| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 1g | 电议 |
| 5g | 电议 |
Cell lines | HEL, Mono Mac 6 and RAW 264.7 cells |
Preparation method | The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below - 20 ℃ for several months. |
Reacting condition | 0.025 ~ 300 μM |
Applications | In HEL cells (COX-1) and LPS-induced Mono Mac 6 cells (COX-2), Ketorolac tromethamine salt inhibited eicosanoid formation with the IC50 value of 0.025 μM and 0.039 μM, respectively. However, in supernatants of LPS-induced RAW 264.7 cells, it did not significantly inhibit NO accumulation at the dose up to 300 μM. |
Animal models | Male Wistar rats |
Dosage form | 0.3 ~ 30 mg/kg; p.o. |
Applications | At all doses, Ketorolac tromethamine salt significantly inhibited COX-1 activity and gastric PG synthesis. At the doses ≥ 1 mg/kg, Ketorolac tromethamine salt inhibited COX-1 activity by 95% and gastric PG synthesis by >88%, without causing obvious gastric damage. At the dose ≤ 3 mg/kg, Ketorolac tromethamine salt did not significantly affect COX-2 activity, but at the doses of 10 and 30 mg/kg, it inhibited COX-2 activity by 75% and 91%, respectively. Meanwhile, it caused significant gastric damage as well. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| 产品描述 | Ketorolac tromethamine salt (RS37619 tromethamine salt) is a non-steroidal anti-inflammatory agent, acting as a nonselective COX inhibitor, with IC50s of 20 nM for COX-1 and 120 nM for COX-2. Ketorolac is a non-steroidal anti-inflammatory agent, acting as a nonselective COX inhibitor, with IC50s of 20 nM for COX-1 and 120 nM for COX-2[1]. Ketorolac tromethamine (0.4%) causes nearly complete inhibition on LPS endotoxin-induced increases in FITC-dextran in the anterior chamber, and increases in aqueous PGE2 concentrations in the aqueous humor in rabbits[1].Ketorolac (30 mg/kg, i.v.) rapidly reverses hyperalgesia in rats. Ketorolac also reduces carrageenan-induced hyperalgesia and paw PG production, and causes reduction in PGE2 levels in rats[1]. Ketorolac (4 mg/kg/day, p.o.) has no detrimental effect in the volume fraction of bone trabeculae formed inside the alveolar socket in rats[2]. Ketorolac (60 μg/10 μL) reduces the histological changes such as ischemic cell death, including cytoplasmic eosinophilia with disintegration of cytoarchitecture and nuclear pyknosis in rats. Ketorolac also effectively reduces neuronal death and improves hindlimb motor function, and the long-term survival is similar to that in the control group[3]. References: |
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