Bacterial cell wall synthesis
Bacterial cell wall peptidoglycan precursor (D-alanyl-D-alanine [D-Ala-D-Ala] terminal motif); [2]

万古霉素是一种大糖肽化合物，分子量为1450 Da。万古霉素是一种独特的糖肽，在结构上与任何目前可用的抗生素无关。它还具有独特的作用方式，抑制敏感细菌细胞壁合成的第二阶段。万古霉素对多种革兰氏阳性菌具有活性，例如金黄色葡萄球菌、葡萄球菌。表皮，Str。无乳链，Str。博维斯海峡变形链球菌、草绿色链球菌、肠球菌。

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Vancomycin HCl 对革兰氏阳性菌具有强效体外活性，包括金黄色葡萄球菌（MIC范围：0.5-2 μg/mL）、凝固酶阴性葡萄球菌（MIC范围：0.25-1 μg/mL）、肺炎链球菌（MIC范围：0.125-0.5 μg/mL）和粪肠球菌（MIC范围：1-4 μg/mL）[2]
- 其通过结合肽聚糖前体的D-Ala-D-Ala末端发挥作用，阻止肽聚糖链的交联反应，最终导致细菌细胞裂解，从而抑制细菌细胞壁合成 [2]
- 由于无法穿透外膜，对革兰氏阴性菌无显著活性 [2]

万古霉素通过静脉注射，标准输注时间至少为 1 小时，以尽量减少输注相关的不良反应。对于肌酐清除率正常的受试者，万古霉素的 α-分布期为 30 分钟至 1 小时，β-消除半衰期为 6-12 小时。分布容积为0.4-1 L/kg。万古霉素与蛋白质的结合率为 10% 至 50%。影响万古霉素整体活性的因素包括其组织分布、接种量和蛋白质结合效应。万古霉素对感染小鼠的治疗与临床、腹泻和组织病理学评分以及治疗期间生存率的改善有关。

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在艰难梭菌感染（CDI）小鼠模型中，腹腔注射Vancomycin HCl（10 mg/kg/天，连续5天）可减轻急性CDI严重程度，但与延迟性肠道组织损伤相关（感染后第10天观察到）[3]
- CDI小鼠经Vancomycin HCl处理（10 mg/kg/天，腹腔注射，连续5天）后，结肠内梭菌过度生长，治疗后第7天艰难梭菌菌落形成单位（CFUs）较未处理对照组增加3.2倍 [3]
- 45%的Vancomycin HCl处理小鼠在治疗后14天内出现CDI复发，显著高于未处理小鼠的复发率（12%）[3]

万古霉素是一种独特的糖肽，在结构上与目前可用的任何抗生素都无关。它还有一种独特的作用模式，可以抑制易感细菌细胞壁合成的第二阶段。还有证据表明，万古霉素改变了细胞膜的通透性，并选择性地抑制核糖核酸的合成。用万古霉素从易感生物体中诱导细菌L相变体是极其困难的，并且这种变体是不稳定的。由其他药物诱导的稳定L相变体对万古霉素敏感。万古霉素对大量革兰氏阳性菌具有活性，如金黄色葡萄球菌（包括耐甲氧西林菌株）、葡萄球菌。表皮葡萄球菌（包括多重耐药菌株）、肺炎链球菌（包括多重耐药性菌株）、化脓性链球菌、无乳链球菌、牛链球菌、变形链球菌、绿色链球菌、肠球菌、梭菌属、白喉杆菌、单核细胞增生李斯特菌、放线菌属和乳杆菌属。在过去的三十年里，对万古霉素的耐药性没有增加。万古霉素和一种氨基糖苷类药物联合对抗葡萄球菌的抗菌活性得到了增强。金黄色葡萄球菌、牛链球菌、肠球菌和绿色链球菌。万古霉素和利福平的组合对大多数葡萄球菌菌株具有拮抗作用。金黄色葡萄球菌，虽然表现出冷漠和偶尔的协同作用，但对葡萄球菌菌株具有协同作用。表皮病。它显示出对肠球菌的漠不关心。万古霉素和fusidic酸对葡萄球菌无明显作用。金黄色葡萄球菌[2]。

