Mefenamic AcidAnti-inflammatory agent CAS# 61-68-7 |
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Quality Control & MSDS
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| Cas No. | 61-68-7 | SDF | Download SDF |
| PubChem ID | 4044 | Appearance | Powder |
| Formula | C15H15NO2 | M.Wt | 241.29 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : ≥ 100 mg/mL (414.44 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 2-(2,3-dimethylanilino)benzoic acid | ||
| SMILES | CC1=C(C(=CC=C1)NC2=CC=CC=C2C(=O)O)C | ||
| Standard InChIKey | HYYBABOKPJLUIN-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C15H15NO2/c1-10-6-5-9-13(11(10)2)16-14-8-4-3-7-12(14)15(17)18/h3-9,16H,1-2H3,(H,17,18) | ||
| 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 | Mefenamic acid is a non-steroidal anti-inflammatory agent, which is an inhibitor of cyclooxygenase.
Target: COX
Mefenamic acid is a non-steroidal anti-inflammatory drug used to treat pain, including menstrual pain. It is typically prescribed for oral administration. Mefenamic acid ingestion, usually in excess and over prolonged period is known to produce interstitial nephritis, or less commonly papillary necrosis, with acute renal failure [1]. Mefenamic acid is typically prescribed for oral administration. Mefenamic acid decreases inflammation and uterine contractions by a still-unknown mechanism. However it is thought to be related to the inhibition of prostaglandin synthesis. There is also evidence that supports the use of mefenamic acid for perimenstrual migraine headache prophylaxis, with treatment starting 2 days prior to the onset of flow or 1 day prior to the expected onset of the headache and continuing for the duration of menstruation [2, 3]. References: | |||||
Mefenamic Acid Dilution Calculator
Mefenamic Acid Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 4.1444 mL | 20.722 mL | 41.4439 mL | 82.8878 mL | 103.6098 mL |
| 5 mM | 0.8289 mL | 4.1444 mL | 8.2888 mL | 16.5776 mL | 20.722 mL |
| 10 mM | 0.4144 mL | 2.0722 mL | 4.1444 mL | 8.2888 mL | 10.361 mL |
| 50 mM | 0.0829 mL | 0.4144 mL | 0.8289 mL | 1.6578 mL | 2.0722 mL |
| 100 mM | 0.0414 mL | 0.2072 mL | 0.4144 mL | 0.8289 mL | 1.0361 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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Mefenamic acid is a non-steroidal anti-inflammatory agent, which is an inhibitor of cyclooxygenase.Mefenamic acid is a non-steroidal anti-inflammatory drug used to treat pain, including menstrual pain. It is typically prescribed for oral administration. M
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Molecular docking, synthesis and biological screening of mefenamic acid derivatives as anti-inflammatory agents.[Pubmed:28259712]
Eur J Pharmacol. 2017 Apr 15;801:28-34.
Drug induced gastrointestinal ulceration, renal side effects and hepatotoxicity are the main causes of numerous Non-Steroidal Anti-inflammatory Drugs (NSAIDs). Cyclooxygenase-2 (COX-2) inhibitors discovered to decrease the gastrointestinal issues, but unfortunately, most of them are associated with major cardiovascular adverse effects. Along these lines, various new strategies and frameworks were developed wherein basic alterations of the present medications were accounted for. The aim of the study was to prepare derivatives of Mefenamic Acid to evaluate anti-inflammatory activity with fewer adverse reactions. In this study, molecular docking investigations of outlined derivatives were done utilizing Protein Data Bank (PDB ID-4PH9). Synthesis of heterocyclic compounds was carried out utilizing Dicyclohexylcarbodiimide/4-Dimethylaminopyridine (DCC/DMAP) coupling. Acute toxicity prediction was performed using free online GUSAR (General Unrestricted Structure-Activity Relationships) software. The study indicated most of the compounds under safe category. In-vitro pharmacological assessment of heterocyclic compounds was done for COX-1 and COX-2 enzymes for the determination of selectivity. In vivo pharmacological screening for anti-inflammatory activity and ED50 value were determined utilizing carrageenan induced rat paw edema. Gastro intestinal safety study was carried out on selected compounds and found to be devoid of any gastric ulcer toxicity. Most of the compounds indicated high scores as compared to standard during molecular modelling, analysis and displayed interactions with active amino acids of a COX-2 enzyme. The pharmacological screening uncovered that compound substituted with p-bromophenyl indicated maximum potency.
Mefenamic acid enhances anticancer drug sensitivity via inhibition of aldo-keto reductase 1C enzyme activity.[Pubmed:28259989]
Oncol Rep. 2017 Apr;37(4):2025-2032.
