Carbocisteine is a mucolytic, a substance that assists in breaking up mucus in the airways. It is used as adjunctive therapy in respiratory tract disorders associated with thick mucus in the absence of an infection. It is often prescribed in the treatment of bronchitis and chronic obstructive pulmonary disease, reducing mucus viscosity, allowing the sufferer to bring up mucus more easily.
Carbocysteine is a muco-active drug with free radical scavenging and anti-inflammatory properties. It is actually approved for clinical use as adjunctive therapy of respiratory tract disorders characterized by excessive, viscous mucus, including chronic obstructive airways disease (COPD).
Macciò, A., Madeddu, C., Panzone, F., & Mantovani, G. (2009). Carbocysteine: clinical experience and new perspectives in the treatment of chronic inflammatory diseases. Expert opinion on pharmacotherapy, 10(4), 693-703.
Cough, one of the main symptoms of bronchial asthma, is a chronic airway inflammatory disease with functionally damaged bronchial epithelium. Recently, we established an animal model with cough hypersensitivity after antigen challenge and clearly showed the protective effect of carbocysteine in this model. This study was designed to investigate the clinical effect of carbocysteine for cough sensitivity in patients with bronchial asthma.
Ishiura, Y., Fujimura, M., Yamamori, C., Nobata, K., Myou, S., Kurashima, K., ... & Takegoshi, T. (2003). Effect of carbocysteine on cough reflex to capsaicin in asthmatic patients. British journal of clinical pharmacology, 55(6), 504-510.
The aim of the study was to examine the effects of a mucolytic drug, carbocisteine, on rhinovirus (RV) infection in the airways. Human tracheal epithelial cells were infected with a major-group RV, RV14. RV14 infection increased virus titres and the cytokine content of supernatants. Carbocisteine reduced supernatant virus titres, the amount of RV14 RNA in cells, cell susceptibility to RV infection and supernatant cytokine concentrations, including interleukin (IL)-6 and IL-8, after RV14 infection. Carbocisteine reduced the expression of mRNA encoding intercellular adhesion molecule (ICAM)-1, the receptor for the major group of RVs. It also reduced the supernatant concentration of a soluble form of ICAM-1, the number and fluorescence intensity of acidic endosomes in the cells before RV infection, and nuclear factor-kappaB activation by RV14. Carbocisteine also reduced the supernatant virus titres of the minor group RV, RV2, although carbocisteine did not reduce the expression of mRNA encoding a low density lipoprotein receptor, the receptor for RV2. These results suggest that carbocisteine inhibits rhinovirus 2 infection by blocking rhinovirus RNA entry into the endosomes, and inhibits rhinovirus 14 infection by the same mechanism as well as by reducing intercellular adhesion molecule-1 levels. Carbocisteine may modulate airway inflammation by reducing the production of cytokines in rhinovirus infection.
Yasuda, H., Yamaya, M., Sasaki, T., Inoue, D., Nakayama, K., Yamada, M., ... & Sasaki, H. (2006). Carbocisteine inhibits rhinovirus infection in human tracheal epithelial cells. European Respiratory Journal, 28(1), 51-58.