C.艰难梭菌毒素测定。艰难梭菌毒素A和B使用Tech Lab毒素A/B II ELISA试剂盒的改良方案进行检测。对每个粪便样品进行称重，并将每个样品的稀释剂量标准化，以提供每个样品相同的粪便质量与稀释剂的比例。通过研磨和涡流将稀释剂-样品混合物均化，并对样品进行1:10、1:100和1:1000系列稀释。将每个样品的1:1000稀释液总计150μl添加到试剂盒中提供的预涂孔中。阴性对照由150μl稀释剂组成，阳性对照由135μl稀释剂加3滴试剂盒中提供的阳性对照毒素A-B混合物组成。向每个孔中加入一滴缀合物，并将平板在37°C下孵育50分钟。用试剂盒中提供的150μl 1倍稀释液洗涤每个孔三次。向每个孔中加入两滴基质。10分钟后，向每个孔中加入1滴停止溶液。在ELISA读取器中读取之前，将板放置2分钟[3]。

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微量肉汤稀释法测定MIC：将细菌菌株接种到含有系列两倍稀释Vancomycin HCl（0.0625-64 μg/mL）的Mueller-Hinton肉汤中。培养物在37°C孵育18-24小时，MIC定义为抑制细菌可见生长的最低Vancomycin HCl浓度 [2]
- 细菌细胞壁合成抑制试验：向经Vancomycin HCl（0.5-4 μg/mL）处理的细菌培养物中加入放射性标记的肽聚糖前体。37°C孵育2小时后，裂解细菌细胞，通过闪烁计数法定量放射性标记的肽聚糖，以评估合成抑制效果 [2]

50 mg/kg; i.v.
Mice Murine model of C. difficile infection and treatment.[3]
The infection model is a modification of the published protocol of Chen et al. This protocol has been approved by the Center for Comparative Medicine at University of Virginia. C57BL/6 mice, male, 8 weeks old, were used. From 6 to 4 days prior to infection, mice were given an antibiotic cocktail containing vancomycin (0.0045 mg/g), colistin (0.0042 mg/g), gentamicin (0.0035 mg/g), and metronidazole (0.0215 mg/g) in drinking water. One day prior to infection, clindamycin (32 mg/kg of body weight) was injected subcutaneously. The mice were divided into the following groups: control uninfected, control infected, infected and treated with vancomycin (20 mg/kg), and infected and treated with comparator drugs—nitazoxanide, fidaxomicin, and metronidazole (all drugs given at 20 mg/kg/day). Food and water were allowed ad libitum. Although each mouse or treatment group was housed in a separate cage, all mice were housed in the same pod of the vivarium. Infection was performed with VPI 10463 (ATCC) as an inoculum of 104 or 105 administered by oral gavage. This strain produces both C. difficile toxins A (TcdA) and B (TcdB). One day postinfection, treated mice were given either vancomycin or nitazoxanide at 20 mg/kg each by oral gavage daily for 5 days and monitored for either 1 or 2 weeks postinfection. One set of experiments was performed in which infected mice were treated with vancomycin (50 mg/kg) daily for 1, 2, 3, or 5 days and were observed for 21 days postinfection or with vancomycin (20 mg/kg) daily for either 5 or 10 days and monitoring for 15 days postinfection. In a separate experiment, mice given a preinfection antibiotic regimen described above were treated with either vancomycin, fidaxomicin, or metronidazole at 20 mg/kg/day for 5 days and infected another 5 days later. Except when indicated, all comparator drugs were administered using the same dosage (20 mg/kg/day for 5 days) to equally compare efficacies, outcomes, and effects on selected gut floras between treatment groups as previously described. From another study, a group of control mice was given vancomycin but was not infected. A clinical scoring system was developed on the basis of weight loss, diarrhea, activity level, and appearance of eyes and hair (each parameter scored from 0 to 3, where 0 is normal and 3 is the worst; maximum score of 20). Stool specimens were collected daily. Diarrhea was scored as follows: 1 for soft or color change (yellow), 2 for wet tail or mucoid, and 3 for liquid or no stool (ileus). Mice judged moribund by the clinical score (score of >14) at any day and all surviving mice at the end of the experiment were sacrificed, and intestinal tissues and cecal contents were collected as described below. A separate set of experiments was performed for harvesting cecal contents for clostridial bacterial and toxin burdens at days 3, 6, 9, and 12 to 13 postinfection to follow changes at different time points of the study. Histopathology. Upon euthanasia, cecal and colonic tissues were fixed in 10% zinc formalin overnight and then placed in 10% ethanol before being sent for paraffin embedding and hematoxylin and eosin (H&E) staining at the University of Virginia Histology Research Core.
Histopathologic scoring was performed coded (C.A.W. and M.S.R.). H&E-stained tissues were scored for mucosal disruption, mucosal hypertrophy, inflammation, vascular congestion and exudates, and submucosal edema (each parameter was graded from 0 to 3, with 0 as normal and 3 worst; maximum score of 15) as we previously described in detail.

