Colistin
(Synonyms: 抗敌素; Polymyxin E) 目录号 : GC43298
An antibiotic
Cas No.:1066-17-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Colistin is a complex antibiotic containing greater than 30 components, with the cyclic polypeptide antibiotics polymyxins E1 (colistin A) and E2 (colistin B) as the major components. It was originally isolated from B. polymyxa. Colistin inhibits the growth of the Gram-negative bacteria E. coli, P. aeruginosa, P. fluorescens, and S. enterica (MICs = 0.04-2.08 μg/ml) and Gram-positive L. ivanovii and L. monocytogenes (MICs = 2.5-10 μg/ml) but is not active against Gram-positive L. lactis, P. polymyxa, P. acidilactici, or S. aureus at concentrations up to 5 μg/ml. It also inhibits the growth of clinical isolates of both susceptible and multidrug-resistant P. aeruginosa (MICs = 1-2 mg/l). Colistin binds selectively to LPS from susceptible strains of K. pneumoniae compared to resistant strains (Kis = 0.56 and 2.83 μM, respectively), which may contribute to its mechanism of action against Gram-negative bacteria. In vivo, colistin slows the growth of P. aeruginosa and A. baumannii in a neutropenic mouse model of thigh infection.
| Cas No. | 1066-17-7 | SDF | |
| 别名 | 抗敌素; Polymyxin E | ||
| 分子式 | C53H100N16O13 (for E1) | 分子量 | 1169.5 |
| 溶解度 | PBS (pH 7.2): 10 mg/ml | 储存条件 | Store at -20°C |
| 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 | 0.8551 mL | 4.2753 mL | 8.5507 mL |
| 5 mM | 0.171 mL | 0.8551 mL | 1.7101 mL |
| 10 mM | 0.0855 mL | 0.4275 mL | 0.8551 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。
Colistin and its role in the Era of antibiotic resistance: an extended review (2000-2019)
Emerg Microbes Infect 2020 Dec;9(1):868-885.PMID:32284036DOI:10.1080/22221751.2020.1754133.
Increasing antibiotic resistance in multidrug-resistant (MDR) Gram-negative bacteria (MDR-GNB) presents significant health problems worldwide, since the vital available and effective antibiotics, including; broad-spectrum penicillins, fluoroquinolones, aminoglycosides, and β-lactams, such as; carbapenems, monobactam, and cephalosporins; often fail to fight MDR Gram-negative pathogens as well as the absence of new antibiotics that can defeat these "superbugs". All of these has prompted the reconsideration of old drugs such as polymyxins that were reckoned too toxic for clinical use. Only two polymyxins, polymyxin E (Colistin) and polymyxin B, are currently commercially available. Colistin has re-emerged as a last-hope treatment in the mid-1990s against MDR Gram-negative pathogens due to the development of extensively drug-resistant GNB. Unfortunately, rapid global resistance towards Colistin has emerged following its resurgence. Different mechanisms of Colistin resistance have been characterized, including intrinsic, mutational, and transferable mechanisms.In this review, we intend to discuss the progress over the last two decades in understanding the alternative Colistin mechanisms of action and different strategies used by bacteria to develop resistance against Colistin, besides providing an update about what is previously recognized and what is novel concerning Colistin resistance.
Colistin Resistance in Aeromonas spp
Int J Mol Sci 2021 Jun 1;22(11):5974.PMID:34205867DOI:10.3390/ijms22115974.
The increase in the use of antimicrobials such as Colistin for the treatment of infectious diseases has led to the appearance of Aeromonas strains resistant to this drug. However, resistance to Colistin not only occurs in the clinical area but has also been determined in Aeromonas isolates from the environment or animals, which has been determined by the detection of mcr genes that confer a resistance mechanism to Colistin. The variants mcr-1, mcr-3, and mcr-5 have been detected in the genus Aeromonas in animal, environmental, and human fluids samples. In this article, an overview of the resistance to Colistin in Aeromonas is shown, as well as the generalities of this molecule and the recommended methods to determine Colistin resistance to be used in some of the genus Aeromonas.
Colistin, mechanisms and prevalence of resistance
Curr Med Res Opin 2015 Apr;31(4):707-21.PMID:25697677DOI:10.1185/03007995.2015.1018989.
