Carbocisteine
(Synonyms: S-(羧甲基)-L-半胱氨酸,S-(Carboxymethyl)-L-cysteine) 目录号 : GC60099
Carbocisteine (S-carboxymethyl-l-cysteine) is a very important pharmaceutical product with mucolitic activity and is normally used for the treatment of bronchitis and colds.
Cas No.:638-23-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Carbocisteine (S-carboxymethyl-l-cysteine) is a very important pharmaceutical product with mucolitic activity and is normally used for the treatment of bronchitis and colds.
| Cas No. | 638-23-3 | SDF | |
| 别名 | S-(羧甲基)-L-半胱氨酸,S-(Carboxymethyl)-L-cysteine | ||
| Canonical SMILES | N[C@@H](CSCC(O)=O)C(O)=O | ||
| 分子式 | C5H9NO4S | 分子量 | 179.19 |
| 溶解度 | 储存条件 | 4°C, protect from light | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.5807 mL | 27.9033 mL | 55.8067 mL |
| 5 mM | 1.1161 mL | 5.5807 mL | 11.1613 mL |
| 10 mM | 0.5581 mL | 2.7903 mL | 5.5807 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Carbocisteine as a Modulator of Nrf2/HO-1 and NFκB Interplay in Rats: New Inspiration for the Revival of an Old Drug for Treating Ulcerative Colitis
Front Pharmacol 2022 Jun 8;13:887233.PMID:35754464DOI:10.3389/fphar.2022.887233.
Ulcerative colitis (UC), an inflammatory bowel disease, is a chronic condition of a multifaceted pathophysiology. The incidence of UC is increasing internationally. The current therapies for UC lack relative effectiveness and are associated with adverse effects. Therefore, novel therapeutic options should be developed. It has been well documented that modulating the Nrf2/NFκB is a promising therapeutic target in inflammation. Carbocisteine is a mucoregulatory medication and its efficacy in COPD was found to be more closely related to its antioxidant and anti-inflammatory properties. Carbocisteine has not yet been examined for the management of UC. Hence, our approach was to investigate the potential coloprotective role of Carbocisteine in acetic acid-induced colitis in rats. Our results revealed that Carbocisteine improved colon histology and macroscopic features and subdued the disease activity as well. Additionally, Carbocisteine attenuated colon shortening and augmented colon antioxidant defense mechanisms via upregulating catalase and HO-1 enzymes. The myeloperoxidase activity was suppressed indicating inhibition of the neutrophil infiltration and activation. Consistent with these findings, Carbocisteine boosted Nrf2 expression along with NFκB inactivation. Consequently, Carbocisteine downregulated the proinflammatory cytokines IL-6 and TNF-α and upregulated the anti-inflammatory cytokine IL-10. Concomitant to these protective roles, Carbocisteine displayed anti-apoptotic properties as revealed by the reduction in the Bax: BCL-2 ratio. In conclusion, Carbocisteine inhibited oxidative stress, inflammatory response, and apoptosis in acetic acid-induced UC by modulating the Nrf2/HO-1 and NFκB interplay in rats. Therefore, the current study provides a potential basis for repurposing a safe and a commonly used mucoregulator for the treatment of UC.
Carbocisteine inhibits the expression of Muc5b in COPD mouse model
Drug Des Devel Ther 2019 Sep 16;13:3259-3268.PMID:31571828DOI:10.2147/DDDT.S198874.
Background: Cigarette smoke (CS) results in chronic mucus hypersecretion and airway inflammation, contributing to COPD pathogenesis. Mucin 5B (MUC5B) and mucin 5 AC (MUC5AC) are major mucins implicated in COPD pathogenesis. Carbocisteine can reduce mucus viscosity and elasticity. Although Carbocisteine decreased human elastase-induced MUC5AC expression in vitro and reduced MUC5AC expression that alleviated bacteria adhesion and improved mucus clearance in vivo, the roles of Carbocisteine in inducing MUC5B expression in COPD remain unclear. Methods: To investigate the Muc5b/Muc5ac ratio and the gene and protein levels of Muc5b in COPD and Carbocisteine intervention models. C57B6J mice were used to develop COPD model by instilling intratracheally with lipopolysaccharide on days 1 and 14 and were exposed to CS for 2 hr twice a day for 12 weeks. Low and high doses of Carbocisteine 112.5 and 225 mg/kg/d, respectively, given by gavage administration were applied for the treatment in COPD models for the same duration, and carboxymethylcellulose was used as control. Carbocisteine significantly attenuated inflammation in bronchoalveolar lavage fluid and pulmonary tissue, improved pulmonary function and protected against emphysema. Results: High-dose Carbocisteine significantly decreased the overproduction of Muc5b (P<0.01) and Muc5ac (P<0.001), and restored Muc5b/Muc5ac ratio in COPD model group (P<0.001). Moreover, the Muc5b/Muc5ac ratio negatively correlated with pro-inflammatory cytokines such as IL-6 and keratinocyte-derived cytokine, mean linear intercept, functional residual capacity and airway resistance, but positively correlated with dynamic compliance. Conclusions: These findings suggest that Carbocisteine attenuated Muc5b and Muc5ac secretion and restored Muc5b protein levels, which may improve mucus clearance in COPD.
