Cyclooxygenase (COX) is a key step in the conversion of arachidonic acid to PGH2. Specifically, PGH2 is a direct substrate for a series of cell-specific prostaglandin and thromboxane syntheses. Besides, COX isomers have been named constitutive (COX-1) and inducible (COX-2). Moreover, COX-1 is expressed in most tissues, while COX-2 is induced by a variety of physiological stimuli. Furthermore, COX-1 and COX-2 catalyze the formation of prostaglandins, thromboxanes, and levulinic anhydride. The expression of COX-1 isoforms is a functional component of homeostasis.
Meanwhile, COX enzymes are clinically important. This inhibition of Cox can alleviate inflammation, fever, thrombosis, neurodegeneration and tumor diseases. Nonetheless, the main function of non-steroidal anti-inflammatory drugs (NSAIDs) is to inhibit cyclooxygenase. Therefore, NSAIDs damage arachidonic acid and eventually convert it into its metabolites. Importantly, the effect of NSAIDs is to the lack of these arachidonic acids. Specifically, thromboxanes play a role in platelet adhesion, prostaglandins cause vasodilation, raise the temperature set point of hypothalamus. Particularly, they play a role in anti-nociception. Most NSAIDs are non-selective and inhibit COX-1 and COX-2. Here, we will introduce an NSAID and a selective COX-1 inhibitor, Tenidap.
Tenidap, a Non-Steroidal Anti-Inflammatory Drug, is a Selective COX-1 Inhibitor.
First of all, Tenidap is a non-steroidal anti-inflammatory drug. Tenidap is a selective COX-1 inhibitor, with IC50 values of 0.03 µM and 1.2 µM for COX-1 and COX-2, respectively. Additionally, Tenidap has anti-inflammatory and antirheumatic properties. Tenidap is also a specific SLC26A3 inhibitor.
In the second place, Tenidap inhibited the hyperpolarization by about 30%, with an estimated IC50 of 2.6 μM about spermatozoa during capacitation. Interestingly, Tenidap blocked ~50% of the HCO3−-induced hyperpolarization.
All in all, Tenidap, a non-steroidal anti-inflammatory drug, is a selective COX-1 inhibitor.