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Mouse Clostridium difficile infection model: Female C57BL/6 mice (6-8 weeks old) were pretreated with a cocktail of antibiotics (oral gavage) for 5 days to disrupt gut microbiota. Two days after antibiotic withdrawal, mice were challenged with C. difficile spores (oral gavage). Vancomycin HCl was dissolved in sterile saline and administered via intraperitoneal injection at 10 mg/kg/day for 5 days, starting 24 hours post-challenge. Mice were euthanized at day 5 (end of treatment) or day 10 (post-treatment) for tissue collection and bacterial CFU counting [3]

Oral bioavailability of Vancomycin HCl is <5% in humans, as it is poorly absorbed from the gastrointestinal tract [1]
- After intravenous administration (1 g every 12 hours in adults), Vancomycin HCl reaches a Cmax of 25-40 μg/mL, with a terminal half-life (t1/2) of 6-10 hours [1]
- Volume of distribution (Vd) is 0.4-1.0 L/kg in adults, primarily distributing to extracellular fluid [1]
- Vancomycin HCl is not metabolized in the body; approximately 90-95% is excreted unchanged in urine via glomerular filtration [1]
- Plasma protein binding rate of Vancomycin HCl is 10-50%, with lower binding in patients with renal impairment [1]

Vancomycin HCl treatment in mice was associated with delayed intestinal epithelial injury, characterized by villous atrophy and increased inflammatory cell infiltration in the colon [3]
- Nephrotoxicity (reversible tubular damage) has been reported in humans at high plasma concentrations (>80 μg/mL) [1]

[1]. The pharmacokinetic and pharmacodynamic properties of vancomycin. Clin Infect Dis. 2006 Jan 1;42 Suppl 1:S35-9.

[2]. Mode of action and in-vitro activity of vancomycin. J Antimicrob Chemother. 1984 Dec;14 Suppl D:7-18.

[3]. Vancomycin treatment's association with delayed intestinal tissue injury, clostridial overgrowth, and recurrence of Clostridium difficile infection in mice. Antimicrob Agents Chemother. 2013 Feb;57(2):689-96.

Vancomycin hydrochloride is an antibacterial prescription medicine approved by the U.S. Food and Drug Administration (FDA) for the treatment of certain bacterial infections, such as infections caused by Clostridium difficile and Staphylococcus aureus.
Clostridium difficile and Staphylococcus aureus are bacteria that can cause opportunistic infections (OIs) of HIV. An OI is an infection that occurs more frequently or is more severe in people with weakened immune systems—such as people with HIV—than in people with healthy immune systems.
Vancomycin Hydrochloride is the hydrochloride salt of vancomycin, a branched tricyclic glycosylated peptide with bactericidal activity against most organisms and bacteriostatic effect on enterococci. At a site different from that of penicillins and cephalosporins, vancomycin binds tightly to the D-alanyl-D-alanine portion of cell wall precursors, thereby interfering with bacterial cell wall synthesis. This leads to activation of bacterial autolysins that destroy the cell wall by lysis. Vancomycin may also alter the permeability of bacterial cytoplasmic membranes and may selectively inhibit RNA synthesis.
Antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to RISTOCETIN that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear.
See also: Vancomycin (has active moiety).