Background: Infections caused by multi-drug-resistant Gram-negative bacteria, particularly Acinetobacter baumannii, Pseudomonas aeruginosa and Klebsiella pneumoniae, that cause nosocomial infections, represent a growing problem worldwide. The rapid increase in the prevalence of Gram-negative pathogens that are resistant to fluoroquinolones and aminoglycosides as well as all β-lactams, including carbapenems, monobactam, cephalosporins and broad-spectrum penicillins, has prompted the reconsideration of Colistin as a valid therapeutic option. Colistin is an old class of cationic, which act by disrupting the bacterial membranes resulting in cellular death. Although there has been a significant recent increase in the data gathered on Colistin, focusing on its chemistry, antibacterial activity, mechanism of action and resistance, pharmacokinetics, pharmacodynamics and new clinical application, the prevalence of Colistin resistance has been very little reported in the literature. This review concentrates on recent literature aimed at optimizing the clinical use of this important antibiotic. Methods: The available evidence from various studies (microbiological and clinical studies, retrieved from the PubMed, and Scopus databases) regarding the mechanisms and prevalence of resistance was evaluated. Results: Increasing use of Colistin for treatment of infections caused by these bacteria has led to the emergence of Colistin resistance in several countries worldwide. Although resistance to polymyxins is generally less than 10%, it is higher in the Mediterranean and South-East Asia (Korea and Singapore), where Colistin resistance rates are continually increasing. Conclusion: There is a critical need for effective infection prevention and control measures and strict use of antibiotics in the world to control the rise and spread of Colistin resistance.
Clinical Pharmacokinetics and Pharmacodynamics of Colistin
Clin Pharmacokinet 2017 Dec;56(12):1441-1460.PMID:28550595DOI:10.1007/s40262-017-0561-1.
In this review, we provide an updated summary on Colistin pharmacokinetics and pharmacodynamics. Colistin is an old molecule that is frequently used as last-line treatment for infections caused by multidrug-resistant Gram-negative bacteria. Colistin is a decapeptide administered either as a prodrug, Colistin methanesulfonate (CMS), when used intravenously, or as Colistin sulfate when used orally. Because Colistin binds to laboratory materials, many experimental issues are raised and studies on Colistin can be tricky. Due to its large molecular weight and its cationic properties at physiological pH, Colistin passes through physiological membranes poorly and is mainly distributed within the extracellular space. Renal clearance of Colistin is very low, but the dosing regimen should be adapted to the renal function of the patient because CMS is partly eliminated by the kidney. Therapeutic drug monitoring of Colistin is warranted because the pharmacokinetics of Colistin are very variable, and because its therapeutic window is narrow. Resistance of bacteria to Colistin is increasing worldwide in parallel to its clinical and veterinary uses and a plasmid-mediated resistance mechanism (MCR-1) was recently described in animals and humans. In vitro, bacteria develop various resistance mechanisms rapidly when exposed to Colistin. The use of a loading dose might reduce the emergence of resistance but the use of Colistin in combination also seems necessary.
Dosing guidance for intravenous Colistin in critically-ill patients
Clin Infect Dis 2017 Mar 1;64(5):565-571.PMID:28011614DOI:10.1093/cid/ciw839.
Background: Intravenous Colistin is difficult to use because plasma concentrations for antibacterial effect overlap those causing nephrotoxicity, and there is large inter-patient variability in pharmacokinetics. The aim was to develop dosing algorithms for achievement of a clinically desirable average steady-state plasma Colistin concentration (Css,avg) of 2mg/L. Methods: Plasma concentration-time data from 214 adult critically-ill patients (creatinine clearance 0-236mL/min; 29 receiving renal replacement therapy (RRT)) were subjected to population pharmacokinetic analysis. Development of an algorithm for patients not receiving RRT was based upon the relationship between the dose of colistimethate that would be needed to achieve a desired Css,avg and creatinine clearance. The increase in Colistin clearance when patients were on RRT was determined from the population analysis and guided the supplemental dosing needed. To balance potential antibacterial benefit against risk of nephrotoxicity the algorithms were designed to achieve target attainment rates of >80% for Css,avg ≥2 and <30% for Css,avg ≥4mg/L. Results: When algorithm doses were applied back to individual patients not on RRT (including patients prescribed intermittent dialysis on a non-dialysis day), >80% of patients with creatinine clearance <80mL/min achieved Css,avg ≥2mg/L; but for patients with creatinine clearance ≥80mL/min target attainment was <40%, even with the maximum allowed daily dose of 360mg Colistin base activity. For patients receiving RRT, target attainment rates were >80% with the proposed supplemental dosing. In all categories of patients, <30% of patients attained Css,avg ≥4mg/L. Conclusions: The project has generated clinician-friendly dosing algorithms and pointed to circumstances where intravenous monotherapy may be inadequate.