Resistance to anticancer medications often leads to poor outcomes. The present study explored an effective approach for enhancing chemotherapy targeted against human cancer cells. Real-time quantitative real-time polymerase chain reaction (qRT-PCR) analysis revealed overexpression of members of aldo-keto reductase (AKR) 1C family, AKR1C1, AKR1C2, AKR1C3, and AKR1C4, in cisplatin, cis-diamminedichloroplatinum (II) (CDDP)-resistant human cancer cell lines, HeLa (cervical cancer cells) and Sa3 (oral squamous cell carcinoma cells). The genes were downregulated using small-interfering RNA (siRNA) transfection, and the sensitivity to CDDP or 5-fluorouracil (5-FU) was investigated. When the genes were knocked down, sensitivity to CDDP and 5-FU was restored. Furthermore, we found that administration of Mefenamic Acid, a widely used non-steroidal anti-inflammatory drug (NSAID) and a known inhibitor of AKR1Cs, enhanced sensitivity to CDDP and 5-FU. The present study suggests that AKR1C family is closely associated with drug resistance to CDDP and 5-FU, and Mefenamic Acid enhances their sensitivity through its inhibitory activity in drug-resistant human cancer cells. Thus, the use of Mefenamic Acid to control biological function of AKR1C may lead to effective clinical outcomes by overcoming anticancer drug resistance.
Biodegradability of fluoxetine, mefenamic acid, and metoprolol using different microbial consortiums.[Pubmed:28091995]
Environ Sci Pollut Res Int. 2017 Mar;24(7):6779-6793.
The biodegradation of fluoxetine, Mefenamic Acid, and metoprolol using ammonium-nitrite-oxidizing consortium, nitrite-oxidizing consortium, and heterotrophic biomass was evaluated in batch tests applying different retention times. The ammonium-nitrite-oxidizing consortium presented the highest biodegradation percentages for Mefenamic Acid and metoprolol, of 85 and 64% respectively. This consortium was also capable to biodegrade 79% of fluoxetine. The heterotrophic consortium showed the highest ability to biodegrade fluoxetine reaching 85%, and it also had a high potential for biodegrading Mefenamic Acid and metoprolol, of 66 and 58% respectively. The nitrite-oxidizing consortium presented the lowest biodegradation of the three pharmaceuticals, of less than 48%. The determination of the selected pharmaceuticals in the dissolved phase and in the biomass indicated that biodegradation was the major removal mechanism of the three compounds. Based on the obtained results, the biodegradation kinetics was adjusted to pseudo-first-order for the three pharmaceuticals. The values of k biol for fluoxetine, Mefenamic Acid, and metoprolol determined with the three consortiums indicated that ammonium-nitrite-oxidizing and heterotrophic biomass allow a partial biodegradation of the compounds, while no substantial biodegradation can be expected using nitrite-oxidizing consortium. Metoprolol was the less biodegradable compound. The sorption of fluoxetine and Mefenamic Acid onto biomass had a significant contribution for their removal (6-14%). The lowest sorption coefficients were obtained for metoprolol indicating that the sorption onto biomass is poor (3-4%), and the contribution of this process to the global removal can be neglected.
Mefenamic acid decreases inflammation but not joint lesions in experimental osteoarthritis.[Pubmed:28370591]
Int J Exp Pathol. 2016 Dec;97(6):438-446.
Mefenamic Acid is a non-steroidal anti-inflammatory drug able to control the symptoms of osteoarthritis (OA), but its effects on protection of cartilage and bone are still unclear. This study aimed to investigate whether the control of inflammation by Mefenamic Acid translates into decreased joint lesions in experimental OA in rats. OA was induced by injecting 1 mg of monosodium iodoacetate (MIA) into the joints of rats. The animals were treated with Mefenamic Acid (50 mg/kg, daily, oral gavage) either pre-MIA injection (preventive) or post-MIA injection (therapeutic). Joint swelling and hyperalgesia were evaluated at baseline and 1, 3, 14 and 28 days after induction of OA. Intra-articular lavage and kinetics of cell migration into the synovium were measured 3 and 28 days after OA induction. Histopathological analysis, Osteoarthritis Research Society International (OARSI) score, total synovium cells count, cartilage area and levels of proteoglycans in joints were also evaluated. Mefenamic Acid prevented joint oedema and hyperalgesia induced by MIA in the acute phase (3 days) of the disease. In the chronic phase (28 days), preventive and therapeutic regimens decreased the number of mononuclear cells in the joint cavity. In contrast, thickening of the synovium, bone resorption, loss of cartilage and levels of proteoglycans were unaffected by Mefenamic Acid when it was administered either preventively or therapeutically. Thus, Mefenamic Acid had anti-inflammatory effects but did not reduce the progression of OA lesions, thereby indicating that it is only effective for symptomatic control of OA.