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Vancomycin HCl is a glycopeptide antibiotic primarily indicated for the treatment of serious infections caused by methicillin-resistant Staphylococcus aureus (MRSA) and other multidrug-resistant Gram-positive bacteria [1][2]
- Its mode of action involves binding to D-Ala-D-Ala residues of bacterial peptidoglycan precursors, blocking the transpeptidation and transglycosylation steps of cell wall synthesis, resulting in bacterial cell death [2]
- The association between Vancomycin HCl treatment and CDI recurrence may be related to its disruption of gut microbiota and selection for C. difficile spores [3]

C66H75CL2N9O24.HCL

1485.71

1483.406

C, 53.36; H, 5.16; Cl, 7.16; N, 8.48; O, 25.84

1404-93-9

Vancomycin;1404-90-6; 1404-93-9 (HCl); 123409-00-7 (HCl hydrate)

6420023

White to off-white solid powder.

1.7±0.1 g/cm3

>190°C (dec.)

87℃

1.735

-1.44

530.49

20

26

13

102

2960

18

C[C@@H]1O[C@@]([H])(O[C@@H]2[C@@H](O)[C@H](O)[C@@H](CO)O[C@H]2OC3=C(OC4=C(Cl)C=C([C@@H](O)[C@](NC([C@]5([H])NC6=O)=O)(C(N[C@]([H])(C(O)=O)C7=CC(O)=CC(O)=C7C8=C(O)C=CC5=C8)=O)[H])C=C4)C=C([C@@]6([H])NC([C@H](CC(N)=O)NC9=O)=O)C=C3OC%10=CC=C([C@@H](O)[C@H]9NC([C@H](NC)C(C)(C)C)=O)C=C%10Cl)C[C@](C)(N)[C@@H]1O.[H]Cl

LCTORFDMHNKUSG-XTTLPDOESA-N

InChI=1S/C66H75Cl2N9O24.ClH/c1-23(2)12-34(71-5)58(88)76-49-51(83)26-7-10-38(32(67)14-26)97-40-16-28-17-41(55(40)101-65-56(54(86)53(85)42(22-78)99-65)100-44-21-66(4,70)57(87)24(3)96-44)98-39-11-8-27(15-33(39)68)52(84)50-63(93)75-48(64(94)95)31-18-29(79)19-37(81)45(31)30-13-25(6-9-36(30)80)46(60(90)77-50)74-61(91)47(28)73-59(89)35(20-43(69)82)72-62(49)92;/h6-11,13-19,23-24,34-35,42,44,46-54,56-57,65,71,78-81,83-87H,12,20-22,70H2,1-5H3,(H2,69,82)(H,72,92)(H,73,89)(H,74,91)(H,75,93)(H,76,88)(H,77,90)(H,94,95);1H/t24-,34+,35-,42+,44-,46+,47+,48-,49+,50-,51+,52+,53+,54-,56+,57+,65-,66-;/m0./s1

(1S,2R,18R,19R,22S,25R,28R,40S)- 48- {[(2S,3R,4S,5S,6R)- 3- {[(2S,4S,5S,6S)- 4- amino- 5- hydroxy- 4,6- dimethyloxan- 2- yl]oxy}- 4,5- dihydroxy- 6- (hydroxymethyl)oxan- 2- yl]oxy}- 22- (carbamoylmethyl)- 5,15- dichloro- 2,18,32,35,37- pentahydroxy- 19- [(2R)- 4- methyl- 2- (methylamino)pentanamido]- 20,23,26,42,44- pentaoxo- 7,13- dioxa- 21,24,27,41,43- pentaazaoctacyclo[26.14.2.23,6.214,17.18,12.129,33.010,25.034,39]pentaconta- 3,5,8(48),9,11,14,16,29(45),30,32,34,36,38,46,49- pentadecaene- 40- carboxylic acid hydrochloride

Vancomycin HCl; Vanco-saar; Vancocin; Vancocin HCl; Vancocine.

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

注意： 请将本产品存放在密封且受保护的环境中，避免吸湿/受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~33.33 mg/mL (~22.43 mM ) DMSO : ~24 mg/mL (~16.15 mM )

配方 1 中的溶解度: ≥ 2.08 mg/mL (1.40 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 20.8 mg/mL澄清DMSO储备液加入400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.08 mg/mL (1.40 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.08 mg/mL (1.40 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 20.8 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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配方 4 中的溶解度: 10% DMSO+40% PEG300+5% Tween-80+45% Saline: ≥ 2.08 mg/mL (1.40 mM)

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配方 5 中的溶解度: 130 mg/mL (87.50 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶.

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。