Non-steroidal anti-inflammatory drugs ibuprofen

Castell, J.V, Larrauri, A. and Gomez-Lechon, M.J. (1988). A study of the relative hepatotoxi-city in vitro of the non-steroidal anti-inflammatory drugs ibuprofen, flurbiprofen and butibufen. Xenobiotica 18 737-745. 

Analysis of non-steroidal anti-inflammatory drugs (ibuprofen, ketoprofen, naproxen, fenoprofen, flurbiproen, and suprofen) Impurity profiling of ketorolac, a chiral nonsteroidal antiinflammatory drug Impurity profiling of a non-steroidal analgesic drug... 

Shah SJ, Bhandarkar SD, Satoskar RS. Drug interaction between chlorpropamide and non-steroidal anti-inflammatory drugs, ibuprofen and phenylbutazone. Int J Clin Pharmacol Ther Toxicol 1984 22(9) 470-2. 

In 2007, Li and List reported the asymmetric hydrogenation of a-arylaldehydes catalysed by [RuCl2(Xyl-BINAP)(DPEN)], providing the corresponding primary alcohols in excellent enantioselectivities and yields, as shown in Scheme 2.40. As an application of this reaction, the biologically active (5)-enantiomer of the non-steroidal anti-inflammatory drug, ibuprofen, could be... 

Electropherograms of a urine sample (8 ml) spiked with non-steroidal anti-inflammatory drugs (10 p-g/ml each) after direct CE analysis (b) and at-line SPE-CE (c). Peak identification is as follows I, ibuprofen N, naproxen K, ketoprofen P, flurbiprofen. Reprinted from Journal of Chromatography, 6 719, J. R. Veraait et al., At-line solid-phase exti action for capillary electrophoresis application to negatively charged solutes, pp. 199-208, copyright 1998, with permission from Elsevier Science. 

However, it is important to note that the addition of nephrotoxic agents, such as amphotericin B, aminoglysides (e.g., gentamicin, tobramidn, or amikacin), and non-steroidal anti-inflammatory drugs (NSAIDs e.g., naproxen, ibuprofen, or ketorolac) may potentiate the nephrotoxic effects of the calcineurin inhibitors. 

Prostaglandins Arachidonic acid/ damaged cells Cyclooxygenase Sensitization Non-steroidal anti-inflammatory drugs (e.g. aspirin, ibuprofen)... 

Juvenile chronic arthritis is defined as a group of systemic inflammatory disorders affecting children below the age of 16 years. Pharmacotherapy is aimed to reduce pain and non-steroidal anti-inflammatory drugs are used. Ibuprofen is used at a dose of 30-40 mg/kg daily up to a maximum of 2.4 g. Other agents used include diclofenac at a dose of 1-3 mg/kg daily. 

Indometacin, which is a non-steroidal anti-inflammatory drug, inhibits the enzyme cyclo-oxygenase implicated in inflammatory reactions. Indometacin is more effective as an anti-inflammatory agent than ibuprofen and tends to have a higher side-effect profile, including headache, diarrhoea and gastrointestinal disturbances. Rectal administration reduces but does not prevent gastrointestinal tract disturbances. 

Some non-steroidal anti-inflammatory drugs (NSAIDs) were found to have the following capacity factors in a particular mobile on a reverse-phase column aspirin 0.4, naproxen 3.6, ibuprofen 14.5, diclofenac 10.4, paracetamol 0.2. Given that the column had a t of 2 min determine the retention times of the NSAIDs. 

Rovensky J et al Treatment of knee osteoarthritis with a topical non-steroidal anti-inflammatory drug. Results of a randomized, double-blind, placebo-controlled study on the efficacy and safety of a 5% ibuprofen cream. Drugs Exp Clin Res 2001 27 209. [PMID 11951579]... 

Ibuprofen, a well-known, non-steroidal, anti-inflammatory drug (NSAID) used as a common painkiller and marketed under brand names such as Advil and Motrin , provides an example of the switching of processes from one chemical route to another. 

Arylpropionic acids are important class of non-steroidal anti-inflammatory drugs (NSAID). Their pharmacological activity is mainly in one of both enantiomers. Thus, efforts had been made to access to the enantiomerically pure substance. The kinetic resolution of racemic 2-(2-fluoro-4-biphenyl) propanoic acid 56 and 2(4-isobutylphenyl) propanoic acid 59 (Ibuprofen) was performed via enzymatic esterification and transesterification using an alcohol and vinyl acetate, respectively in a membrane reactor. The unreacted acid is obtained in highly enantiomerically enriched form. A consecutive approach consisting of the enzymatic hydrolysis of the resulted esters is needed to achieve the alcohol in optically pure form.77... 

The well known, beneficial influence of non-steroidal anti-inflammatory drugs (NSAID) on the progress of Alzheimer s disease has been confirmed for some NSAID subtypes. The work by Weggen et al. indicates the potential of COX 1 inhibitors (e.g. Diclofenac, Sulindac, Indomethacin, Ibuprofen, but not the most prominent, Aspirin) in PS inhibition [17]. 

An important example is the resolution of the enantiomers of naproxen. Naproxen is a member of a family of compounds known as Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) which are 2-aryl propionic acids. This class also includes ibuprofen, the painkiller developed by Boots and marketed as Nurofen. 

Moclobemide may enhance the effects of non-steroidal anti-inflammatory drugs such as ibuprofen... 

ASA = aspirin NSAIDs = non-steroidal anti-inflammatory drugs, such as ibuprofen, naproxen, and diclofenac CNS stimulants include drugs such as pseudoephedrine, dextroamphetamine, theophylline, and caffeine MAO = monoamine oxidase CNS depressants include drugs such as benzodiazepines, barbiturates, and ethanol SSRIs = selective serotonin reuptake inhibitors, such as fluoxetine, sertraline, and paroxetine. Antidiabetic agents include drugs such as insulin, glipizide, glyburide, and metformin. 

Non-steroidal anti-inflammatory drugs (NSAIDs) are often reported to interfere with the blood pressurelowering action of thiazide diuretics (SED-14, 667). In 17 women with arthritis and hypertension taking fosinopril and hydrochlorothiazide, ibuprofen, sulindac, and nabu-metone, each for 1 month, had no effect on mean arterial pressure (47). These results suggest that the ACE inhibitor fosinopril may neutralize the tendency of NSAIDs to increase blood pressure in thiazide-treated hypertensive patients. However, the design of this study precluded such a conclusion, since no evidence was provided that any of the NSAIDs increased blood pressure in the absence of fosinopril. Furthermore, the numbers were small and the precision of the comparison is likely to have been low. Careful monitoring of blood pressure is necessary when NSAIDs are introduced in thiazide-treated hypertensive patients, even when ACE inhibitors are co-prescribed. 

---