폴리(S-카르복시메틸시스테인)

Pharmaceuticals -> Used in Switzerland

Pharmaceuticals -> Listed in ZINC15

141.13 Ų [M+H]+ [CCS Type: DT; Method: stepped-field]

137.2 Ų [M+H]+ [CCS Type: DT; Method: single field calibrated with Agilent tune mix (Agilent)]

130 Ų [M-H]-

This chemical does not meet GHS hazard criteria for 88.9% (16 of 18) of all reports.

Danger

H314 (11.1%): Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]

P260, P264, P280, P301+P330+P331, P302+P361+P354, P304+P340, P305+P354+P338, P316, P321, P363, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 18 reports by companies from 2 notifications to the ECHA C&L Inventory.

R05CB03

R - Respiratory system

QR - Respiratory system

Due to its mucolytic effects, carbocisteine significantly reduces sputum viscosity, cough, dyspnea and fatigue. Additionally, it prevents pulmonary infections by decreasing accumulated mucus in the respiratory tract; this is especially beneficial in preventing exacerbations of COPD caused by bacteria and viruses. It has in-vitro anti-inflammatory activity with some demonstrated action against free radicals.

The hypersecretion of mucus characterizes serious respiratory conditions including asthma, cystic fibrosis (CF), and chronic obstructive pulmonary disease (COPD). It blocks bacterial adherence to cells, preventing pulmonary infections. Glycoproteins (fucomucins, sialomucins and sulfomucins) regulate the viscoelastic properties of bronchial mucus. Increased fucomucins can be found in the mucus of patients with COPD. Carbocisteine serves to restore equilibrium between sialomucins and fucomucins, likely by intracellular stimulation of sialyl transferase enzyme, thus reducing mucus viscosity. A study found that L-carbocisteine can inhibit damage to cells by hydrogen peroxide (H2O2) by activating protein kinase B (Akt) phosphorylation, suggesting that carbocisteine may have antioxidant effects and prevent apoptosis of lung cells. There is some evidence that carbocisteine suppresses NF-κB and ERK1/2 MAPK signalling pathways, reducing TNF-alpha induced inflammation in the lungs, as well as other inflammatory pathways. An in-vitro study found that L-carbocisteine reduces intracellular adhesion molecule 1 (ICAM-1), inhibiting rhinovirus 14 infection, thereby reducing airway inflammation.

Metabolic pathways for carbocisteine include acetylation, decarboxylation, and sulfoxidation, leading to the formation of pharmacologically inactive carbocisteine derivatives. Significant variability exists in metabolism due to genetic polymorphism in sulfoxidation capacity. Two cytosolic enzymes are responsible for the metabolism of carbocisteine: cysteine dioxygenase and phenylalanine 4-hydroxylase. Reduced metabolism can cause increased exposure to carbocisteine, explaining variable clinical response between patients who may polymorphisms affecting the enzymes responsible for carbocisteine metabolism. It is generally accepted that sulfodixation is the main metabolic pathway of carbocisteine, however, one group of researchers found a novel urinary metabolite, S-(carboxymethylthio)-L-cysteine (CMTC). No cysteinyl sulfoxide metabolites were found in the urine of patients taking carbocisteine in this study.

Substances used on humans and other animals that destroy harmful microorganisms or inhibit their activity. They are distinguished from DISINFECTANTS, which are used on inanimate objects.

Agents that increase mucous excretion. Mucolytic agents, that is drugs that liquefy mucous secretions, are also included here.

Carbocisteine is rapidly absorbed in the gastrointestinal tract when taken orally with peak serum concentrations achieved within 1 to 1.7 hours.

About 30% to 60% of an orally administered dose is detected unchanged in the urine.

Carbocisteine penetrates well into the lung and bronchial secretions.

Clearance information for carbocisteine is not readily available in the literature.