia. Local peripheral pre-treatment with metformin (800 microg/paw) partially inhibited the anti-hyperalgesic effect of indomethacin (200 microg/paw) and metamizole (200 microg/paw), but not that of Ketorolac (200 microg/paw). In contrast, systemic pre-treatment with metformin (200 mg/kg) attenuated the antihyperalgesic effect of metamizole (10 mg/kg), but not that observed with either indomethacin (10 mg/kg) or Ketorolac (10 mg/kg). These findings suggest that some but not all NSAIDs have effects mediated by metformin-dependent mechanisms. Drug Dev Res 78 : 98-104, 2017. (c)2017 Wiley Periodicals, Inc.
