Vancomycin
(Synonyms: 万古霉素) 目录号 : GC37885
万古霉素（Vancomycin）是干扰肠道微生物群的有效抗生素之一。
Cas No.:1404-90-6
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
|
Cell lines |
B. burgdorferi |
|
Preparation Method |
Vancomycin was added at a final concentration of 0.5 -2.0 µg/mL into exponentially growing Borrelia spirochetes and incubated for up to 48 h. |
|
Reaction Conditions |
0.5-2.0 µg/mL Vancomycinfor 48 h |
|
Applications |
Low to moderate doses of vancomycin ( 2.0 µg/mL for 24 h) produced small alterations in cell shape and that as the dose was increased, cell speed decreased. Vancomycin concentrations >1.0 µg/mL also inhibited cell growth and led to bleb formation on a fraction of the cells. |
| Animal experiment [2]: | |
|
Animal models |
C57BL/6 (Th1) and BALB/c (Th2) of 6-8 weeks |
|
Preparation Method |
Both Th1 (C57BL/6)- and Th2 (BALB/c)-biased mice were treated with vancomycin (at 50 mg per kg of body weight) for six consecutive days. 0.5 ml of vancomycin was orally gavaged twice daily at a gap of 12 h. Following the withdrawal of 6 days of treatment with vancomycin, mice were observed for 60 days. |
|
Dosage form |
50 mg/kg twice daily at a gap of 12 h,oral |
|
Applications |
The gut microbiome profiling, behavior, and immune responses varied significantly between Th1- and Th2-biased mice. By withdrawing the treatment with vancomycin of major gut microbes, important physiological and behavioral changes of both mice strains returned to the normal (untreated control) level. |
|
References: [1]. Harman MW, Hamby AE, et,al. Vancomycin Reduces Cell Wall Stiffness and Slows Swim Speed of the Lyme Disease Bacterium. Biophys J. 2017 Feb 28;112(4):746-754. doi: 10.1016/j.bpj.2016.12.039. PMID: 28256234; PMCID: PMC5340155. |
|
Vancomycin is one of the potent antibiotics to perturb the gut microbiota [1]. Vancomycin treatment caused a significant alteration in the composition and diversity of the commensal gut microbiota of the host[2].Vancomycin specifically blocks peptide cross-linking in the bacterial peptidoglycan by recognizing terminal peptide sequences and blocking their binding site to enzymatic cross-linkers. Vancomycin has previously been shown to be active against B. burgdorferi in vitro[5,6].
Low to moderate doses of vancomycin ( 2.0 μg/mL for 24 h) produced small alterations in cell shape and that as the dose was increased, cell speed decreased. Vancomycin concentrations >1.0 μg/mL also inhibited cell growth and led to bleb formation on a fraction of the cells[3]. The addition of vancomycin at a concentration of 10ug/ml-1 to the wash solution of the cell-saver achieved similar concentrations in the autologous blood concentrate recovered allowing for bacterial removal, with negative blood cultures in all cases[4].
Metagenomic analysis of gut microbiota revealed that the treatment with vancomycin caused a significant decrease in the relative abundance of Firmicutes and Bacteroidetes phyla with a time-dependent increase in Proteobacteria and Verrucomicrobia phyla. Maximum restoration (> 70%) of gut microbiota happened by the 15th day of withdrawal of vancomycin. BALB/c mice showed a more efficient restoration of gut microbiota compared to C57BL/6 mice[7]. Mice treated with vancomycin alone had a better clinical outcome in the treatment phase of CDI than mice treated with metronidazole alone[8].
References:
[1]. Carding S, Verbeke K, et,al.Dysbiosis of the gut microbiota in disease. Microb Ecol Health Dis. 2015 Feb 2;26:26191. doi: 10.3402/mehd.v26.26191. PMID: 25651997; PMCID: PMC4315779.
[2]. Vrieze A, Out C, et,al. Impact of oral vancomycin on gut microbiota, bile acid metabolism, and insulin sensitivity. J Hepatol. 2014 Apr;60(4):824-31. doi: 10.1016/j.jhep.2013.11.034. Epub 2013 Dec 6. PMID: 24316517
[3]. Harman MW, Hamby AE, et,al. Vancomycin Reduces Cell Wall Stiffness and Slows Swim Speed of the Lyme Disease Bacterium. Biophys J. 2017 Feb 28;112(4):746-754. doi: 10.1016/j.bpj.2016.12.039. PMID: 28256234; PMCID: PMC5340155.