Effect of Carbocisteine on patients with COPD: a systematic review and meta-analysis
Int J Chron Obstruct Pulmon Dis 2017 Aug 2;12:2277-2283.PMID:28814855DOI:10.2147/COPD.S140603.
Background: COPD is the fourth leading cause of death in the world. It is a common, progressive, treatable and preventable disease. The exacerbation of COPD is associated with the peripheral muscle force, forced expiratory volume in 1 second (FEV1), the quality of life and mortality. Many studies indicated that the mucoactive medicines could reduce the exacerbations of COPD. This study summarized the efficacy of Carbocisteine as a treatment for COPD. Methods: We searched the randomized controlled trials (RCTs) following electronic bibliographic databases: MedLine, Embase, Cochrane Library and Web of Science. We additionally searched gray literature database: OpenSIGLE. We also additionally searched the clinical trial registers: ClinicalTrials.gov register and International Clinical Trials Registry Platform Search Portal. We used RCTs to assess the efficacy of the treatments. We included studies of adults (older than 18 years) with COPD. We excluded studies that were published as protocol or written in non-English language (Number 42016047078). Findings: Our findings included data from four studies involving 1,357 patients. There was a decrease in the risk of the rate of total number of exacerbations with Carbocisteine compared with placebo (-0.43; 95% confidence interval [CI] -0.57, -0.29, P<0.01). Carbocisteine could also improve the quality of life (-6.29; 95% CI -9.30, -3.27) and reduce the number of patients with at least one exacerbation (0.86; 95% CI 0.78, 0.95) compared with placebo. There was no significant difference in the FEV1 and adverse effects and the rate of hospitalization. Interpretation: Long-term use of Carbocisteine (500 mg TID) may be associated with lower exacerbation rates, the smaller number of patients with at least one exacerbation and higher quality of life of patients with COPD.
The role for S-carboxymethylcysteine (Carbocisteine) in the management of chronic obstructive pulmonary disease
Int J Chron Obstruct Pulmon Dis 2008;3(4):659-69.PMID:19281081doi
Prescription of mucoactive drugs for chronic obstructive pulmonary disease (COPD) is increasing. This development in clinical practice arises, at least in part, from a growing understanding of the important role that exacerbation frequency, systemic inflammation and oxidative stress play in the pathogenesis of respiratory disease. S-carboxymethylcysteine (Carbocisteine) is the most frequently prescribed mucoactive agent for long-term COPD use in the UK. In addition to its mucoregulatory activity, Carbocisteine exhibits free-radical scavenging and anti-inflammatory properties. These characteristics have stimulated interest in the potential that this and other mucoactive drugs may offer for modification of the disease processes present in COPD. This article reviews the pharmacology, in vivo and in vitro properties, and clinical trial evidence for Carbocisteine in the context of guidelines for its use and the current understanding of the pathogenic processes that underlie COPD.
Carbocisteine attenuates hydrogen peroxide-induced inflammatory injury in A549 cells via NF-κB and ERK1/2 MAPK pathways
Int Immunopharmacol 2015 Feb;24(2):306-313.PMID:25533503DOI:10.1016/j.intimp.2014.12.018.
Carbocisteine is a mucolytic drug with anti-oxidative effect, we had previously proved that Carbocisteine remarkably reduced the rate of acute exacerbations and improved the quality of life in patients with chronic obstructive pulmonary disease (COPD), however, very little is known about its mechanisms. In this study, we aimed to investigate the anti-inflammatory effects of Carbocisteine against hydrogen peroxide (H2O2). A549 cells were cultured in vitro and treated with H2O2 as damaged cell models, Carbocisteine was administered 24h prior to or after H2O2 exposure, and the protective effects of Carbocisteine were determined by MTT, qRT-PCR, ELISA, western blot and immunofluorescence assays. The results showed that Carbocisteine could increase cell viability and decrease LDH, IL-6 and IL-8 levels in the supernatant. Additionally, Carbocisteine decreased IL-6, IL-8, TNF-α, IP-10 and MIP-1β mRNA in a dose-dependent manner. Moreover, Carbocisteine could attenuate phosphorylation of NF-κB p65 and ERK1/2 and inhibit the nuclear translocation of pNF-κB p65 induced by H2O2. In conclusion, Carbocisteine inhibited H2O2-induced inflammatory injury in A549 cells, NF-κB and ERK1/2 MAPK were the target pathways.