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Development of novel drugs with the anti-inflammatory effect of the chemical origin is an up to date and strategic research area for modern medicinal science. This article represents the results of the experimental anti-inflammatory study of the substance with L486-0021 code using the model of the acute pulmonary edema induced by ammonium chloride toxicosis (the model where exudation dominates). Ammonium chloride irritates the walls of alveoli in the lungs, as the result, the acute hypoxia and acidosis increase permeability of the haemato-pleural barrier and finally results in the alveolar pulmonary edema. The study was performed using Wistar albino female rats weighing 180-200 g. The clinical monitoring included the visual assessment of the state of the animals and their survival value. The effectiveness of therapy was also monitored by biochemical indices (ceruleoplasmin, С-reactive protein, interleukin-1β). The test compound administered in the dose of 10 mg/kg showed the high anti-edemic effect; it also increased the survival of animals and decreased the values of the main indices of acute inflammation. The level of C-reactive protein was decreased by 4 times and interleukin-1β by 2.6 times in relation to the intact control group; as to the value of the therapeutic action substance L486-0021 showed 1.8 times higher effect than the reference drug Xefocam. The substance with L486-0021 code is promising for further study as a potent novel domestic non-steroidal anti-inflammatory drug.

The study of the effect of substance L486-0021 on the course of the experimental pulmonary edema in rats