[4]. Perez-Ferrer A, Gredilla-Díaz E, et,al. Vancomycin added to the wash solution of the cell-saver. Effect on bacterial contamination. Rev Esp Anestesiol Reanim. 2017 Apr;64(4):185-191. English, Spanish. doi: 10.1016/j.redar.2016.10.002. Epub 2017 Jan 13. PMID: 28094033.
[5]. Dever LL, Jorgensen JH, et,al. In vitro activity of vancomycin against the spirochete Borrelia burgdorferi. Antimicrob Agents Chemother. 1993 May;37(5):1115-21. doi: 10.1128/AAC.37.5.1115. PMID: 8517700; PMCID: PMC187913
[6]. Hunfeld KP, Weigand J, et,al.In vitro activity of mezlocillin, meropenem, aztreonam, vancomycin, teicoplanin, ribostamycin and fusidic acid against Borrelia burgdorferi. Int J Antimicrob Agents. 2001 Mar;17(3):203-8. doi: 10.1016/s0924-8579(00)00342-3. PMID: 11282265.
[7]. Ray P, Pandey U, et,al.Vancomycin-Induced Changes in Host Immunity and Behavior: Comparative Genomic and Metagenomic Analysis in C57BL/6 and BALB/c Mice. Dig Dis Sci. 2021 Nov;66(11):3776-3791. doi: 10.1007/s10620-020-06729-x. Epub 2021 Jan 1. PMID: 33386517.
[8]. Erikstrup LT, Aarup M, et,al.Treatment of Clostridium difficile infection in mice with vancomycin alone is as effective as treatment with vancomycin and metronidazole in combination. BMJ Open Gastroenterol. 2015 Nov 2;2(1):e000038. doi: 10.1136/bmjgast-2015-000038. PMID: 26568840; PMCID: PMC4641438.
万古霉素是扰乱肠道微生物群的强效抗生素之一[1]。万古霉素处理引起宿主肠道共生菌群组成和多样性的显着改变[2]。万古霉素通过识别末端肽序列并阻断它们的结合，特异性阻断细菌肽聚糖中的肽交联酶促交联剂的位点。万古霉素先前已被证明在体外对伯氏疏螺旋体具有活性[5,6]。
低至中等剂量的万古霉素（2.0 μg/mL，持续 24 小时）使细胞形状发生微小变化，并且随着剂量增加，细胞速度降低。万古霉素浓度 >1.0 μg/mL 也抑制细胞生长并导致部分细胞形成气泡[3]。将浓度为 10ug/ml-1 的万古霉素添加到细胞保护剂的洗涤液中，在回收的自体血液浓缩液中达到相似的浓度，允许去除细菌，所有情况下血培养均为阴性[4].
肠道微生物群的宏基因组分析显示，万古霉素治疗导致厚壁菌门和拟杆菌门的相对丰度显着降低，而变形菌门和疣微菌门的相对丰度随时间增加。肠道微生物群的最大恢复 (> 70%) 发生在停用万古霉素的第 15 天。与 C57BL/6 小鼠相比，BALB/c 小鼠肠道菌群恢复更有效[7]。单独使用万古霉素治疗的小鼠在 CDI 治疗阶段的临床结果优于单独使用甲硝唑治疗的小鼠[8]。
| Cas No. | 1404-90-6 | SDF | |
| 别名 | 万古霉素 | ||
| 分子式 | C66H75Cl2N9O24 | 分子量 | 1449.25 |
| 溶解度 | 125 mg/mL in DMSO(ultrasonic and warming and heat to 60°C) | 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 0.69 mL | 3.4501 mL | 6.9001 mL |
| 5 mM | 0.138 mL | 0.69 mL | 1.38 mL |
| 10 mM | 0.069 mL | 0.345 mL | 0.69 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。
Renaissance of Vancomycin: approaches for breaking antibiotic resistance in multidrug-resistant bacteria
Can J Microbiol 2020 Jan;66(1):11-16.PMID:31545906DOI:10.1139/cjm-2019-0309.
