Nonsteroidal anti-inflammatory drugs (NSAIDs), used in the treatment of numerous diseases, can cause a number of side effects, the main of which is an ulcerogenic effect on the mucous membranes of the gastrointestinal tract. NSAIDs can also cause side effects in the hepato-biliary, cardiovascular, excretory systems, affect the functioning of the liver and lungs [1]. The mechanism of action of NSAIDs is based on the inhibition of the activity of cyclooxygenase (COX), which exists in two main isoforms COX-1 and COX-2, differ structurally and functionally [2, 3]. COX-1 is a constitutive isoform that is expressed throughout the body and synthesizes prostaglandins involved in numerous physiological processes. In particular, with the participation of COX-1, prostaglandins are formed. They regulate the secretion of hydrochloric acid and stimulate the formation of protective mucus in the stomach, influence the process of proliferation and intercellular integration in various organs, regulate vascular homeostasis, platelet aggregation, and kidney function. COX-2 is an inducible form of the enzyme, which expression increases during inflammation, ensuring the synthesis of relatively large concentrations of prostaglandins, that act as the inflammation mediators [4, 5]. Considering the numerous side effects of currently existing NSAIDs, the development of new anti-inflammatory drugs devoid of side effects is actively underway. In this sense, the compounds capable of simultaneous inhibiting the cyclooxygenase and lipoxygenase (LOX) pathways of arachidonic acid metabolism are of significant interest. Dual-acting COX/LOX inhibitors could provide multiple...