Abstract
A class of drugs called coxibs (COX-2 inhibitors) were created to help relieve pain and inflammation of osteoarthritis and rheumatoid arthritis with the lowest amount of side effects possible. The presented paper describes a new developed, optimized and validated thin layer chromatographic (TLC)-densitometric procedure for the simultaneous assay of five coxibs: celecoxib, etoricoxib, firecoxib, rofecoxib and cimicoxib. Chromatographic separation was conducted on HPTLC F254 silica gel chromatographic plates as a stationary phase using chloroform–acetone–toluene (12:5:2, v/v/v) as a mobile phase. Densitometric detection was carried out at two wavelengths of 254 and 290 nm. The method was tested according to ICH guidelines for linearity, recovery and specificity. The presented method was linear in a wide range of concentrations for all analyzed compounds, with correlation coefficients greater than 0.99. The method is specific, precise (%RSD < 1) and accurate (more than 95%, %RSD < 2). Low-cost, simple and rapid, it can be used in laboratories for drug monitoring and quality control.
Highlights
The search for new non-steroidal anti-inflammatory drugs (NSAIDs), since the synthesis of salicylic acid, has been carried out simultaneously in two main directions, obtaining compounds with higher anti-inflammatory effects, and compounds with weaker side effects
The goal of the creation of NSAIDs was to stop prostaglandin production as the main cause of inflammation, pain and fever. The mechanism of their action is the inhibition of the cyclooxygenase enzyme responsible for the transformation of arachidonic acid, and the formation of signal molecules—prostaglandins
The elementary description of the differences between the two isoforms is that COX-1 occurs mainly physiologically in the human body, while COX-2 is a constitutive isoform arising primarily in places of tissue damage and dysfunction
Summary
The search for new non-steroidal anti-inflammatory drugs (NSAIDs), since the synthesis of salicylic acid, has been carried out simultaneously in two main directions, obtaining compounds with higher anti-inflammatory effects, and compounds with weaker side effects. The goal of the creation of NSAIDs was to stop prostaglandin production as the main cause of inflammation, pain and fever. The mechanism of their action is the inhibition of the cyclooxygenase enzyme responsible for the transformation of arachidonic acid, and the formation of signal molecules—prostaglandins. As it turned out in later studies, there are two isoforms of this enzyme, COX-1 (along with the COX-3 subtype) and COX-2, and prostaglandins performs many varied and physiologically important functions in the body. The elementary description of the differences between the two isoforms is that COX-1 occurs mainly physiologically in the human body, while COX-2 is a constitutive isoform arising primarily in places of tissue damage and dysfunction
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