The emergence of multidrug-resistant bacteria demands innovations in the development of new antibiotics. For decades, the glycopeptide antibiotic Vancomycin has been considered as the "last resort" treatment of severe infections caused by Gram-positive bacteria. Since the discovery of the first vancomycin-resistant enterococci strains in the late 1980s, the number of resistances has been steadily rising, with often life-threatening consequences. As an alternative to the generation of completely new substances, novel approaches focus on structural modifications of established antibiotics such as Vancomycin to overcome these resistances. Here, we provide an overview of several promising modifications of Vancomycin to restore its efficacy against vancomycin-resistant enterococci.
Vancomycin
Mayo Clin Proc 1991 Nov;66(11):1165-70.PMID:1943250DOI:10.1016/s0025-6196(12)65799-1.
Vancomycin is a glycopeptide antibiotic that is active against staphylococci, streptococci, and other gram-positive bacteria. It is the drug of choice for the treatment of infections due to methicillin-resistant staphylococci, Corynebacterium jeikeium, and multiply resistant strains of Streptococcus pneumoniae. Vancomycin is an alternative treatment for serious staphylococcal and streptococcal infections, including endocarditis, when allergy precludes the use of penicillins and cephalosporins. Vancomycin is bactericidal against most strains of staphylococci and nonenterococcal streptococci. Although rare strains of staphylococci and enterococci that are resistant to Vancomycin have been reported, bacterial resistance has thus far not emerged as a major clinical problem despite widespread use of Vancomycin. When therapy is monitored by periodic determinations of serum concentrations of the drug and rapid infusion rates are avoided, Vancomycin is rarely associated with serious toxicity.
The pharmacokinetic and pharmacodynamic properties of Vancomycin
Clin Infect Dis 2006 Jan 1;42 Suppl 1:S35-9.PMID:16323118DOI:10.1086/491712.
Vancomycin is one of only a few antibiotics available to treat patients infected with methicillin-resistant Staphylococcus aureus and methicillin-resistant, coagulase-negative Staphylococcus species. Therefore, understanding the clinical implications of the pharmacokinetic and pharmacodynamic properties of Vancomycin is a necessity for clinicians. Vancomycin is a concentration-independent antibiotic (also referred to as a "time-dependent" antibiotic), and there are factors that affect its clinical activity, including variable tissue distribution, inoculum size, and emerging resistance. This article reviews the pharmacokinetic and pharmacodynamic data related to Vancomycin and discusses such clinical issues as toxicities and serum concentration monitoring.
Vancomycin: a history
Clin Infect Dis 2006 Jan 1;42 Suppl 1:S5-12.PMID:16323120DOI:10.1086/491709.
Vancomycin became available for clinical use >50 years ago but was soon discarded in favor of other antibiotics that were deemed to be more efficacious and less toxic. The advent of pseudomembranous enterocolitis, coupled with the spread of methicillin-resistant Staphylococcus aureus, led to a resurgence in the use of Vancomycin. Almost immediately, concerns arose with regard to its therapeutic utility. In addition, resistance to Vancomycin developed, first in enterococci and later in staphylococci. Several types of resistance have now been identified, each with a unique effect on infections treated with Vancomycin. Recent studies have rekindled interest in the best way to administer the antibiotic. The findings of future studies may result in a return to measuring levels of Vancomycin in serum, to assure a successful therapeutic outcome.
A Moving Target-Vancomycin Therapeutic Monitoring
J Pediatric Infect Dis Soc 2020 Sep 17;9(4):474-478.PMID:32716487DOI:10.1093/jpids/piaa078.
Therapeutic drug monitoring (TDM) has been a common practice to optimize efficacy and safety of Vancomycin. While Vancomycin trough-only TDM has widely been integrated into pediatric clinical practice since 2009, recently updated Vancomycin TDM guidelines published in March 2020 recommend area under the curve (AUC) based TDM for Vancomycin instead of trough-only TDM. In this review, we discuss the rationale behind the change in TDM recommendations, describe two approaches for calculating Vancomycin AUC in clinical practice, and address considerations for integrating Vancomycin AUC TDM into pediatric clinical practice. Our primary goal is to provide pediatric clinicians with a resource for implementing Vancomycin AUC monitoring into clinical care.