Pharmacological effectsLung surface-active substances are a mixture of phospholipids and specific proteins as the main components, distributed on the inner surface of alveoli. Its main function is to reduce the surface tension of the lung. The surface tension-reducing properties of pulmonary surfactants are essential for maintaining alveolar stability, avoiding alveolar atrophy at the end of expiration, and maintaining adequate gas exchange throughout the entire ventilatory cycle. Severe respiratory failure in preterm infants due to lung surfactant deficiency, regardless of the cause, is referred to as respiratory distress syndrome (RDS) or pulmonary hyaline membrane disease (HMD).RDS is a major cause of acute morbidity and mortality in preterm infants, and also causes long-term respiratory and neurologic sequelae. This product was developed with the aim of intratracheal titration of exogenous surface-active substances to alternatively compensate for the lack of endogenous pulmonary surface-active substances. The surface activity of this product helps it to be evenly distributed in the lungs, unfolding along the air-liquid interface of the alveoli. The physiologic and therapeutic effects of this product for the treatment of surfactant deficiency have been demonstrated in different animal models. Preterm fetal rabbits delivered by cesarean section and immediately put to death showed a significant improvement in lung expansion after immediate administration of the product. Preterm neonatal rabbits ventilated with 100% oxygen and given the product via endotracheal intubation showed significant improvement in tidal volume and pneumothoracic compliance compared to control animals. Treatment of preterm neonatal rabbits with this product (maintaining a standardized tidal volume of approximately 10 mg/kg) improves lung-thoracic system compliance to a level similar to that of mature neonatal animals. Large-scale international open and controlled clinical trials have demonstrated the therapeutic effect of Solidus in children with RDS and preterm infants at risk for RDS. In preterm neonates with a single dose of the product (1.25-2.5 ml/kg equals 100-200 mg/kg), there was a rapid and significant improvement in oxygenation, with a decrease in the concentration of inspired oxygen (F1O2) and an increase in the ratios of PaO2, PaO2/FiO2, and a/APO2; and a decrease in the rate of morbidity, mortality, and the incidence of major pulmonary comorbidities. A second or third administration of 100 mg/kg further reduced the incidence of pneumothorax and morbidity and mortality. Toxicological studies of acute toxicity in animals of different species administered intraperitoneally and intratracheally revealed no signs of pulmonary or systemic toxicity, and no deaths occurred. Subacute (14-day) endotracheal toxicity studies in dogs, rabbits, and rats showed neither clinical effects nor hematologic nor gross changes related to treatment. Furthermore, there was no evidence of any direct toxicity in rats administered via the intraperitoneal route (4 weeks). Administration via the parenteral route in guinea pigs neither triggered active allergic reactions nor stimulated antibody production in passive skin sensitization tests. No allergic reactions were observed with intratracheal administration. Moreover, there was no evidence of skin sensitization potential (Magnusson and Kligman test) The product does not have any mutagenic or teratogenic activity.